PTEN mutation

In the CAPItello-291 trial, capivasertib and fulvestrant demonstrated efficacy in patients with up to two prior lines endocrine therapy, but its use in late-line settings has not yet been reported. In this article, we report a case of a woman with metastatic recurrent breast cancer who was treated with capivasertib and fulvestrant was used as the late-line treatment, resulting in a progression-free survival of 8 months.

P2, N=124, Recruiting, Alliance for Clinical Trials in Oncology | Trial primary completion date: Jan 2026 --> Jan 2027

The study particularly focuses on the combined use of immunotherapy (checkpoint inhibitors), chemotherapy (docetaxel), and androgen deprivation therapy (ADT), which are designed to break through the resistance-generating mechanisms and increase clinical efficacy...The current discussion also investigates the emerging areas of focus and perfection of combination regimens. The combination of all these developments makes it clear that the PI3K/AKT/mTOR signalling pathway is a key strategic point for developing therapeutics.

ESCAT tiers I-III alterations were reported in 79 % YA with MBC which supports the role of molecular profiling in YA. The differences detected in the genomic profiles of YA with BC and older patients may allude to potential different underlying disease biology.

In 20 % of breast cancer patients with LM, genetic alterations in the CSF were discordant from the primary tumor and/or systemic metastases. These genetic alterations involved in particular the PTEN-PI3K-AKT pathway in TN breast cancer. No ESR1 mutation limited to CSF only was found in HR+/HER2-breast cancer. Divergence of genetic alterations in LM from breast cancer must be considered for optimization of future target treatment strategy.

Here, we review the molecular pathogenesis, clinical features, histologic spectrum, and diagnostic strategies associated with familial follicular cell-derived thyroid tumors caused by DICER1 and PTEN germline alterations. Increased awareness of these entities by pathologists and clinicians is critical to ensure timely diagnosis, risk-appropriate surveillance, and cascade testing in affected families.

TAS-117 at the RP2D of 16 mg o.d. was tolerable, with a manageable safety profile. Clinical benefit, although durable, was only observed in a single patient with a germline PTEN mutation.

Clinical-radiomics ML models based on PSMA PET imaging show promising accuracy in predicting actionable genomic alterations in mPCa. These findings support further investigation into radiogenomics modelling as a complementary, non-invasive tool to inform molecular profiling and treatment stratification.

Despite the implementation of multimodal treatment involving surgery, radiotherapy, and chemotherapy with temozolomide, the average survival time of patients is only about 15 months...Despite these advancements, GBM remains a major therapeutic challenge due to its high heterogeneity and treatment resistance. The integration of molecular diagnostics, artificial intelligence, and personalized therapeutic strategies that may enhance survival and quality of life for GBM patients.

The analysis of material obtained from the biological fluids of oncology patients enabled disease prognosis, risk assessment of progression, and the determination of optimal approaches to personalised therapy, ultimately improving treatment efficacy. The collected data may serve as a foundation for clinically valuable laboratory studies and practical research.

While mechanistic target of rapamycin complex 1 (mTORC1) inhibitors show limited efficacy as single agents in EC, previous studies suggest that they may sensitize the PAM-mutant cancer cells to ferroptosis, a regulated form of necrosis dependent on iron-catalyzed lipid peroxidation...In vivo, combination treatment with RMC-6272 and the GPX4 inhibitor JKE-1674 significantly suppressed xenograft growth, with evidence of both ferroptosis and apoptosis in tumors. Our study highlights the therapeutic potential of dual targeting of mTORC1 and ferroptosis to trigger multi-modal cell death in PAM pathway-activated EC, with broader implications for other cancers exhibiting mTORC1 hyperactivation.

Overall, our findings highlight recurrent somatic ACTB mutations in more than half of sporadic TABs. CS-associated TABs but not sporadic TABs showed loss of PTEN expression. The presence of bilateral and/or multiple TABs should prompt PTEN IHC to rule out the possibility of CS.