Oncotarget

BUFFALO, NY - February 24, 2025 – A new #research paper was #published in Oncotarget, Volume 16, on February 18, 2025, titled “Robust p53 phenotypes and prospective downstream targets in telomerase-immortalized human cells."

Researchers Jessica J. Miciak, Lucy Petrova, Rhythm Sajwan, Aditya Pandya, Mikayla Deckard, Andrew J. Munoz, and Fred Bunz from the Sidney Kimmel Comprehensive Cancer Center and Johns Hopkins University School of Medicine studied the tumor-suppressing protein p53, which plays a key role in preventing cancer. Their findings reveal how p53 affects cancer cell growth, treatment resistance, and potential drug targets, providing new insights that could improve future cancer therapies.

The p53 protein plays a crucial role in preventing cancer by stopping uncontrolled cell growth. However, many cancers mutate or suppress p53, allowing tumors to develop and resist treatment. In this study, researchers restored p53 function in colorectal cancer cells, which led to slower cellular growth, increased cellular aging (senescence), and greater sensitivity to radiation therapy. These findings suggest that p53 status influences cancer progression and response to treatment, making it a promising target for new therapies.

The study also examined hTERT-RPE1 cells; a type of non-cancerous human cell used in research. When the TP53 gene was disrupted in these cells, they grew faster and became more resistant to radiation, reinforcing the idea that p53 helps prevent cancerous growth.

Another key discovery was a previously unnoticed p53 mutation (A276P) found in a subset of hTERT-RPE1 cells. This mutation weakened p53’s ability to regulate certain genes but did not affect its ability to control calcium signaling, a process important for cell survival. The unexpected appearance of this mutation suggests that even non-cancerous cells can acquire genetic changes that mimic early cancer development. This insight could help scientists better understand how cancers evolve and become resistant to treatment.

"Cancers that retain wild type TP53 presumably harbor other clonal alterations that permitted their precursors to bypass p53-mediated growth suppression."

A breakthrough in the study was the identification of two new p53-regulated genes that could be important for cancer treatment. The first, ALDH3A1, helps detoxify harmful substances and may impact cancer cell resistance to oxidative stress. The second, NECTIN4, is a protein found in many aggressive cancers, including bladder and breast cancer. Notably, NECTIN4 is the target of enfortumab vedotin, an FDA-approved drug for bladder cancer. These discoveries provide new potential drug targets and could lead to improved therapies for cancers that still retain some p53 function.

In conclusion, this research highlights the critical role of p53 in cancer biology and suggests that restoring p53 function could make tumors more vulnerable to radiation and chemotherapy. The discovery of new p53-controlled genes provides new opportunities for targeted cancer therapies. With further research, these findings could lead to new precision medicine strategies that leverage p53’s natural tumor-suppressing abilities.

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

Correspondence to - Fred Bunz - [email protected]

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

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BUFFALO, NY - February 25, 2025 – A new #research paper was #published in Oncotarget, Volume 16, on February 18, 2025, titled “Leukopenia, weight loss and oral mucositis induced by 5-Fluorouracil in hamsters’ model: A regenerative approach using electrospun poly(Lactic-co-Glycolic Acid) membrane."

Researchers from the Federal University of Rio de Janeiro and Brazilian Center for Research in Physics have investigated a novel approach to treating oral mucositis, a painful and debilitating side effect of chemotherapy. Led by first author and corresponding author Ana Chor, the study examined the effectiveness of an electrospun poly (Lactic-co-Glycolic Acid) (PLGA) membrane in promoting tissue regeneration in an animal model of chemotherapy-induced oral mucositis. The findings suggest that PLGA membranes, particularly when combined with the body's own healing cells, significantly accelerate the recovery process and reduce inflammation. This promising discovery could lead the way for improved treatments for cancer patients experiencing severe mouth ulcers during chemotherapy.

Oral mucositis affects many cancer patients undergoing 5-Fluorouracil (5-FU) chemotherapy, often leading to difficulty in eating, drinking, and speaking. Despite its prevalence, effective treatments remain limited. In this study, researchers applied electrospun PLGA membranes to 5-FU-induced ulcers in hamsters. Some of these membranes were infused with autologous mesenchymal cells—cells taken from the animal itself—to enhance the healing process.

The study showed significant results, as ulcers treated with PLGA membranes containing autologous cells healed completely within six days, along with reduced inflammation and the formation of new blood vessels essential for tissue repair. While PLGA membranes without added cells also contributed to healing, the recovery process was slower.

"This innovative approach holds significant therapeutic potential, as it utilizes the host’s mesenchymal cells and nanotechnology tools to design a scaffold that mimics the organism’s microenvironment."

These findings highlight the potential of using bioengineered materials to treat chemotherapy-induced oral lesions. While further research is necessary before this approach can be tested in clinical settings, the study provides a strong foundation for future investigations. If successfully translated to human treatment, this technique could significantly improve the quality of life for cancer patients by offering a more effective solution for managing chemotherapy-related mouth ulcers.

DOI - https://doi.org/10.18632/oncotarget.28685

Correspondence to - Ana Chor - [email protected]

Video short - https://www.youtube.com/watch?v=0hGgRAlcBQA

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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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BUFFALO, NY - February 18, 2025 – A new #researchpaper was #published in Oncotarget, Volume 16, on February 12, 2025, titled “Could Panitumumab with very low dose Capecitabine be an option as a maintenance regimen."

In this study, researchers Doaa A. Gamal, Aiat Morsy, and Mervat Omar from Assiut University Hospital, evaluated a new maintenance treatment for metastatic colorectal cancer (mCRC). Their findings suggest that a combination of two drugs—Panitumumab, a targeted therapy that blocks a protein called epidermal growth factor receptor to slow cancer growth, and low-dose Capecitabine, a chemotherapy drug that converts into 5-fluorouracil (5-FU) inside the body to stop cancer cells from growing and dividing—could help extend survival in patients with mCRC. This regimen appears to be both effective and well-tolerated, especially for patients with wild-type KRAS mCRC who had previously responded to treatment.

Colorectal cancer is one of the leading causes of cancer-related deaths worldwide. Standard treatment often involves a combination of chemotherapy and targeted therapies, but many patients face challenges related to treatment toxicity and resistance, which can lead to treatment interruptions. This study tested whether a lower-intensity maintenance treatment could help keep the cancer under control after initial treatment.

The study involved 25 mCRC patients with wild-type KRAS and BRAF, who first received six rounds of standard 5-FU-based chemotherapy with Panitumumab. Patients who responded well then switched to a maintenance treatment of Panitumumab every two weeks and a low, continuous dose of Capecitabine. The results showed that patients had a median progression-free survival of 18 months and a median overall survival of 45 months, indicating a strong potential benefit.

Patients with metastases detected at the same time as the primary tumor showed a longer progression-free survival than those with metastases appearing later. The treatment was also well tolerated, with only 8% of patients experiencing severe side effects such as skin rash or diarrhea, which were managed with standard treatments.

"In our research, the toxicity profile was very acceptable, and no patients needed to stop treatment or had a dose modification due to toxicity."

Finding a way to keep cancer under control while reducing side effects is a major goal in cancer treatment. While other maintenance therapies like Bevacizumab and Cetuximab have been studied, this research suggests that Panitumumab with low-dose Capecitabine could be a promising new option. Panitumumab is already an FDA-approved drug, but its role in maintenance therapy had not been extensively explored. The results of this study suggest that this combination may help delay disease progression while keeping side effects manageable, ultimately improving patients’ quality of life.

Although larger studies are needed, these findings open the door for further clinical trials to confirm the benefits of this regimen. If validated, this approach could change the standard of care for mCRC patients, particularly those who cannot tolerate more intensive chemotherapy.

DOI - https://doi.org/10.18632/oncotarget.28687

Correspondence to - Doaa A. Gamal - [email protected]

Video short - https://www.youtube.com/watch?v=wuPSS0EdK-8

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BUFFALO, NY – February 14, 2025 – A new #review was #published in Oncotarget, Volume 16, on February 12, 2025, titled “SETDB1 amplification in osteosarcomas: Insights from its role in healthy tissues and other cancer types.”

Authors Elodie Verdier, Nathalie Gaspar, Maria Eugenia Marques Da Costa, and Antonin Marchais from the Gustave Roussy Cancer Campus analyzed recent studies on a gene called SETDB1, which may play a key role in osteosarcoma, a type of bone cancer that mostly affects teenagers and young adults. Their review highlights how SETDB1 helps cancer cells grow, resist treatment, and avoid the immune system. Because of this, blocking SETDB1 could be a promising new way to treat osteosarcoma.

Osteosarcoma is a fast-growing bone cancer that is usually treated with surgery and chemotherapy. However, if the cancer spreads or returns, treatment options are very limited. Scientists are searching for new ways to stop this disease, and recent studies have found that osteosarcoma cells often have extra copies of the SETDB1 gene. This seems to make the cancer more aggressive and harder to treat.

“Whole exome sequencing of osteosarcoma samples from both diagnosis and relapses has highlighted several factors, including SETDB1, that are amplified in the most aggressive forms of the disease.”

SETDB1 is involved in epigenetics, meaning it affects how genes are turned on and off without changing the DNA itself. The review explains that SETDB1 helps tumors hide from the immune system, making it difficult for the body to fight the cancer naturally. The researchers believe that blocking SETDB1 could help the immune system recognize and attack osteosarcoma cells. Some experimental drugs that target SETDB1 are already being tested in the lab.

The review also describes how SETDB1 influences key cancer pathways, such as Wnt signaling, which helps cancer cells grow, and epithelial-mesenchymal transition (EMT), a process that allows cancer to spread. The authors suggest that combining SETDB1-blocking drugs with immunotherapy or radiation could be an effective new strategy for treating osteosarcoma.

Another key finding is that SETDB1 may help cancer cells become resistant to chemotherapy, making treatment less effective. This means that drugs targeting SETDB1 could not only slow cancer growth but also make existing treatments work better.

While more research is needed, this review brings attention to SETDB1 as a potential treatment target. Scientists hope that a deeper understanding of SETDB1 will lead to new therapies that improve survival rates for osteosarcoma patients.

DOI - https://doi.org/10.18632/oncotarget.28688

Correspondence to - Antonin Marchais - [email protected], and Maria Eugenia Marques Da Costa - [email protected]

Video short - https://www.youtube.com/watch?v=f9WgaDoEubs

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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For years, breast cancer has been classified as either HER2-positive or HER2-negative, determining whether a patient could receive HER2-targeted therapies like trastuzumab (Herceptin). However, a growing body of research suggests a middle category—HER2-low breast cancer—which has led to important changes in how clinicians approach treatment.

A recent review published in Oncotarget, titled “Evolving Concepts in HER2-Low Breast Cancer: Genomic Insights, Definitions, and Treatment Paradigms,” explores what this means for both patients and clinicians​.

Full blog - https://www.oncotarget.org/2025/02/12/her2-low-breast-cancer-a-new-understanding/

Paper DOI - https://doi.org/10.18632/oncotarget.28680

Correspondence to - Andrew A. Davis - [email protected]

Video short - https://www.youtube.com/watch?v=dn54UrHCUNQ

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Keywords - cancer, breast cancer, HER2-low, 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.

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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 - [email protected]

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

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BUFFALO, NY - February 6, 2025 – A new #casereport was #published in Volume 16 of Oncotarget on February 5, 2025, titled “Acquired RUFY1-RET rearrangement as a mechanism of resistance to lorlatinib in a patient with CD74-ROS1 rearranged non-small cell lung cancer: A case report."

In this case report, Jenny L. Wu from Vanderbilt University School of Medicine and Wade T. Iams from Vanderbilt-Ingram Cancer Center describe a rare case of drug resistance in a patient with advanced non-small cell lung cancer (NSCLC). The patient, a 42-year-old man who had never smoked, initially responded well to lorlatinib, a targeted therapy designed to treat cancer driven by specific genetic alterations. However, after six months, his cancer began to grow again. Clinicians discovered that this was due to a new genetic change, known as the RUFY1-RET fusion. This finding highlights how cancers can adapt to treatment and the importance of ongoing genetic testing to guide therapy decisions.

NSCLC is the most common type of lung cancer, and in some cases, it is driven by genetic changes that can be targeted with specific drugs. The patient’s cancer originally had a ROS1 gene rearrangement, which made it responsive to lorlatinib. But as time went on, the cancer started to grow again, and tests revealed a new genetic alteration called RUFY1-RET fusion, which likely caused resistance to lorlatinib.

This new genetic change was identified using RNA next-generation sequencing (RNA NGS), an advanced test that can find mutations that standard genetic tests might miss. After discovering the RUFY1-RET gene fusion, the patient was treated with a combination of lorlatinib and pralsetinib, a drug that specifically targets RET gene alterations. While this combination helped control the cancer for about four months, the patient’s condition unfortunately worsened after four months.

“This is the first reported case of a RET fusion as a potential mechanism of resistance to lorlatinib, it identifies a novel RET fusion partner, and it emphasizes the importance of testing for acquired resistance mutations with both DNA and RNA at the time of progression in patients with targetable oncogenic drivers.”

Understanding cases like this can help clinicians and researchers develop more effective treatment strategies, including combination therapies that target multiple genetic changes to combat drug resistance. While the combined therapy in this case provided only temporary benefits, it offers important insights for future research and patient care, particularly for cancers that no longer respond to standard treatments.

DOI: https://doi.org/10.18632/oncotarget.28682

Correspondence to: Wade T. Iams, [email protected]

Keywords: cancer, ROS1 rearrangement, RET rearrangement, non-small cell lung cancer, targeted therapy, case report

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An unexpected link between KLRG1 and PD-1, two key immune system proteins, was revealed in a study recently published in Oncotarget. This discovery could help explain why some cancer immunotherapy treatments are less effective for certain patients and lead to new therapeutic strategies.

How the Immune System Fights Cancer

The immune system is a powerful defense mechanism against cancer, with CD8 T cells acting as the primary soldiers. These specialized immune cells identify and destroy tumor cells. However, cancer can cleverly evade this attack by manipulating immune checkpoints—natural “breaks” on the immune system that prevent it from overreacting and damaging healthy tissue.

One of the most studied checkpoints is PD-1 (Programmed Death-1), a receptor on T cells that acts as an “off switch” when activated by tumor cells. This mechanism suppresses the immune response, allowing cancer to grow without control. In response, researchers have developed treatments called PD-1 inhibitors, which block this “off switch” and keep T cells active.

The Study: Investigating KLRG1 and PD-1 in Tumor-Fighting T Cells

In the study titled “Anti-correlation of KLRG1 and PD-1 expression in human tumor CD8 T cells,” Dr. Steven A. Greenberg from Harvard Medical School analyzed publicly available gene expression data from various cancer types, including lung cancer, melanoma, and colorectal cancer. His goal was to identify immune-related proteins that could complement existing therapies, such as PD-1 inhibitors.

Full blog - https://www.oncotarget.org/2025/01/28/a-new-approach-for-cancer-treatment-the-surprising-relationship-between-klrg1-and-pd-1/

Paper DOI - https://doi.org/10.18632/oncotarget.28679

Correspondence to - Steven A. Greenberg - [email protected]

Video short - https://www.youtube.com/watch?v=PME2xfyYN18

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Keywords - cancer, immunotherapy, KLRG1

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BUFFALO, NY - January 27, 2025 – A new #research paper was #published in Oncotarget's Volume 16 on January 21, 2025, titled “Assessment of cfDNA release dynamics during colorectal cancer surgery."

Researchers from the University of Brasília investigated how cell-free DNA (cfDNA) levels in the blood change before, during, and after colorectal cancer surgery. The study found that cfDNA levels increase significantly during and after surgery. The findings suggest that cfDNA could help clinicians evaluate surgery effectiveness and monitor patient outcomes.

cfDNA consists of small DNA fragments released into the bloodstream when cells die and break apart. In healthy individuals, cfDNA usually comes from normal cell turnover, while in cancer patients, some of it originates from tumor cells. Measuring cfDNA levels offers valuable insights into a patient’s condition and is already being used to track disease progression and treatment response in cancers such as lung, breast, and colorectal cancer.

Colorectal cancer is one of the most common cancers worldwide, affecting millions of people each year. Surgery is often the primary treatment, but up to 50% of patients experience cancer recurrence afterward. In this study, the research team, led by first author Mailson Alves Lopes and corresponding author Fabio Pittella-Silva, analyzed blood samples from 30 patients at three key time points: before, during, and after surgery.

It was found that cfDNA levels increased nearly threefold during surgery and doubled after surgery compared to pre-surgery levels. The increases were even higher in individuals over 60, those with preexisting conditions such as diabetes or heart disease, and patients with elevated levels of carcinoembryonic antigen (CEA), a common cancer marker. Patients with the highest cfDNA levels were those with larger or more aggressive tumors, likely due to greater tissue damage during surgery. Additionally, longer surgeries were linked to higher cfDNA levels.

“[...]we observed that cfDNA concentration may rise in correlation with the duration of the surgery, highlighting its potential as a marker of surgical quality.”

These findings suggest that cfDNA could be a valuable, non-invasive biomarker for clinicians to monitor colorectal cancer patients. Tracking cfDNA levels may help better evaluate surgical outcomes and determine whether patients require closer follow-up care.

While these findings are promising, further research is needed to standardize cfDNA testing and validate its usefulness. Larger studies could help establish cfDNA testing as a reliable tool for cancer care and postoperative monitoring, with the potential to become a routine part of clinical practice in the future.

DOI - https://doi.org/10.18632/oncotarget.28681

Correspondence to - Fabio Pittella-Silva - [email protected]

Video short - https://www.youtube.com/watch?v=jC5_xqIrbtA

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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BUFFALO, NY - January 22, 2025 – A new #review was #published in Oncotarget's Volume 16 on January 20, 2025, titled “Evolving concepts in HER2-low breast cancer: Genomic insights,

definitions, and treatment paradigms."

Researchers Whitney L. Hensing, Emily L. Podany, James J. Sears, Shaili Tapiavala, and Andrew A. Davis from the University of Missouri-KC School of Medicine and Washington University in St. Louis School of Medicine explore HER2-low breast cancer, a recently recognized type of breast cancer that is changing the way clinicians should approach treatment. The review explains what makes HER2-low breast cancer different and highlights new treatment options that are helping patients.

“Breast cancer, which has been historically classified as HER2-positive versus HER2-negative, is currently facing a paradigm shift in both the definition of HER2 status and in the existing treatment algorithms.”

Breast cancer is usually classified into two main types based on the HER2 protein: HER2-positive or HER2-negative. HER2-low breast cancer falls somewhere in between. Thanks to new targeted treatments, such as a drug called trastuzumab deruxtecan, patients with HER2-low breast cancer now have more options and better chances of responding to treatment.

The review looks at recent studies on the genetics of HER2-low breast cancer. Researchers found that these tumors are often hormone receptor (HR)-positive, meaning they respond to hormones like estrogen. Some tumors also carry a common genetic change called a PIK3CA mutation, which could affect how well treatments work. However, experts say HER2-low breast cancer is not a completely separate breast cancer type but rather an opportunity for more personalized treatment.

“Despite evidence from existing literature that HER2-low breast cancer does not represent a distinct biologic and prognostic subtype, the introduction of HER2-low expression as a therapeutic target has expanded patient eligibility for a potent class of anti-HER2 drugs, HER2-directed ADCs, with potential for significant efficacy.”

Despite these advances, diagnosing HER2-low breast cancer can still be difficult. Current testing methods are not always accurate, and different laboratories may get different results. The review calls for better detection methods to make sure patients who can benefit from these new treatments are correctly identified.

With cancer treatments becoming more personalized, the review also explains how clinicians can fit HER2-low treatments into existing guidelines to help patients. The success of targeted therapies is changing how breast cancer is treated, especially for patients whose cancer has metastasized.

In conclusion, experts believe ongoing research will continue to improve the way HER2-low breast cancer is diagnosed and treated. However, they stress the need for better detection methods and continued exploration of new therapies to help patients get the best possible care.

DOI - https://doi.org/10.18632/oncotarget.28680

Correspondence to - Andrew A. Davis - [email protected]

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