BRAF V600E

This case expands the known clinical and radiological spectrum of PXA, highlighting that it can occur in older patients, in uncommon locations, and with atypical imaging features. It underscores the importance of histopathological and molecular analysis for definitive diagnosis and supports gross total resection as the mainstay of treatment.

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.

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.

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.

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.

Notably, transgenic Fosl1 expression alone was sufficient to induce tumors with a BRAF V600E-like serrated morphology and transcriptional profile. These findings reveal a mechanism through which oncogenic BRAF-driven ERK signaling reprograms transcription to drive serrated neoplasia.

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.

Critically, the 3D microenvironment induced a more aggressive phenotype, characterized by upregulated expression of the BRAF V600E oncogene and the induction of epithelial-mesenchymal transition (EMT), and conferred significantly increased resistance to both cisplatin and vemurafenib. These findings indicate that our tissue-specific, TAS-based 3D model successfully recapitulates key pathophysiological hallmarks of thyroid cancer, representing a more clinically relevant and predictive platform for investigating tumor mechanisms and for the preclinical evaluation of novel therapeutic agents.

Using a cut-off value of 0.229, the nomogram achieved a sensitivity of 0.829 and a specificity of 0.793. A nomogram with strong predictive performance has been successfully developed and validated, which may assist clinicians in estimating the risk of lung metastasis in young patients with PTC.