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BUFFALO, NY- August 5, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on July 12, 2024, entitled, “INT-1B3, an LNP formulated miR-193a-3p mimic, promotes anti-tumor immunity by enhancing T cell mediated immune responses via modulation of the tumor microenvironment and induction of immunogenic cell death.”

In this study, researchers Chantal L. Duurland, Thijs de Gunst, Harm C. den Boer, Marion T.J. van den Bosch, Bryony J. Telford, Rogier M. Vos, Xiaolei Xie, Mingfa Zang, Fang Wang, Yingying Shao, Xiaoyu An, Jingjing Wang, Jie Cai, Ludovic Bourré, Laurens A.H. van Pinxteren, Roel Q.J. Schaapveld, Michel Janicot, and Sanaz Yahyanejad from InteRNA Technologies BV, Utrecht, The Netherlands, and Crown Bioscience Inc., in San Diego, examined the effect of their lipid nanoparticle (LNP) formulated, chemically modified, synthetic miR-193a-3p mimic (INT-1B3) on anti-tumor immunity.

“In this study, we examined the effect of our lipid nanoparticle (LNP) formulated, chemically modified, synthetic miR-193a-3p mimic (INT-1B3) on animal survival, tumor microenvironment (TME) and induction of anti-tumor immune responses.”

The data presented within the study demonstrates for the first time that miR-193a-3p induces long-term immunity against tumor development via modulation of the tumor microenvironment and induction of immunogenic cell death.

Additionally, the data show that systemic administration of INT-1B3 to 4T1 and H22 tumor bearing immunocompetent mice prolonged animal survival by reducing metastasis compared to phosphate buffered saline (PBS) or anti-programmed death (PD) 1 treatment.

DOI - https://doi.org/10.18632/oncotarget.28608

Correspondence to - Sanaz Yahyanejad - sanaz.yah@gmail.com

Video short - https://www.youtube.com/watch?v=pK_Bs5vMBCQ

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Keywords - cancer, miR-193a-3p, microRNA mimic, T cell mediated immunity, immunogenic cell death

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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Oncotarget

INT-1B3 miR-193a-3p Mimic Boosts T Cell Immunity and Induces Tumor Cell Death

BUFFALO, NY- August 8, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on August 5, 2024, entitled, “Chemical complementarity of tumor resident, T-cell receptor CDR3s and renalase-1 correlates with increased melanoma survival.”

As mentioned in the Abstract of this study, overexpression of the secretory protein renalase-1 negatively impacts the survival of melanoma and pancreatic cancer patients, while inhibition of renalase-1 signaling drives tumor rejection by promoting T-cell activation. 

Thus, researchers Saif Zaman, Fred S. Gorelick, Andrea Chrobrutskiy, Boris I. Chobrutskiy, Gary V. Desir, and George Blanck from Yale School of Medicine, Veteran’s Administration Healthcare System, Oregon Health and Science University Hospital, Morsani College of Medicine, and H. Lee Moffitt Cancer Center and Research Institute, investigated the chemical complementarity between melanoma-resident, T-cell receptor (TCR) complementarity-determining region 3 (CDR3) amino acid sequences (AAs) and the renalase-1 protein.

“In this study, we asked whether the RNLS protein could potentially be a tumor antigen by examining chemical complementarity between melanoma tumor-resident TCR CDR3s and the AA sequence of RNLS.”

The results suggest that there could be biologically relevant antigenic interaction between RNLS epitopes and T-cell receptors (TCRs).

“We hypothesize that RNLS protein could be recognized by TCRs, leading to local immune responses against melanoma, similar to what we have previously demonstrated with wildtype cancer antigens in the melanoma and glioblastoma settings.”

DOI - https://doi.org/10.18632/oncotarget.28633

Correspondence to - George Blanck - gblanck@usf.edu

Video short - https://www.youtube.com/watch?v=p3X9IgPQFJw

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Keywords - cancer, RNLS, melanoma, T-cell receptor CDR3s, chemical complementarity

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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TCR CDR3s and Renalase-1 Linked to Increased Melanoma Survival

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

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

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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.

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

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

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

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

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

BUFFALO, NY- October 21, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on October 1, 2024, entitled, “Next-generation cell-penetrating antibodies for tumor targeting and RAD51 inhibition.”

As highlighted in the abstract, monoclonal antibody therapies for cancer have shown extraordinary clinical success in recent years. However, these strategies are primarily limited to targeting specific cell surface antigens, despite many disease targets being located intracellularly.

In their paper, researchers Madison Rackear, Elias Quijano, Zaira Ianniello, Daniel A. Colón-Ríos, Adam Krysztofiak, Rashed Abdullah, Yanfeng Liu, Faye A. Rogers, Dale L. Ludwig, Rohini Dwivedi, Franziska Bleichert, and Peter M. Glazer from the Departments of Therapeutic Radiology and Genetics at Yale University School of Medicine, Gennao Bio, and the Department of Molecular Biophysics and Biochemistry at Yale University report on the humanization of the full-length, nucleic acid-binding monoclonal lupus-derived autoantibody 3E10, which exhibits a novel mechanism for cell penetration and tumor-specific targeting.

The authors compare humanized variants of 3E10 and demonstrate that cell uptake relies on the nucleoside transporter ENT2. They also find that faster cell uptake and superior in vivo tumor targeting are associated with higher affinity nucleic acid binding.

“We show that one human variant retains the ability of the parental 3E10 to bind RAD51, serving as a synthetically lethal inhibitor of homology-directed repair in vitro.”

DOI - https://doi.org/10.18632/oncotarget.28651

Correspondence to - Peter M. Glazer - peter.glazer@yale.edu

Video short - https://www.youtube.com/watch?v=sTHjJ0Qq0YQ

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Keywords - cancer, 3E10, cell penetration, nucleic acid binding, nucleic acid delivery, RAD51

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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Next-Gen Cell-Penetrating Antibodies for Tumor Targeting and RAD51 Inhibition

Cancer research has made remarkable progress in recent years, with monoclonal antibody (mAb) therapy emerging as one of the most promising advancements. These treatments are designed to precisely target cancer cells, offering a more focused approach that helps patients fight different malignancies with fewer side effects compared to traditional chemotherapy.

Despite this progress, a major challenge remains: targeting cancer-related molecules inside cells rather than on the surface, which has been the main focus of available mAb therapies until now. This is where the groundbreaking research in the paper “Next-generation cell-penetrating antibodies for tumor targeting and RAD51 inhibition,” published in Volume 15 of Oncotarget on October 1, 2024, comes into play.

Full blog - https://www.oncotarget.org/2024/10/24/next-generation-antibodies-for-cancer-therapy/

Paper DOI - https://doi.org/10.18632/oncotarget.28651

Correspondence to - Peter M. Glazer - peter.glazer@yale.edu

Video short - https://www.youtube.com/watch?v=sTHjJ0Qq0YQ

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Keywords - cancer, 3E10, cell penetration, nucleic acid binding, nucleic acid delivery, RAD51

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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Next-Generation Antibodies for Cancer Therapy

lyrics:

chorus
dead braincells in my head
sorry to mom for the moments i forget
i cant describe how its feel
to lost some time from my mind

dead braincells in my head
sorry to mom for the moments i forget
i cant describe how its feel
to lost some time from my mind

verse
met my schoollove
i forgot whats her name
and my schoollove
ye she think im the same

but the time brought changes in my life, lost memories
after psychiatry feelin like empty gallery

so many situations i don't remember
burning cells in my head, guess no one surrendered
friends ask me bout moments, i dont know what to say
a lie is all what i can say

chorus
dead braincells in my head
sorry to mom for the moments i forget
i cant describe how its feel
to lost some time from my mind

dead braincells in my head
sorry to mom for the moments i forget
i cant describe how its feel
to lost some time from my mind

braincells

BUFFALO, NY - November 12, 2024 – A new #review was #published in Oncotarget's Volume 15 on November 7, 2024, entitled “Understanding the interplay between extracellular matrix topology and tumor-immune interactions: Challenges and opportunities.”

This comprehensive review by researchers Yijia Fan, Alvis Chiu, Feng Zhao, and Jason T. George from Texas A&M University, Rice University, and MD  Anderson Cancer Center sheds light on how the structural properties of the extracellular matrix (ECM) within tumors impact immune cell behavior and influence the effectiveness of cancer immunotherapies. The ECM, a network of proteins surrounding cells, often transforms in cancer, becoming denser and more aligned. These changes create physical barriers that can prevent immune cells, especially T cells, from effectively accessing and attacking tumors, thereby limiting the success of immunotherapies.

The team emphasizes the role of specific ECM configurations, known as Tumor-Associated Collagen Signatures (TACS), in cancer progression and immune evasion. TACS1 and TACS2 patterns create "immune deserts" around tumors, limiting immune cell movement and preventing T cells from recognizing and attacking cancer cells, which is essential for successful immunotherapy. In advanced stages, TACS3 aligns ECM fibers in ways that both promote tumor spread and create additional barriers, further obstructing immune cell access to the tumor.

These insights lead the way for ECM-targeted therapies designed to modify these barriers, potentially transforming “cold” (immune-non-responsive) tumors into “hot” (immune-responsive) ones, thereby improving immune cell infiltration and enhancing treatment outcomes. 

“Understanding the complex interplay is relevant for developing more accurate model of tumor evasion and the identification of corresponding therapeutic intervention.”


The review highlights advanced computational models that simulate interactions between the ECM, immune cells, and tumors, offering valuable insights for developing ECM-targeted therapies. These models illustrate how modifying ECM properties could enhance immune cell migration and function, potentially overcoming immune resistance and expanding the effectiveness of immunotherapies.

The authors also suggest that targeting ECM structure could significantly enhance the effectiveness of immunotherapy, especially for cancers like breast, pancreatic, and ovarian, which often feature dense ECM regions. By reshaping the ECM, such treatments could enable immune cells to access previously unreachable tumor areas, presenting a promising strategy to combat tumors that are resistant to standard therapies.

In conclusion, the review underscores the need for continued research into ECM-focused strategies, which could support more integrated approaches to cancer treatment. By targeting the ECM’s physical barriers and immune evasion mechanisms, these strategies hold promise for improving outcomes in difficult-to-treat cancers.

DOI - https://doi.org/10.18632/oncotarget.28666

Correspondence to - Jason T. George - jason.george@tamu.edu

Video short - https://www.youtube.com/watch?v=7Wm-SMLJadk

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Extracellular Matrix and Tumor-Immune Interactions: Challenges & Opportunities

BUFFALO, NY- November 13, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), on October 25, 2024, Volume 16, Issue 20, titled, ”Canonical ligand-dependent and non-canonical ligand-independent EphA2 signaling in the eye lens of wild-type, knockout, and aging mice.“

Researchers from the School of Optometry and Vision Science Program at Indiana University have uncovered important new insights into how the aging affects the eye lens and contributes to cataract formation, a condition impacting millions worldwide. This study focuses on the EphA2 protein, traditionally associated with cancer, which researchers have now identified as essential for maintaining the lens’s clarity and function as it ages.

Cataracts are the leading cause of blindness worldwide, primarily affecting older adults, yet the precise biological mechanisms behind their formation remain unclear. This research sheds light on the role of the EphA2 protein receptor in the eye lens, revealing that it operates through two distinct signaling pathways: a canonical (ligand-dependent) and a non-canonical (ligand-independent) pathway. By studying various groups of mice, including those lacking the EphA2 protein receptor and its ligand partner ephrin-A5, scientists observed how these signaling pathways change with age, affecting the organization and maturation of lens cells.

Researchers Jenna L. Horner, Michael P. Vu, Jackson T. Clark, Isaiah J. Innis, and Catherine Cheng observed that EphA2’s canonical signaling, which organizes lens cells, remains stable in aging lens tissue, particularly in epithelial cells. They found that the non-canonical signaling pathway—previously associated primarily with aggressive cancer cells—increases with age in normal lens cells. This increase suggests that non-canonical signaling plays a crucial role in helping lens fiber cells mature and maintain their structure over time.

“Here, we report that canonical ligand-mediated EphA2 activation is restricted to the lens epithelial cells and show the first evidence of physiological non-canonical EphA2 activity in a normal tissue.”

This understanding could lead to new therapies targeting EphA2 to delay or prevent cataracts.

In conclusion, this study represents a significant advance in understanding the cellular mechanisms behind lens aging and cataract development, potentially paving the way for new non-surgical cataract treatments.

DOI - https://doi.org/10.18632/aging.206144

Corresponding author - Catherine Cheng - ckcheng@iu.edu

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

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Keywords - aging, fiber cells, epithelial cells, Y588, Y589, S897, phosphorylation, maturation, ephrin

About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

Please visit our website at https://www.Aging-US.com​​ and connect with us:

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Aging (Aging-US)

EphA2 Signaling in Eye Lens Aging: Wild-Type, Knockout, and Aging Mice

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/

Cancer and aging are two sides of age-related tumorigenesis.

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

Read about the Aging (Aging-US) Scientific Integrity Process: https://aging-us.com/scientific-integrity

im lost... idk 

pls comment/repost for survive, thank you:(

you wanna Feature, need help or something.. write a dm


every 10 seconds a child dies of hunger.
Please google for an organization of your choice and donate 10 bucks.... Don't go to McDonalds for once, dont cut one nose coke, don't poison yourself with a pack of cigarettes for once.... 
We often feel like a piece of shit, but others die while we cry

~youngsad

New tracks tagged #cells