NRAS mutation

P2, N=92, Beijing Cancer Hospital (Peking University Cancer Hospital); Beijing Cancer Hospital (Peking University Cancer Hospital)

Combined use of PRAME and H3K27me3 can be utilized to discriminate MM from PN arising in LCMN/GCMN if validated on larger cohorts.

The TP53 gene mutation plays a significant role in the pathogenesis of OKC and supports its neoplastic nature. Bilateral OKC showed additional NRAS mutation, and sporadic cases demonstrated MET and BRAF mutations.

We report the case of a patient with metastatic foot melanoma enrolled in a clinical trial of the anti-RAS agent RMC-6236 who developed chronic bilateral corneal epithelial defects and thinning, likely secondary to the systemic effects of targeted therapy. This case highlights the ocular surface toxicity associated with systemic anticancer therapies affecting rapidly dividing cells and the overall importance of multidisciplinary medical management of these systemic therapeutics.

cfDNA from fine-needle aspiration rinses provides a highly reliable and efficient substrate for molecular testing in metastatic melanoma, outperforming CB-based analysis in terms of sample adequacy. This approach preserves cellular material for ancillary studies and may reduce false-negative results. Prospective studies using broader next generation sequencing panels are warranted to confirm analytical robustness and clinical utility.

STAT3/STAT5 mutations are early, dominant, and potentially pathogenic events in plasma cell myeloma. Their association with adverse clinical features and inferior survival supports their routine assessment and potential therapeutic targeting.

The NRAS and CEBPA co-mutation defines a distinct molecular subtype with independently poor prognosis in AML. Routine NRAS mutation screening in patients with CEBPA-mutated AML is warranted to refine risk stratification, particularly for identifying this high-risk subgroup, which may benefit from more intensive or novel therapeutic approaches.

P1/2, N=24, Active, not recruiting, M.D. Anderson Cancer Center | Recruiting --> Active, not recruiting | N=44 --> 24

HG-PFP treatment inhibited NF1 mutant PDOs growth by reducing cells viability and impaired organoids formation and growth in NRAS mutant samples, while showing no effects in BRAF mutant samples. Taking together these findings provide a preclinical perspective on therapeutic potential of HG-PFP across different melanoma subtypes.

Genetic loss of KLF4 or AXL depletion reduced melanoma cell migration and invasion, suggesting a key role of KLF4 in the regulation of invasiveness. Our study describes a novel ERK5/KLF4/AXL signaling axis that drives MEKi resistance and metastatic potential in NRAS-mutant melanoma and highlights this axis as a potential target to improve MAPK-directed and potentially immune therapies.

In this study, targeted next-generation sequencing using the AmpliSeq for Illumina Cancer HotSpot Panel identified pathogenic mutations in canonical cancer driver genes: tumor protein p53 (TP53) NM_000546.6:c.730G>T (p.Gly244Cys) and platelet-derived growth factor receptor alpha (PDGFRA) NM_006206.6:c.2525A>T (p.Asp842Val) mutations in renal leiomyosarcoma and NRAS proto-oncogene, GTPase (NRAS) NM_002524.5:c.35G>T (p.Gly12Val) mutation in the ovarian tumor. These findings suggest a potential benefit of personalized therapies for XP patients with internal malignancies.

The patient received postoperative radiotherapy. At 6 months of follow-up, metastasis to the right inguinal lymph nodes was identified.