Human chromosome 11 contains two different growth suppressor genes for embryonal rhabdomyosarcoma

Willington E. Loh, Heidi J. Scrable, Elizabeth Livanos, Marie J. Arboleda, Webster K. Cavenee, Mitsuo Oshimura, Bernard E. Weissman

Research output: Contribution to journalArticle

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Abstract

The identification of acquired homozygosity in human cancers implies locations of tumor suppressor genes without providing functional evidence. The localization of a defect in embryonal rhabdomyosarcomas to chromosomal region 11p15 provides one such example. In this report, we show that transfer of a normal human chromosome 11 into an embryonal rhabdomyosarcoma cell line elicited a dramatic loss of the proliferative capacity of the transferrants. Indeed, the majority of the viable microcell hybrids had either eliminated genetic information on the short arm of the transferred chromosome 11 or increased the copy number of the rhabdomyosarcoma-derived chromosomes 11. Cells that possessed only the long arm of chromosome 11 also demonstrated a decreased growth rate. In contrast, all microcell hybrids retained the ability to form tumors upon inoculation into animals. These functional data support molecular studies indicating loss of genetic information on chromosome 11p15 during the development of embryonal rhabdomyosarcoma. In addition, our studies demonstrate the existence of a second gene on the long arm. previously unrecognized by molecular analyses, which negatively regulates the growth of embryonal rhabdomyosarcoma cell lines.

Original languageEnglish (US)
Pages (from-to)1755-1759
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume89
Issue number5
StatePublished - 1992
Externally publishedYes

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Embryonal Rhabdomyosarcoma
Chromosomes, Human, Pair 11
Human Chromosomes
Tumor Suppressor Genes
Cell Line
Rhabdomyosarcoma
Growth
Neoplasms
Chromosomes
Genes

Keywords

  • Loss of heterozygosity
  • Microcell hybridization
  • Recessive cancer genes

ASJC Scopus subject areas

  • Genetics
  • General

Cite this

Loh, W. E., Scrable, H. J., Livanos, E., Arboleda, M. J., Cavenee, W. K., Oshimura, M., & Weissman, B. E. (1992). Human chromosome 11 contains two different growth suppressor genes for embryonal rhabdomyosarcoma. Proceedings of the National Academy of Sciences of the United States of America, 89(5), 1755-1759.

Human chromosome 11 contains two different growth suppressor genes for embryonal rhabdomyosarcoma. / Loh, Willington E.; Scrable, Heidi J.; Livanos, Elizabeth; Arboleda, Marie J.; Cavenee, Webster K.; Oshimura, Mitsuo; Weissman, Bernard E.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 89, No. 5, 1992, p. 1755-1759.

Research output: Contribution to journalArticle

Loh, WE, Scrable, HJ, Livanos, E, Arboleda, MJ, Cavenee, WK, Oshimura, M & Weissman, BE 1992, 'Human chromosome 11 contains two different growth suppressor genes for embryonal rhabdomyosarcoma', Proceedings of the National Academy of Sciences of the United States of America, vol. 89, no. 5, pp. 1755-1759.
Loh, Willington E. ; Scrable, Heidi J. ; Livanos, Elizabeth ; Arboleda, Marie J. ; Cavenee, Webster K. ; Oshimura, Mitsuo ; Weissman, Bernard E. / Human chromosome 11 contains two different growth suppressor genes for embryonal rhabdomyosarcoma. In: Proceedings of the National Academy of Sciences of the United States of America. 1992 ; Vol. 89, No. 5. pp. 1755-1759.
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AU - Cavenee, Webster K.

AU - Oshimura, Mitsuo

AU - Weissman, Bernard E.

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N2 - The identification of acquired homozygosity in human cancers implies locations of tumor suppressor genes without providing functional evidence. The localization of a defect in embryonal rhabdomyosarcomas to chromosomal region 11p15 provides one such example. In this report, we show that transfer of a normal human chromosome 11 into an embryonal rhabdomyosarcoma cell line elicited a dramatic loss of the proliferative capacity of the transferrants. Indeed, the majority of the viable microcell hybrids had either eliminated genetic information on the short arm of the transferred chromosome 11 or increased the copy number of the rhabdomyosarcoma-derived chromosomes 11. Cells that possessed only the long arm of chromosome 11 also demonstrated a decreased growth rate. In contrast, all microcell hybrids retained the ability to form tumors upon inoculation into animals. These functional data support molecular studies indicating loss of genetic information on chromosome 11p15 during the development of embryonal rhabdomyosarcoma. In addition, our studies demonstrate the existence of a second gene on the long arm. previously unrecognized by molecular analyses, which negatively regulates the growth of embryonal rhabdomyosarcoma cell lines.

AB - The identification of acquired homozygosity in human cancers implies locations of tumor suppressor genes without providing functional evidence. The localization of a defect in embryonal rhabdomyosarcomas to chromosomal region 11p15 provides one such example. In this report, we show that transfer of a normal human chromosome 11 into an embryonal rhabdomyosarcoma cell line elicited a dramatic loss of the proliferative capacity of the transferrants. Indeed, the majority of the viable microcell hybrids had either eliminated genetic information on the short arm of the transferred chromosome 11 or increased the copy number of the rhabdomyosarcoma-derived chromosomes 11. Cells that possessed only the long arm of chromosome 11 also demonstrated a decreased growth rate. In contrast, all microcell hybrids retained the ability to form tumors upon inoculation into animals. These functional data support molecular studies indicating loss of genetic information on chromosome 11p15 during the development of embryonal rhabdomyosarcoma. In addition, our studies demonstrate the existence of a second gene on the long arm. previously unrecognized by molecular analyses, which negatively regulates the growth of embryonal rhabdomyosarcoma cell lines.

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