PubMed Health⌕ Search

PubMed · 3368666

[Medical genetics and migration].

Abstract

Any migration results in the transfer of normal and pathological genes from one population to another. The frequency of pathological genes may vary according to the population, sickle cell anaemia, for instance, being frequent in Africa and cystic fibrosis in Europe. It follows that the hereditary pathology of migrants is not the same as that of the host population, at least during the immediate post-migration years; subsequently, all depends on the degree of cross-breeding. In epidemiological genetics the study of the frequency of some diseases in the original population, among migrants and in the host population enables the effects of genes and environment on the aetiology of these diseases to be investigated.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J Feingold. [Medical genetics and migration].. https://doi.org/10.1016/s0248-8663(88)80049-3

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Are genome-wide association studies all that we need to dissect the genetic component of complex human diseases?

With the availability of dense maps of anonymous and frequent SNPs spanning the whole human genome, genome-wide association studies are now becoming a reality. In this paper, we discuss the utility of these approaches to detect genetic risk variants involved in complex disease susceptibility and, in the best case scenario where a signal is detected, how helpful it will be to the understanding of the pathological process.

Genetic Diseases, Inborn↗

Mutations in the NF-kappaB signaling pathway: implications for human disease.

The nuclear factor-kappa B (NF-kappaB) signaling pathway is a multi-component pathway that regulates the expression of hundreds of genes that are involved in diverse and key cellular and organismal processes, including cell proliferation, cell survival, the cellular stress response, innate immunity and inflammation. Not surprisingly, mis-regulation of the NF-kappaB pathway, either by mutation or epigenetic mechanisms, is involved in many human and animal diseases, especially ones associated with chronic inflammation, immunodeficiency or cancer. This review describes human diseases in which mutations in the components of the core NF-kappaB signaling pathway have been implicated and discusses the molecular mechanisms by which these alterations in NF-kappaB signaling are likely to contribute to the disease pathology. These mutations can be germline or somatic and include gene amplification (e.g., REL), point mutations and deletions (REL, NFKB2, IKBA, CYLD, NEMO) and chromosomal translocations (BCL-3). In addition, human genetic diseases are briefly described wherein mutations affect protein modifiers or transducers of NF-kappaB signaling or disrupt NF-kappaB-binding sites in promoters/enhancers.

Genetic Diseases, Inborn↗