Hormones play key roles in the regulation of animal and plant life histories, particularly in the timing of transitions between prematurational stages and in the scheduling of reproduction. Furthermore, hormonal mechanisms are subject to information about the external and internal environment of the individual. Within an evolutionary radiation, the same hormone subsets often regulate the schedules of development as well as adult reproduction and related activities and, moreover, are involved in mechanisms of senescence. We propose that the pleiotropic and epistatic effects from hormonal and neural mechanisms are an important substratum for life history evolution. This analysis of hormonal mechanisms in senescence implicates a role for antagonistic pleiotropy in selection for particular subsets of hormonal mechanisms that can be traced throughout prematurational and postmaturational stages. In the example of the vertebrate MHC (major histocompatibility complex), polymorphic loci have been assembled with pleiotropic actions on several regulatory axes affecting reproduction and other fitness components. We argue that the MHC and other complex loci may be considered as life history gene complexes, with pleiotropic influences throughout the lifespan. While analyses of this kind might suggest that life histories could in our interpretation the population genetics that is involved provides a theoretical basis for great flexibility in hormonal regulation during life history evolution. It is possible that life history evolution among taxonomic groups may sometimes be chaotic, which would frustrate strong inferences by the comparative method in the study of life histories between taxonomic groups. [References: 420]. Label: 7441

To test the hypothesis that susceptibility to leukemia can be governed by (a) recessive gene(s) associated with the major histocompatibility complex (MHC) in man, we performed an analysis of the inheritance of HLA antigens in 55 families in which one of the children developed ALL. We found among the parents of affected children a highly significant increased compatibility at the DR locus (p = 0.003). A similar increase was observed in sharing HLA antigens of the B locus (p = 0.02). The observed number of homozygotes among the patients was twice the expected value in families where the parents shared a B and a DR antigen. In segregation analysis, heterozygotes for the shared parental HLA antigen were significantly more prevalent among the healthy siblings. Our genetical analysis indicates that mating of certain shared alleles of the HLA system (especially of the DR locus) is associated with the risk for the offspring to develop ALL in childhood. This situation favors the expression of recessive genes associated with the MHC, and presumably those involved in the susceptibility to acute leukemia. Because familial leukemia is a rare event, the susceptibility to childhood ALL must also implicate genes outside the MHC and important environmental factors. Label: 7895