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BIOMARKER:

PIK3CA overexpression

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Other names: PIK3CA, Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha, Phosphoinositide-3-kinase, catalytic, alpha polypeptide, Serine/threonine protein kinase PIK3CA, PtdIns-3-kinase subunit P110-alpha, PI3K-alpha, Phosphatidylinositol-4,5-bisphosphate 3-kinase 110 KDa catalytic subunit alpha, Phosphatidylinositol 3-kinase, Catalytic, 110-KD, alpha, PI3-kinase P110 subunit alpha, PI3-kinase subunit alpha, PtdIns-3-kinase subunit alpha, PI3Kalpha, P110alpha, PI3K
Entrez ID:
Related biomarkers:
11ms
Potential Contribution of Epithelial Growth Factor Receptor to PI3K/AKT Pathway Dysregulation in Canine Soft Tissue Sarcoma. (PubMed, In Vivo)
EGFR over-expression, rather than PTEN loss or PIK3CA mutations, may contribute to PI3K/AKT pathway dysregulation in canine STS. Further studies with larger sample sizes and additional validation techniques are necessary to confirm these findings.
Journal
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EGFR (Epidermal growth factor receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog)
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EGFR mutation • PIK3CA mutation • EGFR expression • PTEN expression • EGFR positive • EGFR mutation + PIK3CA mutation • PIK3CA expression • PIK3CA overexpression
12ms
MiR-592 Attenuates Tamoxifen Resistance in Breast Cancer Through PIK3CA-Mediated PI3K/AKT/mTOR Signaling Pathway. (PubMed, Appl Biochem Biotechnol)
PIK3CA overexpression partially reversed these reductions. In conclusion, our study demonstrates that miR-592 attenuates TAM resistance by inhibiting the PIK3CA-driven PI3K/AKT/mTOR signaling pathway, representing a promising strategy to address chemoresistance in BC.
Journal
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • CDH1 (Cadherin 1) • CASP3 (Caspase 3)
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CDH1 expression • PIK3CA expression • PIK3CA overexpression
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tamoxifen
1year
Use of 3' Rapid Amplification of cDNA Ends (3' RACE)-Based Targeted RNA Sequencing for Profiling of Druggable Genetic Alterations in Urothelial Carcinomas. (PubMed, Int J Mol Sci)
Overall, more than half of the UCs had potentially druggable genetic alterations. The proposed NGS panel permits comprehensive and cost-efficient analysis of UC-specific molecular targets and may be considered in clinical routine.
Journal • PD(L)-1 Biomarker • IO biomarker
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HER-2 (Human epidermal growth factor receptor 2) • PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • NRAS (Neuroblastoma RAS viral oncogene homolog) • MSI (Microsatellite instability) • FGFR2 (Fibroblast growth factor receptor 2) • FGFR3 (Fibroblast growth factor receptor 3) • FGFR1 (Fibroblast growth factor receptor 1)
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PD-L1 expression • HER-2 overexpression • BRAF mutation • PIK3CA mutation • HER-2 expression • FGFR2 mutation • FGFR2 fusion • FGFR2 amplification • RAS mutation • PIK3CA overexpression
1year
miR-29a Downregulates PIK3CA Expression and Inhibits Cervical Cancer Cell Dynamics: A Comparative Clinical Analysis. (PubMed, Curr Issues Mol Biol)
These findings indicate that miR-29a can slow the progression of cervical cancer by targeting PIK3CA and potentially aid in its treatment. miR-29a shows promise as a therapeutic agent for inhibiting oncogene expression and controlling cervical cancer progression, especially in advanced-stage cases.
Journal
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MIR29A (MicroRNA 29a)
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PIK3CA expression • PIK3CA overexpression
1year
Vertical inhibition of p110α/AKT and N-cadherin enhances treatment efficacy in PIK3CA-aberrated ovarian cancer cells. (PubMed, Mol Oncol)
Importantly, co-targeting N-cadherin and p110α/AKT caused additive reduction in cell migration in vitro and metastases formation in vivo. Together, this study reveals the molecular pathways driven by the PIK3CA aberrations and the exploitable vulnerabilities in PIK3CA-aberrated serous ovarian cancer cells.
Journal
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • YAP1 (Yes associated protein 1) • RAC1 (Rac Family Small GTPase 1) • CDH2 (Cadherin 2) • MAPK3 (Mitogen-Activated Protein Kinase 3)
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PIK3CA mutation • PIK3CA E545K • PIK3CA amplification • PIK3CA E545 • PIK3CA expression • AKT1 amplification • PIK3CA overexpression
almost2years
Targeting MEK/COX-2 axis improve immunotherapy efficacy in dMMR colorectal cancer with PIK3CA overexpression. (PubMed, Cell Oncol (Dordr))
Our results identified that the PIK3CA hyperactivation in dMMR CRC upregulated COX-2 through MEK signaling, which inhibited CD8+ T cells infiltration and promoted tumor growth, together led to immunotherapy resistance. COX-2 or MEK inhibition may relieve therapy resistance and promote therapy efficacy of anti-PD-1/PD-L1 immunotherapy for treating dMMR CRC with PIK3CA overexpression or activating mutation.
Journal • PD(L)-1 Biomarker • IO biomarker
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • CD8 (cluster of differentiation 8) • MLH1 (MutL homolog 1) • PTGS2 (Prostaglandin-Endoperoxide Synthase 2)
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MSI-H/dMMR • PIK3CA mutation • CD8 expression • PIK3CA expression • PTGS2 expression • PIK3CA overexpression
2years
Matched multi-analyte and multi-omic liquid biopsy of cell-free DNA, circulating tumor cells and extracellular vesicles in HER2-positive metastatic breast cancer patients (SABCS 2023)
We successfully established a workflow for parallel isolation of multiple liquid biopsy analytes from a minimized blood volume in HER2+ mBC. Preliminary mRNA profile results for CTCs and EVs show the complementary nature of these two liquid biopsy analytes. Besides the multi-analyte nature of this workflow, the pending results for genomic and epigenomic information will show which one of the analytes, alone or in combination, will help to optimize therapy management in HER2+ mBC patients.
Clinical • Circulating tumor cells • Liquid biopsy • PARP Biomarker • Circulating tumor DNA • Tumor cell • Metastases • Biopsy • Cell-free DNA
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3) • mTOR (Mechanistic target of rapamycin kinase) • ERCC1 (Excision repair cross-complementation group 1) • PARP1 (Poly(ADP-Ribose) Polymerase 1) • PTPRC (Protein Tyrosine Phosphatase Receptor Type C) • AURKA (Aurora kinase A) • EPCAM (Epithelial cell adhesion molecule) • AKT2 (V-akt murine thymoma viral oncogene homolog 2)
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HER-2 positive • HR positive • HER-2 negative • PIK3CA expression • PIK3CA overexpression • PTEN mutation + HR positive
2years
THE EFFECT OF TCGA MOLECULAR TYPING AND IMMUNOHISTOCHEMICAL MARKERS ON THE PROGNOSIS OF ENDOMETRIOD CARCINOMA WITH FERTILITY-SPARING TREATMENT (IGCS 2023)
There were 2 MSI-H subtypes、1 high copy-number subtype、 68 low copy-number subtypes and no POLE mutations. Univariate and multivariate logistic analysis showed those PTEN-positive、ER and PR high-expression were more likely to achieve 3-month CR (OR=24.811、P=0.034; OR=9.428、 P=0.025; OR=29.178、P=0.011). Univariate and multivariate COX regression analysis showed that patients with high-expression PIK3CA were more likely to recurrence (OR=12.750、P=0.017).
MSi-H Biomarker
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MSI (Microsatellite instability) • PTEN (Phosphatase and tensin homolog) • ARID1A (AT-rich interaction domain 1A) • POLE (DNA Polymerase Epsilon)
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MSI-H/dMMR • PTEN mutation • POLE mutation • PGR expression • PIK3CA overexpression • PTEN positive
over2years
Identification of PIK3CA mutation as a novel predictor of efficacious immunotherapy in head and neck cancer (ESMO 2023)
Survival analysis shows PIK3CA-Mut have a good link with longer OS after immunotherapy. These findings indicate that PIK3CA mutation may serve as a potential predictive biomarker for ICIs in HNSC.
Tumor mutational burden • IO biomarker
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • CD8 (cluster of differentiation 8) • CD4 (CD4 Molecule)
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TMB-H • PIK3CA mutation • MTOR mutation • PIK3CA overexpression
over2years
Targeted treatment in a case series of AR+, HRAS/PIK3CA co-mutated salivary duct carcinoma. (PubMed, Front Oncol)
One patient each was treated with immune checkpoint inhibition (Mixed Response) and combination therapies of tipifarnib and ADT (SD) and alpelisib and ADT (PR). Combination therapies, PI3K-inhibitors and immune therapy warrant further investigation, ideally in clinical trials. Future research should consider this rare subgroup of SDC.
Journal • Tumor mutational burden • PD(L)-1 Biomarker • IO biomarker
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PD-L1 (Programmed death ligand 1) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • AR (Androgen receptor) • HRAS (Harvey rat sarcoma viral oncogene homolog)
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PD-L1 expression • PIK3CA mutation • HRAS mutation • AR overexpression • AR expression • PIK3CA expression • HRAS overexpression • PIK3CA overexpression
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Piqray (alpelisib) • Zarnestra (tipifarnib)
over2years
The adaptor protein VEPH1 interacts with the kinase domain of ERBB2 and impacts EGF signaling in ovarian cancer cells. (PubMed, Cell Signal)
Importantly, we found that loss of VEPH1 expression rendered ES2 cells less sensitive to BRAF and MEK inhibition. This study extends the range of adaptor function of VEPH1 to ERBB2, and indicates VEPH1 has differential effects on EGF signaling in ovarian cancer cells that may be influenced by driver gene mutations.
Journal
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HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • CDH1 (Cadherin 1) • EGF (Epidermal growth factor) • CDH2 (Cadherin 2) • SNAI2 (Snail Family Transcriptional Repressor 2)
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KRAS mutation • HER-2 overexpression • BRAF mutation • HER-2 amplification • PIK3CA mutation • HER-2 expression • PIK3CA expression • PIK3CA overexpression
over2years
KAT7 promotes radioresistance through upregulating PI3K/AKT signaling in breast cancer. (PubMed, J Radiat Res)
Moreover, overexpression of KAT7, but not KAT7 acetyltransferase activity-deficient mutants promoted AKT phosphorylation at the Ser473 site, PIK3CA expression and radioresistance suppression due to KAT7 inhibition. In conclusion, KAT7 has huge prospects for clinical application as a new target for predicting radioresistance in breast cancer patients.
Journal
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • AKT1 (V-akt murine thymoma viral oncogene homolog 1)
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PIK3CA mutation • AKT1 overexpression • PIK3CA expression • PIK3CA overexpression