PTEN
PTEN is the brake on the PI3K growth pathway; when a tumour loses it the pathway runs unchecked, which is why PTEN loss now selects patients for the AKT inhibitor capivasertib.
Overview
PTEN is a lipid phosphatase that converts PIP3 back to PIP2, opposing PI3K and switching off AKT signalling. Loss through deletion, mutation or promoter silencing is common in prostate, endometrial, breast and brain tumours and in Cowden syndrome when inherited. Capivasertib's labels name PTEN alterations (with PIK3CA and AKT1) in breast cancer and PTEN deficiency by immunohistochemistry in prostate cancer, so the readout pages under this target carry both the sequencing and the IHC rules.
- Target · the protein and the cell it sits on
- Drug · antibody, small molecule, cell or radioligand
- Effect · signal, damage or kill
In plain words · PTEN is the brake on the PI3K growth pathway; when a tumour loses it the pathway runs unchecked, which is why PTEN loss now selects patients for the AKT inhibitor capivasertib.
- 1 · What it is
PTEN is the brake on the PI3K growth pathway; when a tumour loses it the pathway runs unchecked, which is why PTEN loss now selects patients for the AKT inhibitor capivasertib.
- 2 · What goes wrong in cancer
PTEN loss raises PIP3 and constitutively activates AKT and mTOR; it also has nuclear roles in genome stability, so PTEN-null tumours accumulate further damage.
- 3 · How drugs use it
No product in this corpus aims at PTEN yet. Because the protein is lost rather than overactive, drugs either restore its function or exploit the weakness its loss leaves (synthetic lethality).
External identifiers
What a pathology or genomic report can say about this target, each with the thresholds approvals use.
Biology
PTEN loss raises PIP3 and constitutively activates AKT and mTOR; it also has nuclear roles in genome stability, so PTEN-null tumours accumulate further damage.
- Prostate cancer (loss in about 40 percent of metastatic disease)
- Endometrial cancer
- Glioblastoma
- Breast cancer (PI3K pathway alterations)
Latest papers
topQuery for this target: (TITLE:"PTEN" OR ABSTRACT:"PTEN" OR TITLE:"phosphatase and tensin homolog" OR ABSTRACT:"phosphatase and tensin homolog" OR TITLE:"MMAC1" OR ABSTRACT:"MMAC1" OR TITLE:"TEP1" OR ABSTRACT:"TEP1") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about PTEN, not a curated reading list.
Similar pages
not linked directly; found by shared links- TargetHistone H3.3 (H3-3A)
Shares CIViC, IntOGen, Open Targets Platform and the tag biomarker-parent.
- TargetMYCN (N-myc)
Shares CIViC, IntOGen, Open Targets Platform and the tag biomarker-parent.
- TargetMGMT (O6-methylguanine-DNA methyltransferase)
Shares Glioma & glioblastoma, CIViC and the tag biomarker-parent.
- TargetKi-67 (MKI67)
Shares CIViC, HR-positive / HER2-negative breast cancer and the tag biomarker-parent.
- TargetMismatch repair proteins (MLH1, MSH2, MSH6, PMS2)
Shares Endometrial cancer and the tag biomarker-parent.
- BiomarkerAKT1 E17K mutation
Shares PTEN alteration (sequencing) and PTEN loss (IHC), Capivasertib, Endometrial cancer, HR-positive / HER2-negative breast cancer.
- BiomarkerPIK3CA mutation
Shares PTEN alteration (sequencing) and PTEN loss (IHC), Capivasertib, Endometrial cancer, HR-positive / HER2-negative breast cancer.
- TrialCAPItello-281
Shares Capivasertib, Metastatic hormone-sensitive prostate cancer.