A companion to "Managing Manuscript Edits", in this track I discuss how and what to communicate with the editor when you resubmit your manuscript.

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Communicating manuscript edits

In a groundbreaking study, researchers have unlocked a new frontier in the fight against aging and age-related diseases. The study, conducted by a team of scientists at Harvard Medical School, has published the first chemical approach to reprogram cells to a younger state. Previously, this was only achievable using a powerful gene therapy.

On July 12, 2023, researchers Jae-Hyun Yang, Christopher A. Petty, Thomas Dixon-McDougall, Maria Vina Lopez, Alexander Tyshkovskiy, Sun Maybury-Lewis, Xiao Tian, Nabilah Ibrahim, Zhili Chen, Patrick T. Griffin, Matthew Arnold, Jien Li, Oswaldo A. Martinez, Alexander Behn, Ryan Rogers-Hammond, Suzanne Angeli, Vadim N. Gladyshev, and David A. Sinclair from Harvard Medical School, University of Maine and Massachusetts Institute of Technology (MIT) published a new research paper in Aging, titled, “Chemically induced reprogramming to reverse cellular aging.”

The team's findings build upon the discovery that the expression of specific genes, called Yamanaka factors, could convert adult cells into induced pluripotent stem cells (iPSCs). This Nobel Prize-winning discovery raised the question of whether it might be possible to reverse cellular aging without causing cells to become too young and turn cancerous.

In this new study, the researchers screened for molecules that could, in combination, reverse cellular aging and rejuvenate human cells. They developed high-throughput cell-based assays to distinguish young cells from old and senescent cells, including transcription-based aging clocks and a real-time nucleocytoplasmic protein compartmentalization (NCC) assay. In an exciting discovery, the team has identified six chemical cocktails that restore NCC and genome-wide transcript profiles to youthful states and reverse transcriptomic age in less than a week.

The Harvard researchers previously demonstrated that it is indeed possible to reverse cellular aging without uncontrolled cell growth by virally-introducing specific Yamanaka genes into cells. Studies on the optic nerve, brain tissue, kidney, and muscle have shown promising results, with improved vision and extended lifespan observed in mice and, recently, a report of improved vision in monkeys.

The implications of this new discovery are far-reaching, opening avenues for regenerative medicine and, potentially, whole-body rejuvenation. By developing a chemical alternative to age reversal via gene therapy, this research could revolutionize the treatment of aging, injuries and age-related diseases and offers the potential for lower costs and shorter timelines in development. On the heels of positive results in reversing blindness in monkeys in April 2023, preparations for human clinical trials of the lab’s age reversal gene therapy are in progress.

“Until recently, the best we could do was slow aging. New discoveries suggest we can now reverse it,” said David A. Sinclair, A.O., Ph.D., Professor in the Department of Genetics and co-Director of the Paul F. Glenn Center for Biology of Aging Research at Harvard Medical School and lead scientist on the project. “This process has previously required gene therapy, limiting its widespread use.”

The team at Harvard envisions a future where age-related diseases can be effectively treated, injuries can be repaired more efficiently, and the dream of whole-body rejuvenation becomes a reality. “This new discovery offers the potential to reverse aging with a single pill, with applications ranging from improving eyesight to effectively treating numerous age-related diseases,” Sinclair said.

Press Release: https://www.aging-us.com/news_room/NEW-STUDY-Discovery-of-Chemical-Means-to-Reverse-Aging-and-Restore-Cellular-Function

DOI: https://doi.org/10.18632/aging.204896 

Corresponding Author: David A. Sinclair - david_sinclair@hms.harvard.edu  

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Aging (Aging-US)

NEW STUDY: Discovery of Chemical Means to Reverse Aging and Restore Cellular Function

BUFFALO, NY- November 1, 2023 – A new research perspective was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 20, entitled, “Cholinergic centro-cingulate network in Parkinson disease and normal aging.”

In their new perspective, researchers Nicolaas I. Bohnen, Sygrid van der Zee and Roger Albin from University of Michigan, Veterans Administration Ann Arbor Healthcare System, University of Groningen, and the University Medical Center Groningen discussed Parkinson disease (PD). Decreased cholinergic binding within the recently identified centro-cingulate brain network has been shown to robustly correlate with the severity of cognitive impairment in PD. This network with key hubs within the cingulum, operculum and peri-central cortical regions also correlates with elements of parkinsonian motor impairments, including postural instability and gait difficulties, such as falls or freezing. 

“We recently reported novel data-driving findings suggesting that cholinergic innervation deficits in centro-cingulate brain regions may be an important contributor to cognitive impairments in PD [1].”

MRI neuroimaging studies have shown that the anterior midcingulate cortex is a key node for cognitive aspects of movement generation, i.e., intentional motor control. Recent evidence also suggests a novel aspect of organization of primary motor cortex, describing “effector” regions for fine movement control intercalated with interlinked “inter-effector” regions devoted to whole-body control. 

A distinguishing feature of inter-effector regions is tight linkage to the cingular and opercular regions. Such inter-effector regions have been proposed to be part of a greater somato-cognitive action network necessary for integration of goals and movement. Recent evidence also points to vulnerabilities of cholinergic nerve terminals in the centro-cingulate network in older non-PD adults. These features of normal aging underscore that cortical cholinergic terminal losses in age-associated neurodegenerative disorders are likely not exclusively the result of disease-specific etiologies but also related to otherwise normal aging. 

“Practical implications of this overlap are that addressing disease-specific and general aging etiologies involved in neurodegeneration, may be of benefit in age-associated neurodegenerative disorders where significant cholinergic systems degeneration is present.”

DOI - https://doi.org/10.18632/aging.205209

Corresponding author - Nicolaas I. Bohnen - nbohnen@umich.edu

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Keywords - aging, centro-cingulate network, cholinergic, cognition, motor, Parkinson disease

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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Parkinson Disease and Normal Aging

BUFFALO, NY - February 10, 2025 – A new #casereport was #published in Volume 16 of Oncotarget on February 5, 2025, titled “A case report of donor cell–derived hematologic neoplasms 9 years after allogeneic hematopoietic cell transplantation."

In this case report, Aleksandra Mroczkowska-Bękarciak and Tomasz Wróbel from Wroclaw Medical University describe a rare and serious complication after a stem cell transplant. The case involves a patient who, nine years after receiving a stem cell transplant for acute myeloid leukemia (AML), developed a new, aggressive blood cancer originating from donor cells. Despite receiving treatment, the disease progressed to myelodysplastic syndrome/acute myeloid leukemia (MDS/AML), ultimately leading to the patient’s death.

Stem cell transplants are a life-saving treatment for many blood cancers, including AML. While relapse of the original cancer is the most common concern, this case highlights another rare but serious complication: the development of donor cell-derived hematologic neoplasms (DCHN).

The report details the case of a 23-year-old woman who remained in remission for nearly 10 years following a successful hematopoietic stem cell transplant from an unrelated donor. However, she later developed a new form of leukemia, driven by genetic mutations in the ASXL1, SETBP1, and EZH2 genes—biomarkers linked to highly aggressive blood cancers. Over the next two years, the disease progressed despite intensive treatment, ultimately proving fatal.

This case highlights the need for continued monitoring of transplant recipients, even years after the procedure. Although DCHN is extremely rare, its occurrence raises critical questions about the process by which donor cells transform into leukemia.

Some stem cell donors may unknowingly carry genetic mutations that are harmless in their own bodies but could trigger cancer in recipients. Additionally, factors such as immunosuppressive therapy, bone marrow stress, and transplantation procedures may contribute to these rare but deadly outcomes.

“Early diagnosis and intervention are crucial to improving patient prognosis.” 

Ongoing research is focused on improving donor screening methods to help predict and prevent these complications. In the future, routine genetic testing for stem cell donors could become a standard part of the transplant process, helping clinicians identify potential risks before transplantation.

More studies are needed to fully understand why donor-derived cancers develop and how they can be prevented. With continued progress in precision medicine and genetic diagnostics, researchers aim to make stem cell transplants safer and more effective for all patients.

DOI - https://doi.org/10.18632/oncotarget.28686

Correspondence to - Aleksandra Mroczkowska-Bękarciak - omroczkowska@interia.pl

Video short - https://www.youtube.com/watch?v=G2zd0UqWzeE

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

Rare Case of Donor Cell-Derived Blood Cancer Discovered Nine Years After Stem Cell Transplant

BUFFALO, NY - March 17, 2025 – Impact Journals (Oncotarget’s publisher), is pleased to announce its participation as an exhibitor at the American Association for Cancer Research (AACR) Annual Meeting 2025. The meeting is scheduled for April 25-30, 2025, at the McCormick Place Convention Center in Chicago, Illinois.

The 2025 AACR Annual Meeting's central theme, "Unifying Cancer Science and Medicine: A Continuum of Innovation for Impact," highlights major breakthroughs and innovative developments transforming cancer research. Oncotarget aligns directly with this vision, being always committed to rapidly publishing and disseminating impactful research findings across diverse areas of cancer science and thus advancing cancer treatment and patient care.

Conference attendees are warmly invited to visit Booth 2815 to meet members of the Oncotarget, discover notable recent publications, and discuss collaborative opportunities. Oncotarget, assisted by its publisher Impact Journals, remains focused on accelerating the sharing of crucial oncology research, fostering innovation, and maintaining excellence in cancer research.

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 to Participate at the AACR Annual Meeting 2025

BUFFALO, NY — March 17, 2025 —  Impact Journals (Aging’s publisher) is pleased to announce its participation as an exhibitor at theAmerican Association for Cancer Research (AACR) Annual Meeting 2025. The meeting is scheduled for April 25-30, 2025, at the McCormick Place Convention Center in Chicago, Illinois.

This 2025 AACR Annual Meeting theme, “Unifying Cancer Science and Medicine: A Continuum of Innovation for Impact,” highlights significant advancements and groundbreaking discoveries in cancer research. Aging closely aligns with this mission, dedicated to disseminating impactful scientific research at the intersection of oncology and gerontology.

Visit Booth 2815 to meet directly with members of the Aging team, explore the latest research publications, and discuss opportunities for collaboration and manuscript submissions. Aging, supported by its publisher Impact Journals, remains dedicated to promoting innovation, collaboration, and advancing scientific knowledge in aging-related cancer research.

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.)

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Aging (Aging-US) to Participate at the AACR Annual Meeting 2025

A new study from the Sidney Kimmel Comprehensive Cancer Center and Johns Hopkins University School of Medicine, published in Oncotarget, reveals that the gene p53, long known as the “guardian of the genome,” may be even more powerful than previously thought. By studying it in non-cancerous human cells, researchers discovered how p53 stops risky cell growth and uncovered two new potential targets for cancer therapy.

Understanding p53: The Genome’s Guardian Against Cancer

The p53 gene is one of the most important natural defenses our body has against cancer. When functioning properly, p53 detects damage in a cell’s DNA and either stops the cell from dividing or pushes it to self-destruct. This process helps prevent potentially dangerous mutations from spreading. However, many cancers find ways to silence or mutate p53, allowing uncontrolled growth and resistance to treatments.

Studying p53 in a clear and accurate way has long been a challenge. Most cancer cell models used in research already carry numerous genetic mutations, which can mask or alter how p53 truly functions. To fully understand this vital tumor-suppressing gene, scientists needed a model that closely resembled healthy, genetically stable human cells—yet could still be maintained and studied over time in the laboratory.

The Study: Exploring p53 in Normal and Cancer Cell Models

Researchers Jessica J. Miciak, Lucy Petrova, Rhythm Sajwan, Aditya Pandya, Mikayla Deckard, Andrew J. Munoz, and Fred Bunz explored p53 activity using a uniquely suitable cell line: hTERT-RPE1. These non-cancerous human cells are immortalized using telomerase, meaning they continue dividing like cancer cells, but without the chaotic mutations seen in tumors. This makes them an excellent model for studying how p53 operates in near-normal conditions.

Full blog - https://www.oncotarget.org/2025/04/22/new-insights-into-p53-a-powerful-genes-role-in-cancer-therapy/

Paper DOI - https://doi.org/10.18632/oncotarget.28690

Correspondence to - Fred Bunz - fredbunz@jhmi.edu

Video short - https://www.youtube.com/watch?v=Psxj3ctbTuk

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Keywords - cancer, p53, ionizing radiation, immortalized cells, ALDH3A1, NECTIN4

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 Insights into p53: A Powerful Gene’s Role in Cancer Therapy

BUFFALO, NY - April 28, 2025 – A new #research paper was #published in Oncotarget, Volume 16, on April 24, 2025, titled “PD-L1 and FOXP3 expression in high-grade squamous intraepithelial lesions of the anogenital region."

Researchers Humberto Carvalho Carneiro, Rodrigo de Andrade Natal, José Vassallo and Fernando Augusto Soares from the Instituto D’Or de Pesquisa e Ensino and Rede D’Or studied early tissue changes caused by human papillomavirus (HPV) in the anal, vulvar, and penile regions. They found that high-grade pre-cancer lesions triggered stronger immune responses and showed higher levels of two immune-related markers, PD-L1 and FOXP3. These findings are important because they help explain how some HPV-related lesions progress to cancer while others heal on their own.

High-risk HPV is known to cause several types of anogenital cancers. Before these cancers appear, the virus often leads to abnormal tissue changes known as high-grade squamous intraepithelial lesions. Many of these lesions disappear without treatment, but some become cancer—especially in people with weakened immune systems. This study explored how immune activity may play a role in this progression.

The researchers examined tissue from 157 patients—95 males and 55 females—with either high-grade or low-grade HPV-related lesions. They found that T-regulatory cells, marked by the FOXP3 protein, were more common in high-grade lesions. These immune cells are known to suppress immune responses, which can allow infected or abnormal cells to grow. The team also found higher expression of PD-L1, a protein that helps cells evade immune detection, particularly in inflammatory immune cells.

"Dense inflammatory infiltrates and high counts of FOXP3+ cells were significantly more frequent in patients with HSILs than in those with LSILsHR (p = 0.04 and 0.02, respectively). HSILs also exhibited higher PD-L1 expression (padj < 0.01 and < 0.01 for the SP142 and 22C3 clones, respectively), based on the Poisson generalized linear model.”

These findings suggest that HPV may begin avoiding the immune system early in infection, even before cancer develops. The combination of high FOXP3 and PD-L1 levels may create a protective environment for infected cells, making them harder for the body to eliminate. This immune evasion may allow the lesions to remain and, over time, become cancerous.

The study also compared patients with and without HIV to assess whether immune health influenced the results. While those with compromised immune systems had more extensive lesions, PD-L1 and FOXP3 expression was also found in patients with healthy immune systems. This evidence shows that immune evasion by HPV can happen regardless of a person’s immune status.

Understanding how PD-L1 and FOXP3 function in early HPV-related lesions may help clinicians predict which lesions are more likely to become cancer. These insights could lead to new strategies for monitoring, treating, or preventing HPV-related precancerous lesions and cancer in the anogenital region. The study highlights how early immune system changes can play a key role in the development of HPV-related cancers.

DOI - https://doi.org/10.18632/oncotarget.28715

Correspondence to - Humberto Carvalho Carneiro - humberto.carneiro@rededor.com.br

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Early Immune Evasion Found in HPV-Related Pre-Cancer Lesions of the Anogenital Region

BUFFALO, NY - May 14, 2025 – A new #review paper was #published in Volume 16 of Oncotarget on May 9, 2025, titled “Relationship between ABO blood group antigens and Rh factor with breast cancer: A systematic review and meta-analysis."

A comprehensive study, led by first authors Rahaf Alchazal from Yarmouk University and Khaled J. Zaitoun from Johns Hopkins University School of Medicine and Jordan University of Science and Technology, examined the potential link between blood type and breast cancer. The research team conducted a systematic review and meta-analysis of 29 previously published studies, involving more than 13,000 breast cancer patients and over 717,000 controls. 

“Researchers searched for studies on breast cancer patients and ABO blood groups across four major databases: PubMed, Scopus, Web of Science, and Google.“

Breast cancer is the most common cancer among women worldwide. Identifying risk factors is vital for early detection and prevention. While many studies have explored lifestyle and genetic causes, this analysis focused on the ABO blood group system. By pooling global data, the researchers found that blood type A was the most common among breast cancer patients and was significantly associated with an 18% increased risk compared to type O.

The study did not find a significant association between breast cancer and blood types B, AB, or Rh factor. Although the results do not prove causation, they point to a biological pattern worth further investigation. Blood group antigens are proteins found on the surface of cells, including breast tissue. These molecules may influence how cancer develops and spreads by interacting with the immune system or affecting cell behavior.

This meta-analysis is the most extensive review to date on this topic, based on studies conducted across Asia, Europe, Africa, and the Americas. While previous research found unclear conclusions, this large-scale evaluation provides stronger evidence for a possible connection between blood type A and breast cancer risk.

Researchers note that regional differences, genetic diversity, and study quality may affect individual results. Nevertheless, the overall trend supports considering blood type A as a potential risk marker. This insight could help shape screening guidelines, encouraging earlier or more frequent checkups for women with this blood type.

Further research is needed to understand why blood type A may play a role in cancer development. Future studies may explore genetic mechanisms, immune responses, and other biological pathways. These efforts could lead the way for more personalized cancer prevention and care strategies.

DOI - https://doi.org/10.18632/oncotarget.28718

Correspondence to - Khaled J. Zaitoun - kzaitou1@jh.edu

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Keywords - cancer, breast cancer, cancer risk factors, blood group antigens, tumor

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Blood Type A Identified as Potential Breast Cancer Risk Factor

Releasing documents old and new in honor of Spring and the impending gala by Peer Review. A recent blossoming of friendship has unearthed the treasures of talent, passion and hunger this crew is lavishing on Denver. They're tight ... they're real ... they're beyond ... and I will be joining them on Saturday 4.27.19 for a night of after hours mayhem.

35mm Film: 
Dani B. Cruz

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Spring Disclosure

AlalaOne PeerReview SpringDisclosure

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

Academic career guide. I firmly believe that your academic career has the potential for joy as well as success. I help academics build their confidence to do the work they find meaningful and find the time to do the important work.

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