1979
DOI: 10.1002/1097-0142(197902)43:2<679::aid-cncr2820430240>3.0.co;2-5
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Genetic mechanisms in cancer predisposition.Report of a cancer family

Abstract: A family is described in which four children developed cancer affecting different organs: lymphoma, meningeal sarcoma, osteogenic sarcoma, and adenocarcinoma of the cecum. Since there was only one other case of cancer in previous generations of this family, an hypothesis is put forth to explain this unusual aggregation on the basis of recombination of common genes. It is postulated that each parent carried a different combination of genes which, though not associated with increased cancer predisposition in the… Show more

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Cited by 20 publications
(1 citation statement)
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“…In the case of Li-Fraumeni and congenital retinoblastoma syndromes, two high-penetrance cancer-prone conditions with a predisposition for OS, a subset of the affected patients had not been found to carry germline mutations in the prototypical TP53 gene [ 8 ] or in the RB1 coding sequence [ 9 ]. It is therefore likely that phenocopies of these OS linked syndromes are caused by mutations in other genes affecting the same pathways, or that yet undiscovered hypomorphic allelic variants of established susceptibility genes modify tumor risk [ 9 , 10 ]. The presence of such low-penetrance gene variants would imply that a much larger than previously estimated fraction of tumors may be due to a congenital predisposition [ 11 , 12 ].…”
Section: Introductionmentioning
confidence: 99%
“…In the case of Li-Fraumeni and congenital retinoblastoma syndromes, two high-penetrance cancer-prone conditions with a predisposition for OS, a subset of the affected patients had not been found to carry germline mutations in the prototypical TP53 gene [ 8 ] or in the RB1 coding sequence [ 9 ]. It is therefore likely that phenocopies of these OS linked syndromes are caused by mutations in other genes affecting the same pathways, or that yet undiscovered hypomorphic allelic variants of established susceptibility genes modify tumor risk [ 9 , 10 ]. The presence of such low-penetrance gene variants would imply that a much larger than previously estimated fraction of tumors may be due to a congenital predisposition [ 11 , 12 ].…”
Section: Introductionmentioning
confidence: 99%