BRAF V600E

ABM-1310 showed a favorable safety profile and encouraging intracranial activity. These findings support continued evaluation for CNS tumors and in cancer patients with prior BRAF inhibitor exposure.

Advances in lipidomics technologies, particularly mass spectrometry-based approaches, have enabled comprehensive profiling of lipid alterations at bulk, spatial, and single-cell levels, offering new opportunities for biomarker discovery and therapeutic stratification. Targeting lipid metabolic vulnerabilities represents a promising strategy to improve melanoma diagnosis, prognosis, and treatment efficacy.

Demonstrating the mutation carried by the tumor is very critical in this regard. The purpose of this article is to focus on the treatment of thalamic glioma in pediatric patients in light of molecular information.

These molecular insights have been incorporated into updated risk stratification frameworks, preoperative surgical planning, and treatment algorithms, informing the selection of kinase inhibitors, redifferentiation strategies, and enrollment in genotype-directed clinical trials for radioiodine-refractory disease. This review synthesizes recent evidence connecting genomic alterations to clinical behavior and highlights their translation into evolving approaches for thyroid cancer management.

Precursors of SD-iCCA, if they exist, may be included in the second category, and the third category may represent unique carcinomas possibly associated with or followed by conventional SD-iCCA. In conclusion, this novel approach to categorize BLNPs into three categories guarantees further studies of precursors of and their progression to conventional SD-iCCA.

P1/2, N=16, Active, not recruiting, National Cancer Institute (NCI) | N=58 --> 16 | Trial completion date: Nov 2025 --> Jan 2027

Recurrent alterations included NF1 (87.5%), PTEN (62.5%), and TERT promoter mutations (25%), with a single BRAF V600E-mutant tumor, while the classical +7/ - 10 signature was infrequent and MGMT promoter methylation was largely absent in GBM, IDH-wildtype. This study demonstrates that a substantial subset of pediatric and AYA HGGs harbor molecularly adult-type signatures, revealing the limitations of conventional histopathology and immunohistochemistry, challenging age-based diagnostic paradigms, and highlights the value of methylation profiling for diagnostic refinement, detection of targetable alterations in younger patients.

Using a panel of BRAFV600E positive YUMM lines, we find that, following chronic vemurafenib treatment, SOX10 is lost whereas SOX9 is induced...Overall, our data show that the loss of SOX10 and SOX9 induction are critical to program drug resistance. Furthermore, we show that the YUMM cell lines represent a good murine model to investigate transitions to an acquired drug resistant state.

Erdheim-Chester disease causes symptomatic pleuropulmonary disease, which may be the initial presenting feature. Erdheim-Chester disease characteristically manifests interlobular septal thickening with ground-glass and/or small nodular opacities, often combined with pleural thickening and/or pleural effusions. Targeted therapy may provide durable therapeutic responses.

P2, N=56, Recruiting, SWOG Cancer Research Network | Trial completion date: May 2029 --> May 2028

Nonmetastatic BRAFmut CRC carries a dismal prognosis, irrespective of MMR status. Routine testing for BRAFV600E mutation alongside MMR assessment is advocated to inform personalized management, potentially impacting surveillance, adjuvant therapy decisions, and eligibility for targeted therapies.

P2, N=66, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Jan 2026 --> May 2026 | Trial primary completion date: Jan 2026 --> May 2026