TP53 mutation

The mOS of the EGFR-TP53 co-mutant group who received second-line TKIs combined with platinum-containing double-drug chemotherapy and bevacizumab after the progression of first-line single-drug TKIs was 27.0 months versus 6.0 months compared with those who did not receive second-line therapy (P = .019). In first-line EGFR-TKIs monotherapy in patients with EGFR-TP53 co-mutation, osimertinib was clearly superior to gefitinib. In first-line EGFR-TKIs monotherapy progression, TKIs combined with chemotherapy and antiangiogenesis therapy could prolong patients' survival.

The 4 signature genes showed abnormal expression in HCC tissues at multiple levels. This study identified 2 PRG subtypes and a robust 4-gene prognostic signature for HCC, which accurately predicts prognosis, reflects tumor immune microenvironment features, and guides precision therapy selection, highlighting PRGs' potential as HCC biomarkers and therapeutic targets.

Specific genomic alterations may help stratify immunotherapy outcomes in recurrent or metastatic cervical cancer. The proposed genomic risk model remains exploratory and requires validation in larger, independent cervical cancer cohorts.

Our findings highlight the potential of cisplatin-alpelisib treatment in a subset of HGSOC patients with PIK3CA overexpression, mediated either through gene amplification or transcriptional modulation, reflecting the wider application of alpelisib in PIK3CA-non-mutated ovarian cancer.

RNA-triggered chromatin shredding may offer a new way to attack cancers driven by mutations that have resisted conventional drugs, two new studies show. In mouse models, upon activation by a target transcript, the CRISPR enzyme Cas12a2 can selectively eliminate tumor cells carrying mutations in TP53, MYC, and other hard-to-drug cancer genes.

Our data show that TP53 isoforms are dysregulated in B-ALL at diagnosis as well as at relapse. Short TP53 isoforms, particularly Δ133p53 is associated with better prognosis suggesting its potential role in refining risk stratification of B-ALL.

Cases harboring biallelic TET2 inactivation or TET2+SRSF2 co-mutation show the highest bone marrow monocyte burden, frequent classical monocyte (MO1; CD14+/CD16-) elevation, and highest progression risk representing biologically true OM-CMML, whereas SF3B1-mutated and biallelic TP53 mutated cases show MDS-directed biology and warrant reclassification. This review synthesizes current diagnostic frameworks, molecular heterogeneity, risk stratification approaches, and evolving classification proposals, thereby providing a practical guide for pathologists navigating OM-CMML in the modern genomic era.

This refinement operates at the cellular level without displacing the tissue-level Correa sequence documented in long-term human cohorts. It nominates the remodelled stem-cell niche as a tractable pharmacological target and warrants molecular profiling of at-risk progenitor populations to complement, rather than replace, histopathological surveillance.

Inactivation of the pRB/p16 pathway is common, with 2/3 showing pRB loss. They present as advanced tumors and behave aggressively.

Using clinical samples, we show that the DNAe panel with analysis using DNAe's pipeline detects mutations comparably to the commercial Oncomine-Assay. This paves the way for development of the DNAe panel into a test for the LiDia-SEQ platform.

These findings demonstrate that mTORi with everolimus reverses multiple mechanisms of immune resistance in TP53 -mutant HNSCC by promoting immune cell recruitment, suppressing immunosuppressive pathways, and enhancing anti-tumor T cell activity. Collectively, these results support mTORi as a mechanistically rational strategy for reprogramming immune resistance in TP53 -mutant HNSCC and provide a strong preclinical rationale for combining everolimus with immune therapy in patients who are likely to fail immunotherapy.