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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.
20779 Ensembl ENSG00000197122 ENSMUSG00000027646 UniProt P12931 P05480 RefSeq (mRNA) NM_005417 NM_198291 NM_001025395 NM_009271 RefSeq (protein) NP_005408 NP_938033 NP_001020566 NP_033297 Location (UCSC) Chr 20: 37.34 – 37.41 Mb Chr 2: 157.42 – 157.47 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Proto-oncogene tyrosine-protein kinase Src, also known as proto-oncogene c-Src, or ...
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.
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
Printable version; In other projects ... Antileukemic drugs, anticancer drugs that are used to treat one or more types of leukemia, include: [1] 6-Mercaptopurine;
Idelalisib (trade name Zydelig; codenamed CAL-101, GS-1101; PIK3CD inhibitor): FDA-approved in July 2014 for treatment of three types of blood cancers: treatment of relapsed or refractory chronic lymphocytic leukemia (CLL) in combination with rituximab, treatment of relapsed small lymphocytic lymphoma after at least two prior systemic therapies, and treatment of follicular lymphoma (FL) after ...
Many of these mutations cause the kinase to be more active. It is the single most mutated kinase in glioblastoma, the most malignant primary brain tumor. [22] The PtdIns(3,4,5)P 3 phosphatase PTEN that antagonises PI3K signaling is absent from many tumours.
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 ...