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Significance Fanconi anemia (FA) is a devastating disease associated with a progressive bone marrow failure (BMF) and clonal proliferation of primitive hematopoietic cells that leads to leukemia. In an effort to understand the molecular basis of BMF and leukemogenesis in FA, we recently uncovered a unique function of proteins associated with FA in transcriptional regulation that translates into elevated levels of the signaling molecule Dickkopf-1 (DKK1). Overproduction of DKK1 has been shown to alter functions in hematopoiesis and to promote hematologic malignancies. Thus, our findings represent a crucial step in the development of strategies aimed at preventing BMF and/or clonal hematopoiesis in patients with FA.

The Fanconi anemia pathway has a dual function in Dickkopf-1 transcriptional repression