PIK3CA mutation

In vitro experiments further demonstrated that ITGB2 knockdown led to inactivation of Akt and ERK signaling and suppression of cell aggressiveness in ER+/HER2- breast cancer cells. ITGB2 gain represents an unfavorable prognostic marker for early recurrence in luminal HER2-negative high proliferative breast cancer, with potential therapeutic implications.

Patients with metastatic HR+HER2- IBC demonstrated a shorter time on treatment suggesting shorter duration of response on CDKI + HT, which is markedly inferior to reported data for non-IBC patients from phase III trials.

We described the genomic landscape of KRASG12D-mutant CRC and PDAC, demonstrating that cases often have additional oncogenic alterations linked to resistance to KRAS inhibition. These alterations are also associated with a worse prognosis. Recognizing these alterations may inform new therapeutic strategies. Further studies are warranted to validate these findings in ongoing clinical trials.

Olaparib and temozolomide (OT) combination therapy is in clinical trial evaluation for rhabdomyosarcoma (RMS). The combination of OT + alpelisib also kills RMS cells which are resistant to standard-of-care combination chemotherapy and was effective in preclinical xenograft mouse models at curbing tumor growth. Our work defines a common resistance pathway in RMS and has credentialled PIK3CA/AKT inhibition as a preclinical strategy to kill therapy resistant RMS.

Thus, we characterize a pattern of large genomic events that had remained hidden by the insensitivity of the molecular and analytical methods previously used. Finally, we propose that similar events may be found in other vascular malformations or PIK3CA overgrowth syndromes that have yet to be analyzed in this manner.

Histopathological evaluation may aid risk stratification alongside KRAS status. Prognostic assessment in clinical settings should take both TNM staging and KRAS status into account.

Our findings reveal that SUMOylation subtypes in breast cancer exhibit distinct prognostic, immunological and pharmacogenomic profiles. These insights may provide candidate biomarkers for future personalized treatment strategies for breast cancer and potentially for other malignancies.

POLE mutations, especially non-EDMs, are frequent in MSI-L CRC and often co-occur with MLH3, MSH3, KRAS, PIK3CA, and BRAF, highlighting their potential role in tumor biology and as biomarkers for personalized treatment. Functional validation and multicenter studies are needed.

Early postoperative persistent ctDNA positivity (especially TP53 mutation) combined with Lauren diffuse-type classification and serosal invasion can effectively identify patients at high risk of peritoneal metastasis. This integrated model provides a new strategy for precise postoperative surveillance and intervention in advanced gastric cancer.

Consistent with this, bioinformatics analysis demonstrated that miR-124-3p expression is significantly lower in tumor tissues than in adjacent normal lung and further decreases in advanced T stage (T3-T4) compared to early stage (T1-T2). These findings indicate that miR-124-3p inhibits NSCLC progression via the ITGB1/PI3K/p-AKT axis and remains functional despite PIK3CA activation, supporting its potential as a therapeutic candidate.

These findings indicate that metformin synergistically enhances the antitumor activity of alpelisib in HER2-positive breast cancer by inhibiting oncogenic signaling and stemness pathways. Beyond its metabolic benefit in mitigating hyperglycemia, metformin may potentiate PI3K-targeted therapies, supporting further preclinical and clinical evaluation of this combination strategy.

P2, N=7, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Aug 2025 --> Feb 2027