Asian Pacific Journal of Cancer Biology

The Relationship Between Kirsten Rat Sarcoma Mutations and Mismatch Repair Status in Colorectal Cancer Patients: A Preliminary Study

2025-07-14T04:51:52+00:00

Background: Chromosomal instability (CIN) is a key pathway in colorectal cancer (CRC) tumorigenesis, occurring in 80%-85% of cases and leading to aneuploidy. CIN tumors often harbor mutations in APC, KRAS, and TP53, which drive tumor progression. Another crucial pathway, microsatellite instability (MSI), results from DNA mismatch repair (MMR) defects, leading to a hypermutable phenotype. MSI-CRC has distinct clinicopathologic features and a better prognosis than proficient MMR (pMMR) CRC. KRAS mutations, found in approximately 40% of CRC cases, drive tumor progression via the RAS/RAF/MAPK pathway. This study investigates the relationship between KRAS mutations and MMR status in CRC patients.

Methods: A preliminary cross-sectional study was conducted on CRC patients. KRAS mutations were analyzed using PCR, while MMR status was determined via immunohistochemistry and microsatellite testing. Clinical variables, including cancer stage, tumor category, and location, were analyzed.

Results: Among 55 patients, 91.3% had pMMR and 8.7% had deficient MMR (dMMR). KRAS mutations were more frequent in pMMR patients (80% of cases). Patients with pMMR and KRAS mutations exhibited aggressive tumors but responded to conventional therapy, whereas dMMR patients with KRAS mutations showed complex molecular profiles, potentially benefiting from immunotherapy.

Conclusion: KRAS mutations are primarily associated with pMMR in CRC, indicating distinct molecular pathways. Personalized treatment strategies should consider MMR status and KRAS mutations to optimize therapeutic outcomes. Further research is needed to explore their clinical implications.

Comparative Efficacy of Prostate Tumor Induction Methods in Wistar Rats

2025-07-14T04:54:29+00:00

Objectives: This study aims to evaluate and compare the efficacy of three methods for inducing prostate tumors in male Wistar rats: hormonal induction using testosterone propionate, chemical induction with cadmium chloride, and a combination of both agents. The research seeks to enhance understanding of the interactions between environmental and hormonal factors in prostate cancer development.

Materials and Methods: Twenty-five male Wistar rats (180-220 grams) were randomly assigned to five groups: a control group (no induction), a low-dose cadmium chloride group (1 mg/kg), a high-dose cadmium chloride group (2 mg/kg), a testosterone propionate group (5 mg/kg), and a combination group (1 mg/kg cadmium chloride + 5 mg/kg testosterone). Each treatment was administered over four weeks, followed by a four-week observation period. Histopathological analyses were conducted on prostate tissues using Hematoxylin and Eosin (H&E) staining to assess tumor characteristics and progression.

Results: Histopathological examination revealed that the control group exhibited normal prostate architecture. The low-dose cadmium chloride group showed mild hyperplasia, while the high-dose group displayed significant dysplastic changes. The testosterone propionate group demonstrated hyperplastic and pleomorphic epithelium, indicative of early tumorigenesis. The combination group exhibited the most aggressive tumors, characterized by severely dysplastic epithelium and stromal invasion. Survival rates were notably lower in the combination group, indicating increased health risks associated with dual exposure.

Conclusions: The study concludes that the combination of cadmium chloride and testosterone propionate results in a more aggressive tumor phenotype compared to either agent alone, suggesting a synergistic effect in prostate carcinogenesis. These findings underscore the importance of using combined hormonal and chemical induction models to better replicate human prostate cancer for experimental research. Further studies are recommended to explore molecular mechanisms and optimize induction protocols for improved translational relevance in prostate cancer research.

Advances in Uveal Melanoma: From Molecular Pathogenesis to Precision Diagnostics and Personalized Therapies: Narrative Overview

2025-07-14T05:01:43+00:00

Objective: This review aims to summarize recent progress in the molecular understanding, diagnostic strategies, and treatment innovations in uveal melanoma (UM), the most common primary intraocular malignancy in adults. Emphasis is placed on the integration of precision diagnostics and emerging therapies that may improve clinical outcomes in high-risk cases.

Materials and Methods: A narrative literature review was conducted using databases including PubMed, Scopus, Web of Science, and Google Scholar, covering the years 2020 to 2024. Keywords used included “uveal melanoma,” “liquid biopsy,” “circulating tumor cells,” “gene mutations,” “immunotherapy,” and “precision oncology.” Relevant peer-reviewed articles, clinical trials, and reviews were selected based on methodological quality and relevance to the scope of the review.

Results: Uveal melanoma most frequently arises in the choroid and is genetically distinct from cutaneous melanoma. It is primarily driven by mutations in guanine nucleotide-binding protein G(q) subunit alpha (GNAQ), guanine nucleotide-binding protein G(q) subunit alpha-11 (GNA11), BRCA1 associated protein-1 (BAP1), eukaryotic translation initiation factor 1A X-linked (EIF1AX), and splicing factor 3B subunit 1 (SF3B1). These mutations activate key signaling pathways such as mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT), influencing prognosis and therapeutic response. Diagnostic advancements include high-resolution imaging and liquid biopsy techniques, which enable detection of circulating tumor cells, circulating tumor DNA, and microRNAs. Standard treatments include radiation therapy (plaque brachytherapy) and surgical interventions. Novel therapeutic approaches such as tebentafusp (a T-cell receptor therapy), oncolytic viruses, chimeric antigen receptor (CAR) T-cell therapy, suicide gene constructs, and RNA interference show promise in clinical and preclinical settings.

Conclusion: A precision medicine approach that integrates molecular diagnostics, artificial intelligence-enhanced liquid biopsy, and novel systemic therapies is transforming the management of uveal melanoma. These innovations may enable earlier detection, more accurate risk stratification, and targeted treatment, potentially improving survival and preserving vision in affected patients.