NRAS (Neuroblastoma RAS viral oncogene homolog)

Our findings indicate that while relapse after allo-HCT in AML is genetically diverse, timing of recurrence remains the most critical determinant of outcome. Given that certain genetic changes may inform therapeutic options, these findings highlight the relevance of longitudinal molecular monitoring especially during the early post-transplant period.

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.

After a median follow-up of 33.5 months, 36% of patients developed distant metastases, and 2 patients died of disease 8 and 32 months, respectively, after initial diagnosis. These findings expand the molecular diversity of DPN-like melanomas and provide valuable insights into their clinical outcomes.

The discovery that the non-selective beta-blocker propranolol induces rapid regression of proliferating IHs established the first widely adopted systemic pharmacologic therapy in vascular anomaly care and provided a clinical proof-of-concept that targeting lesion-specific endothelial biology can alter disease course. In parallel, recurrent somatic variants affecting PI3K/AKT/mTOR (e.g., PIK3CA, TEK/TIE2, AKT1) and RAS/MAPK (e.g., KRAS, NRAS) signalling have reframed many malformations as mosaic disorders amenable to targeted inhibition with agents such as sirolimus, alpelisib, AKT inhibitors and MEK inhibitors. This review synthesizes translational mechanisms, clinical evidence and safety considerations for beta-blockers and emerging targeted therapies, emphasizing lesion phenotype, timing of intervention and molecular stratification as determinants of response. We highlight current limitations, including toxicity, durability and pathway escape, and outline future directions for precision therapy and genotype-guided trial design in vascular anomalies.

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.

Differences between canonical encoders were modest relative to task-specific variability. GOLDMARK establishes a shared experimental substrate for computational pathology, enabling reproducible benchmarking and direct comparison of methods across datasets and models.

This study identified tumor genomic alterations associated with clinical outcomes in melanoma patients treated with neoadjuvant ipilimumab, suggesting their potential role in anti-tumor immunity. These findings warrant further investigation in larger cohorts and across other ICIs in melanoma and other malignancies.

This review explores the mutations and co-mutations most relevant to CRC, their prevalence, prognostic significance, and implications for precision oncology. By focusing on these genetic and epigenetic alterations, we aim to contextualize how biomarker-driven strategies are reshaping the management of CRC in both early and advanced disease settings.