BRAF (B-raf proto-oncogene)

RN are characterized by architectural asymmetry and a trizonal pattern. Nuclear atypia and a pagetoid distribution may be observed. RN cells have a low proliferative index and are positive for HMB-45 and tyrosinase. BRAF expression occurs in most recurrences and is heterogeneous in RN melanocytes.

This case highlights the potential of ctDNA to improve monitoring of concurrent malignancies, especially during immunotherapy, where PET/CT may lead to false-positive results. It is the first reported case of nivolumab treatment for chemo-refractory relapsed HL and OC, demonstrating the utility of ctDNA in managing dual malignancies.

RICTOR mutations in lung adenocarcinoma define a molecularly distinct subgroup characterized by preferential co-occurrence with EGFR, KRAS, and TP53, as well as a broader spectrum of genomic alterations. These findings support the view that RICTOR functions within complex oncogenic contexts and warrant further investigation in larger, multi-institutional cohorts.

This review will highlight the molecular and genetic underpinnings of these tumors and how targeted therapeutic strategies led to the US Food and Drug Administration's approvals of combination therapy with dabrafenib and trametinib for pediatric patients with BRAF V600E mutant low-grade glioma; tovorafenib, a pan-RAF inhibitor, for pediatric BRAF mutant glioma; and vorasidenib, an inhibitor of mutant IDH1/2 enzymes, for patients with mutant IDH low-grade glioma. Integration of these targeted therapies into currently accepted treatment paradigms remains to be fully understood, along with the long-term impact on patient quality of life and prognosis.

From 36 HER2 positive cases, 32(32,5%) were with score 2+, and 4(4,4%) with score 3+. Continued research into molecular mechanisms and biomarkers holds the promise of further improving CRC outcomes through personalized and effective interventions.

The POE+ACC+NDA or MI+NDA method provided high diagnostic performance for predicting BRAFV600E mutation in PTC. Texture analysis of tumor calcified area can also be used to predict BRAFV600E mutation.

Molecular docking studies suggest that nemtabrutinib preferentially binds in the ATP-binding pocket of MEK1. Combined cancer cell panel and biochemical profiling reveals previously underappreciated cross-reactivities of nemtabrutinib indicating a potential application in MAPK-driven cancers.

In vivo studies further validated these findings, showing that the combination treatment inhibited tumor growth and significantly prolonged survival in mouse models bearing patient-derived NRAS-mutated melanoma tumors. Given the tolerability of this combination in vivo, our results suggest that brimarafenib and mirdametinib represent a promising therapeutic strategy for patients with NRAS-mutated melanomas and potentially other RAS-mutated solid tumors.

These higher rates persisted in patients without a 20% or more increase in sCr at drug start and without exposure to chemotherapy or immunotherapy. In this cohort study of patients treated with molecularly targeted anticancer medications associated with an acute rise in sCr, we observed higher incidence and relative rate for kidney dysfunction among treated patients, compared with matched cancer-free patients.

The clinical and molecular stratification of tumors enables differential treatment. Organ-preserving strategies after a complete response to therapy are an important area of current research.

P=N/A, N=600, Recruiting, City of Hope Medical Center

P1, N=51, Active, not recruiting, Institut de Recherches Internationales Servier | Trial completion date: Jun 2025 --> Mar 2026