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Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors
Published on: July 17, 2020
Genetic alterations of protein tyrosine phosphatases in human cancers
11] Division of Gastroenterology and Hepatology and Shanghai Institution of Digestive Disease, Shanghai Jiao-Tong University School of Medicine Renji Hospital, Shanghai, China [2] Department of Genetics and Genome Sciences, Case Western Reserve University, Cleveland, OH, USA [3] Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, OH, USA.
Abstract:
Protein tyrosine phosphatases (PTPs) are enzymes that remove phosphate from tyrosine residues in proteins. Recent whole-exome sequencing of human cancer genomes reveals that many PTPs are frequently mutated in a variety of cancers. Among these mutated PTPs, PTP receptor T (PTPRT) appears to be the most frequently mutated PTP in human cancers. Beside PTPN11, which functions as an oncogene in leukemia, genetic and functional studies indicate that most of mutant PTPs are tumor suppressor genes. Identification of the substrates and corresponding kinases of the mutant PTPs may provide novel therapeutic targets for cancers harboring these mutant PTPs.
Insights
Protein tyrosine phosphatases (PTPs) are enzymes frequently mutated in cancer. Most mutated PTPs act as tumor suppressors, and identifying their targets could reveal new cancer therapies.
Area of Science:
- Biochemistry
- Molecular Biology
- Oncology
Background:
- Protein tyrosine phosphatases (PTPs) are crucial enzymes regulating protein dephosphorylation.
- Whole-exome sequencing reveals frequent mutations in PTPs across diverse human cancers.
- PTP receptor T (PTPRT) is the most commonly mutated PTP in human cancers.
Purpose of the Study:
- To investigate the role of mutated PTPs in cancer development.
- To identify potential therapeutic targets based on PTP mutations.
Main Methods:
- Analysis of whole-exome sequencing data from human cancer genomes.
- Review of genetic and functional studies on mutant PTPs.
Main Results:
- A significant number of PTPs are recurrently mutated in various cancers.
- PTPRT is identified as the most frequently mutated PTP.
- Evidence suggests most mutated PTPs function as tumor suppressors, unlike PTPN11 in leukemia.
Conclusions:
- Mutations in PTPs, particularly PTPRT, are prevalent in human cancers.
- Understanding the substrates and kinases of mutant PTPs is key to developing novel cancer therapeutics.
- Targeting pathways affected by mutant PTPs offers a promising strategy for cancer treatment.
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