ARID1A mutation

This case highlights the diagnostic challenges of PPCCC and offers valuable insights into the clinical and pathological spectrum of this underrecognized malignancy.

The interpretable DeepSurv model, integrating multimodal features, enables quantitative survival prediction and risk stratification in advanced NSCLC, facilitating personalized decision-making.

P1, N=34, Not yet recruiting, University of California, Irvine | Initiation date: Nov 2025 --> Apr 2026

P1/2, N=254, Recruiting, Haihe Biopharma Co., Ltd. | Trial completion date: Dec 2025 --> Dec 2028 | Trial primary completion date: Dec 2025 --> Dec 2027

P1, N=161, Active, not recruiting, EMD Serono Research & Development Institute, Inc. | Trial completion date: Jan 2026 --> Jan 2027 | Trial primary completion date: Jan 2026 --> Jan 2027

P2, N=18, Not yet recruiting, Harbin Medical University Affiliated Cancer Hospital; Harbin Medical University Affiliated Cancer Hospital

Our data highlights mutational variation across demographic cohorts. These patterns are vital to future studies into identifying diagnostic markers or therapeutic targets.

This study validates the primary drivers of cervical adenocarcinoma and reveals novel findings, including notable racial disparities in TP53 mutation frequency and unique patterns of co-occurring mutations. These findings highlight the genomic heterogeneity of the disease and suggest that ancestry and tumor evolution may influence its molecular pathogenesis, offering potential avenues for the development of targeted therapies and personalized biomarkers.

Gene panel testing identified TMEM178B-BRAF fusion and subclonal PIK3CA mutations in the liver metastasis, in addition to ARID1A and CTNNB1 mutations that were shared with the endometrial tumour. This is the first report of an endometrioid carcinoma transforming into a high-grade neuroendocrine tumour associated with TMEM178B-BRAF fusion.

Here we show that combination of niraparib and lenvatinib exhibits significant synergistic inhibitory effects against platinum-resistant OCCC cell lines, xenografts, patient-derived tumoroid (PDT) models, and prolonged survival in the platinum-refractory patient-derived xenograft (PDX) model. RNA sequencing revealed that the most differentially expressed genes in PDX models treated with this combination were associated with structural ribosomal components. This combination suppresses Src phosphorylation, NPM1 expression, and ribosomal protein levels in OCCC.

These findings reveal criticalmolecular and prognostic differences between LCC and RCC and highlight SMAD4 and SETD2 asimportant prognostic biomarkers, suggesting the potential value of location-and mutation-guided precision therapies in CRC.

Together, these results highlight distinct tumorigenic mechanisms in HIV+ DLBCL and underscore the need for mutational profiling of HIV+ DLBCL cohorts worldwide to identify biomarkers and therapeutic targets.