| First Author | Tijchon E | Year | 2013 |
| Journal | Leukemia | Volume | 27 |
| Issue | 3 | Pages | 541-52 |
| PubMed ID | 23047478 | Mgi Jnum | J:196798 |
| Mgi Id | MGI:5489959 | Doi | 10.1038/leu.2012.293 |
| Citation | Tijchon E, et al. (2013) B-lineage transcription factors and cooperating gene lesions required for leukemia development. Leukemia 27(3):541-52 |
| abstractText | Differentiation of hematopoietic stem cells into B lymphocytes requires the concerted action of specific transcription factors, such as RUNX1, IKZF1, E2A, EBF1 and PAX5. As key determinants of normal B-cell development, B-lineage transcription factors are frequently deregulated in hematological malignancies, such as B-cell precursor acute lymphoblastic leukemia (BCP-ALL), and affected by either chromosomal translocations, gene deletions or point mutations. However, genetic aberrations in this developmental pathway are generally insufficient to induce BCP-ALL, and often complemented by genetic defects in cytokine receptors and tyrosine kinases (IL-7Ralpha, CRLF2, JAK2 and c-ABL1), transcriptional cofactors (TBL1XR1, CBP and BTG1), as well as the regulatory pathways that mediate cell-cycle control (pRB and INK4A/B). Here we provide a detailed overview of the genetic pathways that interact with these B-lineage specification factors, and describe how mutations affecting these master regulators together with cooperating lesions drive leukemia development. |
