Human chromosome 7 carries a putative tumor suppressor gene(s) involved in choriocarcinoma

Matsuda, Takao; Sasaki, Masahiro; Kato, Hidenori; Yamada, Hidetoshi; Cohen, Michael B.; Jc, Barrett; Oshimura, Mitsuo; Wake, Norio

doi:10.1038/sj.onc.1201461

Cited by 53 publications

(22 citation statements)

References 32 publications

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“…Cytogenetic studies on choriocarcinomas identified certain consistently affected regions including deletion of 7p12-7q11.2 [21], amplification of 7q21-q31 and loss of 8p12-p21 [17]. Loss of heterozygosity for 8p12-p21 [22] or 7q11.2 [21,22] in choriocarcinoma suggests the possible existence of tumor suppressor genes in these two regions.…”

Section: Cytogenetic Compositionmentioning

confidence: 99%

Pathogenesis of Choriocarcinoma: Clinical, Genetic and Stem Cell Perspectives

et al. 2009

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Choriocarcinoma is a unique malignant neoplasm composed of mononuclear cytotrophoblasts and multinucleated syncytiotrophoblasts that produce human chorionic gonadotrophin. Choriocarcinoma can occur after a pregnancy, as a component of germ cell tumors, or in association with a poorly differentiated somatic carcinoma, each with distinct clinical features. Cytogenetic and molecular studies, predominantly on gestational choriocarcinoma, revealed the impact of oncogenes, tumor suppressor genes and imprinting genes on its pathogenesis. The role of stem cells in various types of choriocarcinoma has been studied recently. This review will discuss how such knowledge can enhance our understanding of the pathogenesis of choriocarcinoma, enable exploration of novel anti-choriocarcinoma targeted therapy and possibly improve our insight on embryological and placental development.

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Section: Cytogenetic Compositionmentioning

confidence: 99%

Pathogenesis of Choriocarcinoma: Clinical, Genetic and Stem Cell Perspectives

et al. 2009

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“…Functional assays have demonstrated that the introduction of an intact copy of hchr7 can restore senescence to immortalized human ®broblast cell lines having LOH at 7q31-q32 (Ogata et al, 1993) and can inhibit the tumorigenic phenotype of a murine-derived squamous cell carcinoma cell line (Zenklusen et al, 1994c). Recently, introduction of hchr7 into a choriocarcinoma cell line delayed tumorigenicity of the microcell hybrids (Matsuda et al, 1997). However, the critical region of LOH in the latter type of tumor is typically 7p12-q11.3, suggesting an additional TSG may be present on hchr7 that is relevant to the tumorigenesis of a dierent group of neoplasias, as previously suggested (Zenklusen and Conti, 1996).…”

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confidence: 99%

Definitive functional evidence for a tumor suppressor gene on human chromosome 7q31.1 neighboring the Fra7G site

et al. 2000

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We have previously shown that loss of heterozygosity (LOH) on human chromosome (hchr) 7 at q31.1 is common in a variety of tumors of epithelial origin. Frequent LOH of a speci®c chromosomal marker is indicative of a closely linked tumor suppressor gene (TSG). However, recent reports have also indicated that such a high frequency of LOH could be due to the presence in this region of the second most common aphidicolin-inducible fragile site in the human genome (Fra7G). To address this controversy, we introduced single copies of hchr7 or hchr12 into a highly aggressive human prostate carcinoma cell line (PC3) by microcellmediated transfer. The tumorigenicity of six clones of PC3/hchr7 hybrids and three clones of PCRhchr12 hybrids, obtained in four separate fusion experiments, were studied in BALB/c nude mice. All but one of the PC3/hchr7 hybrids increased tumor latency by at least twofold, whereas none of the PC3/hchr12 hybrids delayed tumor onset. No dierences in the in vitro growth rate were observed among any of the cell lines assayed (parental and hybrids) suggesting that the observed tumor suppression was due to factors other than cell cycle regulation. Deletion mapping of the PC3/ hchr7 tumors obtained after reversion to the malignant phenotype revealed a common region of loss centred around 7q31.1, supporting the TSG hypothesis. The smallest commonly deleted region was *1.5 Mb in size and¯anked by the markers D7S486 and D7S655.

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“…Une approche originale combinant cytogénétique et biologie cellulaire a été effectuée par Matsuda et al [54] qui ont utilisé le principe de la complémentation génétique au sein des hybrides somatiques. Ils ont réalisé des fusions entre des cellules de lignées de choriocarcinomes et des microcaryoplastes.…”

Section: 1 Un Segment Chromosomique Hébergeant Un Anti-oncogène Misunclassified

“…Le gène N33 (putative prostate cancer tumor supressor) a été proposé pour la perte en 8p et KOX 18 et 20 qui codent pour des protéines en doigt de zinc putativement impliquées dans la régulation, pour le gain en 7q. Les délétions en 7p12q21, rapportées par Matsuda et al [54], n'ont été confirmées que sur un seul cas par CGH. Les observations de Xue et al [42] (voir plus haut) sur Tim P3, E cad et p16 sont documentées par un (Tim P3, E Cad) ou deux (p16) cas de perte (sur 15) ce qui donne de l'importance à ces antioncogènes.…”

Section: Les Choriocarcinomesunclassified

Des andro- et parthénogénotes humains (môles hydatiformes et tératomes ovariens) au cancer

Coullin

2005

Gynécologie Obstétrique & Fertilité

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Human chromosome 7 carries a putative tumor suppressor gene(s) involved in choriocarcinoma

Cited by 53 publications

References 32 publications

Pathogenesis of Choriocarcinoma: Clinical, Genetic and Stem Cell Perspectives

Pathogenesis of Choriocarcinoma: Clinical, Genetic and Stem Cell Perspectives

Definitive functional evidence for a tumor suppressor gene on human chromosome 7q31.1 neighboring the Fra7G site

Des andro- et parthénogénotes humains (môles hydatiformes et tératomes ovariens) au cancer

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