TP53 mutation

Notably, MAP2K1 E102-I103 deletion was frequently observed in pre-invasive samples, which endowed alveolar type II cells with increased growth potential and initiated tumor formation, suggesting that it is a potential driver mutation of LUAD. In summary, our study highlights key molecular changes during the stepwise progression of LUAD, provides insights into the identification of novel therapeutic targets, and helps to define the curative time window for this disease.

Our results indicate that integrated morpho-molecular FIGO 2023 staging significantly impacts both stage and risk group stratification, and will benefit EC patients, particularly in high-grade early stage ECs, with potential treatment implications. Further comprehensive studies are needed to fully establish the implications of molecular classification in the FIGO 2023 staging system.

OS was additionally negatively affected when the ten genes were unmutated. Notably, outcomes were excellent for SAR mutations (2-year LFS 76%, OS 84%), indicating allo-HCT in CR1 can overcome their adverse risk at diagnosis.

Trastuzumab-based therapy has shown survival benefit in HER2-positive SEC, leading to its inclusion in current treatment guidelines...The prognostic value remains debated, though recent trials of antibody-drug conjugates (e.g., T-DXd) show promise...Diagnostic challenges include variable scoring systems, intratumoral heterogeneity, and HER2-low classification. Standardization of testing criteria and further clinical validation of HER2-targeted strategies across gynecologic tumors are essential to guide personalized therapy and improve outcomes.

P2, N=490, Recruiting, Merck Sharp & Dohme LLC | Trial completion date: Mar 2027 --> Jan 2029 | Trial primary completion date: Mar 2027 --> Jan 2029

Endometrial carcinomas with SB-GN represent a distinct and aggressive tumor group characterized by solid growth pattern, prominent necrosis, frequent basaloid morphology, high rates of CTNNB1 mutations, and aberrant β-catenin staining. Our results demonstrate that endometrial carcinomas with SB-GN and PiMHECs share similar clinicopathologic and molecular profiles, supporting a unified biological spectrum.

These proof-of-concept results support the utility of integrating intrasubject dynamics, "biological knowledge"-based feature reduction (pathway-level feature reduction grounded in prior biological knowledge; eg, N-of-1-pathway analytics), and reproducible MLOp workflows can overcome cohort size limitations in infrequent disease, offering a scalable, interpretable solution for high-dimensional transcriptomic classification. Future work will extend these advances across various therapeutic and small cohort designs.

After induction therapy with the lenalidomide-dexamethasone (RD) regimen, ASCT is performed and partial remission is achieved. The pathogenesis of secondary MDS in POEMS syndrome is discussed from three aspects: cytotoxic therapy, genetic predisposition, and SARS-CoV-2 infection. This case underscores the importance of prolonged surveillance for secondary myeloid neoplasms (sMN) in POEMS patients and suggests that early genomic profiling and individualized treatment may improve outcomes.

CD5+ diffuse large B-cell lymphoma (DLBCL) is aggressive, and Rituximab-Cyclophosphamide Hydroxydaunorubicin Vincristine Prednisone (R-CHOP) combined with radiotherapy is recommended, but prognosis is affected by age, Lactate Dehydrogenase (LDH) levels, and molecular characteristics such as TP53 mutations. Radiotherapy and chemotherapy are the first choice for treatment. It is very important to formulate a reasonable treatment plan according to the results of pathology and molecular analysis.

ECs with MECOM amplification are associated with poor clinical outcomes, even in the absence of CCNE1 or ERBB2 amplification. The current literature is limited, and further studies are warranted to determine the role of MECOM amplification in ECs.

Emerging therapeutic strategies targeting redox-sensitive nodes, including GPX4 degraders, mitophagy inducers (urolithin A) and chronotherapy, have the potential to overcome resistance. By elucidating the crosstalk between mitochondrial quality control and ferroptotic signaling, the present review provides a mechanistic framework for precision oncology in EC, emphasizing subtype-specific vulnerabilities and spatiotemporal redox profiling.

A TRGs-based prognostic model effectively predicts survival in EC and reveals associations with somatic mutations, immune infiltration, and drug sensitivity. Functional validation of PTGES3 further supports its potential as a therapeutic target.