Chemotherapy often causes damage to hematopoietic tissues, leading to acute bone marrow suppression and the long term development of
leukemias.
Niacin deficiency, which is common in
cancer patients, causes dramatic
genomic instability in bone marrow cells in an in vivo rat model. From a mechanistic perspective,
niacin deficiency delays excision repair and causes double strand break accumulation, which in turn favors
chromosome breaks and translocations.
Niacin deficiency also impairs cell cycle arrest and apoptosis in response to DNA damage, which combine to encourage the survival of cells with leukemogenic potential. Conversely, pharmacological supplementation of rats with
niacin increases bone marrow
poly(ADP-ribose) formation and apoptosis. Improvement of
niacin status in rats significantly decreased nitrosourea-induced
leukemia incidence. The data from our rat model suggest that
niacin supplementation of
cancer patients may decrease the severity of short- and long-term side effects of
chemotherapy, and could improve
tumor cell killing through activation of
poly(ADP-ribose)-dependent apoptosis pathways.