Identification of a chromosome carrying a putative tumor suppressor gene in human choriocarcinoma by microcell-mediated chromosome transfer

S. Miyamoto, Masayuki Sasaki, M. Nishida, N. Wake

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3 Citations (Scopus)

Abstract

There are two main mechanisms of origin for complete hydatidiform mole; a) fertilization of an empty egg by a haploid sperm followed by duplication, and b) fertilization of such an egg by two haploid spermatozoa. It is widely accepted that, of all forms of pregnancy that had to choriocarcinoma, the risk associated with moles is by far the highest. Homozygous expression of a recessive mutation of moles has been assumed to associate with this propensity to malignancies. Alterations of several tumor suppressor genes together with activation of oncogenes are assumed to be necessary for choriocarcinogenesis. Genetic characteristics shown in the moles suggest that the former alterations are especially important to explore the multistep conversions to malignancies. Thus, individual chromosomes derived from normal cells were introduced into choriocarcinoma cells via microcell fusion. Evaluation of tumorigenicity in microcell hybrids suggested that chromosome #7 carried a putative tumor suppressor gene for choriocarcinoma. The gene imprinting or recessive mutation may be responsible for the inactivation of such a gene, being able to correspond with the high propensity to malignancy of moles.

Original languageEnglish
Pages (from-to)38-43
Number of pages6
JournalHuman cell : official journal of Human Cell Research Society
Volume4
Issue number1
Publication statusPublished - Jan 1 1991

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Choriocarcinoma
Tumor Suppressor Genes
Chromosomes
Haploidy
Fertilization
Ovum
Spermatozoa
Hydatidiform Mole
Neoplasms
Mutation
Chromosomes, Human, Pair 7
Oncogenes
Genes
Pregnancy

All Science Journal Classification (ASJC) codes

  • Cell Biology
  • Cancer Research

Cite this

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title = "Identification of a chromosome carrying a putative tumor suppressor gene in human choriocarcinoma by microcell-mediated chromosome transfer",
abstract = "There are two main mechanisms of origin for complete hydatidiform mole; a) fertilization of an empty egg by a haploid sperm followed by duplication, and b) fertilization of such an egg by two haploid spermatozoa. It is widely accepted that, of all forms of pregnancy that had to choriocarcinoma, the risk associated with moles is by far the highest. Homozygous expression of a recessive mutation of moles has been assumed to associate with this propensity to malignancies. Alterations of several tumor suppressor genes together with activation of oncogenes are assumed to be necessary for choriocarcinogenesis. Genetic characteristics shown in the moles suggest that the former alterations are especially important to explore the multistep conversions to malignancies. Thus, individual chromosomes derived from normal cells were introduced into choriocarcinoma cells via microcell fusion. Evaluation of tumorigenicity in microcell hybrids suggested that chromosome #7 carried a putative tumor suppressor gene for choriocarcinoma. The gene imprinting or recessive mutation may be responsible for the inactivation of such a gene, being able to correspond with the high propensity to malignancy of moles.",
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AU - Miyamoto, S.

AU - Sasaki, Masayuki

AU - Nishida, M.

AU - Wake, N.

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N2 - There are two main mechanisms of origin for complete hydatidiform mole; a) fertilization of an empty egg by a haploid sperm followed by duplication, and b) fertilization of such an egg by two haploid spermatozoa. It is widely accepted that, of all forms of pregnancy that had to choriocarcinoma, the risk associated with moles is by far the highest. Homozygous expression of a recessive mutation of moles has been assumed to associate with this propensity to malignancies. Alterations of several tumor suppressor genes together with activation of oncogenes are assumed to be necessary for choriocarcinogenesis. Genetic characteristics shown in the moles suggest that the former alterations are especially important to explore the multistep conversions to malignancies. Thus, individual chromosomes derived from normal cells were introduced into choriocarcinoma cells via microcell fusion. Evaluation of tumorigenicity in microcell hybrids suggested that chromosome #7 carried a putative tumor suppressor gene for choriocarcinoma. The gene imprinting or recessive mutation may be responsible for the inactivation of such a gene, being able to correspond with the high propensity to malignancy of moles.

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