The American Association for Cancer Research (AACR) organizes an annual meeting program covering some of the most recent discoveries in cancer research. The conference aims to highlight work from the best minds in research and medicine from institutions all over the world. Oncotarget, exhibited by its publisher Impact Journals, will be participating virtually at the AACR Annual Meeting this year. 
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As of June 2020, Scopus released their latest 2019 Journal Rankings on Oncology. Oncotarget is among their highest rated (Q1) journals and ranked number one in total citations in oncology. The journal has published outstanding papers and reviews by authors including Bert Vogelstein, Peter K. Vogt, Pier Paolo Pandolfi, Arnold J. Levine, Brian Druker, and Carol Prives. Founding Oncotarget Editorial Board members include Nobel Laureates Andrew V. Schally and Gregg L. Semenza; Lasker Award recipients Alexander Varshavsky, Brian J. Druker, and Gregg L. Semenza; and 16 members of the US National Academy of Sciences. Oncotarget is indexed and archived in PubMed, PubMed Central, Scopus, EMBASE, and META (Chan Zuckerberg Initiative).

The 2021 AACR conference, a two-week online event, will take place from April 10-15 and May 17-21, 2021. Topics include population science and prevention, cancer biology, translational and clinical studies, survivorship, and advocacy. 

In 2019, Oncotarget participated in the AACR Annual Meeting at the Georgia World Congress Center in Atlanta, Georgia, USA, and "AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics," at the Hynes Convention Center in Boston, Massachusetts, USA. The total registration count from the 2019 AACR Annual Meeting was over 21,000—nearly 16,000 of which were scientific attendees from all over the world. 

Follow the Oncotarget Twitter account (@Oncotarget) for live updates about the conference using the #AACR21 hashtag.

About Oncotarget:

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Oncotarget: Participating in the AACR Annual Meeting

BUFFALO, NY- January 3, 2024 – A new #editorial paper was #published in Oncotarget's Volume 14 on December 20, 2023, entitled, “Therapeutically harnessing cancer stem cell-derived exosomes.”

In this editorial, researcher Yong Teng from Emory University discusses cancer stem cell-derived exosomes. Cancer stem cells (CSCs), a small population of cancer cells capable of self-renewal, are thought to serve as a central hub for tumor initiation, growth, metastasis, and recurrence. The potential for using CSCs in the diagnosis and treatment of cancer is gaining recognition. Exosomes are formed when multivesicular endosomes or multivesicular bodies fuse with the outer membrane of the cell, releasing various components such as DNA, RNA, lipids, metabolites, and cytosolic and cell surface proteins. 

“Over the past decade, our understanding of the characteristics and function of cancer-associated exosomes has expanded rapidly.”

As the major messengers, exosomes present in the tumor microenvironment (TME) play a critical role in maintaining the delicate balance between CSCs and non-CSCs. Given the importance of CSCs, it is reasonable to believe that CSC-derived exosomes (CSC-Exos) are essential for communication between CSCs and other cells in the TME. Accumulating evidence has demonstrated that CSC-Exos contribute significantly to almost all fundamental aspects of cancer, including maintaining a continuous cycle of self-renewal within the TME, exerting control over neighboring or distant cells, enabling cancer cells to evade immune surveillance, and promoting immune tolerance. 

“A deeper understanding of the characteristics and functions of CSC-Exos has the potential to lay the foundation for the development of novel clinical tools for diagnosis and prognosis, as well as therapies aimed at preventing tumor progression and recurrence.”

DOI - https://doi.org/10.18632/oncotarget.28542

Correspondence to - Yong Teng - yong.teng@emory.edu

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Keywords - cancer, cancer stem cells, exosomes, the tumor microenvironment, therapeutic target, anticancer strategy

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Therapeutically Harnessing Cancer Stem Cell-derived Exosomes

BUFFALO, NY- January 8, 2024 – A new #review paper was #published in Oncotarget's Volume 14 on December 22, 2023, entitled, “Transformation-associated recombination (TAR) cloning and its applications for gene function; genome architecture and evolution; biotechnology and biomedicine.”

Transformation-associated recombination (TAR) cloning represents a unique tool to selectively and efficiently recover a given chromosomal segment up to several hundred kb in length from complex genomes (such as animals and plants) and simple genomes (such as bacteria and viruses). The technique exploits a high level of homologous recombination in the yeast Sacharomyces cerevisiae. 

“TAR cloning has become a valuable procedure for the selective and efficient isolation and manipulation of large DNA molecules. [...] The ability to isolate individual gene alleles will help to clarify whether a particular allele is associated with predisposition to different diseases, including cancer.”

In this new review, researchers Natalay Kouprina and Vladimir Larionov from the National Cancer Institute's Developmental Therapeutics Branch summarized multiple applications of the pioneering TAR cloning technique, developed previously for complex genomes, for functional, evolutionary, and structural studies, and extended the modified TAR versions to isolate biosynthetic gene clusters (BGCs) from microbes, which are the major source of pharmacological agents and industrial compounds, and to engineer synthetic viruses with novel properties to design a new generation of vaccines. TAR cloning was adapted as a reliable method for the assembly of synthetic microbe genomes for fundamental research. 

“In this review, we also discuss how the TAR cloning in combination with HAC (human artificial chromosome)- and CRISPR-based technologies may contribute to the future.”

DOI - https://doi.org/10.18632/oncotarget.28546

Correspondence to - Natalay Kouprina - kouprinn@mail.nih.gov

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Keywords - cancer, transformation-associated recombination, TAR, microbes, biomedicine, biotechnology

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Transformation-associated Recombination (TAR) Cloning and Its Applications

BUFFALO, NY- January 10, 2024 – A new #editorial paper was #published in Oncotarget's Volume 14 on December 22, 2023, entitled, “One more step toward treatment of PARP inhibitor-resistant ovarian cancers.”

Over 80% of ovarian cancer cases experience recurrence, resulting in roughly 12,000 annual deaths in the United States. While targeted therapies like poly (ADPribose) polymerase inhibitors (PARPis) have received FDA approval for both initial and recurrent treatments, extending median progression-free survival for individuals with homologous recombination repair (HRR) deficiency, the emergence of PARPi resistance remains a common challenge among patients. Consequently, addressing resistance to PARPi treatment in ovarian cancer has become a pressing therapeutic dilemma, necessitating innovative strategies. 

In this editorial, researchers Upasana Ray, Prabhu Thirusangu and Viji Shridhar from Mayo Clinic School of Medicine and Science responded to this unmet need with their current study, which unveiled promising findings related to the Pixatimod (PG545) drug, a sulfated small molecule compound. Engineered with a core structure mimicking heparan sulfate, this compound targets heparanase and heparin binding growth factor (HB-GF) signaling. 

“Our present study has revealed a previously unknown effect of PG545 in ovarian cancer cells, inducing DNA damage. The investigation unveiled that PG545 induces both single- and double-strand breaks in DNA while also promoting the autophagic degradation of RAD51, a critical DNA repair protein, thereby impeding the homologous recombination repair (HRR) pathway in cancer cells.”

DOI - https://doi.org/10.18632/oncotarget.28545

Correspondence to - Viji Shridhar - Shridhar.Vijayalakshmi@mayo.edu

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Keywords - cancer, ovarian cancer, PARP inhibitors, PG545, DNA damage, cell death

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One More Step Toward Treatment of PARP Inhibitor-resistant Ovarian Cancers

BUFFALO, NY- January 17, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on January 16, 2024, entitled, “ATR inhibition using gartisertib enhances cell death and synergises with temozolomide and radiation in patient-derived glioblastoma cell lines.”

Glioblastoma cells can restrict the DNA-damaging effects of temozolomide (TMZ) and radiation therapy (RT) using the DNA damage response (DDR) mechanism which activates cell cycle arrest and DNA repair pathways. Ataxia-telangiectasia and Rad3-Related protein (ATR) plays a pivotal role in the recognition of DNA damage induced by chemotherapy and radiation causing downstream DDR activation. 

In this new study, researchers Mathew Lozinski, Nikola A. Bowden, Moira C. Graves, Michael Fay, Bryan W. Day, Brett W. Stringer, and Paul A. Tooney from University of Newcastle, Hunter Medical Research Institute, GenesisCare, QIMR Berghofer Medical Research Institute, and Griffith University investigated the activity of the ATR inhibitor gartisertib alone, and in combination with TMZ and/or RT, in multiple patient-derived glioblastoma cell lines. 

“Using a panel of 12 patient-derived glioblastoma cell lines, we investigated the chemo- and radio-sensitizing effect of gartisertib, a potent and selective inhibitor of ATR [26] that was explored in a phase 1 clinical trial for patients with advanced solid tumors (NCT02278250).”

The team showed that gartisertib alone potently reduced the cell viability of glioblastoma cell lines, where sensitivity was associated with the frequency of DDR mutations and higher expression of the G2 cell cycle pathway. ATR inhibition significantly enhanced cell death in combination with TMZ and RT and was shown to have higher synergy than TMZ+RT treatment. MGMT promoter unmethylated and TMZ+RT resistant glioblastoma cells were also more sensitive to gartisertib. Analysis of gene expression from gartisertib treated glioblastoma cells identified the upregulation of innate immune-related pathways. 

“Overall, this study identifies ATR inhibition as a strategy to enhance the DNA-damaging ability of glioblastoma standard treatment, while providing preliminary evidence that ATR inhibition induces an innate immune gene signature that warrants further investigation.”

DOI - https://doi.org/10.18632/oncotarget.28551

Correspondence to - Paul A. Tooney - paul.tooney@newcastle.edu.au

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Keywords - cancer, glioblastoma, DNA damage response, ataxia-telangiectasia and rad3-related protein, radiation therapy, temozolomide

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ATR Inhibition Using Gartisertib in Patient-derived Glioblastoma Cell Lines

BUFFALO, NY- January 24, 2024 – A new #case report was #published in Oncotarget's Volume 15 on January 16, 2024, entitled, “Lazarus effect in a patient initially empirically treated with osimertinib for EGFR L858R mutant non-small cell lung cancer with leptomeningeal disease: a case report.”

Osimertinib has been shown to be effective for patients with non-small cell lung cancer (NSCLC) with activating EGFR mutations. These patients are also at risk for leptomeningeal disease (LMD). LMD is characterized by central nervous system metastases with spread to the cerebrospinal fluid or leptomeninges. In patients with NSCLC with EGFR activating mutations, there is an increased occurrence of LMD, which occurs in 9% of patients.

In this new report, researchers Shreya Bhatia, Manuel G. Cortez, Spencer Lessans, and Wade T. Iams from Vanderbilt-Ingram Cancer Center present a patient of East Asian descent whose initial presentation included severe, progressive leptomeningeal carcinomatosis and a small lung mass, with limited tissue available for molecular testing. She responded to empiric, urgent initiation of osimertinib, repeat tissue sampling revealed an EGFR L858R mutation, and she has experienced durable disease improvement for 18 months on osimertinib monotherapy.

“Our case demonstrates the nuances of decision-making in starting osimertinib in urgent clinical settings. Given our patient’s progressively worsening functional status and spread of disease to her CNS upon presentation, there was a need to begin treatment imminently. Time constraints, financial constraints, and lack of sufficient tissue for analysis ultimately led to the empiric use of osimertinib. Through the urgent initiation of appropriate anti-cancer therapy, she experienced both a life saving improvement in functional status and improvement in her LUL primary tumor one month into treatment.”

DOI - https://doi.org/10.18632/oncotarget.28550

Correspondence to - Wade T. Iams - wade.t.iams@vumc.org

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Keywords - cancer, EGFR mutation, leptomeningeal disease, non-small cell lung cancer, osimertinib

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Lazarus Effect in Patient Treated with Osimertinib for NSCLC with Leptomeningeal Disease

BUFFALO, NY- February 5, 2024 – A new #editorial paper was #published in Oncotarget's Volume 15 on January 24, 2024, entitled, “The fate of drug discovery in academia; dumping in the publication landfill?”

In this new editorial, researchers Uzma Saqib, Isaac S. Demaree, Alexander G. Obukhov, Mirza S. Baig, Amiram Ariel, and Krishnan Hajela, from Devi Ahilya Vishwavidyalaya, Indore, discuss drug discovery—a tedious process that is time consuming in both divulging whether a molecule is efficacious and specific in hitting the target and also in confirming that the potential drug does not cause severe adverse effects. Many drug candidates fail crossing multiple checkpoints of this long journey; they lag in one or several aspects and never move beyond the research bench to contribute to public health. These setbacks make the process of drug discovery very time consuming, expensive, and tedious. 

“This viewpoint is focused on delineating how and why the multi-million [dollar] research efforts in the field of drug discovery often fail to reach its full potential.”

There is no shortage of studies focusing on drug discovery. They are published on a daily basis describing the efforts encompassing conventional and/or modern drug discovery technology, including structure-based drug design (SBDD), virtual screening, high-throughput screening (HTS), Artificial Intelligence (AI), and cell-based screening approaches (Figure 1). However, many drug development strategies are rather fuzzy in their advancement. 

Thus, there is a large gap between drug “discovery” and “development.” This part could be attributed to the lack of synergy between Academia and Industry at multiple levels. A significant part of this failure results from the lack of streamlining of drug development process. 

“In the current perspective, we discussed why many therapeutic molecules never make it to clinical studies despite being proven efficacious pre-clinically. Additionally, we discussed the possible solutions to overcome this défaut of the drug development process.”

DOI - https://doi.org/10.18632/oncotarget.28552

Correspondence to - Krishnan Hajela - hajelak@gmail.com

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Keywords - cancer, drug discovery and development, clinical trials, academia-industry collaboration, translational research, drug database

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Drug Discovery in Academia; Dumping in the Publication Landfill?

BUFFALO, NY- February 7, 2024 – A new #research perspective was #published in Oncotarget's Volume 15 on February 5, 2024, entitled, “Preclinical and clinical evaluation of the Janus Kinase inhibitor ruxolitinib in multiple myeloma.”

In this new paper, researchers Ashley Del Dosso, Elizabeth Tadevosyan, and James R. Berenson from ONCOtherapeutics, Berenson Cancer Center, and Institute for Myeloma and Bone Cancer Research discussed multiple myeloma (MM) — the most common primary malignancy of the bone marrow. No established curative treatment is currently available for patients diagnosed with MM. 

In recent years, new and more effective drugs have become available for the treatment of this B-cell malignancy. These new drugs have often been evaluated together and in combination with older agents. However, even these novel combinations eventually become ineffective; and, thus, novel therapeutic approaches are necessary to help overcome resistance to these treatments. 

Recently, the Janus Kinase (JAK) family of tyrosine kinases, specifically JAK1 and JAK2, has been shown to have a role in the pathogenesis of MM. Preclinical studies have demonstrated a role for JAK signaling in direct and indirect growth of MM and downregulation of anti-tumor immune responses in these patients. Also, inhibition of JAK proteins enhances the anti-MM effects of other drugs used to treat MM. These findings have been confirmed in clinical studies which have further demonstrated the safety and efficacy of JAK inhibition as a means to overcome resistance to currently available anti-MM therapies. Additional studies will provide further support for this promising new therapeutic approach for treating patients with MM.

“The following sections of this article will be focused on studies of RUX [Ruxolitinib] in the preclinical [21–24] and clinical settings [18–20] focused on the treatment of relapsed/refractory (RR) MM.”

DOI - https://doi.org/10.18632/oncotarget.28547

Correspondence to - James R. Berenson - jberenson@berensoncancercenter.com

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Keywords - cancer, multiple myeloma, ruxolitinib, JAK/STAT, cytokine, clinical trial

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Evaluation of Ruxolitinib, a Janus Kinase Inhibitor, in Multiple Myeloma

BUFFALO, NY- February 14, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on February 5, 2024, entitled, “Genetic and therapeutic landscapes in cohort of pancreatic adenocarcinomas: next-generation sequencing and machine learning for full tumor exome analysis.”

About 7% of all cancer deaths are caused by pancreatic cancer (PCa). PCa is known for its lowest survival rates among all oncological diseases and heterogenic molecular profile. Enormous amount of genetic changes, including somatic mutations, exceeds the limits of routine clinical genetic laboratory tests and further stagnates the development of personalized treatments. 

In this new study, researchers P.A. Shatalov, N.A. Falaleeva, E.A. Bykova, D.O. Korostin, V.A. Belova, A.A. Zabolotneva, A.P. Shinkarkina, A. Yu Gorbachev, M.B. Potievskiy, V.S. Surkova, Zh V. Khailova, N.A. Kulemin, Denis Baranovskii, A.A. Kostin, A.D. Kaprin, and P.V. Shegai from the Ministry of Health of the Russian Federation, Pirogov Russian National Research Medical University, Federal Medical-Biological Agency, Moscow, and the Peoples Friendship University of Russia (RUDN University) aimed to build a mutational landscape of PCa in the Russian population based on full exome next-generation sequencing (NGS) of the limited group of patients. 

“Applying a machine learning model on full exome individual data, we received personalized recommendations for targeted treatment options for each clinical case and summarized them in the unique therapeutic landscape.”

DOI - https://doi.org/10.18632/oncotarget.28512

Correspondence to - Denis Baranovskii - doc.baranovsky@gmail.com

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Keywords - cancer, pancreatic cancer, tumor mutation burden, somatic mutations, artificial intelligence, machine learning

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Genetic and Therapeutic Landscapes in Cohort of Pancreatic Cancer Using NGS and Machine Learning

BUFFALO, NY- March 18, 2024 – A new #researchpaper was #published in Oncotarget's Volume 15 on March 14, 2024, entitled, “G-quadruplex landscape and its regulation revealed by a new antibody capture method.”

In this new study, researchers Subhamoy Datta, Manthan Patel, Chakkarai Sathyaseelan, Chandrama Ghosh, Akanksha Mudgal, Divyesh Patel, Thenmalarchelvi Rathinavelan, and Umashankar Singh from the Indian Institute of Technology Gandhinagar, Indian Institute of Technology Hyderabad, Queen Mary University of London, Bar-Ilan University, Medical University of Lublin, and the University of Helsinki discuss a secondary structure of DNA that has attracted wide interest, G-quadruplexes or G4s.

“Our understanding of DNA G-quadruplexes (G4s) from in vitro studies has been complemented by genome-wide G4 landscapes from cultured cells.”

Conventionally, the formation of G4s is accepted to depend on G-repeats such that they form tetrads. However, genome-wide G4s characterized through high-throughput sequencing suggest that these structures form at a large number of regions with no such canonical G4-forming signatures. Many G4-binding proteins have been described with no evidence for any protein that binds to and stabilizes G4s. 

“It remains unknown what fraction of G4s formed in human cells are protein-bound.” 

The G4-chromatin immunoprecipitation (G4-ChIP) method hitherto employed to describe G4 landscapes preferentially reports G4s that get crosslinked to proteins in their proximity. The current understanding of the G4 landscape is biased against representation of G4s which escape crosslinking as they are not stabilized by protein-binding and presumably transient. The researchers reported a protocol that captures G4s from the cells efficiently without any bias as well as eliminates the detection of G4s formed artifactually on crosslinked sheared chromatin post-fixation. They discovered that G4s form sparingly at SINEs (short interspersed nuclear elements). An application of this method shows that depletion of a repeat-binding protein CGGBP1 enhances net G4 capture at CGGBP1-dependent CTCF-binding sites and regions of sharp interstrand G/C-skew transitions. 

“The AbC G4-ChIP presents a powerful technique to decipher the cellular G4 landscape and its regulation and it has the potential to be adapted for discovering any DNA secondary structures genome-wide against which reliable antibodies are available.”

DOI - https://doi.org/10.18632/oncotarget.28564

Correspondence to - Umashankar Singh - usingh@iitgn.ac.in

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Keywords - cancer, DNA G-quadruplexes, G4-ChIP, CGGBP1, CTCF, G/C-skew

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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A New Antibody Capture Method Reveals G-quadruplex Landscape and its Regulation

BUFFALO, NY- March 19, 2024 – A new #research perspective was #published by Mikhail V. Blagosklonny M.D., Ph.D., from Roswell Park Comprehensive Cancer Center in Oncotarget's Volume 15 on March 15, 2024, entitled, “From osimertinib to preemptive combinations.”

“Here, I suggest that while first-line osimertinib extends median progression-free survival (PFS) in EGFR-mutant lung cancer compared to first-generation TKIs, it reduces individual PFS in 15–20% of patients compared to first-generation TKIs. Since detecting a single resistant cell before treatment is usually impossible, osimertinib must be used in all patients as a first-line treatment, raising median PFS overall but harming some. 

The simplest remedy is a preemptive combination (PC) of osimertinib and gefitinib. A comprehensive PC (osimertinib, afatinib/gefitinib, and capmatinib) could dramatically increase PFS for 80% of patients compared to osimertinib alone, without harming anyone. This article also explores PCs for MET-driven lung cancer.”

DOI - https://doi.org/10.18632/oncotarget.28569

Correspondence to - Mikhail V. Blagosklonny - Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com

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Keywords - cancer, lung cancer, NSCLC, EGFR, resistance, afatinib, gefitinib, capmatinib

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Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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“From Osimertinib to Preemptive Combinations” by Dr. Blagosklonny

BUFFALO, NY- March 20, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on March 14, 2024, entitled, “Analytical validation of NeXT Personal®, an ultra-sensitive personalized circulating tumor DNA assay.”

In this new study, researchers Josette Northcott, Gabor Bartha, Jason Harris, Conan Li, Fabio C.P. Navarro, Rachel Marty Pyke, Manqing Hong, Qi Zhang, Shuyuan Ma, Tina X. Chen, Janet Lai, Nitin Udar, Juan-Sebastian Saldivar, Erin Ayash, Joshua Anderson, Jiang Li, Tiange Cui, Tu Le, Ruthie Chow, Randy Jerel Velasco, Chris Mallo, Rose Santiago, Robert C. Bruce, Laurie J. Goodman, Yi Chen, Dan Norton, Richard O. Chen, and John M. Lyle from Personalis, Inc. describe the analytical validation of NeXT Personal®, an ultra-sensitive, tumor-informed circulating tumor DNA (ctDNA) assay for detecting residual disease, monitoring therapy response, and detecting recurrence in patients diagnosed with solid tumor cancers. 

“NeXT Personal uses whole genome sequencing of tumor and matched normal samples combined with advanced analytics to accurately identify up to ~1,800 somatic variants specific to the patient’s tumor.” 

A personalized panel is created, targeting these variants and then used to sequence cell-free DNA extracted from patient plasma samples for ultra-sensitive detection of ctDNA. The NeXT Personal analytical validation is based on panels designed from tumor and matched normal samples from two cell lines, and from 123 patients across nine cancer types. Analytical measurements demonstrated a detection threshold of 1.67 parts per million (PPM) with a limit of detection at 95% (LOD95) of 3.45 PPM. NeXT Personal showed linearity over a range of 0.8 to 300,000 PPM (Pearson correlation coefficient = 0.9998). Precision varied from a coefficient of variation of 12.8% to 3.6% over a range of 25 to 25,000 PPM. The assay targets 99.9% specificity, with this validation study measuring 100% specificity and in silico methods giving a confidence interval of 99.92 to 100%.

“In summary, this study demonstrates NeXT Personal as an ultra-sensitive, highly quantitative and robust ctDNA assay that can be used to detect residual disease, monitor treatment response, and detect recurrence in patients.”

DOI - https://doi.org/10.18632/oncotarget.28565

Correspondence to - John M. Lyle - john.lyle@personalis.com 

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Keywords - cancer, circulating tumor DNA, whole genome sequencing, molecular residual disease, tumor-informed assay, analytical validation

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Analytical Validation of an Ultra-sensitive Personalized Circulating Tumor DNA Assay: NeXT Personal®

BUFFALO, NY- March 25, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on March 14, 2024, entitled, “ABT199/venetoclax synergism with thiotepa enhances the cytotoxicity of fludarabine, cladribine and busulfan in AML cells.”

ABT199/venetoclax, an inhibitor of the pro-survival BCL-2 protein, has improved AML treatment. Its efficacy in hematopoietic stem cell transplantation (HSCT), when combined with other chemotherapeutic drugs, has not been thoroughly investigated. In this new study, researchers Benigno C. Valdez, Bin Yuan, David Murray, Jeremy L. Ramdial, Uday Popat, Yago Nieto, and Borje S. Andersson from The University of Texas MD Anderson Cancer Center and the University of Alberta demonstrate the synergistic cytotoxicity of ABT199/venetoclax with the DNA alkylator thiotepa (Thio) in AML cells. 

“The results may provide relevant information for the design of clinical trials using these drugs to circumvent recognized drug-resistance mechanisms when used as part of pre-transplant conditioning regimens for AML patients undergoing allogenic HSCT.”

Cleavage of Caspase 3, PARP1 and HSP90, as well as increased Annexin V positivity, suggest potent activation of apoptosis by this two-drug combination; increased levels of γ-H2AX, P-CHK1 (S317), P-CHK2 (S19) and P-SMC1 (S957) indicate an enhanced DNA damage response. Likewise, the increased level of P-SAPK/JNK (T183/Y185) and decreased P-PI3Kp85 (Y458) suggest enhanced activation of stress signaling pathways. These molecular readouts were synergistically enhanced when ABT199/venetoclax and Thio were combined with fludarabine, cladribine and busulfan. 

The five-drug combination decreased the levels of BCL-2, BCL-xL and MCL-1, suggesting its potential clinical relevance in overcoming ABT199/venetoclax resistance. Moreover, this combination is active against P53-negative and FLT3-ITD-positive cell lines. Enhanced activation of apoptosis was observed in leukemia patient-derived cell samples exposed to the five-drug combination, suggesting a clinical relevance. 

“The results provide a rationale for clinical trials using these two- and five-drug combinations as part of a conditioning regimen for AML patients undergoing HSCT.”

DOI - https://doi.org/10.18632/oncotarget.28563

Correspondence to - Benigno C. Valdez - mbalasik@yahoo.com

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Keywords - cancer, acute myeloid leukemia, aml, pre-transplant regimens, venetoclax, thiotepa, busulfan

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.
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ABT199/Venetoclax Synergism With Thiotepa in Acute Myeloid Leukemia (AML) Cells

BUFFALO, NY- April 16, 2024 – A new #researchpaper was #published in Oncotarget's Volume 15 on April 12, 2024, entitled, “Novel therapeutic bispecific antibodies for B-cell lymphoma targeting IgM and other antigens on the B-cell surface.”

The B-cell receptor regulates B-cell proliferation and apoptosis. Aberrations in BCR signaling are associated with the development and progression of B-cell malignancies, such as mantle cell lymphoma, diffuse large B-cell lymphoma, and chronic lymphocytic leukemia, many of which express the IgM type of BCR on their cellular surface. 

Therefore, IgM is an attractive target for therapeutic antibodies against B-cell malignancies. However, soluble IgM competitively binds to anti-IgM antibodies in the serum, and these antibodies show insufficient cytotoxic activity. Thus, antibody therapy targeting IgM is hindered by the presence of soluble IgM in the blood. In this new study, researchers Takahiro Ohashi, Sayuri Terada, Shinsuke Hiramoto, Yuko Nagata, Hirokazu Suzuki, Hitoshi Miyashita, Tetsuo Sasaki, Yasukatsu Tsukada, and Keiko Fukushima from ZENOAQ (Zenyaku Kogyo Co., Ltd.) used a bispecific antibody to address this problem. 

“In this study, we aimed to produce IgM-dependent bispecific antibodies targeting IgM and the other B-cell antigens such as CD20, CD32b (FcγRIIB), CD79b, and human leukocyte antigen (HLA)-DR using the Cys1m technology [10, 43–45]. Additionally, the correct IgG-like bispecific antibody structures were confirmed and their efficacies in the presence of soluble IgM were analyzed.”

The researchers generated bispecific antibodies bound to IgM and other B-cell antigens such as CD20 and HLA-DR using their own bispecific antibody-producing technology, Cys1m. These bispecific antibodies directly inhibited cell proliferation via cell-cycle arrest and apoptosis in vitro, although large amounts of soluble IgM were present. Additionally, a bispecific antibody bound to IgM and HLA-DR (BTA106) depleted B-cells in cynomolgus monkeys. 

“These data suggest that anti-IgM/B-cell surface antigen-binding specific antibodies are promising therapeutic agents for B-cell malignancies. Moreover, the bispecific antibody modality can potentially overcome problems caused by soluble antigens.”

DOI - https://doi.org/10.18632/oncotarget.28578

Correspondence to - Keiko Fukushima - keiko_fukushima@mail.zenyaku.co.jp

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Keywords - cancer, bispecific antibody, Cys1m, IgM, lymphoma, cynomolgus monkey

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Novel Therapeutic Bispecific Antibodies for B-cell Lymphoma

BUFFALO, NY- April 29, 2024 – Oncotarget is a contributing #sponsor at the 19th International p53 Workshop, organized by the International Center for Genetic Engineering and Biotechnology (ICGEB), which takes place from May 13–16, 2024, in Trieste, Italy.

“Groundbreaking research and cutting-edge advancements in the field of the most studied human gene and most frequently mutated gene in cancer, will take center stage at the 19th International p53 Workshop.” – ICGEB.org

Among the 24 invited speakers at the 19th International p53 Workshop, 18 speakers have published new research on p53 in Oncotarget. These distinguished speakers who have published with Oncotarget include Dr. Andrei Gudkov — one of Oncotarget’s founding Editors-in-Chief. Dr. Gudkov will be speaking in the session on “p53 Inflammation and Immunity” and moderating the session on “Targeting p53 in Human Disease.”

“The event will gather leading scientists, clinicians, and researchers from around the world providing a unique opportunity to delve into the latest discoveries and innovations related to TP53 biology and explore the intricate role of TP53 in cancer and its potential for transformative impact in oncology.” – ICGEB.org

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Oncotarget Sponsors 19th International p53 Workshop in Italy

BUFFALO, NY- May 6, 2024 – A new research paper was published in Oncotarget's Volume 15 on May 3, 2024, entitled, “Transfected SARS-CoV-2 spike DNA for mammalian cell expression inhibits p53 activation of p21(WAF1), TRAIL Death Receptor DR5 and MDM2 proteins in cancer cells and increases cancer cell viability after chemotherapy exposure.”

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and COVID-19 infection has led to worsened outcomes for patients with cancer. SARS-CoV-2 spike protein mediates host cell infection and cell-cell fusion that causes stabilization of tumor suppressor p53 protein. In-silico analysis previously suggested that SARS-CoV-2 spike interacts with p53 directly but this putative interaction has not been demonstrated in cells. In this new study, researchers Shengliang Zhang and Wafik S. El-Deiry from Brown University and Lifespan Health System examined the interaction between SARS-CoV-2 spike, p53 and MDM2 (E3 ligase, which mediates p53 degradation) in cancer cells using an immunoprecipitation assay. 

“We observed that SARS-CoV-2 spike protein interrupts p53-MDM2 protein interaction but did not detect SARS-CoV-2 spike bound with p53 protein in the cancer cells.”

The researchers further observed that SARS-CoV-2 spike suppresses p53 transcriptional activity in cancer cells including after nutlin exposure of wild-type p53-, spike-expressing tumor cells and inhibits chemotherapy-induced p53 gene activation of p21(WAF1), TRAIL Death Receptor DR5 and MDM2. The suppressive effect of SARS-CoV-2 spike on p53-dependent gene activation provides a potential molecular mechanism by which SARS-CoV-2 infection may impact tumorigenesis, tumor progression and chemotherapy sensitivity. In fact, cisplatin-treated tumor cells expressing spike were found to have increased cell viability as compared to control cells. 

Further observations on γ-H2AX expression in spike-expressing cells treated with cisplatin may indicate altered DNA damage sensing in the DNA damage response pathway. The preliminary observations reported here warrant further studies to unravel the impact of SARS-CoV-2 and its various encoded proteins including spike on pathways of tumorigenesis and response to cancer therapeutics. More efforts should be directed at studying the effects of the SARS-CoV-2 spike and other viral proteins on host DNA damage sensing, response and repair mechanisms. 

“A goal would be to understand the structural basis for maximal anti-viral immunity while minimizing suppression of host defenses including the p53 DNA damage response and tumor suppression pathway. Such directions are relevant and important including not only in the context of viral infection and mRNA vaccines in general but also for patients with cancer who may be receiving cytotoxic or other cancer treatments.”

DOI - https://doi.org/10.18632/oncotarget.28582

Correspondence to - Wafik S. El-Deiry - wafik@brown.edu

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Transfected SARS-CoV-2 Spike DNA Suppresses Cancer Cell Response to Chemotherapy

The profound impact of the COVID-19 pandemic, caused by the SARS-CoV-2 virus, has been felt across various domains, including the realm of cancer research and treatment. As scientists delve deeper into the intricate mechanisms of this viral pathogen, intriguing revelations have emerged regarding its potential influence on cellular processes pivotal to cancer development and progression. 

In a new study, researchers Wafik S. El-Deiry and Shengliang Zhang from Brown University and Lifespan Health System shed light on the intricate interplay between the SARS-CoV-2 spike protein and the tumor suppressor p53, a key guardian of genomic integrity. On May 3, 2024, they published their new research paper in Oncotarget’s Volume 15, entitled, “Transfected SARS-CoV-2 spike DNA for mammalian cell expression inhibits p53 activation of p21(WAF1), TRAIL Death Receptor DR5 and MDM2 proteins in cancer cells and increases cancer cell viability after chemotherapy exposure.”

In this study, researchers El-Deiry and Zhang uncovered a hitherto unknown facet of the SARS-CoV-2 spike protein’s impact on cancer cells. Their findings, meticulously detailed in their research paper, have ignited a newfound curiosity within the scientific community.

Full blog - https://www.oncotarget.org/2024/05/09/sars-cov-2-spike-protein-disrupts-p53-tumor-suppressor-pathway/

Paper DOI - https://doi.org/10.18632/oncotarget.28582

Correspondence to - Wafik S. El-Deiry - wafik@brown.edu

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Keywords - cancer, SARS-COV2 spike, p53, MDM2, chemotherapy

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SARS-CoV-2 Spike Protein Disrupts p53 Tumor Suppressor Pathway

BUFFALO, NY- May 13, 2024 – BUFFALO, NY- May 13, 2024 – Impact Journals publishes scholarly journals in the biomedical sciences, with a focus on all areas of cancer and aging research. Oncotarget is one of the most prominent journals published by Impact Journals.

Impact Journals is proud to participate at the Society for Scholarly Publishing (SSP) 46th Annual Meeting, which convenes in Boston, Massachusetts, at the Westin Boston Seaport District from May 29–31, 2024. This year, the SSP Annual Meeting theme is “Inflection Point: Setting the Course for the Future of Scholarly Communication.”

Visit booth #212 at the SSP 46th Annual Meeting 2024 to connect with members of the Oncotarget team.

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Oncotarget at SSP 46th Annual Meeting

BUFFALO, NY- May 15, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on May 14, 2024, entitled, “Cyclin D1 expression in penile cancer.”

In this new study, researchers Wesliany Everton Duarte, Jaqueline Diniz Pinho, Syomara Pereira da Costa Melo, Denner Rodrigo Diniz Duarte, Juliana Martins da Guia Ribeiro do Carmo, André Salim Khayat, José Ribamar Rodrigues Calixto, Marcos Adriano Garcia Campos, Rita da Graça Carvalhal Frazão Correa, Antonio Machado Alencar Júnior, Antônio Augusto Lima Teixeira-Júnior, and Gyl Eanes Barros Silva from Federal University of Maranhão, State University of Maranhão, Federal University of Pará, São Paulo State University, and University of São Paulo analyzed the expression profile of cyclin D1 in patients with PC, and to determine possible correlations with clinical and histopathological features. 

“Regarding PC, however, few studies have assessed the role of cyclin D1, reinforcing the necessity for initiatives that aim to investigate its actual role in the pathophysiology of this disease. As such, the present study aimed to characterize the expression of cyclin D1 in patients with PC, and to determine possible correlations with the clinical and histopathological features of the disease.”

A survey was conducted with 100 patients diagnosed with PC, who were treated at two reference hospitals in São Luís, Maranhão, Brazil, between 2013 and 2017. A review of clinical, epidemiological, and histopathological data was performed, Human Papillomavírus (HPV) DNA was detected using polymerase chain reaction (PCR) and cyclin D1 expression analysis was performed using immunohistochemical techniques. The data revealed that the absence of cyclin D1 expression was significantly associated with HPV-positive histological subtypes (p = 0.001), while its expression was associated with high-grade tumors (p = 0.014), histological subtype (p = 0.001), presence of sarcomatoid transformation (p = 0.04), and perineural invasion (p = 0.023). Patients with cyclin D1 expression exhibited lower disease-free survival compared to the cyclin D1-negative group, although the difference was not statistically significant. 

“The results suggest that cyclin D1 may be a potential biomarker for PC, especially for poorer prognosis.”

DOI - https://doi.org/10.18632/oncotarget.28584

Correspondence to - Gyl Eanes Barros Silva - gyl.silva@ufma.br

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Keywords - cancer, immunohistochemistry, biomarkers, cyclin D1, penile neoplasms

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Expression of Cyclin D1 in Penile Cancer

BUFFALO, NY- May 20, 2024 – A new research paper was published in Oncotarget's Volume 15 on May 16, 2024, entitled, “The anticancer potential of the CLK kinases inhibitors 1C8 and GPS167 revealed by their impact on the epithelial-mesenchymal transition and the antiviral immune response.”

The diheteroarylamide-based compound 1C8 and the aminothiazole carboxamide-related compound GPS167 inhibit the CLK kinases, and affect the proliferation of a broad range of cancer cell lines. A chemogenomic screen previously performed with GPS167 revealed that the depletion of components associated with mitotic spindle assembly altered sensitivity to GPS167.
 
In this new study, researchers Lulzim Shkreta, Johanne Toutant, Aurélie Delannoy, David Durantel, Anna Salvetti, Sophie Ehresmann, Martin Sauvageau, Julien A. Delbrouck, Alice Gravel-Trudeau, Christian Comeau, Caroline Huard, Jasmin Coulombe-Huntington, Mike Tyers, David Grierson, Pierre-Luc Boudreault, and Benoit Chabot from Université de Sherbrooke, Université de Lyon, Institut de recherches cliniques de Montréal, Université de Montréal, and University of British Columbia a similar screen performed with 1C8 also established the impact of components involved in mitotic spindle assembly. 

“Accordingly, transcriptome analyses of cells treated with 1C8 and GPS167 indicated that the expression and RNA splicing of transcripts encoding mitotic spindle assembly components were affected.” 

The functional relevance of the microtubule connection was confirmed by showing that subtoxic concentrations of drugs affecting mitotic spindle assembly increased sensitivity to GPS167. 1C8 and GPS167 impacted the expression and splicing of transcripts in pathways relevant to tumor progression, including MYC targets and the epithelial mesenchymal transition (EMT). Finally, 1C8 and GPS167 altered the expression and alternative splicing of transcripts involved in the antiviral immune response. Consistent with this observation, depleting the double-stranded RNA sensor DHX33 suppressed GPS167-mediated cytotoxicity on HCT116 cells. 

“Our study uncovered molecular mechanisms through which 1C8 and GPS167 affect cancer cell proliferation as well as processes critical for metastasis."

DOI - https://doi.org/10.18632/oncotarget.28585

Correspondence to - Benoit Chabot - benoit.chabot@usherbrooke.ca

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Keywords - cancer, CLK kinases inhibitors, EMT, antiviral immune response, microtubules, metastasis

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Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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Anticancer Potential of CLK Kinase Inhibitors 1C8 and GPS167 via EMT and Antiviral Immune Response

BUFFALO, NY- May 22, 2024 – A new research paper was published in Oncotarget's Volume 15 on May 17, 2024, entitled, “GZ17-6.02 kills PDX isolates of uveal melanoma.”

In this new study, researchers Laurence Booth, Jane L. Roberts, Ivan Spasojevic, Kaitlyn C. Baker, Andrew Poklepovic, Cameron West, John M. Kirkwood, and Paul Dent from Virginia Commonwealth University, Duke University School of Medicine, Genzada Pharmaceuticals, Texas Tech University Health Sciences Center, and University of Pittsburgh Cancer Institute defined the biology of GZ17-6.02 in UM cells and in parallel determined its interaction with irreversible ERBB inhibitors (afatinib, neratinib) and with the cytotoxic agent doxorubicin. 

“GZ17-6.02 is a novel compound, containing the synthetically manufactured components: curcumin, harmine and isovanillin and has undergone phase I safety evaluation in cancer patients (NCT03775525).”

GZ17-6.02 has undergone phase I evaluation in patients with solid tumors (NCT03775525). The RP2D is 375 mg PO BID, with an uveal melanoma patient exhibiting a 15% reduction in tumor mass for 5 months at this dose. Studies in this manuscript have defined the biology of GZ17-6.02 in PDX isolates of uveal melanoma cells. 

GZ17-6.02 killed uveal melanoma cells through multiple convergent signals including enhanced ATM-AMPK-mTORC1 activity, inactivation of YAP/TAZ and inactivation of eIF2α. GZ17-6.02 significantly enhanced the expression of BAP1, predictive to reduce metastasis, and reduced the levels of ERBB family RTKs, predicted to reduce growth. GZ17-6.02 interacted with doxorubicin or ERBB family inhibitors to significantly enhance tumor cell killing which was associated with greater levels of autophagosome formation and autophagic flux. 

Knock down of Beclin1, ATG5 or eIF2α were more protective than knock down of ATM, AMPKα, CD95 or FADD, however, over-expression of FLIP-s provided greater protection compared to knock down of CD95 or FADD. Expression of activated forms of mTOR and STAT3 significantly reduced tumor cell killing. GZ17-6.02 reduced the expression of PD-L1 in uveal melanoma cells to a similar extent as observed in cutaneous melanoma cells whereas it was less effective at enhancing the levels of MHCA. The components of GZ17-6.02 were detected in tumors using a syngeneic tumor model. 

“Our data support future testing GZ17-6.02 in uveal melanoma as a single agent, in combination with ERBB family inhibitors, in combination with cytotoxic drugs, or with an anti-PD1 immunotherapy.”

DOI - https://doi.org/10.18632/oncotarget.28586

Correspondence to - Paul Dent - paul.dent@vcuhealth.org

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Keywords - cancer, autophagy, ER stress, GZ17-6.02, doxorubicin, afatinib, neratinib

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GZ17-6.02 Kills Uveal Melanoma Cells

BUFFALO, NY- May 28, 2024 – A new review paper was published in Oncotarget's Volume 15 on May 23, 2024, entitled, “The importance of integrated therapies on cancer: Silibinin, an old and new molecule.”

In this new review, researchers Elisa Roca, Giuseppe Colloca, Fiorella Lombardo, Andrea Bellieni, Alessandra Cucinella, Giorgio Madonia, Licia Martinelli, Maria Elisa Damiani, Ilaria Zampieri, and Antonio Santo from Perderzoli Hospital and Fondazione Policlinico Universitario “A. Gemelli” begin their abstract by noting that the efficacy of coadjuvant molecules, in the landscape of cancer treatments, remains a focus of attention for clinical research with the aim of reducing toxicity and achieving better outcomes.

“Most of the pathogenetic processes causing tumour development, neoplastic progression, ageing, and increased toxicity involve inflammation.”

Inflammatory mechanisms can progress through a variety of molecular patterns. As is well known, the ageing process is determined by pathological pathways very similar and often parallel to those that cause cancer development. Among these complex mechanisms, inflammation is currently much studied and is often referred to in the geriatric field as ‘inflammaging’. In this context, treatments active in the management of inflammatory mechanisms could play a role as adjuvants to standard therapies.

Among these emerging molecules, Silibinin has demonstrated its anti-inflammatory properties in different neoplastic types, also in combination with chemotherapeutic agents. Moreover, this molecule could represent a breakthrough in the management of age-related processes. Thus, Silibinin could be a valuable adjuvant to reduce drug-related toxicity and increase therapeutic potential.

“For this reason, the main aim of this review is to collect and analyse data presented in the literature on the use of Silibinin, to better understand the mechanisms of the functioning of this molecule and its possible therapeutic role.”

DOI - https://doi.org/10.18632/oncotarget.28587

Correspondence to - Elisa Roca - elisaroca@gmail.com

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Keywords - cancer, silibinin, anti-inflammatory, inflammation, toxicity, integrated therapy

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Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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The Importance of Integrated Therapies on Cancer: Silibinin, an Old and New Molecule

BUFFALO, NY- June 4, 2024 – A new research perspective was published in Oncotarget's Volume 15 on June 3, 2024, entitled, “Bruton’s tyrosine kinase inhibitor-related cardiotoxicity: The quest for predictive biomarkers and improved risk stratification.”

In this new perspective, researchers Jai N. Patel, Jai Singh, and Nilanjan Ghosh from Atrium Health discuss Ibrutinib — the first Bruton's tyrosine kinase (BTK) inhibitor approved for the treatment of patients with chronic lymphocytic leukemia (CLL). 

“While producing durable responses and prolonging survival, roughly 20–25% of patients experience dose limiting side effects, mostly consisting of cardiovascular toxicities like severe hypertension and atrial fibrillation.”

While clinical predictors of BTK inhibitor-related cardiotoxicity have been proposed and may aid in risk stratification, there is no routine risk model used in clinical practice today to identify patients at highest risk. A recent study investigating genetic predictors of ibrutinib-related cardiotoxicity found that single nucleotide polymorphisms in KCNQ1 and GATA4 were significantly associated with cardiotoxic events. If replicated in larger studies, these biomarkers may improve risk stratification in combination with clinical factors. 

“A clinicogenomic risk model may aid in identifying patients at highest risk of developing BTK inhibitor-related cardiotoxicity in which further risk mitigation strategies may be explored.”

DOI - https://doi.org/10.18632/oncotarget.28589

Correspondence to - Nilanjan Ghosh - nilanjan.ghosh@atriumhealth.org

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Keywords - cancer, BTK inhibitor, cardiotoxicity, biomarkers, risk, genetics

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BTK Inhibitor-related Cardiotoxicity: Quest for Predictive Biomarkers, Improved Risk Stratification

BUFFALO, NY- June 5, 2024 – A new research paper was published in Oncotarget's Volume 15 on June 3, 2024, entitled, “Synergistic cytotoxicity of histone deacetylase and poly-ADP ribose polymerase inhibitors and decitabine in pancreatic cancer cells: Implications for novel therapy.”

Histone deacetylase inhibitors (HDACi) can modulate the acetylation status of proteins, influencing the genomic instability exhibited by cancer cells. Poly (ADP ribose) polymerase (PARP) inhibitors (PARPi) have a direct effect on protein poly (ADP-ribosyl)ation, which is important for DNA repair. Decitabine is a nucleoside cytidine analogue, which when phosphorylated gets incorporated into the growing DNA strand, inhibiting methylation and inducing DNA damage by inactivating and trapping DNA methyltransferase on the DNA, thereby activating transcriptionally silenced DNA loci.

In this new study, researchers Benigno C. Valdez, Apostolia M. Tsimberidou, Bin Yuan, Yago Nieto, Mehmet A. Baysal, Abhijit Chakraborty, Clark R. Andersen, and Borje S. Andersson from The University of Texas MD Anderson Cancer Center explored various combinations of HDACi and PARPi +/− decitabine (hypomethylating agent) in pancreatic cancer cell lines BxPC-3 and PL45 (wild-type BRCA1 and BRCA2) and Capan-1 (mutated BRCA2). 

“[...] we explored various combinations of HDACis and PARPis, with or without decitabine, in pancreatic cancer cell lines.”

The combination of HDACi (panobinostat or vorinostat) with PARPi (talazoparib or olaparib) resulted in synergistic cytotoxicity in all cell lines tested. The addition of decitabine further increased the synergistic cytotoxicity noted with HDACi and PARPi, triggering apoptosis (evidenced by increased cleavage of caspase 3 and PARP1). 

The 3-drug combination treatments (vorinostat, talazoparib, and decitabine; vorinostat, olaparib, and decitabine; panobinostat, talazoparib, and decitabine; panobinostat, olaparib, and decitabine) induced more DNA damage (increased phosphorylation of histone 2AX) than the individual drugs and impaired the DNA repair pathways (decreased levels of ATM, BRCA1, and ATRX proteins). The 3-drug combinations also altered the epigenetic regulation of gene expression (NuRD complex subunits, reduced levels). 

“This is the first study to demonstrate synergistic interactions between the aforementioned agents in pancreatic cancer cell lines and provides preclinical data to design individualized therapeutic approaches with the potential to improve pancreatic cancer treatment outcomes.”

DOI - https://doi.org/10.18632/oncotarget.28588

Correspondence to - Apostolia M. Tsimberidou - atsimber@mdanderson.org

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Synergistic Cytotoxicity of HDAC and PARP Inhibitors and Decitabine in Pancreatic Cancer Cells

BUFFALO, NY- June 11, 2024 – The Ride for Roswell is one of the nation’s largest cycling events—hosted by Roswell Park Comprehensive Cancer Center—to raise awareness and funds for cancer research and patient care. This charity bike ride, based out of Buffalo, New York, has brought people together for 28 years to celebrate cancer survivors, pay tribute to lives that have been lost, and to work together to support research and find a cure.

THE ORIGIN OF THE RIDE

The Ride for Roswell started in 1989 when Mitch Flynn, owner of the advertising agency Flynn & Friends, met Katherine Gioia. Katherine was a four-year-old patient battling a rare form of cancer. After Katherine’s death (less than a year after her diagnosis), Katherine’s mother, Anne Gioia, and aunt, Donna Gioia, founded the Roswell Park Alliance Foundation in her memory to raise money for cancer research and treatment. On June 29, 1996, Mitch and Alliance Foundation staff launched the first Ride for Roswell.

In the 28 years since then, thanks to over 135,000 riders and thousands of volunteers, the Ride for Roswell has raised over $72 million to fund cancer research. The event has become one of the largest charity rides in the United States.

THIS YEAR

This year, Ride Day is on Saturday, June 22, 2024, and will once again begin at the University at Buffalo North Campus. There are nine routes to choose from, ranging from five to 100 mile distances. All riders are encouraged to check in on the Thursday or Friday before Ride Day.

Learn more about The Ride, check in, and routes: www.rideforroswell.org/routes/

JOIN A TEAM: TEAM OPEN ACCESS

Impact Journals has been a part of this event since 2018 and continues to sponsor captain Sergei Kurenov’s peloton, Team Open Access. Team Open Access was named in honor of all open-source online medical journals, such as Oncotarget, Aging, Genes & Cancer, and Oncoscience. Sergei works at Roswell Park Comprehensive Cancer Center to create, develop, and implement innovative diagnostic and surgical pre-planning software used in cancer treatment. He has been riding in the event since 2016.

“I am proud to [say] that our team is supported again by open source cancer-related scientific journals: Oncotarget and Aging! Both of these journals publish high-impact research papers of general interest and biological significance in all fields of cancer research,” Sergei said.

There is still time to join Team Open Access in the Ride for Roswell. You can also support the team by giving a donation of any size. Any avenue of support you may choose to donate to the Ride for Roswell will make a difference and change lives.

“Finding a cure for cancer is something we are all incredibly passionate about, and we are so thankful and grateful for your support. Together, we can make a difference!” Sergei said. “Thank you so much for your donations, your support, and well wishes!”

Visit the Open Access team page to join or donate today:
give.roswellpark.org/site/TR/Specia…eam&fr_id=1940

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Impact Journals Sponsors 2024 Ride for Roswell

BUFFALO, NY- June 18, 2024 – A new #research perspective was #published in Oncotarget's Volume 15 on June 13, 2024, entitled, “When does a melanoma metastasize? Implications for management.”

In this new perspective, researchers John F. Thompson and Gabrielle J. Williams from The University of Sydney, Royal Prince Alfred Hospital, and the University of Western Australia discussed melanoma and timing treatment. Selecting which patients with clinically localized melanoma require treatment other than wide excision of the primary tumor is based on the risk or presence of metastatic disease. This in turn is linked to survival. 

“Knowing if and when a melanoma is likely to metastasize is therefore of great importance.” 

Several studies employing a range of different methodologies have suggested that many melanomas metastasize long before the primary lesion is diagnosed. Therefore, waiting for dissemination of metastatic disease to become evident before making systemic therapy available to these patients may be less effective than giving them post-operative adjuvant therapy initially if the metastatic risk is high. The identification of these high-risk patients will assist in selecting those to whom adjuvant systemic therapy can most appropriately be offered. 

“Further studies are required to better identify high-risk patients whose primary melanoma is likely to have already metastasized.”

DOI - https://doi.org/10.18632/oncotarget.28591

Correspondence to - John F. Thompson - john.thompson@melanoma.org.au

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Keywords - cancer, melanoma, metastasis, time, adjuvant systemic therapy, tumor doubling time

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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When Does a Melanoma Metastasize? Implications for Management

BUFFALO, NY- June 19, 2024 – A new research paper was published in Oncotarget's Volume 15 on June 13, 2024, entitled, “Assessment of serum tumor markers CEA, CA-125, and CA19-9 as adjuncts in non-small cell lung cancer management.”

Conventional tumor markers may serve as adjuncts in non-small cell lung cancer (NSCLC) management. In this new study, researchers Scott Strum, Mark Vincent, Meghan Gipson, Eric McArthur, and Daniel Breadner from the Schulich School of Medicine and Dentistry, London Health Sciences Centre, and Royal College of Surgeons in Ireland analyzed whether three tumor markers (CEA, CA19-9, and CA-125) held associations with radiographic and clinical outcomes in NSCLC. 

“The aim of this retrospective study was to provide additional evidence for the clinical use of conventional serum tumor markers CEA, CA19-9, and CA-125 in NSCLC management.”

It constituted a single-center study of NSCLC patients treated with systemic therapy at the London Regional Cancer Program. Serum tumor markers were analyzed for differences in radiographic responses (RECIST v1.1 or iRECIST), associations with clinical characteristics, and all-cause mortality. A total of 533 NSCLC patients were screened, of which 165 met inclusion criteria. A subset of 92 patients had paired tumor markers and radiographic scans. 

From the latter population, median (IQR) fold-change from nadir to progression was 2.13 (IQR 1.24–3.02; p < 0.001) for CEA, 1.46 (IQR 1.13–2.18; p < 0.001) for CA19-9, and 1.53 (IQR 0.96–2.12; p < 0.001) for CA-125. Median (IQR) fold-change from baseline to radiographic response was 0.50 (IQR 0.27, 0.95; p < 0.001) for CEA, 1.08 (IQR 0.74, 1.61; p = 0.99) for CA19-9, and 0.47 (IQR 0.18, 1.26; p = 0.008) for CA-125. 

“In conclusion, tumor markers are positioned to be used as adjunct tools in clinical decision making, especially for their associations with radiographic response (CEA/CA-125) or progression (CEA/CA-125/CA-19-9).”

DOI - https://doi.org/10.18632/oncotarget.28566

Correspondence to - Daniel Breadner - daniel.breadner@lhsc.on.ca

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Keywords - cancer, tumor marker, biomarker, lung cancer; NSCLC, translational research

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Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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Assessment of CEA, CA-125, and CA19-9 as Adjuncts in Non-small Cell Lung Cancer Management

BUFFALO, NY- June 24, 2024 – A new editorial paper was published in Oncotarget's Volume 15 on June 14, 2024, entitled, “Leveraging gold nanostars for precision laser interstitial thermal therapy.”

In this new editorial, researchers Aden P. Haskell-Mendoza, Ethan S. Srinivasan, Tuan Vo-Dinh and Peter E. Fecci from Duke University discuss laser interstitial thermal therapy (LITT). Over the past decade, LITT has become an important tool for the neurosurgical treatment of a variety of intracranial pathologies, including focal epilepsies, vascular malformations, and central nervous system (CNS) tumors [1]. LITT involves the minimally invasive, stereotactically-guided placement of a laser catheter into a target lesion for subsequent thermal ablation via the delivery of infrared radiation, typically at wavelengths of 980–1064 nm [1, 2]. Following transfer of the patient to a scanner, real-time magnetic resonance (MR) thermometry is employed to track tissue hyperthermal ablation. 

“For patients with primary and metastatic brain tumors who are suboptimal candidates for craniotomy due to clinical status, wound healing concerns, or tumor location, LITT represents a particularly favorable option for reducing tumor burden.” 

However, successful ablation is limited by the (1) inability to precisely sculpt heat to cover or conform to large (typically, ≥3 cm) or irregular lesions, (2) the presence of various intracranial heat sinks, including cerebrospinal fluid (CSF) spaces and blood vessels, and (3) the sensitivity of uninvolved white and gray matter structures to inadvertent thermal damage [1–3]. 

“To aid in the performance of more efficient, conformal, and accordingly, safe ablations, we recently developed procedures for the use of gold nanostars (GNS, Figure 1) [2]."

DOI -  https://doi.org/10.18632/oncotarget.28592

Correspondence to - Peter E. Fecci - peter.fecci@duke.edu

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Keywords - cancer, laser interstitial thermal therapy, gold nanostars, brain tumors, thermal ablation, immunotherapy

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Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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Leveraging Gold Nanostars for Precision Laser Interstitial Thermal Therapy

BUFFALO, NY- June 26, 2024 – A new research perspective was published in Oncotarget's Volume 15 on June 20, 2024, entitled, “Starving cancer cells to enhance DNA damage and immunotherapy response.”

Prostate cancer (PCa) poses significant challenges in treatment, particularly when it progresses to a metastatic, castrate-resistant state. Conventional therapies, including chemotherapy, radiotherapy, and hormonal treatments, often fail due to toxicities, off-target effects, and acquired resistance. In this new research perspective, researchers Aashirwad Shahi and Dawit Kidane from Howard University define an alternative therapeutic strategy focusing on the metabolic vulnerabilities of PCa cells, specifically their reliance on non-essential amino acids such as cysteine. 

“In this prospective, we will rise the driving questions and potential possibilities how amino acid depletion induced oxidative stress associated DNA damage exploited for DNA repair targeted and immune checkpoint blockade therapy [...].”

Using an engineered enzyme cyst(e)inase to deplete the cysteine/cystine can induce oxidative stress and DNA damage in cancer cells. This depletion elevates reactive oxygen species (ROS) levels, disrupts glutathione synthesis, and enhances DNA damage, leading to cancer cell death. The combinatorial use of cyst(e)inase with agents targeting antioxidant defenses, such as thioredoxins, further amplifies ROS accumulation and cytotoxicity in PCa cells. 

“Overall, this perspective provides a compressive overview of the previous work on manipulating amino acid metabolism and redox balance modulate the efficacy of DNA repair-targeted and immune checkpoint blockade therapies in prostate cancer.”

DOI - https://doi.org/10.18632/oncotarget.28595

Correspondence to - Dawit Kidane - dawit.kidane-mulat@howard.edu

Video short - https://www.youtube.com/watch?v=Zrj24o_-b50

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Keywords - cancer, amino acid depletion, DNA damage, DNA repair, Immunotherapy, tumor immunity

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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Starving Cancer Cells to Enhance DNA Damage and Immunotherapy Response

BUFFALO, NY- July 2, 2024 – A new editorial paper was published in Oncotarget's Volume 15 on June 20, 2024, entitled, “Genomics has more to reveal.”

In this new editorial, researchers Laurène Fenwarth and Nicolas Duployez from the University of Lille and CHU Lille discuss molecular and cytogenetic analyses that are now used to identify mutations and structural variants defining distinct subtypes of acute myeloid leukemias (AML) and myelodysplastic syndromes (MDS). These genetic considerations have become essential for risk stratification and the selection of appropriate treatments, including the use of allogeneic hematopoietic stem cell transplantation. 

“Despite over 15 years of genomic research since the first publication of the AML genome and large studies like The Cancer Genome Atlas (TCGA) [2], around 15% of AML cases remained genetically unclassifiable with current knowledge.”

Notably, several studies in both adults and children identified a subset of AML without known initiating events but particularly enriched in FLT3- ITD and WT1 mutations, and normal karyotypes with an overall unfavorable prognosis. In 2021–2022, notably thanks to advancements in bioinformatic approaches and tools, recurrent somatic tandem duplications (TD) of a portion of the UBTF gene were identified in high-risk pediatric AML cases. 

“With increased screenings of retrospective cohorts, the characteristics associated with this molecular alteration have since been confirmed. UBTF-TD are considered initiating events in leukemogenesis and define a distinct entity of myeloid malignancies.”

DOI -  https://doi.org/10.18632/oncotarget.28596

Correspondence to - Nicolas Duployez - nicolas.duployez@chu-lille.fr

Video short - https://www.youtube.com/watch?v=WVY_ejhr7Fc

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Keywords - cancer, acute myeloid leukemia, genomics, UBTF

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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Editorial: Genomics Has More to Reveal

BUFFALO, NY- July 8, 2024 – A new research paper was published in Oncotarget's Volume 15 on July 2, 2024, entitled, “Regorafenib synergizes with TAS102 against multiple gastrointestinal cancers and overcomes cancer stemness, trifluridine-induced angiogenesis, ERK1/2 and STAT3 signaling regardless of KRAS or BRAF mutational status.”

Single-agent TAS102 (trifluridine/tipiracil) and regorafenib are FDA-approved treatments for metastatic colorectal cancer (mCRC). Researchers previously reported that regorafenib combined with a fluoropyrimidine can delay disease progression in clinical case reports of multidrug-resistant mCRC patients. In this new study, researchers Jun Zhang, Lanlan Zhou, Shuai Zhao, and Wafik S. El-Deiry from Fox Chase Cancer Center and Brown University hypothesized that the combination of TAS102 and regorafenib may be active in CRC and other gastrointestinal (GI) cancers and may in the future provide a treatment option for patients with advanced GI cancer. 

“We investigated the therapeutic effect of TAS102 in combination with regorafenib in preclinical studies employing cell culture, colonosphere assays that enrich for cancer stem cells, and in vivo.”

TAS102 in combination with regorafenib has synergistic activity against multiple GI cancers in vitro including colorectal and gastric cancer, but not liver cancer cells. TAS102 inhibits colonosphere formation and this effect is potentiated by regorafenib. In vivo anti-tumor effects of TAS102 plus regorafenib appear to be due to anti-proliferative effects, necrosis and angiogenesis inhibition. 

Growth inhibition by TAS102 plus regorafenib occurs in xenografted tumors regardless of p53, KRAS or BRAF mutations, although more potent tumor suppression was observed with wild-type p53. Regorafenib significantly inhibits TAS102-induced angiogenesis and microvessel density in xenografted tumors, as well inhibits TAS102-induced ERK1/2 activation regardless of RAS or BRAF status in vivo. TAS102 plus regorafenib is a synergistic drug combination in preclinical models of GI cancer, with regorafenib suppressing TAS102-induced increase in microvessel density and p-ERK as contributing mechanisms. 

“The TAS102 plus regorafenib drug combination may be further tested in gastric and other GI cancers.”
DOI - https://doi.org/10.18632/oncotarget.28602

Correspondence to - Wafik S. El-Deiry - wafik@brown.edu

Video short - https://www.youtube.com/watch?v=tuEmJTkyyGQ

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Keywords - cancer, TAS102, regorafenib, ERK1/2, angiogenesis, microvessel density

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Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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Regorafenib Synergizes With TAS102 Against Multiple Gastrointestinal Cancers

In this research paper, researchers demonstrate a promising new treatment option for refractory metastatic gastrointestinal cancers using a combination of two FDA-approved drugs.

Researchers Jun Zhang, Lanlan Zhou, Shuai Zhao, and Wafik S. El-Deiry from Fox Chase Cancer Center and Brown University explore the potential of combining TAS102 (trifluridine/tipiracil) and regorafenib as a treatment option for gastrointestinal (GI) cancers. Their research paper, published in Oncotarget’s Volume 15 on July 2, 2024, is entitled, “Regorafenib synergizes with TAS102 against multiple gastrointestinal cancers and overcomes cancer stemness, trifluridine-induced angiogenesis, ERK1/2 and STAT3 signaling regardless of KRAS or BRAF mutational status.”

The Study

The combination of two FDA-approved drugs, TAS102 and regorafenib, has shown promising results in preclinical studies. TAS102 is an oral formulation consisting of trifluridine (FTD) and tipiracil hydrochloride (TPI). It has been approved by the US FDA for the treatment of refractory metastatic colorectal cancer and metastatic gastric cancer. Regorafenib is a multi-target tyrosine kinase inhibitor that inhibits tumor angiogenesis and cell proliferation and is approved for the treatment of gastrointestinal cancers.

Recent studies have shown that TAS102, in combination with regorafenib, can lead to improved survival and restrict tumor progression. The combination therapy has been found effective in multiple gastrointestinal cancer cell lines, including colorectal, gastric, and pancreatic cancers.

Full blog - https://www.oncotarget.org/2024/08/09/combining-regorafenib-and-tas102-to-target-gastrointestinal-cancers-and-overcome-cancer-stemness/

Paper DOI - https://doi.org/10.18632/oncotarget.28602

Correspondence to - Wafik S. El-Deiry - wafik@brown.edu

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Keywords - cancer, TAS102, regorafenib, ERK1/2, angiogenesis, microvessel density

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Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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Combining Regorafenib and TAS102 to Target Gastrointestinal Cancers and Overcome Cancer Stemness

BUFFALO, NY- August 12, 2024 – A new research perspective was published in Oncotarget's Volume 15 on July 16, 2024, entitled, “Targeting the multifaceted BRAF in cancer: New directions.”

In cancer patients, BRAF-targeting precision therapeutics are effective against Class I BRAF alterations (p.V600 hotspot mutations) in tumors such as melanoma, thyroid cancer, and colorectal cancer. However, numerous non-Class I BRAF inhibitors are also in development and have been explored in various cancers.

Researchers Eamon Toye, Alexander Chehrazi-Raffle, Justin Hwang, and Emmanuel S. Antonarakis from the Masonic Cancer Center, University of Minnesota-Twin Cities, Department of Medicine, University of Minnesota-Twin Cities, Perelman School of Medicine, University of Pennsylvania, and the City of Hope Comprehensive Cancer Center in Duarte, California, discuss the diverse forms of BRAF alterations found in human cancers and the strategies used to inhibit them in patients with cancers of various origins.

As part of their conclusion, the researchers highlighted that Class I BRAF inhibitors represent a landmark achievement in precision oncology, as demonstrated by the recent tissue-agnostic FDA approval of dabrafenib/trametinib for patients with metastatic BRAF p.V600E-mutant solid tumors. Additionally, the accelerated approval of tovorafenib for patients with relapsed/refractory BRAF-altered pediatric low-grade glioma underscores the therapeutic potential of this and other next-generation strategies targeting aberrant MAPK signaling.

DOI - https://doi.org/10.18632/oncotarget.28612

Correspondence to - Emmanuel S. Antonarakis - anton401@umn.edu, and Justin Hwang - jhwang@umn.edu

Video short - https://www.youtube.com/watch?v=3dRWRvOnssc

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Keywords - cancer, BRAF, MAPK, pan-cancer, precision oncology, genomics

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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New Directions in Targeting the Multifaceted BRAF in Cancer

BUFFALO, NY- August 14, 2024 – A new #casereport was #published in Oncotarget's Volume 15 on July 17, 2024, entitled, “Rapid but nondurable response of a BRAF exon 15 double-mutated spindle cell sarcoma to a combination of BRAF and MEK inhibitors.”

As noted in the introduction of the Abstract, the BRAF V600E substitution predicts a cancer's sensitivity to BRAF inhibitor therapy, though the mutation is rarely found in soft-tissue sarcomas.

Researchers Kseniya Sinichenkova, Iliya Sidorov, Nataliya Kriventsova, Dmitriy Konovalov, Ruslan Abasov, Nataliya Usman, Alexander Karachunskiy, Galina Novichkova, Dmitriy Litvinov, and Alexander Druy from the Dmitriy Rogachev National Medical Research Center of Pediatric Hematology, Oncology, Immunology (Ministry of Healthcare of Russian Federation) and the Research Institute of Medical Cell Technologies in Yekaterinburg, Russia, describe a case of undifferentiated spindle cell sarcoma that exhibited primary insensitivity to standard chemotherapy and a pronounced but non-sustained response to BRAF/MEK inhibitors at recurrence.

The case presentation involved a 13-year-old girl that was diagnosed with low-grade spindle cell sarcoma of pelvic localization, BRAF exon 15 double-mutated: c.1799T>A p.V600E and c.1819T>A p.S607T in cis-position. 

“This is the first report of spindle cell sarcoma BRAF V600E/S607T double-mutated, responding to a combination of B-Raf and MEK inhibitors.”

DOI - https://doi.org/10.18632/oncotarget.28606

Correspondence to - Kseniya Sinichenkova - ksinichenkova@gmail.com

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Keywords - cancer, undifferentiated sarcoma, BRAF V600E mutation, low grade spindle cell sarcoma, abdominal cocoon

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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Response of BRAF-Mutated Spindle Cell Sarcoma to BRAF/MEK Inhibitors

BUFFALO, NY- August 15, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on August 14, 2024, entitled, “A nanobody against the V-ATPase c subunit inhibits metastasis of 4T1-12B breast tumor cells to lung in mice.”

The vacuolar H+-ATPase (V-ATPase) is an ATP-dependent proton pump that functions to control the pH of intracellular compartments as well as to transport protons across the plasma membrane of various cell types, including cancer cells.  

Researchers Zhen Li, Mohammed A. Alshagawi, Rebecca A. Oot, Mariam K. Alamoudi, Kevin Su, Wenhui Li, Michael P. Collins, Stephan Wilkens, and Michael Forgac from Tufts University School of Medicine; Tufts University; Dana Farber Cancer Institute, Harvard Medical School; University of Minnesota School of Medicine; Prince Sattam Bin Abdulaziz University; Korro Bio; SUNY Upstate Medical University; and Foghorn Therapeutics, have previously shown that selective inhibition of plasma membrane V-ATPases in breast tumor cells inhibits the invasion of these cells in vitro. They have now developed a nanobody directed against an extracellular epitope of the mouse V-ATPase c subunit.

“We show that treatment of 4T1-12B mouse breast cancer cells with this nanobody inhibits V-ATPase-dependent acidification of the media and invasion of these cells in vitro.”

The research team further found that injecting this nanobody into mice implanted with 4T1-12B cells orthotopically in the mammary fat pad inhibited the metastasis of tumor cells to the lungs.

“In conclusion, our results indicate that a nanobody directed against an extracellular epitope expressed on the surface of the V-ATPase is able to inhibit activity of cell surface V-ATPases in 4T1-12B breast cancer cells, inhibit in vitro invasion of these cells and inhibit metastasis of these cells to lung following their implantation in the mammary fat pad of mice.”

DOI - https://doi.org/10.18632/oncotarget.28638

Correspondence to - Michael Forgac - michael.forgac@tufts.edu

Video short - https://www.youtube.com/watch?v=4eLGqvSfAgg

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Keywords - cancer, vacuolar ATPase, breast cancer, invasion, tumor metastasis, tumor growth

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Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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Nanobody Inhibits Metastasis of Breast Tumor Cells to Lung in Mice

BUFFALO, NY- August 19, 2024 – A new #review was #published in Oncotarget's Volume 15 on August 14, 2024, entitled, “The gut barrier as a gatekeeper in colorectal cancer treatment.”

Colorectal cancer (CRC) is highly prevalent and a major cause of cancer-related deaths worldwide. The primary curative treatment for CRC is surgical resection of the affected bowel segment. However, postoperative complications often include a weakened gut barrier and the dissemination of bacterial proinflammatory lipopolysaccharides.

Researchers Roy Hajjar, Carole Richard, and Manuela M. Santos from Centre de recherche du Centre hospitalier de l’Université de Montréal (CRCHUM), Québec; Centre hospitalier de l’Université de Montréal (CHUM), Québec; Université de Montréal, Québec; and Institut du cancer de Montréal, Québec, discuss how gut microbiota and microbial metabolites regulate basal inflammation levels in the gut and the healing process of the bowel after surgery.

“We and others have shown in the last few years that gut microbiota influences the healing process of the bowel and the restoration of the gut barrier after surgery.”

The researchers further elaborate on the restoration of gut barrier function in CRC patients and how this potentially impacts the dissemination and implantation of CRC cells in extracolonic tissues, thereby contributing to worse survival outcomes after surgery.

“Based on our recent work, we believe that weakened gut barrier function, namely due to poor healing after surgery, leads to persistent systemic low-grade inflammation and a higher risk of local and systemic cancer recurrence.”

DOI - https://doi.org/10.18632/oncotarget.28634

Correspondence to - Roy Hajjar - roy.hajjar@umontreal.ca

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Keywords - cancer, colorectal cancer, gut microbiome, gut barrier, colorectal surgery, anastomotic leak

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Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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Role of the Gut Barrier in Colorectal Cancer Treatment

BUFFALO, NY- August 21, 2024 – A new #editorial was #published in Oncotarget's Volume 15 on July 17, 2024, entitled, “Strategies to disrupt NKG2A:HLA-E interactions for improved anti-cancer immunity.”

Two studies using CRISPR screens in cancer cells identified HLA-E as a critical negative regulator of NK cell interactions with cancer cells. Consistent with this, IFNγ signaling was associated with NK cell resistance due to increased STAT1 activation and enhanced HLA-E expression. This effect is also evident in the murine homolog of HLA-E, Qa-1b, which was upregulated by inflammatory signals across all cell types tested.

In addition to inflammatory signals, researchers Jack G. Fisher, Lara V. Graham, and Matthew D. Blunt from Clinical and Experimental Sciences, Faculty of Medicine at the University of Southampton, UK, recently demonstrated that surface expression of HLA-E is increased by lymph node-associated signals IL-4 and CD40L on primary chronic lymphocytic leukaemia (CLL) cells.

Additionally, two recent studies have shown that HLA-E can protect circulating tumor cells from NK cell lysis via NKG2A, suggesting that targeting the NKG2A axis could be a promising strategy for preventing metastasis in solid tumors.

“In conclusion, there is strong preclinical evidence that disruption of NKG2A interactions with HLA-E can stimulate both NK cell and cytotoxic T cell effector functions against cancer.”

DOI - https://doi.org/10.18632/oncotarget.28610

Correspondence to - Matthew D. Blunt - m.d.blunt@soton.ac.uk

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Keywords - cancer, Natural killer (NK) cells, immunotherapy, NKG2A, immune checkpoint blockade, HLA-E

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Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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Disrupting NKG2A:HLA-E Interactions for Enhanced Anti-Cancer Immunity

BUFFALO, NY- August 26, 2024 – A new #editorial was #published in Oncotarget's Volume 15 on July 10, 2024, entitled, “Genotype matters: Personalized screening recommendations for germline CHEK2 variants.”

Recognized as a moderate-risk gene, CHEK2—responsible for encoding the CHK2 protein, which plays a crucial role in the repair of DNA double-strand breaks—is associated with a 20–40% lifetime risk of breast cancer (BC) by age 85. While CHEK2 pathogenic variants (PVs) were previously linked to an increased risk of colorectal cancer (CRC), two recent studies have not observed this association.

In their recent work, researchers Adela Rodriguez Hernandez, Rochelle Scheib, Judy E. Garber, Huma Q. Rana and Brittany L. Bychkovsky from Dana-Farber Cancer Institute and Harvard Medical School in Boston, found that a CHEK2 PV does not increase the CRC risk compared with controls (odds ratio 0.62 (0.51–0.76), p < .001).

The cancer risks associated with CHEK2 PVs vary depending on the variant type, and risk management strategies should reflect this variability. The CHEK2 c.1100del is the most studied truncating variant and has been crucial to our understanding of the cancer phenotype. Cancer risks seem to be higher with truncating variants compared to missense variants.

“In our study, we postulated that these differences were driven by three common low-risk (LR) missense variants: p.I157T, p.S428F, and p.T476M, all of which have a BC odds ratio of <1.4.” 

In summary, CHEK2 is recognized as a moderate-risk gene for breast cancer. Further large-scale, prospective studies are needed to clarify its potential associations with prostate, kidney, and thyroid cancers, as well as to establish appropriate screening measures.

DOI - https://doi.org/10.18632/oncotarget.28604

Correspondence to - Brittany L. Bychkovsky - brittany_bychkovsky@dfci.harvard.edu

Video short - https://www.youtube.com/watch?v=KYHCdGz8c3I

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Keywords - cancer, CHEK2, pathogenic or likely pathogenic variants, germline

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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Genotype Matters: Tailored Screening for Germline CHEK2 Variants

BUFFALO, NY- August 27, 2024 – A new #editorial was #published in Oncotarget's Volume 15 on August 26, 2024, entitled, “Artificial intelligence: A transformative tool in precision oncology.”

Artificial intelligence (AI) is revolutionizing society and healthcare, opening new possibilities for precision medicine. In oncology, immunotherapy (IO) has similarly transformed cancer treatment with novel therapeutic mechanisms, but it has also introduced atypical response patterns that challenge traditional evaluation methods.

In this editorial, researchers Jeremy McGale, Matthew J. Liao, Egesta Lopci, Aurélien Marabelle, and Laurent Dercle from the Department of Radiology at Columbia University in New York, explore AI's role in addressing these challenges. They focus on the development of new biomarkers for precise disease characterization, particularly those using imaging for the early response assessment of cancer patients treated with IO.

Additionally, the researchers highlight a comprehensive review that applied AI/radiomics to cross-sectional imaging (PET, CT, MRI) showcasing the current landscape in IO treatment. They also determined that of 87 relevant studies, most utilized algorithms to predict treatment response or prognosticate survival at predetermined time points.

“In conclusion, although AI/Radiomics in IO is a rapidly advancing field, there remains significant room for improvement.”

DOI - https://doi.org/10.18632/oncotarget.28639

Correspondence to - Jeremy McGale - jm4782@cumc.columbia.edu, and Laurent Dercle -  ld2752@cumc.columbia.edu

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Keywords - cancer, immunotherapy, oncology, artificial intelligence, radiomics, lactate, dehydrogenase, PET, MRI, CT, SPECT

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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Artificial Intelligence: Revolutionizing Precision Oncology

BUFFALO, NY- August 28, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on August 26, 2024, entitled, “Inhibition of miR-10b treats metastatic breast cancer by targeting stem cell-like properties.”

As stated within the Abstract of the paper, despite advances in breast cancer screening and treatment, the prognosis for metastatic disease remains dismal, with only a 30% five-year survival rate. This poor outcome is largely due to the failure of current therapeutics to target the unique properties of metastatic cells. One of the key drivers of metastasis is miR-10b, a small noncoding RNA implicated in cancer cell invasion, migration, viability, and proliferation. 

Researchers Alan Halim, Nasreen Al-Qadi, Elizabeth Kenyon, Kayla N. Conner, Sujan Kumar Mondal, Zdravka Medarova, and Anna Moore from Michigan State University’s Precision Health Program, College of Human Medicine, and College of Veterinary Medicine, and Transcode Therapeutics Inc. in Newton, Massachusetts, provide transcriptional evidence that inhibiting miR-10b with MN-anti-miR10b—a nanodrug designed to deliver anti-miR-10b antisense oligomers to cancer cells—activates developmental processes in cancer cells. They observed increased miR-10b expression in stem-like cancer cells.

In mouse models of metastatic triple-negative breast cancer, MN-anti-miR10b has been shown to prevent the onset of metastasis and eliminate existing metastases when combined with chemotherapy, even after treatment has been discontinued.

"Our results demonstrate that inhibition of miR-10b using MN-anti-miR10b decreases the stemness of breast cancer cells, supporting dedifferentiation as a mechanism through which the nanodrug may function as a therapy."

DOI - https://doi.org/10.18632/oncotarget.28641

Correspondence to - Anna Moore - moorea57@msu.edu

Video short - https://www.youtube.com/watch?v=BtaZd_iV8dI

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Keywords - cancer, breast cancer, metastasis, stem-like cells, nanoparticle, miR-10b

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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miR-10b Inhibition: A Strategy for Treating Metastatic Breast Cancer

Macrophage Migration Inhibitory Factor (MIF) and its homolog D-dopachrome Tautomerase (DDT) have been implicated as drivers of tumor progression in various cancers. Recent evidence suggests that MIF could be a therapeutic target in immune checkpoint inhibition (ICI) resistant melanomas; however, clinical evidence for MIF, and particularly for DDT, remains limited.

Researchers Caroline Naomi Valdez, Gabriela Athziri Sánchez-Zuno, Lais Osmani, Wael Ibrahim, Anjela Galan, Antonietta Bacchiocchi, Ruth Halaban, Rajan P. Kulkarni, Insoo Kang, Richard Bucala, and Thuy Tran from Yale University; Oregon Health and Science University; Cancer Early Detection Advanced Research Center (CEDAR); and the Department of Veterans Affairs Portland Health Care System analyzed 97 patients treated at Yale for melanoma between 2002–2020. Their research paper was published in Oncotarget’s Volume 15 on July 19, 2024, entitled, “Prognostic and therapeutic insights into MIF, DDT, and CD74 in melanoma.”

Full blog - https://www.oncotarget.org/2024/08/28/key-roles-of-mif-ddt-and-cd74-in-melanoma-prognosis-and-therapy/

Paper DOI - https://doi.org/10.18632/oncotarget.28615

Correspondence to - Thuy Tran - thuy.tran@yale.edu

Video short - https://www.youtube.com/watch?v=ULlzscn0PvQ

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Keywords - cancer, MIF, DDT, melanoma, immune checkpoint inhibition, cancer transcriptomics

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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Key Roles of MIF, DDT, and CD74 in Melanoma Prognosis and Therapy

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We, the scientists, should change the situation and change the policies of Indexes such as Clarivate's Web of Science, and Medline, and make indexes work for us. Otherwise, why should all of these organizations exist?

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Librarians Against Scientists: Oncotarget lesson

Hundreds of scientific studies, reviews, and analyses are being published from around the world at any given time. This can make reading the latest research literature a time consuming task—depending, of course, on the quantity of papers one hopes to consume. As a tool to help alleviate this important undertaking, many researchers have taken to listening to one of the top open-access podcasts of 2020 and 2021: The Oncotarget Podcast.

After a paper is published, it is added to an enhanced post-publication service provided by Oncotarget, in an effort to help authors reach a wider audience. This podcast series is another way to widely distribute the research that is published with free access by Oncotarget. Oncotarget Podcast episodes regularly include audio readings, press releases, and interviews with authors about their latest and trending papers published by Oncotarget. Player.fm (https://player.fm/podcasts/open-access) rated the Oncotarget Podcast on their lists of Best Open Access Podcasts of 2020 and 2021.

Oncotarget, and Impact Journals as a whole, is constantly expanding the definition of open-access to include a wide variety of accessibility-based audio and visual media to support researchers and readers with disabilities. Creators of the Oncotarget Podcast hope that offering audible renderings of literature from Oncotarget.com, and of blog posts from Oncotarget.org and Oncotarget.net, will be helpful for the vision impaired community.

Stay up-to-date with all of the latest oncology-focused research literature published by Oncotarget by subscribing to the Oncotarget Podcast, which can be found on Soundcloud, Apple, Stitcher, and Blubrry podcast streaming services.

About Oncotarget:

Oncotarget is a bi-weekly, peer-reviewed, open access biomedical journal covering research on all aspects of oncology.

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Oncotarget Podcast Episodes: The Latest in Oncology-Focused Research

Oncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Oncotarget is now indexed by MEDLINE, PubMed and PMC/PubMed.

Read about the Oncotarget Scientific Integrity Process: https://www.oncotarget.com/scientific_integrity/

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