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BIOMARKER:

PIK3CA mutation + PTEN mutation + KRAS mutation

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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, PTEN, Phosphatase and tensin homolog, Mutated In Multiple Advanced Cancers 1, Phosphatase And Tensin Homolog, Phosphatidylinositol 3,4,5-Trisphosphate 3-Phosphatase And Dual-Specificity Protein Phosphatase PTEN, MMAC1, TEP1, MMAC1 Phosphatase And Tensin Homolog Deleted On Chromosome 10, Mitochondrial Phosphatase And Tensin Protein Alpha, Phosphatase And Tensin-Like Protein, Protein Tyrosine Phosphatase, Mitochondrial PTENalpha, PTENbeta, PTEN1, CWS1, GLM2, MHAM, KRAS, KRAS proto-oncogene GTPase, KRAS1, KRAS2, NS, NS3, OES, CFC2, RALD, K-Ras, RASK2, KI-RAS, C-K-RAS, K-RAS2A, K-RAS2B, K-RAS4A, K-RAS4B, K-Ras 2, C-K-RAS, c-Ki-ras, c-Ki-ras2, Kirsten rat sarcoma viral oncogene homolog
Entrez ID:
Related biomarkers:
5years
Somatic mutation profiling in BRCA-negative breast and ovarian cancer patients by multigene panel sequencing. (PubMed, Am J Cancer Res)
In contrast, somatic screening of BRCA mutations in BRCA-negative breast cancer patients has limited value. The results highlight the benefit of somatic testing to guide future research directions on other targeted therapies for breast and ovarian malignancies.
Clinical • Journal • BRCA Biomarker • PARP Biomarker
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • BRCA1 (Breast cancer 1, early onset) • PTEN (Phosphatase and tensin homolog) • RB1 (RB Transcriptional Corepressor 1) • BRCA (Breast cancer early onset)
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TP53 mutation • KRAS mutation • PIK3CA mutation • PTEN mutation • BRCA mutation • PIK3CA mutation + PTEN mutation + KRAS mutation
5years
[VIRTUAL] Study of Potential Mutations in the Genetic Profiles of Rectal Cancer Patients Before and After Neoadjuvant Chemoradiation (CAP 2020)
Our results show reduction in variant heterogeneity with treatment in both groups that was not statistically significant. We identified multiple genetic variations in tumor DNA from rectal cancer patients who are poor responders to neoadjuvant chemoradiation, compared to complete responders. Further investigation is warranted.
Clinical • BRCA Biomarker
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • ABL1 (ABL proto-oncogene 1) • BRCA2 (Breast cancer 2, early onset) • PTEN (Phosphatase and tensin homolog) • FGFR3 (Fibroblast growth factor receptor 3) • RB1 (RB Transcriptional Corepressor 1) • ARID1A (AT-rich interaction domain 1A) • GNAQ (G Protein Subunit Alpha Q) • KMT2D (Lysine Methyltransferase 2D) • MSH6 (MutS homolog 6) • FBXW7 (F-Box And WD Repeat Domain Containing 7) • PMS2 (PMS1 protein homolog 2) • CREBBP (CREB binding protein) • JAK1 (Janus Kinase 1) • KDM6A (Lysine Demethylase 6A) • EP300 (E1A binding protein p300)
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TP53 mutation • KRAS mutation • PIK3CA mutation • ATM mutation • PTEN mutation • ARID1A mutation • FGFR3 mutation • PMS2 mutation • PIK3CA mutation + PTEN mutation + KRAS mutation
5years
Blocking Y-Box Binding Protein-1 through Simultaneous Targeting of PI3K and MAPK in Triple Negative Breast Cancers. (PubMed, Cancers (Basel))
Our data obtained from the experiments, applying pharmacological inhibitors and genetic approaches, shows that YB-1 is a key player in cell proliferation, clonogenic activity, and tumor growth of TNBC cells through the MAPK and PI3K pathways. Therefore, dual inhibition of these two pathways or single targeting of YB-1 may be an effective strategy to treat TNBC.
Journal
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KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog) • YBX1 (Y-Box Binding Protein 1)
|
KRAS mutation • PIK3CA mutation • PIK3CA H1047R • KRAS G13D • KRAS G13 • PIK3CA mutation + PTEN mutation + KRAS mutation • PTEN loss
over5years
[VIRTUAL] KRAS mutations in NSCLC patients who never smoke: definition of a new patient subgroup (DGHO 2020)
Never-smoking NSCLC patients with KRAS mutations represent a subgroup with marked genetic and clinical differences to the well-known smoker-cohort. Further work in the light of new targeted therapy approaches in this patient group is warranted.
Clinical • PD(L)-1 Biomarker • IO biomarker
|
EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • FGFR2 (Fibroblast growth factor receptor 2) • PTEN (Phosphatase and tensin homolog) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • KEAP1 (Kelch Like ECH Associated Protein 1) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • DDR2 (Discoidin domain receptor 2)
|
PD-L1 expression • TP53 mutation • KRAS mutation • EGFR mutation • KRAS G12C • PIK3CA mutation • KRAS G12D • PTEN mutation • KRAS G12V • FGFR2 mutation • ALK mutation • KRAS G12 • KRAS G13 • EGFR mutation + KRAS mutation • KRAS Q61 • PIK3CA mutation + PTEN mutation + KRAS mutation
over5years
Clinical • Next-generation sequencing
|
HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • ER (Estrogen receptor) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • NRAS (Neuroblastoma RAS viral oncogene homolog) • PTEN (Phosphatase and tensin homolog) • HRAS (Harvey rat sarcoma viral oncogene homolog)
|
TP53 mutation • KRAS mutation • ER positive • HER-2 negative • PIK3CA mutation • PTEN mutation • ER mutation • HRAS mutation • PIK3CA mutation + ER positive • AR mutation • ER positive + HER-2 negative • PIK3CA mutation + HRAS mutation • PIK3CA mutation + PTEN mutation + KRAS mutation
over5years
Clinical • Next-generation sequencing
|
HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • ER (Estrogen receptor) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • NRAS (Neuroblastoma RAS viral oncogene homolog) • PTEN (Phosphatase and tensin homolog) • HRAS (Harvey rat sarcoma viral oncogene homolog)
|
TP53 mutation • KRAS mutation • ER positive • HER-2 negative • PIK3CA mutation • PTEN mutation • ER mutation • HRAS mutation • PIK3CA mutation + ER positive • AR mutation • ER positive + HER-2 negative • PIK3CA mutation + HRAS mutation • PIK3CA mutation + PTEN mutation + KRAS mutation
over5years
[VIRTUAL] KRAS mutations in NSCLC patients who never smoke: definition of a new patient subgroup (DGHO 2020)
Never-smoking NSCLC patients with KRAS mutations represent a subgroup with marked genetic and clinical differences to the well-known smoker-cohort. Further work in the light of new targeted therapy approaches in this patient group is warranted.
Clinical • PD(L)-1 Biomarker • IO biomarker
|
EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • FGFR2 (Fibroblast growth factor receptor 2) • PTEN (Phosphatase and tensin homolog) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • KEAP1 (Kelch Like ECH Associated Protein 1) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • DDR2 (Discoidin domain receptor 2)
|
PD-L1 expression • TP53 mutation • KRAS mutation • EGFR mutation • KRAS G12C • PIK3CA mutation • KRAS G12D • PTEN mutation • KRAS G12V • FGFR2 mutation • ALK mutation • KRAS G12 • KRAS G13 • EGFR mutation + KRAS mutation • KRAS Q61 • PIK3CA mutation + PTEN mutation + KRAS mutation
over5years
Clinical • Next-generation sequencing
|
HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • ER (Estrogen receptor) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • NRAS (Neuroblastoma RAS viral oncogene homolog) • PTEN (Phosphatase and tensin homolog) • HRAS (Harvey rat sarcoma viral oncogene homolog)
|
TP53 mutation • KRAS mutation • ER positive • HER-2 negative • PIK3CA mutation • PTEN mutation • ER mutation • HRAS mutation • PIK3CA mutation + ER positive • AR mutation • ER positive + HER-2 negative • PIK3CA mutation + HRAS mutation • PIK3CA mutation + PTEN mutation + KRAS mutation
over5years
Clinical • Next-generation sequencing
|
HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • ER (Estrogen receptor) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • NRAS (Neuroblastoma RAS viral oncogene homolog) • PTEN (Phosphatase and tensin homolog) • HRAS (Harvey rat sarcoma viral oncogene homolog)
|
TP53 mutation • KRAS mutation • ER positive • HER-2 negative • PIK3CA mutation • PTEN mutation • ER mutation • HRAS mutation • PIK3CA mutation + ER positive • AR mutation • ER positive + HER-2 negative • PIK3CA mutation + HRAS mutation • PIK3CA mutation + PTEN mutation + KRAS mutation
over5years
[VIRTUAL] KRAS mutations in NSCLC patients who never smoke: definition of a new patient subgroup (DGHO 2020)
Never-smoking NSCLC patients with KRAS mutations represent a subgroup with marked genetic and clinical differences to the well-known smoker-cohort. Further work in the light of new targeted therapy approaches in this patient group is warranted.
Clinical • PD(L)-1 Biomarker • IO biomarker
|
EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • FGFR2 (Fibroblast growth factor receptor 2) • PTEN (Phosphatase and tensin homolog) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • KEAP1 (Kelch Like ECH Associated Protein 1) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • DDR2 (Discoidin domain receptor 2)
|
PD-L1 expression • TP53 mutation • KRAS mutation • EGFR mutation • KRAS G12C • PIK3CA mutation • KRAS G12D • PTEN mutation • KRAS G12V • FGFR2 mutation • ALK mutation • KRAS G12 • KRAS G13 • EGFR mutation + KRAS mutation • KRAS Q61 • PIK3CA mutation + PTEN mutation + KRAS mutation
over5years
[VIRTUAL] KRAS mutations in NSCLC patients who never smoke: definition of a new patient subgroup (DGHO 2020)
Never-smoking NSCLC patients with KRAS mutations represent a subgroup with marked genetic and clinical differences to the well-known smoker-cohort. Further work in the light of new targeted therapy approaches in this patient group is warranted.
Clinical • PD(L)-1 Biomarker • IO biomarker
|
EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • FGFR2 (Fibroblast growth factor receptor 2) • PTEN (Phosphatase and tensin homolog) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • KEAP1 (Kelch Like ECH Associated Protein 1) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • DDR2 (Discoidin domain receptor 2)
|
PD-L1 expression • TP53 mutation • KRAS mutation • EGFR mutation • KRAS G12C • PIK3CA mutation • KRAS G12D • PTEN mutation • KRAS G12V • FGFR2 mutation • ALK mutation • KRAS G12 • KRAS G13 • EGFR mutation + KRAS mutation • KRAS Q61 • PIK3CA mutation + PTEN mutation + KRAS mutation
over5years
Influence of Concurrent Mutations on Overall Survival in EGFR-mutated Non-small Cell Lung Cancer. (PubMed, Cancer Genomics Proteomics)
Concurrent resistance mutations in genes other than EGFR influenced the outcome of patients with NSCLC, while non-resistance mutations did not alter survival, compared to the absence of co-mutations. This evidence highlights the importance of a careful interpretation of molecular findings. The best treatment options for these patients should be studied in randomized controlled trials.
Clinical • Journal
|
EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog)
|
KRAS mutation • EGFR mutation • PIK3CA mutation • PTEN mutation • EGFR mutation + KRAS mutation • PIK3CA mutation + PTEN mutation + KRAS mutation
|
Tagrisso (osimertinib)