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Myc roles in hematopoiesis and leukemia. Myc roles in hematopoiesis and leukemia. Delgado, M.D and León, J. Genes &Cancer (2010) 1: 605–616. Review2010-06-14T22:00:00Z<p style="text-align:justify;"><span class="ms-rteThemeForeColor-2-5"><strong>​</strong><span class="ms-rteThemeFontFace-1 ms-rteFontSize-2"><strong>Abstract</strong></span></span></p><p style="text-align:justify;"><span class="ms-rteThemeFontFace-1 ms-rteFontSize-2"><span style="color:#985735;"></span><span style="color:#000000;">Hematopoiesis is a process capable of generating millions of cells every second, as distributed in many cell types. The process is regulated by a number of transcription factors that regulate the differentiation along the distinct lineages and dictate the genetic program that defines each mature phenotype. Myc was first discovered as the oncogene of avian leukemogenic retroviruses; it was later found translocated in human lymphoma. From then on, evidence accumulated showing that c-Myc is one of the transcription factors playing a major role in hematopoiesis. The study of genetically modified mice with overexpression or deletion of</span><span style="color:#000000;"> </span><em style="color:#000000;">Myc</em><span style="color:#000000;"> </span><span style="color:#000000;">has shown that c-Myc is required for the correct balance between self-renewal and differentiation of hematopoietic stem cells (HSCs). Enforced</span><span style="color:#000000;"> </span><em style="color:#000000;">Myc</em><span style="color:#000000;"> </span><span style="color:#000000;">expression in mice leads to reduced HSC pools owing to loss of self-renewal activity at the expense of increased proliferation of progenitor cells and differentiation. c-Myc deficiency consistently results in the accumulation of HSCs. Other models with conditional</span><span style="color:#000000;"> </span><em style="color:#000000;">Myc</em><span style="color:#000000;"> </span><span style="color:#000000;">deletion have demonstrated that different lineages of hematopoietic cells differ in their requirement for c-Myc to regulate their proliferation and differentiation. When transgenic mice overexpress c-Myc or N-Myc in mature cells from the lymphoid or myeloid lineages, the result is lymphoma or leukemia. In agreement, enforced expression of c-Myc blocks the differentiation in several leukemia-derived cell lines capable of differentiating in culture. Not surprising,</span><span style="color:#000000;"> </span><em style="color:#000000;">MYC</em><span style="color:#000000;"> </span><span style="color:#000000;">deregulation is recurrently found in many types of human lymphoma and leukemia. Whereas</span><span style="color:#000000;"> </span><em style="color:#000000;">MYC</em><span style="color:#000000;"> </span><span style="color:#000000;">is deregulated by translocation in Burkitt lymphoma and, less frequently, other types of lymphoma,</span><span style="color:#000000;"> </span><em style="color:#000000;">MYC</em><span style="color:#000000;"> is frequently overexpressed in acute lymphoblastic and myeloid leukemia, through mechanisms unrelated to chromosomal translocation, and is often associated with disease progression.</span></span></p><p><span class="ms-rteForeColor-2"><a href="">​[pubmed]</a></span></p>106