HRAS mutation

CD5, CD117 and Glut1 are diffusely expressed in MNC, but not in MNT. The genetic alterations in MNC are more diverse than those of MNT, but MNC lacks the characteristic GTF2I mutation of MNT.

P2, N=34, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Jan 2026 --> Feb 2027

Co-occurring genetic alterations with RAS mutations markedly increased the risk of malignancy compared with isolated RAS mutations (Fisher's exact test, two-tailed p = 0.0026) and were associated with more aggressive tumor phenotypes, whereas isolated RAS mutations were more common in indolent neoplasms. Comprehensive molecular profiling is essential for accurate risk stratification and management of indeterminate thyroid nodules.

P2, N=35, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Dec 2025 --> Jan 2027

While the therapeutic associations are based on a limited cohort and require prospective validation, the integration of comprehensive genomic and single-cell profiling provides an exploratory framework that may potentially enhance diagnostic accuracy in the future. However, these associations remain preliminary and require prospective validation to confirm their clinical utility.

BRAFV600E mutation was the most common alteration observed in gangliogliomas, whereas mutations in other genes, such as FGFR1, H3K27M, KRAS, IDH1, and RAF1, were rare.

Both the breast and lung tumor exhibited the HRAS G13R mutation, which is frequently observed in M-AME. This mutation may be considered a driver mutation in mammary M-AME.

Finally, we examined target DMGs expression in relation to immune checkpoint proteins (ICPs) to identify potential therapeutic targets. THCA specimens with suppressed BRAF expression demonstrated upregulated ICPs expression, indicating potential susceptibility to checkpoint blockade immunotherapy.

P1, N=91, Recruiting, Adlai Nortye Biopharma Co., Ltd. | Not yet recruiting --> Recruiting

Farnesyltransferase (FTase) inhibitors (FTIs), such as tipifarnib, inhibit HRAS membrane localization and blunt RAS effector signaling, leading to an antitumor effect in HRAS-mutant FN-RMS preclinical models...Co-targeting FTase and MEK restrained tumor progression and induced terminal myogenic differentiation. These findings highlight an effective combinatorial strategy and support its preclinical translation for patients with HRAS-mutant RMS.

P1/2, N=370, Recruiting, Revolution Medicines, Inc.

This is similar to well-differentiated NETs of other organs, in particular the small intestine and lung. Overall, our findings support the grouped classification of MeNET within the larger NET scheme.