Abstract
Children suffering from Fanconi anemia (FA) are at an increased risk of developing leukemia. FA is a devastating disease associated with a progressive decline in primitive hematopoietic cells due to accelerated cycling and hypersensitivity to various external cellular cues. These cellular defects favour the development of clonal proliferation and leads to leukemia. In an effort to understand the molecular basis of abnormal hematopoiesis in FA, we recently uncovered a novel function of proteins associated with FA that translates into elevated levels of the signaling molecule, Dickkopf-1 (DKK1).
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