Fanconi anemia (FA) is a heritable disease characterized by bone marrow failure, congenital abnormalities, and a predisposition to develop malignancies, in particular acute myeloid leukemia and squamous cell carcinoma. So far, fifteen FA genes have been identified, the products of which operate in a molecular pathway that preserves genomic stability. The function of the FA proteins in DNA interstrand crosslink repair is emerging, novel FA mouse models that closely recapitulate hematological abnormalities observed in FA patients are available, and strategies for therapeutic intervention to prevent FA-associated hematopoietic symptoms and cancer onset have been outlined. We invite investigators to contribute original research articles as well as review articles that will stimulate the ongoing efforts to understand and treat FA on the basis of underlying molecular and cellular biology.

We are particularly interested in articles describing novel insights in FA protein function, the role of FA genes in hematopoietic stem and progenitor cells, therapeutic intervention by bone marrow transplantation, induced pluripotent stem cells, gene therapy, RNA interference, or small molecules, and the dysfunction of FA genes in sporadic hematological malignancies.Potential topics include, but are not limited to:

• The elucidation of FA gene function in DNA repair, cell cycle regulation, or other molecular processes
• The role of FA genes in stem cell biology
• Advances in molecular diagnostics of FA
• New insights in clinical features of FA
• Strategies for therapeutic intervention to prevent bone marrow failure and cancer onset
• FA gene mutations, silencing, and aberrant FA protein localization in sporadic malignancies
• Management of cancer in FA patients