TP53 mutation

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.

In this review, we summarize the biological roles of p53, examine how TP53 gene alterations drive therapeutic resistance in myeloid neoplasms, and compare contemporary classification frameworks, including their limitations and proposed refinements. We also highlight standard and emerging therapeutic strategies aimed specifically at TP53-mutated myeloid neoplasms.

While these emiPS cells remain transgene-dependent, we inactivated the transgenes and differentiated emiPS cells into all three germ layers via tri-lineage differentiation, embryoid body generation and direct differentiation into putative cell types from all three layers. These methods will open new frontiers for cellular models of nonmodel organisms, including for genetic rescue and conservation.

Single-nucleus RNA sequencing reveals intra-tumoral heterogeneity within this subtype, including divergent inflammatory states. Together, these findings establish a molecular classification framework and identify actionable vulnerabilities in PEComa.

In addition, high NCAPH expression was found to predict reduced 5-year overall survival and exhibited certain diagnostic efficacy (area under the curve=0.628). Overall, NCAPH may promote endometrial carcinogenesis through dysregulation of mitotic processes, induction of chromosomal instability as well as modulation of the tumor immune microenvironment and thus may serve as both a prognostic biomarker and a therapeutic target in EC.

ATAD2 suppresses cellular senescence and SASP phenotypes via the SIRT7-p53/p21 axis, promoting immune-suppressive TME and driving EC progression and immune evasion. ATAD2 represents a promising therapeutic target for EC.

This model provides a robust and interpretable tool for individualized risk stratification in elderly AML. By integrating genomic, immunophenotypic, and therapeutic variables, it may help optimize treatment decisions and improve outcomes for this vulnerable population. Future efforts should focus on external validation and integration of dynamic biomarkers.

The results confirm watch-and-wait as standard of care for early-stage CLL patients, especially in high-risk CLL characterized by del(17p) and/or mutated TP53. EudraCT Number: 2013-003211-22.

A diagnostic algorithm combining endometrial carcinoma molecular classification, SWI/SNF protein testing, and thorough sampling is proposed. This study expands the clinicopathological and molecular spectrum of SMARCA4-deficient uterine tumours, underscoring the need for entity-specific management strategies.

Although TP53 mutations are associated with poor prognosis in patients treated with chemotherapy, their adverse prognostic impact appears to be attenuated in the context of CAR-T cell therapy. These findings suggest that CAR-T therapy may partially mitigate the negative impact of TP53 alterations.