array(1) { [0]=> object(AppBundle\Entity\geneTOpubmed)#307 (6) { ["id":"AppBundle\Entity\geneTOpubmed":private]=> int(10511) ["geneNihId":"AppBundle\Entity\geneTOpubmed":private]=> int(2175) ["pubmedNihId":"AppBundle\Entity\geneTOpubmed":private]=> int(9382107) ["title":"AppBundle\Entity\geneTOpubmed":private]=> string(49) "Evidence for at least eight Fanconi anemia genes." ["urltitle":"AppBundle\Entity\geneTOpubmed":private]=> string(48) "evidence-for-at-least-eight-fanconi-anemia-genes" ["content":"AppBundle\Entity\geneTOpubmed":private]=> string(14621) " 9382107 1997 11 07 2016 10 19
0002-9297 61 4 1997 Oct American journal of human genetics Am. J. Hum. Genet. Evidence for at least eight Fanconi anemia genes. 940-4 Fanconi anemia (FA) is an autosomal recessive chromosomal breakage disorder with diverse clinical symptoms including progressive bone marrow failure and increased cancer risk. FA cells are hypersensitive to crosslinking agents, which has been exploited to assess genetic heterogeneity through complementation analysis. Five complementation groups (FA-A through FA-E) have so far been distinguished among the first 20 FA patients analyzed. Complementation groups in FA are likely to represent distinct disease genes, two of which (FAC and FAA) have been cloned. Following the identification of the first FA-E patient, additional patients were identified whose cell lines complemented groups A-D. To assess their possible assignment to the E group, we introduced selection markers into the original FA-E cell line and analyzed fusion hybrids with three cell lines classified as non-ABCD. All hybrids were complemented for cross-linker sensitivity, indicating nonidentity with group E. We then marked the three non-ABCDE cell lines and examined all possible hybrid combinations for complementation, which indicated that each individual cell line represented a separate complementation group. These results thus define three new groups, FA-F, FA-G, and FA-H, providing evidence for a minimum of eight distinct FA genes. Joenje H H Department of Human Genetics, Free University, Amsterdam, The Netherlands. Oostra A B AB Wijker M M di Summa F M FM van Berkel C G CG Rooimans M A MA Ebell W W van Weel M M Pronk J C JC Buchwald M M Arwert F F eng HL51031 HL NHLBI NIH HHS United States Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.
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1997 10 23 1997 10 23 0 1 1997 10 23 0 0 ppublish 9382107 S0002-9297(07)64204-9 10.1086/514881 PMC1715980
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