PIK3C2B (Phosphatidylinositol-4-Phosphate 3-Kinase Catalytic Subunit Type 2 Beta)

Our findings establish PIK3C2B as a dual-function oncoprotein that promotes lung cancer progression through EMT activation and bioenergetic reprogramming. Its prognostic significance and role in metabolic adaptability highlight PIK3C2B as a promising therapeutic target for disrupting metastasis and enhancing tumor resilience.

The ancillary testing of SMARCB1 (INI-1) should be considered in a subset of patients whose tumor demonstrates bizarre cytomorphology, especially in poorly differentiated or markedly pleomorphic tumors. The cytological recognition is critical for appropriate management.

Dysregulation of class II PI3Ks has been implicated in diverse pathological conditions, including cancer, metabolic disorders, epilepsy, congenital myopathies, vascular dysfunction, and premature aging. These findings establish a framework for understanding how localized phosphoinositide synthesis contributes to cellular homeostasis and disease, and underscore the therapeutic potential of selectively targeting class II PI3K isoforms.

These findings suggest that METTL1-WDR4 might serve as a potential diagnostic and prognostic biomarker and a therapeutic target for GC treatment by regulating m7G level.

Lastly, rapamycin treatment reduced migration and invasion of PI3KC2β KO tumor cells in vitro and their lung metastasis in vivo, supporting an important role of mTORC1 pathway. Together, our results identify PI3KC2β as a suppressor for HER2+ breast cancer metastasis by negatively regulating mTORC1 signalling by affecting its complex formation with ITSN1 and raptor. Implications: Our findings revealed PI3KC2β as a new metastasis suppressor for HER2+ breast cancer, which might serve as a potential diagnostic and therapeutic target for the disease.

P1, N=12, Recruiting, Nader Sanai | Trial completion date: Apr 2026 --> May 2028 | Trial primary completion date: Apr 2025 --> May 2026

The identified blood-based candidate susceptibility genes provide further insights into the genetic basis of PCa risk.

In summary, ENTs arising from GCTs are molecularly heterogeneous; however, a large fraction of testicular ENTs could be stratified by two distinct sets of genetic alterations, including MYCN/MYC amplification with concurrent suppression of the p53 pathway, and activation of the PI3K pathway with co-occurring CDK4 amplification. Moreover, the novel gene fusions identified in a subset of testicular GCT-derived ENTs overlap with molecularly defined tumors of embryonic-type neuroectodermal features in the central nervous system, indicating the potential common driving events for tumorigenesis from different anatomic sites.

Genetic alterations significantly influencing progression-free survival concerned PIK3C2B, ARID1B genes, and concomitant mutations in KMT2B, FAT1, and ARID1B. The findings underscore the potential of gene mutation-based prognostic tools in enhancing clinical decision-making and suggest that further exploration of identified genetic markers could pave the way for improved prognostic stratification and targeted therapeutic interventions in multiple myeloma.

Although PI(3,4)P2 is undetectable in normal mouse or human tissues and common cell lines, it appears in a mouse prostate cancer model and in cells exposed to oxidative stress, indicating that PI(3,4)P2 is involved in the pathogenesis of some diseases. Here, I summarize recent findings on the cellular roles and pathophysiological significance of PI(3,4)P2.

PVL and HL present differential methylation patterns that could be linked to their differential clinical behavior. Our findings show the potential of methylation markers and suggest novel diagnostic biomarkers.

P1, N=12, Recruiting, Nader Sanai | Trial completion date: Apr 2025 --> Apr 2026 | Trial primary completion date: Apr 2024 --> Apr 2025