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Phosphatase and tensin homolog (PTEN) is a phosphatase in humans and is encoded by the PTEN gene. [6] Mutations of this gene are a step in the development of many cancers , specifically glioblastoma, lung cancer, breast cancer, and prostate cancer.
Printable version; In other projects ... Antileukemic drugs, anticancer drugs that are used to treat one or more types of leukemia, include: [1] 6-Mercaptopurine;
Treatment of people aged twelve years of age and older with solid tumors that: have a neurotrophic tyrosine receptor kinase (NTRK) gene fusion, are locally advanced or metastatic or where surgical resection is likely to result in severe morbidity, and have progressed following treatment or have no satisfactory alternative therapy [2] Resmetirom
The genetics of the Bannayan–Riley–Ruvalcaba syndrome is determined, in the majority of cases, via the PTEN gene which presents about 30 mutations in this condition. This gene which regulates cell growth, when not working properly can lead to hamartomas. PTEN chromosomal location is 10q23.31, while the molecular location is 87,863,438 to ...
PTEN also refers to a member of the class, phosphatase and tensin homolog. [ citation needed ] This enzyme participates in 10 metabolic pathways : inositol phosphate metabolism , phosphatidylinositol signaling system , p53 signaling pathway , focal adhesion , tight junction , endometrial cancer , glioma , prostate cancer , melanoma , and small ...
The most common known aberrations include the PIK3CA gene mutation and the loss-of-function mutations or epigenetic silencing of PTEN. [12] The phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway is activated in approximately 30–40% of BC cases.
Patients and their diseases are profiled in order to identify the most effective treatment for their specific case. Targeted therapy or molecularly targeted therapy is one of the major modalities of medical treatment (pharmacotherapy) for cancer, [1] others being hormonal therapy and cytotoxic chemotherapy.
Mutations in the TET2 gene are found in approximately 40–50% of CMML. [12] Inactivating mutations in one of the two parental GATA2 genes lead to a reduction, i.e. a haploinsufficiency, in the cellular levels of the gene's product, the GATA2 transcription factor, and thereby to a rare autosomal dominant genetic disease, GATA2 deficiency.