NRAS (Neuroblastoma RAS viral oncogene homolog)

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.

Clinically, one patient succumbed to disease one month and another patient experienced a recurrence at 43 months, whereas the remaining patients had no evidence of disease at 3-24 months of follow-up. MLA displays unique cytomorphologic features and accurate identification of MLA on cytology should prompt confirmatory tests to exclude potential morphologic mimics and ensure appropriate diagnosis.

Subsequently, multiple hepatic metastases and pelvic dissemination developed, and conventional chemotherapy including bevacizumab was ineffective...Switching to sorafenib led to further progression, but reintroduction of LVB reduced Tg levels...The patient has survived seven years since recurrence, including six years on LVB. The tumor behaved similarly to poorly differentiated thyroid carcinoma, with Tg levels reflecting disease activity and LVB demonstrating the potential for long-term tumor control.

This study identifies NCOA5 and CHD4 as crucial proviral cofactors and NRAS as a potent antiviral factor regulating HBV replication. The findings highlight HBV's profound host dependence, uncover specific molecular mechanisms (involving HNF4A, epigenetic regulation of cccDNA, and cell cycle), and reveal validated host targets for potential therapeutic strategies against HBV infection.

P2, N=34, Active, not recruiting, University of Wisconsin, Madison | Recruiting --> Active, not recruiting | N=71 --> 34 | Trial completion date: Oct 2033 --> Oct 2029 | Trial primary completion date: Oct 2033 --> Oct 2029

Mucosal and vulvovaginal melanomas are biologically and clinically distinct from cutaneous melanoma and continue to have poor survival outcomes. Their rarity restricts high-quality evidence, highlighting the need for collaborative, innovative research to inform effective treatment strategies.

This study delineated the genetic landscape of pAML in Southwest China and explored the prognostic value of gene fusions and mutations in early and long-term outcomes. These findings provide a foundation for understanding the genetic heterogeneity of pAML and offer evidence for the development of precision medicine approaches.

These data support RRAS Q87L and RRAS2 Q72L as bona fide lung cancer drivers and nominate RRAS/RRAS2-mutant tumors as candidates for pan-RAS-targeted therapeutics. Our findings provide a biologic rationale and preclinical evidence to inform molecular testing paradigms and to prioritize enrollment of patients with RRAS/RRAS2-mutant NSCLC into future clinical trials of pan-RAS inhibitors.

Here we show that the BET inhibitor PLX51107 potently suppresses the growth of NRAS -mutant AML cell lines, and that these activities are enhanced by co-treatment with the MEK inhibitor PD0325901. AMLs that relapsed after frontline chemotherapy showed similar transcriptional remodeling. These studies demonstrate transcriptional plasticity in primary AMLs that relapse following in vivo treatment with either targeted agents or chemotherapy, and support evaluating BET inhibition in leukemias with monocytic differentiation and RAS mutations.

Our findings underscore the clinical and genetic diversity of RASopathies in the Indian population and highlight the role of next-generation sequencing in early and accurate diagnosis. While exploratory drug-gene interaction analysis provides hypothesis-generating insights, clinical translation requires rigorous validation in functional studies and clinical trials.