RAS mutation

Collectively, these results indicated that Casticin suppresses and sensitizes non-small-cell lung cancer cells to EGFR-TKIs. Casticin may serve as a sensitizing agent by targeting SMYD2 to improve the efficacy of EGFR-TKIs.

Following the development of resistance, all patients received platinum-based doublet chemotherapy plus immunotherapy; in the second-line setting, median PFS was modestly longer in the co-mutation groups compared with the single-mutation group (EGFR/TP53: 5.2 months; EGFR/KRAS: 5.0 months; EGFR single mutation: 3.9 months; overall log-rank P < 0.0001), with no significant difference between the TP53 and KRAS subgroups (P = 0.174). These associations were evident on Kaplan-Meier curves (with numbers at risk) and log-rank testing, and were supported by multivariable Cox models adjusted for age, sex, smoking history, clinical stage, histology, and ECOG performance status.

dMMR/MSI-H mCRC is an entity with different tumor biology. We consider that dMMR/MSI-H mCRC patients with BRAF wild, MCS and subsequent IO have better outcomes with 1st line 5FU-based treatment with anti-VEGF/anti-EGFRs.

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.

In this cohort, BRAF -mutant AML patients had poor overall survival with currently available treatments, including venetoclax-based regimens...Single-cell multiomic profiling revealed unique co-mutation patterns and immunophenotypes that highlight RAS pathway addiction and nominate BRAF -mutated disease as a distinct subtype within RAS pathway-aberrated leukemias. Drug sensitivity screens suggest broad CDK or HSP90 inhibition in addition to BRAF/RAS-directed inhibition may be effective targeted therapies in this prognostically poor AML subtype.

WT1 overexpression and KIT mutations (in selected cytogenetic contexts) are validated as adverse prognostic indicators in pediatric AML. Conversely, FLT3-ITD and CEBPA mutations require nuanced interpretation due to variable effects and methodological heterogeneity. These findings support the integration of molecular profiling into pediatric AML risk stratification and underscore the need for harmonized, prospective studies to refine prognostic models in this population.

Risk prediction of chemotherapy-associated VTE is a compelling challenge in oncology, as VTE may result in treatment delays, impaired quality of life, and increased mortality. Patients with a single type of metastatic cancer with a high risk of VTE will be selected for study inclusion. For the first time in ambulatory prophylaxis of cancer-associated thrombosis, a precision medicine approach will be used in a clinical trial. If the individualization of antithrombotic prophylaxis can reduce the complications of outpatient cancer treatment and be cost effective, it would be of great value in the future care of patients with metastatic CRC.

This retrospective study included 287 RAS-mutant mCRC patients, all of whom received at least three cycles of chemotherapy combined with bevacizumab...NHHR may serve as a potential prognostic biomarker in patients with RAS-mutant metastatic colorectal cancer. Its putative role in promoting tumor progression through modulation of chronic inflammation warrants further investigation.

Preoperative ctDNA is prognostic for early recurrence and overall survival after local liver treatment in patients with initially unresectable CRLM and KRAS/NRAS/BRAF mutated primary tumors. Further research should determine how to incorporate this parameter into clinical risk scores and therapy management.

Our data suggest that MSI/dMMR CRCs harboring RASmut are less immunogenic and TiME contains a lower inflammatory profile than wild-type or BRAFV600E tumors. Further analysis and validation are required to confirm these findings.

In conclusion, liquid biopsy was a feasible and valuable method for detecting RAS and BRAF mutations in patients with mCRC, offering a less invasive alternative to traditional tissue biopsy in real-world settings. The trial registration number is 2015-A01272-47/NCT02751177 (registered March 3, 2016).

Besides, we identified potential drugs and evaluated the drug sensitivity for GC. In brief, our investigation identified distinct RAS-related subtypes in GC, offering a novel perspective on the disease's underlying prognostic factors and supporting the progression of personalized therapeutic strategies aimed at improving outcomes in GC patients.