Involvement of adenomatous polyposis coli (APC) gene in testicular yolk sac tumor of infants

Kato, Noriko; Shibuya, Hiroyuki; Fukase, Masayuki; Tamura, Gen; Motoyama, Teiichi

doi:10.1016/j.humpath.2005.09.008

Cited by 17 publications

(12 citation statements)

References 24 publications

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“…Cloned cells also represented clear microvilli on cell surfaces up to 25 generations, and possessed strong proliferation. The characteristic cytogenetic abnormality in adult testicular germ cell tumors is the invariable gain of material from chromosome 12p [30], so called isochromosome 12p, i(12p), measured by both conventional cytogenetic and molecular cytogenetic techniques, while the abnormal chromosome of i(12p) hardly occurred in infants [31,32]. Our results on i(12p) from the analysis of G-banding were similar to the findings from previous studies [33].…”

Section: Discussionsupporting

confidence: 88%

Evaluation of cloned cells, animal model, and ATRA sensitivity of human testicular yolk sac tumor

et al. 2012

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The testicular yolk sac tumor (TYST) is the most common neoplasm originated from germ cells differentiated abnormally, a major part of pediatric malignant testicular tumors. The present study aimed at developing and validating the in vitro and vivo models of TYST and evaluating the sensitivity of TYST to treatments, by cloning human TYST cells and investigating the histology, ultra-structure, growth kinetics and expression of specific proteins of cloned cells. We found biological characteristics of cloned TYST cells were similar to the yolk sac tumor and differentiated from the columnar to glandular-like or goblet cells-like cells. Chromosomes for tumor identification in each passage met nature of the primary tumor. TYST cells were more sensitive to all-trans-retinoic acid which had significantly inhibitory effects on cell proliferation. Cisplatin induced apoptosis of TYST cells through the activation of p53 expression and down-regulation of Bcl- expression. Thus, we believe that cloned TYST cells and the animal model developed here are useful to understand the molecular mechanism of TYST cells and develop potential therapies for human TYST.

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Section: Discussionsupporting

confidence: 88%

Evaluation of cloned cells, animal model, and ATRA sensitivity of human testicular yolk sac tumor

et al. 2012

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“…Although deletion and duplication of the APC has been associated with testicular dysgenesis syndrome (TDS) and other testicular abnormities (48), its loss in SCO has heretofore not been described. Additionally, mutations and hypermethylation of the APC gene has been observed in human testicular yolk sac tumor patients (2), and a progressive decrease in male fertility was noted in APC min/ϩ mice, a well-studied mouse model of colon cancer (49). However, the mechanisms involved in APC-mediated infertility were not reported.…”

Section: Discussionmentioning

confidence: 99%

“…M utations in adenomatous polyposis coli (APC), a multifunction tumor suppressor, are associated with development of various human cancers, including colon, liver, ovarian, endometrial, and testicular cancers (1)(2)(3)(4). The most prominent role played by APC in the cell is to inhibit Wnt/␤-catenin signaling by at least three different mechanisms.…”

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confidence: 99%

Adenomatous Polyposis Coli (APC) Is Essential for Maintaining the Integrity of the Seminiferous Epithelium

Tanwar

Zhang

Teixeira

2011

Molecular Endocrinology

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Sertoli cells provide the microenvironment necessary for germ cell development and spermatogenesis; disruption of Sertoli cell morphology or function can lead to germ cell aplasia, which is observed in testicular dysgenesis syndrome. Mutation of the adenomatous polyposis coli (APC) gene has been associated with various human cancers, including testicular cancer, but its involvement in nonmalignant testicular pathologies has not been reported. We have developed a mouse model (APC(cko)) that expresses a truncated form of APC in Sertoli cells. Despite normal embryonic and early postnatal testicular development in APC(cko) mice, premature germ cell loss and Sertoli cell-only seminiferous tubules were observed in mutant testes without affecting Sertoli cell quiescence, apoptosis, or differentiation, which were confirmed by the absence of both proliferating cell nuclear antigen, DNA strand breaks, and anti-Müllerian hormone, respectively. We show that mutant Sertoli cells lose their apical extensions, which would normally enclose germ cells during various stages of spermatogenesis, and were unable to maintain the blood-testis barrier because of disrupted expression of junctional proteins. We also observed an up-regulation of Snail and Slug, markers suggestive of epithelial-mesenchymal transition in the Sertoli cells, but tumorigenesis was not observed. No comparable phenotype was observed with Sertoli cell-specific loss-of-function mutations in β-catenin, leading us to speculate that truncation of APC in Sertoli cells results in progressive degeneration of the seminiferous tubules by a mechanism that disrupts the integrity of Sertoli cell junctions independently of APC-regulated β-catenin activities and leads to development of a Sertoli cell-only phenotype.

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“…To date, the function of APC in human testes is unclear [14]. Most mutations of the APC gene are frameshift mutations, however, it is recognised that a number of tumors demonstrated LOH of this gene.…”

Section: Discussionmentioning

confidence: 99%

Loss of heterozygosity of selected tumor suppressor genes in human testicular germ cell tumors

Vladušić

Hrašćan

Vrhovac

et al. 2010

Pathology - Research and Practice

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Involvement of adenomatous polyposis coli (APC) gene in testicular yolk sac tumor of infants

Cited by 17 publications

References 24 publications

Evaluation of cloned cells, animal model, and ATRA sensitivity of human testicular yolk sac tumor

Evaluation of cloned cells, animal model, and ATRA sensitivity of human testicular yolk sac tumor

Adenomatous Polyposis Coli (APC) Is Essential for Maintaining the Integrity of the Seminiferous Epithelium

Loss of heterozygosity of selected tumor suppressor genes in human testicular germ cell tumors

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