Concerted nonsyntenic allelic loss in human colorectal carcinoma

David J. Law, Sylviane Olschwang, Jean Philippe Monpezat, Danielle Lefrançois, David Jagelman, Nicholas J. Petrelli, Gilles Thomas, Andrew P Feinberg

Research output: Contribution to journalArticle

Abstract

Familial polyposis coli (FPC) is caused by an autosomal dominant gene on chromosome 5, and it has been proposed that colorectal cancer in the general population arises from loss or inactivation of the FPC gene, analogous to recessive tumor genes in retinoblastoma and Wilms' tumor. Since allelic loss can be erroneously scored in nonhomogeneous samples, tumor cell populations were first microdissected from 24 colorectal carcinomas, an additional nine cancers were engrafted in nude mice, and nuclei were flow-sorted from an additional two. Of 31 cancers informative for chromosome 5 markers, only 6 (19%) showed loss of heterozygoshy of chromosome 5 alleles, compared to 19 of 34 (56%) on chromosome 17, and 17 of 33 (52%) on chromosome 18. Therefore, it appears that (i) FPC is a true dominant for adenomatosis but not a common recessive gene for colon cancer; and (ii) simple Mendelian models involving loss of alleles at a single locus may be inappropriate for understanding common human solid tumors.

Original languageEnglish (US)
Pages (from-to)961-965
Number of pages5
JournalScience
Volume241
Issue number4868
StatePublished - 1988
Externally publishedYes

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Loss of Heterozygosity
Colorectal Neoplasms
Chromosomes, Human, Pair 5
Adenomatous Polyposis Coli
Recessive Genes
Neoplasms
Alleles
Chromosomes, Human, Pair 18
Dominant Genes
Chromosomes, Human, Pair 17
Wilms Tumor
Retinoblastoma
Genetic Markers
Nude Mice
Colonic Neoplasms
Population
Genes

ASJC Scopus subject areas

  • General

Cite this

Law, D. J., Olschwang, S., Monpezat, J. P., Lefrançois, D., Jagelman, D., Petrelli, N. J., ... Feinberg, A. P. (1988). Concerted nonsyntenic allelic loss in human colorectal carcinoma. Science, 241(4868), 961-965.

Concerted nonsyntenic allelic loss in human colorectal carcinoma. / Law, David J.; Olschwang, Sylviane; Monpezat, Jean Philippe; Lefrançois, Danielle; Jagelman, David; Petrelli, Nicholas J.; Thomas, Gilles; Feinberg, Andrew P.

In: Science, Vol. 241, No. 4868, 1988, p. 961-965.

Research output: Contribution to journalArticle

Law, DJ, Olschwang, S, Monpezat, JP, Lefrançois, D, Jagelman, D, Petrelli, NJ, Thomas, G & Feinberg, AP 1988, 'Concerted nonsyntenic allelic loss in human colorectal carcinoma', Science, vol. 241, no. 4868, pp. 961-965.
Law DJ, Olschwang S, Monpezat JP, Lefrançois D, Jagelman D, Petrelli NJ et al. Concerted nonsyntenic allelic loss in human colorectal carcinoma. Science. 1988;241(4868):961-965.
Law, David J. ; Olschwang, Sylviane ; Monpezat, Jean Philippe ; Lefrançois, Danielle ; Jagelman, David ; Petrelli, Nicholas J. ; Thomas, Gilles ; Feinberg, Andrew P. / Concerted nonsyntenic allelic loss in human colorectal carcinoma. In: Science. 1988 ; Vol. 241, No. 4868. pp. 961-965.
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AU - Petrelli, Nicholas J.

AU - Thomas, Gilles

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N2 - Familial polyposis coli (FPC) is caused by an autosomal dominant gene on chromosome 5, and it has been proposed that colorectal cancer in the general population arises from loss or inactivation of the FPC gene, analogous to recessive tumor genes in retinoblastoma and Wilms' tumor. Since allelic loss can be erroneously scored in nonhomogeneous samples, tumor cell populations were first microdissected from 24 colorectal carcinomas, an additional nine cancers were engrafted in nude mice, and nuclei were flow-sorted from an additional two. Of 31 cancers informative for chromosome 5 markers, only 6 (19%) showed loss of heterozygoshy of chromosome 5 alleles, compared to 19 of 34 (56%) on chromosome 17, and 17 of 33 (52%) on chromosome 18. Therefore, it appears that (i) FPC is a true dominant for adenomatosis but not a common recessive gene for colon cancer; and (ii) simple Mendelian models involving loss of alleles at a single locus may be inappropriate for understanding common human solid tumors.

AB - Familial polyposis coli (FPC) is caused by an autosomal dominant gene on chromosome 5, and it has been proposed that colorectal cancer in the general population arises from loss or inactivation of the FPC gene, analogous to recessive tumor genes in retinoblastoma and Wilms' tumor. Since allelic loss can be erroneously scored in nonhomogeneous samples, tumor cell populations were first microdissected from 24 colorectal carcinomas, an additional nine cancers were engrafted in nude mice, and nuclei were flow-sorted from an additional two. Of 31 cancers informative for chromosome 5 markers, only 6 (19%) showed loss of heterozygoshy of chromosome 5 alleles, compared to 19 of 34 (56%) on chromosome 17, and 17 of 33 (52%) on chromosome 18. Therefore, it appears that (i) FPC is a true dominant for adenomatosis but not a common recessive gene for colon cancer; and (ii) simple Mendelian models involving loss of alleles at a single locus may be inappropriate for understanding common human solid tumors.

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