BRAF (B-raf proto-oncogene)

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

In combination with external datasets or pretrained models, the resource can help advance data-driven detection and characterisation work. The diverse range of polyps assigned to cancer stages from 201 patients makes this tool valuable for researchers and clinicians in furthering diagnosis and treatment.

Its presence in a substantial portion of AFO/AFD/DO, together with their larger size compared to OD, could support a neoplastic nature in at least a subset of these lesions, though a hamartomatous DO may exist. Further investigation and clinical correlation remain essential to distinguish these entities.

P=N/A, N=5500, Recruiting, University Health Network, Toronto | N=1000 --> 5500 | Trial completion date: Dec 2025 --> Dec 2029 | Trial primary completion date: Dec 2025 --> Dec 2029

The patient received combined dabrafenib, trametinib, and pembrolizumab with close safety monitoring, achieving rapid tumor control and complete remission by six months with manageable toxicity. This case suggests that early integration of PD-1 blockade with BRAF/MEK inhibition treatment may benefit selected patients and underscores the value of comprehensive molecular and immunohistochemical assessment to guide individualized therapy.

Importantly, this resistance mechanism is conserved in human melanoma: combined MEK and Gαq-PLCβ-PKC inhibition markedly enhances trametinib efficacy in BRAF V600E melanoma cells and xenografts, and reverses acquired resistance in trametinib-resistant melanoma sublines. Together, our results identify a conserved Gαq-PLCβ-PKC pathway as a driver of trametinib resistance and provide preclinical evidence for its co-targeting with MEK inhibition as a therapeutic strategy in BRAF V600E melanoma.

P2, N=70, Recruiting, Zhejiang University

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.

BRAF inhibitors yielded only transient responses, and outcomes were poor. These cases underscore the diagnostic and therapeutic value of multigene testing in SCC, highlighting the need to integrate detailed clinical history into precision oncology strategies.

The presence of infiltrative tumor margin, plump pink cells, and myxoid desmoplasia, may serve as active markers associated with the normalized BRAF V600E mutation. These findings suggest that the mutation acts as a driver in both early and late stages of PTC development. Furthermore, a direct relationship between tumor size and clonality underscores the role of BRAF V600E mutation in tumor progression and morphological evolution.

Functional studies reveal that HOMER3 overexpression enhances ECM stiffness, type I collagen deposition, and Aβ accumulation in the tumor stroma, leading to tumor growth and aggressiveness, while HOMER3 knockdown reduces ECM stiffness, disrupts collagen composition, and increases sensitivity to docetaxel. These findings establish HOMER3 as a pivotal regulator of OSCC malignancy and chemoresistance, providing novel insights into its role in orchestrating the tumor microenvironment and identifying it as a promising therapeutic target for OSCC.

ESGDA is a rare benign tumor arising from the esophageal duct, characterized by multiple lobulated cystic proliferation.The key diagnositic point is the presence of double layers and micropapillary/serrated structures lining the cysts. We identified BRAF V600E gene mutations in ESGDA, providing further evidence that it is the esophageal counterpart of ductal tumors and expanding the morphologic spectrum of sialadenoma papilliferum (SP)-like lesions.