Chronic myeloid leukemia
| PAG Title | Chronic myeloid leukemia |
| PAG ID | WAG000610 |
| Type | P |
| Source Link |  KEGG |
| Publication Reference | NA |
| PAG Description | Chronic myelogenous leukemia (CML) origites in a pluripotent hematopoetic stem cell of the bone marrow and is characterized by greatly increased numbers of granulocytes in the blood. Myeloid and other hematopoetic cell lineages are involved in the process of clol proliferation and differentiation. On the cellular level, CML is associated with a specific chromosome abnormality, the t(9; 22) reciprocal translocation that forms the Philadelphia (Ph) chromosome. The Ph chromosome is the result of a molecular rearrangement between the c-ABL proto-oncogene on chromosome 9 and the BCR (breakpoint cluster region) gene on chromosome 22. The BCR/ABL fusion gene encodes p210 BCR/ABL, an oncoprotein, which, unlike the normal p145 c-Abl, has constitutive tyrosine kise activity and is predomintly localized in the cytoplasm. While fusion of c-ABL and BCR is believed to be the primary cause of the chronic phase of CML, progression to blast crisis requires other molecular changes. Common secondary abnormalities include mutations in TP53, RB, and p16/INK4A, or overexpression of genes such as EVI1. Additiol chromosome translocations are also observed,such as t(3;21)(q26;q22), which generates AML1-EVI1. |
| Species | Homo sapiens |
| nCoCo Score | 3,807 |
| Base PAG ID | WAG000610 |
| Human Phenotyte Annotation | |
| Curator | PAGER curation team |
| Curator Contact | PAGER-contact@googlegroups.com |
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