Experimental Compounds Push Cancer-Promoting Pathways Into Overdrive in Pancreatic Cancer Cells

New Analysis Challenges Methods Used to Measure Residual DNA in mRNA Vaccines

BUFFALO, NY – August 25, 2026 – A new precision oncology paper was #published in Volume 17 of Oncotarget on August 14, 2026, titled “Systematic methodological flaws in DNA contamination assessment of mRNA vaccines: A critical analysis of Achs et al. (2025).” The article was led by first and corresponding author Kevin McKernan from Medicinal Genomics, Beverly, Massachusetts, along with co-authors David J. Speicher from Cyrus Scientific Inc, Hamilton, Ontario, Canada, and Jessica Rose from Brownstone Institute, Austin, Texas. Rather than presenting a new experimental vaccine analysis, the paper critically examines the methodology used by Achs et al. in a 2025 study that reported no excessive residual DNA impurities in COVID-19 mRNA vaccines. McKernan and colleagues argue that several methodological choices in that study could systematically underestimate residual DNA and therefore limit its suitability for regulatory safety assessment. One major concern involves how quantitative PCR results were converted from DNA copy numbers into mass. Achs et al. used full-length plasmid molecular weight in their calculations even though their own sequencing data suggested much shorter median DNA fragment sizes. The critique argues that this approach requires fragmentation-correction factors because random DNA breakage can disrupt qPCR target regions and reduce the number of detectable amplicons. Without such correction, the authors contend that residual DNA mass may be underestimated. The paper also highlights the importance of primer and amplicon design. Achs et al. used qPCR targets with substantially different amplicon lengths, including shorter kanamycin-resistance targets and longer spike-encoding targets. Because the reported median DNA fragment sizes were approximately 130–201 base pairs, longer amplicons would be less likely to remain intact after fragmentation. The authors therefore argue that this design could preferentially reduce detection of spike-associated DNA relative to shorter plasmid regions. DOI - https://doi.org/10.18632/oncotarget.28913 Correspondence to - Kevin McKernan - Kevin.McKernan@medicinalgenomics.com Abstract video - https://www.youtube.com/watch?v=xSWS3HDQUus Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28913 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, mRNA vaccines, DNA contamination, qPCR; plasmid DNA, RNA:DNA hybrids 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

Experimental Compounds Push Cancer-Promoting Pathways Into Overdrive in Pancreatic Cancer Cells

Pancreatic cancer remains one of the most difficult cancers to treat, in part because mutations in the KRAS gene are extraordinarily common in pancreatic ductal adenocarcinoma (PDAC). These mutations keep growth-promoting signals switched on, allowing cancer cells to proliferate and survive. Although drugs targeting certain KRAS mutations have emerged in recent years, they work against only a subset of mutant forms, leaving a need for strategies capable of targeting a broader range of KRAS-driven cancers. A research paper published in Volume 17 of Oncotarget, titled “The anticancer effects of PCAIs in pancreatic cancer cells involve MAPK and PI3K/AKT pathways hyperactivation,” investigated a class of experimental compounds known as polyisoprenylated cysteinyl amide inhibitors, or PCAIs. Rather than simply shutting down signaling pathways normally associated with cancer growth, the researchers uncovered a more unexpected effect: PCAIs pushed some of these pathways into unusually high activity while simultaneously promoting oxidative stress, disrupting cell structure, and triggering cancer cell death. Full blog post - https://www.oncotarget.org/2026/08/24/experimental-compounds-push-cancer-promoting-pathways-into-overdrive-in-pancreatic-cancer-cells/ DOI - https://doi.org/10.18632/oncotarget.28879 Correspondence to - Nazarius S. Lamango - nazarius.lamango@famu.edu Abstract video - https://www.youtube.com/watch?v=asbhjME7rFQ Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28879 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, PCAIs, PDAC, MAPK, PI3K/AKT, KRAS To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us on social media: 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

Trk and IGF1R-Related Signaling Linked to Delayed Ewing Sarcoma Growth

BUFFALO, NY – August 10, 2026 – A new #research paper was #published in Volume 17 of Oncotarget on August 7, 2026, titled “Delayed growth of SK-ES-1 Ewing sarcoma tumor xenografts is associated with reduced Trk and IGF1R pathway markers.” The study was led by first author Bruna Almeida dos Santos and corresponding author Caroline Brunetto de Farias, primarily affiliated with the Federal University of Rio Grande do Sul and the National Science and Technology Institute for Children’s Cancer Biology and Pediatric Oncology (INCT BioOncoPed), with de Farias also affiliated with the Children’s Cancer Institute (ICI) in Brazil. The research team investigated whether targeting tropomyosin receptor kinase (Trk) and related signaling pathways could interfere with Ewing sarcoma growth. Ewing sarcoma is an aggressive cancer that primarily affects children and adolescents and can arise in bone or soft tissue. Although modern multimodal treatments have substantially improved outcomes for patients with localized disease, the prognosis remains considerably poorer for metastatic or relapsed Ewing sarcoma. This has driven efforts to identify molecular pathways that could provide additional therapeutic targets. One potential target involves the Trk family of receptor tyrosine kinases. TrkA, TrkB, and TrkC are encoded by the NTRK1, NTRK2, and NTRK3 genes, respectively, and regulate intracellular signaling pathways involved in cell survival, differentiation, and growth. Previous work from the research group showed that TrkA and TrkB are expressed in Ewing sarcoma and that blocking these receptors can reduce tumor-cell proliferation. Full press release - https://www.oncotarget.com/news/pr/trk-and-igf1r-related-signaling-linked-to-delayed-ewing-sarcoma-growth/ DOI - https://doi.org/10.18632/oncotarget.28911 Correspondence to - Caroline Brunetto de Farias - cbfarias@zielbiosciences.com Abstract video - https://www.youtube.com/watch?v=ZG-vhYfHjuw Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28911 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, Ewing sarcoma, K252a, Trk, NTRK, insulin-like growth factor 1 receptor 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

CTHRC1 in the Tumor Microenvironment Drives Colorectal Cancer Growth in Mouse Study

Colorectal cancer does not develop in isolation. Cancer cells exist within a complex tumor microenvironment made up of fibroblasts, immune cells, blood vessels, and extracellular matrix. Increasing evidence suggests that these surrounding cells and structures can influence whether tumors grow, regress, or evade the immune system. A research paper published in Volume 17 of Oncotarget, titled “Microenvironmental CTHRC1 has a pro-tumorigenic role in colorectal cancer,” investigated the role of collagen triple helix repeat containing 1 (CTHRC1), a secreted protein found in cancer-associated stroma. Full blog post - https://www.oncotarget.org/2026/08/10/cthrc1-in-the-tumor-microenvironment-drives-colorectal-cancer-growth-in-mouse-study/ DOI - https://doi.org/10.18632/oncotarget.28878 Correspondence to: Sergey Ryzhov - Sergey.Ryzhov@mainehealth.org; Volkhard Lindner- Volkhard.Lindner@mainehealth.org; Michaela R. Reagan - Michaela.Reagan@mainehealth.org Abstract video - https://www.youtube.com/watch?v=gTbYy6vGd7E Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28878 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, Cthrc1, CRC, colorectal cancer, subcutaneous tumor model, immune analysis 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

Artificial Intelligence Could Transform Nutrition Care for Cancer Patients

Nutrition plays a critical role in cancer care, yet it is often overlooked. Many patients experience weight loss, muscle wasting, treatment-related side effects, and changes in appetite that can affect their ability to tolerate therapy and maintain quality of life. Although nutrition specialists can help manage these challenges, access to specialized nutritional care remains limited in many healthcare settings. An editorial published in Volume 17 of Oncotarget, titled “Artificial intelligence in nutritional oncology: From isolated screening tools to agentic intervention systems,” explores how advances in artificial intelligence (AI) could help address this gap. The editorial was written by Arnab Sarkar and corresponding author Yashbir Singh-Wolkenhauer, who is affiliated with the Department of Radiology, Mayo Clinic, Rochester, Minnesota. Rather than presenting new clinical trial data, the authors outline a future vision in which AI systems move beyond isolated tasks to continuously support nutritional care throughout a patient’s cancer journey. Full blog post - https://www.oncotarget.org/2026/07/28/artificial-intelligence-could-transform-nutrition-care-for-cancer-patients/ DOI - https://doi.org/10.18632/oncotarget.28874 Correspondence to - Yashbir Singh-Wolkenhauer - singh.yashbir@mayo.edu Abstract video - https://www.youtube.com/watch?v=sVKhRSr5xaY Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28874 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, artificial intelligence To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us on social media: 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