A Call to Arms: Wartime Blood Donor Recruitment.

To ensure an adequate blood supply, blood collection agencies must design campaigns to recruit and maintain an active donor pool. Such campaigns generally appeal to altruism and humanitarianism, which donors most commonly cite as their reasons for donating. However, large donor registries and the widespread recruitment campaigns that sustain them did not become a necessity until the technology for the collection, storage, and transfusion of blood had advanced to a point that enabled the establishment of transfusion services that could provide large amounts of stored blood to meet high demands. The realization of these milestones was one of the most important medical achievements of the Great War: the desperate need for blood created by war drove earlier adoption of scientific discoveries that might otherwise have been neglected. The medical advances of the Great War in turn enabled the establishment of wide-ranging transfusion services to aid combatants during the Spanish Civil War and Second World War. These services required the support of large civilian donor bases, and donor campaigns tapped into the patriotic feelings of civilians at home. This review will highlight some of the messages and media that were used to recruit blood donors in Spain, Britain, Canada, and the United States during wartime.

Gene expression and mutation-guided synthetic lethality eradicates proliferating and quiescent leukemia cells.

Quiescent and proliferating leukemia cells accumulate highly lethal DNA double-strand breaks that are repaired by 2 major mechanisms: BRCA-dependent homologous recombination and DNA-dependent protein kinase-mediated (DNA-PK-mediated) nonhomologous end-joining, whereas DNA repair pathways mediated by poly(ADP)ribose polymerase 1 (PARP1) serve as backups. Here we have designed a personalized medicine approach called gene expression and mutation analysis (GEMA) to identify BRCA- and DNA-PK-deficient leukemias either directly, using reverse transcription-quantitative PCR, microarrays, and flow cytometry, or indirectly, by the presence of oncogenes such as BCR-ABL1. DNA-PK-deficient quiescent leukemia cells and BRCA/DNA-PK-deficient proliferating leukemia cells were sensitive to PARP1 inhibitors that were administered alone or in combination with current antileukemic drugs. In conclusion, GEMA-guided targeting of PARP1 resulted in dual cellular synthetic lethality in quiescent and proliferating immature leukemia cells, and is thus a potential approach to eradicate leukemia stem and progenitor cells that are responsible for initiation and manifestation of the disease. Further, an analysis of The Cancer Genome Atlas database indicated that this personalized medicine approach could also be applied to treat numerous solid tumors from individual patients.