Study of the role of protein tyrosine phosphatases in the pathogenesis of acute lymphoblastic leukemia.

@font-face { font-family: "Arial"; }@font-face { font-family: "Courier New"; }p.MsoNormal, li.MsoNormal, div.MsoNormal { margin: 0cm 0cm 0.0001pt; font-size: 12pt; font-family: "Times New Roman"; }div.Section1 { page: Section1; } Over the past 30 years, significant advances have been made in our understanding of the genetics of cancer. Many different types of oncogenes and tumor suppressor genes have been identified and characterized, and some of these insights have been translated towards improved diagnosis and treatment of various tumor types. It is now well established that mutations in RAS signaling proteins or tyrosine kinase proteins are often present in cancer cells, where they provide proliferation and survival advantages to the cancer cells. In addition, loss of tyrosine phosphatase function can further enhance kinase activation and downstream signaling. Recent findings in glioblastoma and lung tumors support an important role for protein tyrosine phosphatases in the pathogenesis of cancer, and we have recently obtained genetic and functional evidence for a tumor suppressor role for the tyrosine phosphatase PTPN2 in a subset of acute lymphoblastic leukemia (ALL). ALL is a genetically complex leukemia that is caused by the accumulation of various genetic defects that affect important cellular functions such as proliferation, survival, differentiation, cell cycle and self-renewal. This study aims to determine the involvement of tyrosine phosphatases in the development of ALL using genetic and functional studies.

Keywords:Leukemia, Cancer, Protein tyrosine phosphatases (PTPs)