Latest Research
All publications from the Cancer3.AI database, newest first.
Molecular signature of SETD2 and m6A modifiers in the pathogenesis of different grades of adult-type diffuse gliomas.
Kumari S, et al
This study investigated the molecular roles of SETD2, a histone H3K36 trimethyltransferase, and m6A RNA modification regulators in the development and graded progression of adult-type diffuse gliomas, a spectrum of primary brain tumors ranging from lower-grade IDH-mutant tumors to the highly aggressive IDH-wildtype glioblastoma. Researchers analyzed how alterations in SETD2 expression and m6A modifier activity — including writers, erasers, and readers of the N6-methyladenosine mark — correlate with tumor grade and contribute to glioma pathogenesis. The findings reveal that dysregulation of both epigenetic chromatin remodeling and epitranscriptomic RNA methylation mechanisms plays a significant role in driving glioma malignancy and grade escalation. These molecular signatures may serve as potential biomarkers for tumor classification, prognosis, or as novel therapeutic targets in adult diffuse gliomas, a disease with notoriously poor outcomes and limited treatment options.
Molecular biology reports
Source →Demographics of malignant melanoma in Trinidad and Tobago.
Ramdass MJ, et al
Researchers conducted a retrospective analysis of all confirmed malignant melanoma (MM) cases in Trinidad and Tobago between 2004 and 2019, aiming to describe the disease's demographics and clinical patterns in this Caribbean nation. Across 16 years and a catchment population of approximately 700,000 people, 54 cases were identified, yielding a low incidence rate of 0.482 per 100,000 persons per year and a prevalence of just 0.01%. Notably, individuals of African ethnicity accounted for 83.3% of cases, contrasting with global patterns where melanoma predominantly affects fair-skinned populations, and the lower limb was the most commonly affected anatomical site, seen in nearly 55% of cases. The most frequently recorded histological subtype was nodular melanoma, followed by acral lentiginous melanoma, a subtype known to occur more commonly in darker-skinned individuals and often diagnosed at a later stage. The authors emphasize that incomplete staging data and inconsistent record-keeping represent significant obstacles to understanding and managing melanoma in the Caribbean, calling for standardized data collection and improved clinical protocols across the region.
Annals of the Royal College of Surgeons of England
Source →Surgical Margins Required for the Complete Excision of Canine Oral Melanomas.
Chinner JR, et al
A new retrospective study published in Veterinary and Comparative Oncology investigated the surgical margins needed to achieve complete, cancer-free excision of oral malignant melanoma (OMM), the most common oral tumor in dogs. Researchers from two referral centers and a veterinary pathology laboratory analyzed 28 tumors — 25 OMMs and three benign melanocytomas — categorized by the width of the surgical margin removed around the tumor. The results showed that surgical margins of 10 to 15 millimeters, combined with a qualitative deep margin such as bone or fascia, achieved a complete excision rate (R0) of 100%, compared to only 56% when margins were narrower than 10 millimeters, a difference that was statistically significant. All three melanocytomas were completely excised even with margins smaller than 10 millimeters, suggesting these less aggressive tumors may require less aggressive surgery. These findings provide veterinary surgeons with the first evidence-based margin recommendations for canine oral melanoma, potentially improving surgical planning and reducing the risk of local tumor recurrence in affected dogs.
Veterinary and comparative oncology
Source →Keratinocyte-derived exosomal miR-31-5p reduces vemurafenib sensitivity in melanoma cells.
Li Y, et al
Researchers investigated a key mechanism behind resistance to vemurafenib, a targeted therapy used in melanoma patients whose tumors carry the BRAFV600E mutation. The study found that keratinocytes — normal skin cells surrounding the tumor — release tiny vesicles called exosomes that carry a small RNA molecule, miR-31-5p, into melanoma cells, reducing the cancer cells' sensitivity to vemurafenib both in laboratory models and in living animals. Paradoxically, vemurafenib treatment itself increased miR-31-5p levels in keratinocyte-derived exosomes, creating a feedback loop that amplifies resistance. Inside melanoma cells, miR-31-5p silences ALKBH1, an enzyme that normally removes a chemical tag called m6A from RNA, causing m6A to accumulate and driving cancer cell proliferation. Blocking miR-31-5p or restoring ALKBH1 expression reversed these effects and re-sensitized melanoma cells to vemurafenib. These findings identify the miR-31-5p/ALKBH1/m6A axis as a promising therapeutic target to overcome drug resistance in BRAF-mutant melanoma patients.
International immunopharmacology
Source →RHOV is a Detachment-Responsive Rho GTPase Necessary for Ovarian Cancer Peritoneal Metastasis.
Elhaw AT, et al
Researchers investigated how epithelial ovarian cancer cells survive detachment from the tissue matrix and spread through the peritoneal cavity — a process called transcoelomic metastasis that is the principal driver of mortality in ovarian cancer patients. By profiling gene expression changes shortly after matrix detachment across multiple ovarian cancer cell lines derived from patient ascites, scientists identified a conserved detachment-sensitive gene signature and pinpointed RHOV, an atypical fast-cycling Rho GTPase, as one of the most strongly induced genes. Functional experiments demonstrated that RHOV is essential for anoikis resistance, multicellular tumor aggregate formation, cell migration, and invasion in vitro, and that its genetic loss completely abolished peritoneal metastasis in animal models. Mechanistically, RHOV was found to promote c-Jun signaling and cytoskeletal remodeling, with both GTP-binding capacity and membrane localization required for its pro-metastatic activity. These findings establish RHOV as a critical and previously underappreciated mediator of the earliest molecular adaptations that prime disseminating ovarian cancer cells for peritoneal spread, opening a potential therapeutic window for intercepting metastasis at its inception.
Cancer research
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