BRAF V600E

P2, N=64, Completed, University of Sydney | Active, not recruiting --> Completed

P2, N=152, Not yet recruiting, The Third Xiangya Hospital of Central South University

Analogous PAX3 positive populations were also identified in mouse and human single-cell transcriptomic datasets. Collectively, these findings establish a critical role for Mitfa-independent melanocyte progenitors in UM pathogenesis.

This pooled analysis of candidates considered optimal for initial anti-EGFR-based therapy supports both stop and go and maintenance as de-intensification strategies to consider in shared decision making. Adequately powered phase III studies are advocated to compare the two strategies.

BRAF inhibitors such as encorafenib are ineffective due to MAPK pathway reactivation driven by BRAF dimerization...dHuR abrogated BRAF expression by inducing its exon 18 skipping, and demonstrated superior suppression of BRAF-mutant CRC tumours including those gaining resistance to BRAF inhibitors. Finally, we performed kinome library CRISPR screening and revealed that inactivation of EGFR or MEK enhanced dHuR cytotoxicity, thus establishing a combinatorial strategy to treat patients with refractory BRAF-mutant CRC.

P1, N=16, Recruiting, Memorial Sloan Kettering Cancer Center

These findings uncover a novel miR-31-5p/CSE/H₂S/Zinc axis that fuels BRAF-driven progression. These findings provide a compelling mechanistic rationale for utilizing H₂S-based interventions as a potential therapeutic strategy against BRAF-driven thyroid cancer metastasis.

P1/2, N=75, Not yet recruiting, Gilead Sciences Inc.

The disease later relapsed as high-grade B-cell lymphoma with MYC and BCL2 rearrangements (HGBCL-MYC/BCL2), still harbouring the BRAF mutation. Complete remission was achieved with Rituximab, Cyclophosphamide, Hydroxydaunorubicin, Oncovin and Prednisone, but the double-hit lymphoma relapsed 14 months later.This case illustrates sequential transformation from FL to BRAF-mutated HDS with excellent response to BRAF/MEK inhibition, followed by evolution into HGBCL-MYC/BCL2 responding transiently to immunochemotherapy, emphasising the value of repeated histological and molecular reassessment in FL evolution.

BRAFV600E and TERT promoter co-mutation, identifiable preoperatively, defines a distinct PTC subtype with a profoundly aggressive clinicopathological profile and a significantly elevated risk of recurrence. This combined molecular signature is a potent preoperative biomarker for stratifying patients into the highest-risk category, potentially guiding more individualized initial therapeutic strategies.

Raising physician awareness, as reflected by the untested rate, is a crucial factor in conducting clinical trials to implement perioperative cancer genomic medicine.

P1/2, N=67, Recruiting, D3 Bio (Wuxi) Co., Ltd | Active, not recruiting --> Recruiting | Trial completion date: Apr 2028 --> Aug 2028 | Trial primary completion date: Apr 2028 --> Aug 2028