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BIOMARKER:

PIK3CA overexpression

i
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:
9ms
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
1year
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
1year
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
over1year
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
over1year
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)
over1year
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
over1year
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)
|
PIK3CA mutation • AKT1 overexpression • PIK3CA expression • PIK3CA overexpression
almost2years
An in vitro carcinogenesis model for cervical cancer harboring episomal form of HPV16. (PubMed, PLoS One)
Thus an in vitro model for progression of cervical neoplasia with episomal HPV16 was established. In the model, constitutively active mutation of PIK3CA, PIK3CAE545K, and overexpression of MYC, in the cells with episomal HPV16 genome were not sufficient, but an additional event such as activation of the RAS-MEK pathway was required for progression to tumorigenicity.
Preclinical • Journal
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KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • MAP2K1 (Mitogen-activated protein kinase kinase 1)
|
PIK3CA mutation • PIK3CA E545K • MYC overexpression • KRAS G12 • MYC expression • PIK3CA E545 • PIK3CA expression • PIK3CA overexpression
almost2years
Anwuligan inhibits the progression of non-small cell lung cancer via let-7c-3p/PI3K/AKT/mTOR axis. (PubMed, Cancer Med)
In summary, ANW inhibits the growth and metastasis of NSCLC cells in vivo and in vitro by upregulating the expression of let-7c-3p, which can regulate the PI3K/AKT/mTOR signaling pathway. PIK3CA is the main target of let-7c-3p.
Journal
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • Let-7c (MicroRNA Let-7c)
|
Let-7c overexpression • PIK3CA overexpression
2years
Multiomics Profiling Characterizes Distinct HER2-low Breast Cancer Subgroups in the East Asian Population (SABCS 2022)
We reported the largest single-center multiomics HER2-low BC cohort in East Asian hitherto, and revealed its molecular nature, internal heterogeneity and ethnic difference. Compared with HR- positive diseases, HER2-low BCs in the HR-negative subgroup were more likely to be a molecularly distinct entity from HER2-0 tumors. Furthermore, HR-negative HER2-low BC also accommodates higher internal heterogeneity, which was ethnicity-specific in our East Asian cohort and may infer a different treatment response.
Clinical • BRCA Biomarker
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HER-2 (Human epidermal growth factor receptor 2) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • BRCA1 (Breast cancer 1, early onset) • AR (Androgen receptor) • NF1 (Neurofibromin 1) • FGFR4 (Fibroblast growth factor receptor 4) • PTK6 (Protein Tyrosine Kinase 6)
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HER-2 positive • HR positive • HER-2 negative • PIK3CA mutation • HER-2 expression • FGFR4 overexpression • PIK3CA expression • PIK3CA overexpression
over2years
Depleting receptor tyrosine kinases EGFR and HER2 overcomes resistance to EGFR inhibitors in colorectal cancer. (PubMed, J Exp Clin Cancer Res)
Our study shows that CRC resistance to EGFR inhibitors results primarily from the inability of the inhibitors to downregulate their target and that a PEPD-based combination treatment overcomes the resistance.
Journal
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HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • ADAM17 (ADAM Metallopeptidase Domain 17) • ADAM10 (ADAM Metallopeptidase Domain 10)
|
KRAS mutation • EGFR mutation • BRAF mutation • PIK3CA mutation • HER-2 mutation • EGFR overexpression • PIK3CA expression • PIK3CA overexpression • KRAS expression
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Erbitux (cetuximab) • 5-fluorouracil • Vectibix (panitumumab) • aderbasib (INCB7839)
over2years
Potential genetic biomarker of Saudi Arabian patients with colorectal cancer. (PubMed, Eur Rev Med Pharmacol Sci)
As well as, lower expression of MLH1, MSH2, MSH6, PMS2, EPCAM and MUTYH genes were recognized in LS patients and future CRC Saudi patients. These gene mutations may be used as diagnostic and/or prognostic genetic markers in CRC Saudi patients and could offer a potential therapeutic target for CRC management.
Review • Journal • PARP Biomarker
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog) • NOTCH1 (Notch 1) • MLH1 (MutL homolog 1) • MSH6 (MutS homolog 6) • ABCB1 (ATP Binding Cassette Subfamily B Member 1) • MSH2 (MutS Homolog 2) • CRLF2 (Cytokine Receptor Like Factor 2) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • FBXW7 (F-Box And WD Repeat Domain Containing 7) • TNFA (Tumor Necrosis Factor-Alpha) • PMS2 (PMS1 protein homolog 2) • CHEK2 (Checkpoint kinase 2) • NOTCH3 (Notch Receptor 3) • ABCC1 (ATP Binding Cassette Subfamily C Member 1) • PARP1 (Poly(ADP-Ribose) Polymerase 1) • CHEK1 (Checkpoint kinase 1) • EPCAM (Epithelial cell adhesion molecule) • MALAT1 (Metastasis associated lung adenocarcinoma transcript 1) • MMP2 (Matrix metallopeptidase 2) • NOTCH4 (Notch 4) • MIR34A (MicroRNA 34a-5p) • TLR9 (Toll Like Receptor 9) • BMI1 (BMI1 proto-oncogene, polycomb ring finger) • MUTYH (MutY homolog) • TLR4 (Toll Like Receptor 4) • FOXM1 (Forkhead Box M1) • IL17A (Interleukin 17A) • MIR182 (MicroRNA 182) • TSLP (Thymic Stromal Lymphopoietin) • XRCC1 (X-Ray Repair Cross Complementing 1) • CYP1A1 (Cytochrome P450 Family 1 Subfamily A Member 1) • MIR29A (MicroRNA 29a)
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NOTCH3 mutation • PIK3CA expression • EPCAM expression • PIK3CA overexpression • MSH6 expression
over2years
A phase 1/2 trial to evaluate the safety and antitumor activity of tipifarnib and alpelisib for patients with PIK3CA-mutated/amplified and/or HRAS-overexpressing recurrent/metastatic head and neck squamous cell carcinoma. (ASCO 2022)
All observed/available data among each cohort will be evaluated before choosing the combination dose for a subsequent cohort. Enrollment into the PIK3CA cohort began in October 2021.
Clinical • P1/2 data
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KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • HRAS (Harvey rat sarcoma viral oncogene homolog)
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PIK3CA mutation • HRAS mutation • HRAS overexpression • PIK3CA overexpression
|
Piqray (alpelisib) • Zarnestra (tipifarnib)
over2years
Targeting the lncRNA DUXAP8/miR-29a/PIK3CA Network Restores Doxorubicin Chemosensitivity via PI3K-AKT-mTOR Signaling and Synergizes With Inotuzumab Ozogamicin in Chemotherapy-Resistant B-Cell Acute Lymphoblastic Leukemia. (PubMed, Front Oncol)
Targeting lncRNA DUXAP8/miR-29a/PIK3CA network synergized with inotuzumab ozogamicin's effect on N6/ADR and 697/ADR cells. Targeting the lncRNA DUXAP8/miR-29a/PIK3CA network not only induced an apoptotic effect on Dox-resistant B-ALL and restored Dox chemosensitivity via PI3K-AKT-mTOR signaling but also showed synergism with inotuzumab ozogamicin treatment.
Journal
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MIR29A (MicroRNA 29a)
|
PIK3CA expression • PIK3CA overexpression
|
doxorubicin hydrochloride • Besponsa (inotuzumab ozogamicin)
over2years
A Phase 1/2 trial to evaluate the safety and antitumor activity of tipifarnib and alpelisib for patients with HRAS-overexpressing and/or PIK3CA-mutated/amplified recurrent/metastatic head and neck squamous cell carcinoma (The KURRENT trial) (AACR 2022)
All observed/available data among each cohort will be evaluated before choosing the combination dose for a subsequent cohort. The trial opened for enrollment in October 2021.
Clinical • P1/2 data
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KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • HRAS (Harvey rat sarcoma viral oncogene homolog)
|
PIK3CA mutation • RAS wild-type • PIK3CA amplification • HRAS mutation • PIK3CA overexpression • HRAS wild-type
|
Piqray (alpelisib) • Zarnestra (tipifarnib)
almost3years
Personalizing first-line treatment in advanced colorectal cancer: Present status and future perspectives. (PubMed, J Clin Transl Res)
Therapies at present approved or under investigation in clinical trials will be thoroughly reviewed, with special emphasis on the molecular rationale behind them. Understanding the molecular status, resistance mechanisms and potential new druggable targets may allow physicians to choose the best therapeutic option in the first-line mCRC.
Clinical • Review • Journal • MSi-H Biomarker • IO biomarker
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HER-2 (Human epidermal growth factor receptor 2) • 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) • HGF (Hepatocyte growth factor)
|
KRAS mutation • MSI-H/dMMR • HER-2 overexpression • BRAF mutation • HER-2 amplification • NRAS mutation • PIK3CA amplification • PIK3CA overexpression
3years
Single cell transcriptomic analysis reveals the effects of BRCA1 and BRCA2 mutations on distinct signaling networks and cancer susceptibility (SABCS 2021)
Our studies provide a high resolution transcriptome atlas of breast epithelial cells of BRCA1 and BRCA2 mutation carriers, which also reveal potentially targetable signaling networks uniquely deregulated in these cells. BRCA2 mutations are associated with distinct susceptibility to PIK3CA mutation-driven transformation. Since PIK3CA mutations are observed in clinically normal breast tissues, screening for such mutations in BRCA2 mutation carriers may help to detect pre-neoplastic or early stage breast cancer.
BRCA Biomarker
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • TERT (Telomerase Reverse Transcriptase) • MYCN (MYCN Proto-Oncogene BHLH Transcription Factor) • IL6 (Interleukin 6) • SMARCA4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4) • YAP1 (Yes associated protein 1) • BRD4 (Bromodomain Containing 4) • FOXO3 (Forkhead box O3)
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BRCA2 mutation • BRCA1 mutation • PIK3CA mutation • PIK3CA H1047R • BRCA1 mutation + BRCA2 mutation • HRAS G12V • PIK3CA overexpression
3years
Qing-Kai-Ling Injection Acts Better Than Shen-Fu Injection in Enhancing the Antitumor Effect of Gefitinib in Resistant Non-Small Cell Lung Cancer Models. (PubMed, Evid Based Complement Alternat Med)
QKL and TRQ, with cooling-heat TCM treatment principle, should be combined with gefitinib in the treatment of NSCLC. Furthermore, warming-yang drug SF should be avoided to be used together with EGFR-TKIs.
Preclinical • Journal
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • AKT1 (V-akt murine thymoma viral oncogene homolog 1)
|
EGFR mutation • PIK3CA mutation • EGFR H1975 • PIK3CA overexpression
|
gefitinib
over3years
Identification and Validation of PIK3CA as a Marker Associated with Prognosis and Immune Infiltration in Renal Clear Cell Carcinoma. (PubMed, J Oncol)
The therapeutic strategies for advanced KIRC are very few, with only sunitinib being widely approved...We identified PIK3CA as a potential biomarker for prognosis correlated with immune infiltrates in KIRC. Further studies should focus on the functions of PIK3CA in KIRC carcinogenesis.
Journal
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
|
PIK3CA mutation • PIK3CA expression • PIK3CA overexpression
|
sunitinib
over3years
Integrative Bioinformatics Study of Tangeretin Potential Targets for Preventing Metastatic Breast Cancer. (PubMed, Evid Based Complement Alternat Med)
Tangeretin inhibits metastasis in breast cancer cells by targeting TP53, PTGS2, MMP9, and PIK3CA and regulating the PI3K/Akt signaling pathway. Further investigation is needed to validate the results of this study.
Journal
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • NOTCH1 (Notch 1) • mTOR (Mechanistic target of rapamycin kinase) • PTGS2 (Prostaglandin-Endoperoxide Synthase 2) • MMP9 (Matrix metallopeptidase 9) • RELA (RELA Proto-Oncogene)
|
TP53 expression • PTGS2 expression • PIK3CA overexpression
over3years
[VIRTUAL] Radiosensitization of PIK3CA wild type triple negative breast cancers with Bcl-family inhibition (AACR 2021)
Single-agent response to pan Bcl-2 family inhibition (ABT-263) or Bcl-xL inhibition (WEHI-539, A-1331852) was more effective in PIK3CA wild type (wt) TNBC (IC50 < 1µM) compared to PIK3CA mutant TNBC...Radiosensitization was observed to be Bcl-xL-dependent, with Bcl-xL inhibitor-specific radiosensitization (rER: 1.12-2.38) but a lack of Bcl-2 inhibitor (ABT-199, rER: 0.94 - 1.21) or MCL-1 inhibitor-mediated radiosensitization (S63845, rER: 0.91 - 1.06)... In this study, we demonstrated that inhibition of Bcl-2 family proteins in combination with RT led to increased levels of apoptosis and cell death in PIK3CA/PTEN wt - but not PIK3CA/PTEN mutant - TNBC and we identified MCL-1 as a critical mediator of this radiosensitIvity. Together, these results indicate that Bcl-xL inhibition may be a feasible clinical strategy for the radiosensitization of PIK3CA/PTEN wild-type TNBC.
PARP Biomarker • IO biomarker
|
PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog) • BCL2L1 (BCL2-like 1)
|
PIK3CA mutation • PTEN expression • MCL1 expression • PIK3CA expression • PIK3CA overexpression
|
Venclexta (venetoclax) • navitoclax (ABT 263) • S63845 • A-1331852
over3years
[VIRTUAL] Possible molecular backgrounds underlying different efficacy of palbociclib over several HNSCC cell lines and TW2.6(betel-nuts related HNSCC cell line) response to different CDK inhibitors for future combination strategies (AACR 2021)
Palbociclib could reverse afatinib, docetaxel, & radiation resistance...CDK7/8/9/12/13 are involved in RNA polymerase II function with RNA elongation pause/release, transcription & onco-histones control, and SWI/SNF superfamily with epigenetic modifications. HNSCC cell lines(SCC4, SCC9, SCC15, SCC25, FaDu, KB, Cal27, SAS, and TW2.6, betel-nuts related) were tested in (1)in vitro sensitivity to CDK inhibitors; (2)synergistic effect of AZD4573(CDK9 inhibitor) with other therapies by MTT assay, colony formation, flow cytometry, & western blotting; (3) NGS studies to elucidate molecular mechanisms. Palbociclib response correlated to CCND1 gain & CDKN2A deletion; but FaDu had poor response with both and TW2.6 had good response without both... CCND1 gain & CDKN2A deletion could not fully predict CDK4/6 inhibitor response. TW2.6 is responsive to CDK4/6 inhibitors(palbociclib>ribociclib>abemaciclib). FAT1 loss, CCND3 amplification, PI3K/AKT/mTOR derangements, & FGFR amplification might imply CDK4/6 inhibitor resistance.
Preclinical • PARP Biomarker • PD(L)-1 Biomarker • IO biomarker
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TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • PTEN (Phosphatase and tensin homolog) • STK11 (Serine/threonine kinase 11) • HRAS (Harvey rat sarcoma viral oncogene homolog) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • AXL (AXL Receptor Tyrosine Kinase) • CCND1 (Cyclin D1) • CDK12 (Cyclin dependent kinase 12) • FAT1 (FAT atypical cadherin 1) • ARID1B (AT-Rich Interaction Domain 1B) • PARP1 (Poly(ADP-Ribose) Polymerase 1) • TNFAIP3 (TNF Alpha Induced Protein 3) • CCND3 (Cyclin D3) • SOX9 (SRY-Box Transcription Factor 9) • BRD4 (Bromodomain Containing 4) • CDK7 (Cyclin Dependent Kinase 7) • DDR2 (Discoidin domain receptor 2) • FGF10 (Fibroblast Growth Factor 10)
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TP53 mutation • TMB-H • PIK3CA mutation • PTEN deletion • PIK3CA H1047R • STK11 mutation • CDKN2A deletion • BCL2 overexpression • CDK12 mutation • EZH2 mutation • HRAS mutation • CDK4 amplification • FAT1 mutation • STK11 deletion • AKT1 amplification • FGF10 amplification • PIK3CA overexpression
|
Gilotrif (afatinib) • Ibrance (palbociclib) • docetaxel • Verzenio (abemaciclib) • Kisqali (ribociclib) • AZD4573
almost4years
Screening for PIK3CA mutations among Saudi women with ovarian cancer. (PubMed, J Obstet Gynaecol)
The Mutated PIK3CA gene was significantly involved in the pathogenesis of EOC among Saudi women. PIK3CA gene mutation and overexpression represent important clinical implications for diagnosis, and prognosis, which can be utilised for better EOC management.
Clinical • Journal
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
|
PIK3CA mutation • PIK3CA overexpression
almost4years
Overexpression of PIK3CA impacts global survival of patients with HER2 subtype breast carcinoma. (PubMed, J BUON)
The PIK3CA expression showed a protective effect in relation to the OS of patients with HER2-positive breast cancer.
Clinical • Journal
|
HER-2 (Human epidermal growth factor receptor 2) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog)
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HER-2 positive • PTEN expression • PIK3CA expression • PIK3CA overexpression • PTEN loss
almost4years
Chemosensitization of HT29 and HT29-5FU Cell Lines by a Combination of a Multi-Tyrosine Kinase Inhibitor and 5FU Downregulates ABCC1 and Inhibits PIK3CA in Light of Their Importance in Saudi Colorectal Cancer. (PubMed, Molecules)
We have combined the PamChip kinase profiling of Saudi CRC samples with in vitro drug combination studies in four CRC cells, highlighting the importance of targeting PIK3CA and ABCC1 for Saudi CRC patients, especially given that the overexpression of PIK3CA mutations was previously linked with the lack of activity for the anti-EGFRs as first line treatment for CRC patients. The combination of HAA and 5FU has selectively sensitized the four CRC cells to 5FU and could be further studied.
Journal
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KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • ABCC1 (ATP Binding Cassette Subfamily C Member 1) • CASP8 (Caspase 8) • CDKN1A (Cyclin-dependent kinase inhibitor 1A)
|
KRAS mutation • PIK3CA mutation • PIK3CA overexpression
|
LY294002
almost4years
Divergent molecular profile of PIK3CA gene in arsenic-associated bladder carcinoma. (PubMed, Mutagenesis)
Finally, AsH patients with the overexpression of PIK3CA or NFκB had the worst overall survival, signifying a strong impact of arsenic on this pathway and outcome of the patients. Thus, our study showed that the arsenic-associated differential molecular profile of PIK3CA/AKT1/NFkB in BlCa has an important role in the molecular pathogenesis of the disease.
Journal
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • NFKB1 (Nuclear factor of kappa light polypeptide gene enhancer in B-cells 1)
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PIK3CA mutation • PIK3CA E545K • PIK3CA E545 • PIK3CA E542 • PIK3CA exon 9 mutation + HR positive • PIK3CA overexpression
almost4years
In-silico prediction of potential inhibitors against phosphatidylinositol 3-kinase catalytic subunit alpha involved in head and neck squamous cell carcinomas. (PubMed, J Biomol Struct Dyn)
The only FDA approved specific inhibitor of p110α is Alpelisib (BYL719)...This study provides a significant in-depth understanding of p110α inhibitors that can be used in the development of potential therapeutics against HNSCC. Communicated by Ramaswamy H. Sarma.
Journal
|
PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
|
PIK3CA mutation • PIK3CA overexpression
|
Piqray (alpelisib)
almost4years
PIK3CA Is Regulated by CUX1, Promotes Cell Growth and Metastasis in Bladder Cancer via Activating Epithelial-Mesenchymal Transition. (PubMed, Front Oncol)
Besides, over-expressed CUX1 could restore the expression of downregulated Snail, β-catenin, Vimentin and E-cadherin which was induced by PIK3CA knockdown. These results revealed that PIK3CA overexpression in bladder cancer was regulated by the transcription factor CUX1, and PIK3CA exerted its biological effects by activating EMT.
Journal
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • CDH1 (Cadherin 1) • CUX1 (cut like homeobox 1) • VIM (Vimentin)
|
CDH1 expression • PIK3CA expression • VIM expression • PIK3CA overexpression
almost4years
The Safe Soluble Compound Dehydroascorbic Acid Inhibits Various Upstream and Downstream Effectors of PI3K and KRAS Signaling Pathways in Undruggable PIK3CA/KRAS-Mutant Colorectal Cancer Stem-Like Cells. (PubMed, Nutr Cancer)
CXCR4, stemness marker genes and metabolic activity appear to be promising targets of L-DHA. Our results may provide a new therapeutic approach to target selectively GLUT-overexpressing PIK3CA/KRAS-mutant CRCSCs using L-DHA with no toxicity on normal cells.
Journal
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KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • CXCR4 (Chemokine (C-X-C motif) receptor 4) • CASP3 (Caspase 3) • POU5F1 (POU Class 5 Homeobox 1) • BMI1 (BMI1 proto-oncogene, polycomb ring finger)
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KRAS mutation • PIK3CA mutation • KRAS overexpression • PIK3CA overexpression
almost4years
TP53, SPOP and PIK3CA Genes Status in Prostate Cancer. (PubMed, Asian Pac J Cancer Prev)
PIK3CA gene overexpression was detected in 6% of the cohort by RT-PCR. TP53 mutation is the most frequent genetic alteration and likely has a major role in the pathogenesis of PC in the Jordanian population..
Journal
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TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
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TP53 mutation • PIK3CA mutation • TP53 expression • PIK3CA overexpression
4years
miR‑10a increases the cisplatin resistance of lung adenocarcinoma circulating tumor cells via targeting PIK3CA in the PI3K/Akt pathway. (PubMed, Oncol Rep)
PIK3CA overexpression attenuated the cisplatin resistance of A549 and H1299 cells induced by miR‑10a. In conclusion, miR‑10a suppressed the PI3K/Akt pathway to strengthen the resistance of CTCs to cisplatin via targeting PIK3CA, providing a new therapeutic target for lung cancer treatment.
Journal • Circulating Tumor Cells
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
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PIK3CA expression • PIK3CA overexpression
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cisplatin
4years
DNA Methylation and Genetic Aberrations in Gastric Cancer. (PubMed, Digestion)
Comprehensive DNA methylation analyses revealed multiple DNA methylation patterns in GCs and classified GC into distinct molecular subgroups: extremely high-methylation epigenotype uniquely observed in GC associated with Epstein-Barr virus (EBV), high-methylation epigenotype associated with microsatellite instability (MSI), and low-methylation epigenotype. In The Cancer Genome Atlas classification, EBV and MSI are extracted as independent subgroups of GC, whereas the remaining GCs are categorized into genomically stable (GS) and chromosomal instability (CIN) subgroups. EBV-positive GC, exhibiting the most extreme DNA hypermethylation in the whole human malignancies, frequently shows CDKN2A silencing, PIK3CA mutations, PD-L1/2 overexpression, and lack of TP53 mutations. MSI, exhibiting high DNA methylation, often has MLH1 silencing and abundant gene mutations. GS is generally a diffuse-type GC and frequently shows CDH1/RHOA mutations or CLDN18-ARHGAP fusion. CIN is generally an intestinal-type GC and frequently has TP53 mutations and genomic amplification of receptor tyrosine kinases. Key Messages: The frequency and targets of genetic aberrations vary depending on the epigenotype. Aberrations in the genome and epigenome are expected to synergistically interact and contribute to gastric carcinogenesis and comprehensive analyses of those in GCs may help elucidate the mechanism of carcinogenesis.
Review • Journal • PD(L)-1 Biomarker
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PD-L1 (Programmed death ligand 1) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MSI (Microsatellite instability) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • MLH1 (MutL homolog 1) • CDH1 (Cadherin 1)
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TP53 mutation • PD-L1 overexpression • PIK3CA mutation • TP53 expression • CDH1 mutation • PIK3CA overexpression • PD-L1 mutation
4years
Clinical Significance of PIK3CA Gene in Non-Small-Cell Lung Cancer: A Systematic Review and Meta-Analysis. (PubMed, Biomed Res Int)
PIK3CA mutation may affect lymph node metastasis and serve as a promising prognostic factor, and smoking may be related with PIK3CA high expression in NSCLC patients. However, more well-designed prospective researches are needed to verify the abovementioned findings.
Retrospective data • Review • Journal
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
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PIK3CA mutation • PIK3CA expression • PIK3CA overexpression
over4years
Actionable co-alterations in breast tumors with pathogenic mutations in the homologous recombination DNA damage repair pathway. (PubMed, Breast Cancer Res Treat)
HR-MT was common across breast cancer subtypes and co-occurred more frequently with markers of response to immunotherapy (MSI-H/dMMR, TMB) compared to HR-WT tumors. Mutations were identified in both HR-MT and HR-WT tumors that suggest other targets for treatment. Clinical trials combining HRD-targeted agents and immunotherapy are underway and could be enriched through comprehensive molecular profiling.
Journal • BRCA Biomarker • MSi-H Biomarker • PARP Biomarker • PD(L)-1 Biomarker
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HER-2 (Human epidermal growth factor receptor 2) • PD-L1 (Programmed death ligand 1) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • MSI (Microsatellite instability) • ATM (ATM serine/threonine kinase) • ARID1A (AT-rich interaction domain 1A) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • BAP1 (BRCA1 Associated Protein 1) • PALB2 (Partner and localizer of BRCA2) • KMT2D (Lysine Methyltransferase 2D) • ATRX (ATRX Chromatin Remodeler) • FANCA (FA Complementation Group A) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • RAD50 (RAD50 Double Strand Break Repair Protein) • CHEK1 (Checkpoint kinase 1) • BARD1 (BRCA1 Associated RING Domain 1) • MRE11A (MRE11 homolog, double strand break repair nuclease) • WRN (WRN RecQ Like Helicase)
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BRCA1 mutation • MSI-H/dMMR • PD-L1 overexpression • PIK3CA mutation • ATM mutation • ARID1A mutation • BAP1 mutation • ATRX mutation • AR overexpression • BRIP1 mutation • FANCA mutation • RAD50 mutation • BARD1 mutation • BLM mutation • CHEK1 mutation • NBN mutation • PIK3CA overexpression • CHEK1 expression
over4years
[VIRTUAL] Genomic and transcriptomic profiling in head and neck tumours to identify treatment options: The WINTHER trial experience (ESMO 2020)
P=N/A | "Morgan Private Bank Clinical Oncology Research Grant, the National Cancer Institute grant P30 P30-CA023100 (R.K.), the Israeli Science Foundation grant 1188/16 (E.R.), Instituto Salud Carlos III—Programa Rio Hortega Contract grant CM15/00255 (I.B.), the Canadian Institutes for Health Research (grant MOP-142281 to W.H.M.) and the Canadian Cancer Society (grant 703811 to W.H.M.). Clinical trial identification: NCT01856296."
PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • FGFR2 (Fibroblast growth factor receptor 2) • FGFR1 (Fibroblast growth factor receptor 1)
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FGFR2 amplification • FGFR1 overexpression • PIK3CA amplification • FGFR2 overexpression • FGFR1 expression • PIK3CA expression • PIK3CA overexpression
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FoundationOne® CDx
over4years
LINC00152 promotes hepatocellular carcinoma progression by regulating PI3k/Akt/mTOR signaling pathway through miR-139/PIK3CA. (PubMed, Am J Pathol)
Similarly, PIK3CA overexpressing plasmid also reversed miR-139-mediated biological functions in HCC cells. Taken together, our study revealed a crucial regulatory network of LINC00152/miR-139/PIK3CA axis in the tumorigenesis of HCC, implying that LINC00152 may be a biomarker and novel therapeutic target for further clinical therapy of HCC.
Journal
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MIR139 (MicroRNA 139)
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PIK3CA overexpression
over4years
ETV5 overexpression contributes to tumor growth and progression of thyroid cancer through PIK3CA. (PubMed, Life Sci)
ETV5 enhanced cell proliferation, migration, and epithelial-mesenchymal transition through the PIK3CA signaling pathway, indicating that ETV5 may be a therapeutic target in thyroid cancer.
Journal
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ER (Estrogen receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • ETV5 (ETS Variant Transcription Factor 5)
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PIK3CA overexpression