Oncotarget

Discover a groundbreaking blood test designed to detect minimal residual disease in B-cell lymphomas. This innovative method uses PhasED-Seq technology, allowing for ultra-sensitive detection of tumor DNA fragments. With the potential to revolutionize monitoring and treatment response, this test offers hope for improving outcomes in patients who face a high risk of relapse. Learn about its accuracy and how it can inform personalized treatment strategies while enhancing early detection efforts.

A fascinating study delves into the connection between blood type and breast cancer risk, highlighting type A blood as a significant factor. Researchers analyzed over 13,000 breast cancer patients and revealed that individuals with type A have an 18% increased risk compared to type O. The analysis draws on extensive global data and calls for further exploration of the biological mechanisms behind this association. Other blood types showed no significant links, making this a compelling area for future research.

Researchers unveil how METTL3 fuels oral squamous cell carcinoma, shedding light on the intricate mechanisms behind this aggressive cancer. The team emphasizes the role of the small RNA molecule miR-146a-5p, which hinders the tumor-suppressing gene SMAD4. This discovery could pave the way for innovative therapies targeting METTL3 and miR-146a, potentially transforming treatment options for patients facing this challenging disease. The findings highlight the urgent need for better strategies against a cancer notorious for late detection and treatment resistance.

Discover groundbreaking research on a new maintenance therapy for metastatic colorectal cancer that combines panitumumab and low-dose capecitabine. This innovative approach aims to extend survival and improve quality of life without the severe side effects of conventional treatments. Learn how this gentler option can make cancer care more accessible for patients around the world, transforming the way doctors manage the challenges of advanced cancer.

BUFFALO, NY - May 5, 2025 – Oncotarget, #published by Impact Journals, is proud to #announce its presence as an #exhibitor at the 47th Annual Meeting of the Society for Scholarly Publishing (SSP), taking place May 28–30, 2025, at the Hilton Baltimore in Maryland. Impact Journals publishes scholarly journals in the biomedical sciences, with a focus on cancer and aging research. Attendees are invited to stop by Booth #209 to meet members of the Oncotarget team and learn more about the journal’s latest initiatives. This year’s conference theme, “Reimagining the Future of Scholarly Publishing at the Intersection of Value and Values,” highlights critical topics such as artificial intelligence, research ethics, and transparency in science—principles that closely align with Oncotarget's commitment to rigorous peer review and scientific integrity. We look forward to connecting with SSP attendees to discuss Oncotarget’s mission, explore potential collaborations, and emphasize the role of open science in advancing cancer research and related fields. To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us on social media at: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

Discover groundbreaking research on early immune evasion in HPV-related pre-cancer lesions. The study reveals how two immune markers, PD-L1 and FOXP3, help predict whether lesions will progress to cancer or resolve on their own. It sheds light on the role of T-regulatory cells in suppressing immune responses in high-grade lesions. This fascinating exploration connects immune activity to the complex behaviors of these lesions, offering hope for targeted prevention strategies.

Researchers reveal groundbreaking findings on the p53 gene, a key player in preventing cancer. This gene, known as the 'guardian of the genome', can halt harmful cell growth and even push damaged cells to self-destruct. New research in healthy cell models uncovers two promising therapeutic targets: ALDH3A1 and Nectin-4. These insights could revolutionize cancer therapy and address challenges faced by many treatments today.

BUFFALO, NY - April 15, 2025 – A new #research paper was #published in Oncotarget, Volume 16, on April 4, 2025, titled “Association between two single nucleotide polymorphisms of the Prostaglandin-Endoperoxide Synthase 1 and 2 genes and cell proliferative prostatic diseases in Lebanon." The team of researchers led by first author Brock J. Sheehan and corresponding author Ruhul H. Kuddus, from Utah Valley University, discovered that a specific genetic variation in the PTGS2 gene is associated with a higher risk of benign prostate hyperplasia (BPH), a common condition in aging men. The study, which focused on Lebanese men, suggests that the C allele of the -765 G>C polymorphism in the PTGS2 gene may increase risk to this non-cancerous but problematic prostate condition. This finding could help identify men at greater risk earlier and lead to better treatment choices. Benign prostate hyperplasia and prostate cancer are two common conditions that involve abnormal cell growth in the prostate gland. While prostate cancer is malignant and potentially life-threatening, BPH is a non-cancerous enlargement that can still significantly affect quality of life. Both conditions are widespread in older men, with BPH affecting over 70% of men above 60. Researchers have long suspected that inflammation-related genes may play a role in their development. In this study, the focus was to study PTGS1 and PTGS2, genes that help produce enzymes involved in inflammation. Using DNA samples from 168 Lebanese men, including 61 with prostate cancer, 51 with BPH, and 56 healthy controls, the researchers analyzed two common gene variants. They found no link between the PTGS1 variant and either condition. However, the PTGS2 variant showed a strong association with BPH. Men carrying the C version of this gene were more than twice as likely to have BPH compared to those without it. While a similar trend was observed in men with prostate cancer, the results were less conclusive. "The C allele of SNP-765G>C of the PTGS2 gene was significantly associated with an increased risk of BPH (OR = 2.30, p-value = 0.01)." This is the first study to report a genetic link between the C allele of the -765 G>C polymorphism in the PTGS2 gene and BPH in Lebanese men. It builds on earlier findings that associated this gene variant with various cancers, including prostate, colon, and stomach cancers. Although based on a relatively small and specific population, the study offers new insight that could help improve genetic screening and guide prevention strategies. The research also points to the potential benefits of COX-2 inhibitors—drugs already used to treat prostate conditions—which may be more effective for men with certain PTGS2 gene types. Further studies in larger and more diverse groups are needed to confirm these results and explore how this gene variant influences prostate disease. In the future, simple genetic tests could help identify men at higher risk before symptoms appear, allowing for earlier and more personalized care. Continue reading: DOI: https://doi.org/10.18632/oncotarget.28710 Correspondence to: Ruhul H. Kuddus — ruhul.kuddus@uvu.edu Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY - April 11, 2025 – A new research perspective was published in Oncotarget, Volume 16, on April 4, 2025, titled “GSK3β activation is a key driver of resistance to Raf inhibition in BRAF mutant melanoma cells." In this work, first author Diana Crisan and corresponding author Abhijit Basu from the University Hospital Ulm led a team that presents experimental evidence pointing to the protein GSK3β as a key contributor to drug resistance in melanoma. Their findings suggest that GSK3β becomes increasingly active in cancer cells during treatment, helping them survive and adapt despite ongoing therapy with BRAF inhibitors. Melanoma is a type of skin cancer in which nearly half of patients have mutations in the BRAF gene that accelerate tumor growth. While treatments targeting BRAF, known as BRAF inhibitors, initially work well, tumors often find ways to fight back. This research perspective explores how GSK3β, a protein involved in metabolism and cell survival, becomes more active in melanoma cells that develop resistance to BRAF inhibitors. Researchers treated melanoma cells with a common BRAF mutation using Dabrafenib, a widely used BRAF inhibitor. Over time, the cancer cells developed resistance and showed a marked increase in GSK3β levels. This pattern was confirmed across multiple melanoma cell models, suggesting that the finding is consistent and reliable. Importantly, the researchers observed that treating resistant cancer cells with a GSK3β inhibitor significantly reduced their growth. This result suggests that blocking this protein could restore sensitivity to treatment, highlighting GSK3β as a promising therapeutic target and supporting the idea of combining GSK3β inhibitors with existing melanoma therapies. “Remarkably, treatment of BRAFi-resistant melanoma cells with the GSK3 inhibitor LY2090314 for three weeks could overcome resistance and significantly decreased melanoma cell growth, confirming the causal role of GSK3 activation for BRAFi resistance development.” The research perspective adds to ongoing efforts to understand and overcome melanoma drug resistance. It shows that resistance is not driven only by genetic mutations but may also involve adaptive changes in the cell’s internal signaling and survival mechanisms. By identifying GSK3β as a potential contributor, the authors offer a new direction for improving the durability of targeted treatments in melanoma. As research continues, GSK3β may be a critical factor in the long-term success of melanoma therapy, particularly for patients who have stopped responding to standard BRAF-targeted drugs. Continue reading: DOI: https://doi.org/10.18632/oncotarget.28711 Correspondence to: Abhijit Basu — abhijit.basu@alumni.uni-ulm.de Video short - https://www.youtube.com/watch?v=G2Tq4_r6xLw Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ 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). To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

Despite decades of research, treatment for osteosarcoma has remained largely unchanged, especially for patients whose cancer spreads or returns. However, a growing body of evidence, summarized in the review “SETDB1 amplification in osteosarcomas: Insights from its role in healthy tissues and other cancer types,” published in Oncotarget, highlights the gene regulator SETDB1 as a potential key player in cancer progression, immune system evasion, and resistance to therapy. Targeting this protein may offer a new direction for developing more effective treatments. Understanding Osteosarcoma Osteosarcoma is a rare but aggressive bone cancer that primarily affects teenagers and young adults. While current treatments like surgery and chemotherapy can help some patients, outcomes are much worse for those with relapsed or advanced disease. One of the reasons osteosarcomas are so difficult to treat is their complex and unstable genetics. Unlike cancers with well-defined mutations, osteosarcomas involve chaotic DNA rearrangements, making it difficult to identify precise drug targets. Adding to the challenge, the immune system often fails to recognize these cancer cells, limiting the success of immunotherapy. Full blog - https://www.oncotarget.org/2025/04/09/targeting-setdb1-a-new-strategy-for-treating-osteosarcoma/ Paper DOI - https://doi.org/10.18632/oncotarget.28688 Correspondence to - Antonin Marchais - antonin.marchais@gustaveroussy.fr, and Maria Eugenia Marques Da Costa - jenny.marquescosta@gustaveroussy.fr Video short - https://www.youtube.com/watch?v=f9WgaDoEubs Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28688 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, SETDB1, cancer epigenetics, tumor immunogenicity, mesenchymal differentiation in osteosarcoma 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). To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM