Polymorphisms in genes involved in homologous recombination repair interact to increase the risk of developing acute myeloid leukemia.

Purpose: Double-strand break repair via homologous recombination is essential in maintaining genetic integrity. RAD51 and XRCC3 are involved in the repair of DNA by this pathway, and polymorphisms have been identified in both the RAD51 (RAD51-G135C) and XRCC3 (XRCC3-Thr241Met) genes. The object of this study was to examine whether these polymorphisms may modulate susceptibility to the development of acute myeloid leukemia (AML), a disease that is characterized by genetic instability.

BAT-25 and BAT-26, two mononucleotide microsatellites, are not sensitive markers of microsatellite instability in acute myeloid leukaemia.

BAT-25 and BAT-26 are mononucleotide microsatellites with quasi-monomorphic allele length distribution in healthy controls but unstable, shortened alleles in solid organ tumours with a mutator phenotype (RER+). Both markers are highly sensitive and specific for RER+ colorectal cancer. This study evaluated three mononucleotide microsatellites, BAT-25, BAT-26 and BAT-40 (a polymorphic mononucleotide microsatellite) in RER+ acute myeloid leukaemia (AML).

BEAM-alemtuzumab reduced-intensity allogeneic stem cell transplantation for lymphoproliferative diseases: GVHD, toxicity, and survival in 65 patients.

We report the outcomes of reduced-intensity allogeneic stem cell transplantation using BEAM-alemtuzumab conditioning (carmustine, etoposide, cytosine arabinoside, melphalan, and alemtuzumab 10 mg/d on days -5 to -1) in 6 United Kingdom transplant centers. Sixty-five patients with lymphoproliferative diseases underwent sibling (n = 57) or matched unrelated donor (n = 8) transplantation. Sustained donor engraftment occurred in 60 (97%) of 62 patients.