BRAF mutation

P1, N=56, Recruiting, Memorial Sloan Kettering Cancer Center | Active, not recruiting --> Recruiting

This PEITC effect could be demonstrated in two further dabrafenib-resistant cell lines, WM164D and 451LuP. These results suggest that the altered redox status is linked to compromised mitochondria and is associated with the development of BRAFi resistance, rendering cells exquisitely sensitive to the actions of selective ROS-inducing therapeutics.

The ferroptosis inducer erastin also inhibits melanoma growth. Combining the ATAD2 inhibitor BAY-850 with the MEK inhibitor trametinib potently suppresses melanoma growth. Our study identifies ATAD2 as a key driver of melanoma and provides a rationale for targeting ATAD2 in conjunction with the MAPK pathway to treat melanoma.

Similar haploidy is found in 3 additional high-grade astrocytoma by literature review, all harbor a single gene mutation in the MAPK pathway. We propose that the massive chromosome loss might serve as a significant mechanism contributing to the unusual malignant transformation of benign brain tumors activated by the MAPK pathway.

About 40% of cutaneous melanomas carry BRAF mutations-more common in younger patients-and these are linked to more aggressive behaviour and a higher risk of brain metastasis. Over the past decade, targeted therapies (TT) using BRAF and MEK inhibitors (BRAFi, MEKi), along with immune checkpoint inhibitors (ICI), have significantly improved response rates and survival in metastatic melanoma.

This case highlights the importance of considering MF in patients presenting with tissue eosinophilia or Langerhans cell infiltration, even when initial biopsies lack definitive features.

Loss of SATB2 staining in CRC is associated with inferior survival outcomes and adverse clinicopathologic features.

The degradation of IRF-8 ultimately contributes to tumor progression enhancement. Clinically, the presence of pS69 on TRIM63 is associated with tumor immunosuppression and poor prognosis among melanoma patients, highlighting its potential as a promising therapeutic target.

Using the American Association for Cancer Research GENIE and MSK-CHORD cohorts, early-onset and late-onset colorectal liver metastases samples had comparable mutation rates in key genes including KRAS, BRAF, APC, TP53, PI3K3CA, and SMAD4 (all q > 0.05) Despite the presence of more aggressive clinicopathologic features, patients with early-onset colorectal liver metastases had outcomes and genomic profiles similar to patients with late-onset colorectal liver metastases. These data highlight how age at disease onset per se should not be considered an indicator of aggressive disease and poor prognosis among patients with colorectal liver metastases.

MSS/EMAST-L tumors aligned with chromosomally stable, KRAS/Wnt-driven CRC. In conclusion, MSS/EMAST-H tumors represent an underrecognized CRC subtype with intermediate genomic instability and a distinctive molecular profile, with potential implications for prognostic assessment and personalized therapeutic strategies.

Future outlooks are outlined with near-term biomarker-drug hypotheses for microsatellite-stable (MSS)-iCMS3 and high fibrosis tumors and key gaps to close for clinical translation. This review outlines a roadmap for precision medicine in colorectal cancer by leveraging the iCMS/IMF framework to integrate pathology and digital pathology, molecular diagnostics, and therapy mapping with FAP-targeted imaging and therapy.

Advances in high-definition endoscopy and chromoendoscopy improve the detection of these subtle, mucus-capped, flat lesions, while endoscopic resection is nowadays feasible in expert hands. Future priorities should include prospective multicenter cohorts integrating molecular profiling to refine surveillance strategies.