Cancer in Young Adutts (Ages 15 to 34)

Silverberg, B S Edwin

doi:10.3322/canjclin.32.1.32

Cited by 43 publications

(8 citation statements)

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“…Testicular cancer is a relatively rare malignancy; however, an estimated 7,400 new cases were reported in the United States in 1999, and it is the most common cancer of men between the ages of 15 and 34 (1,2). Based on morphological features, germ cell tumors are divided into seminoma, yolk sac tumor, embryonal carcinoma, choriocarcinoma, and teratoma according to the WHO International Histological Classification of Testicular Tumors (3).…”

Section: Introductionmentioning

confidence: 99%

Gene Expression Profiling of Early- and Late-Relapse Nonseminomatous Germ Cell Tumor and Primitive Neuroectodermal Tumor of the Testis

Sugimura

Foster

Cummings³

et al. 2004

Clinical Cancer Research

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Purpose: To better understand the molecular mechanisms that underlay the development and progression of nonseminomatous germ cell tumor of testis (NSGCTT) as well as malignant transformation of teratoma and primitive neuroectodermal tumor (PNET).Experimental Design: We studied the gene expression profiles of 17 retroperitoneal NSGCTTs (10 yolk sac tumors, 3 embryonal carcinomas, 4 teratomas) and 2 PNETs obtained from patients with two clinical outcomes. Tissue samples were obtained from the Indiana University. One group of NSGCTT and PNET patients developed metastases within 2 years (early-relapse) of initial successful treatment, and the other group developed metastases after 2 years (late-relapse). Gene expression in these groups of patients was quantified using cDNA microarrays and real-time relative quantitative PCR.Results: We demonstrate that the gene expression profiles of these tumors correlate with histological type. In addition, we identify type-specific genes that may serve as novel diagnostic markers. We also identify a gene set that can distinguish between early-relapse and late-relapse yolk sac tumors. The expression differences of these genes may underlie the differences in clinical outcome and drug response of these tumors.Conclusion: This is the first study that used gene expression profiling to examine the molecular characteristics of the NSGCTTs and drug response in early-and laterelapse tumors. These results suggest that two molecularly distinct forms of NSGCTTs exist and that the integration of expression profile data with clinical parameters could enhance the diagnosis and prognosis of NSGCTTs. More importantly, the identified genes provide insight into the molecular mechanisms of aggressive NSGCTTs and suggest intervention strategies.

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Section: Introductionmentioning

confidence: 99%

Gene Expression Profiling of Early- and Late-Relapse Nonseminomatous Germ Cell Tumor and Primitive Neuroectodermal Tumor of the Testis

Sugimura

Foster

Cummings³

et al. 2004

Clinical Cancer Research

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“…Germ cell tumors (GCTs) are the most common malignant neoplasm of males aged 15-34 and are a major cause of death due to cancer in this age group (Silverberg, 1982). Hypogonadism, cryptorchidism, Klinefelter's syndrome, testicular carcinoma in situ, and prior germ cell tumor are known risk factors for development of GCTs (Krabbe et al, 1979;Einhorn et al, 1986;Lachman et al, 1986).…”

Section: Introductionmentioning

confidence: 99%

Cytogenetic and molecular analysis of human male germ cell tumors: Chromosome 12 abnormalities and gene amplification

Samaniego

Rodríguez

Houldsworth

et al. 1990

Genes Chromosomes & Cancer

149

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We report karyotypic analysis of 24 male germ cell tumors (GCTs) with clonally abnormal karyotypes biopsied from testicular and extragonadal lesions from 20 patients belonging to the histologic categories seminoma, teratoma, embryonal carcinoma, choriocarcinoma, and endodermal sinus tumor. Chromosomes 1, 7, 9, 12, 17, 21, 22, and the X chromosome were nonrandomly gained in these tumors. Nonrandom structural changes affected most frequently chromosomes 1 and 12, the latter as i(12p) and/or del(12)(q13----q22). The i(12p) was seen in 90% of tumors which included all histologic subtypes and gonadal as well as extragonadal presentation. Our present results, along with those from published data on fresh GCT biopsies, establish that i(12p) is a highly nonrandom chromosome marker of all histologic as well as anatomic presentations of GCTs. in contrast, we found del(12)(q13----q22) exclusively in nonseminomatous GCTs (NSGCTs) and mixed GCTs (MGCTs) occurring in 44% of such lesions. Because successful cytogenetic analysis of fresh tumor specimens is not always possible, we developed a method based on DNA analysis to detect i(12p) as increased copy number of 12p. In addition to the changes affecting chromosome 12 identified above, we have detected, for the first time, cytological evidence of gene amplification in the form of homogeneously staining regions (HSRs) and double minute chromosomes (dmins) in treated as well as untreated primary extragonadal and metastatic GCTs and confirmed the presence of amplified DNA in one of these tumors at the molecular level by the in-gel renaturation method. Hybridization of DNA from cultured cells from an HSR-bearing tumor with a panel of probes for genes known to be amplified or otherwise perturbed in diverse tumor systems did not identify the amplified gene, suggesting amplification of a novel gene or genes. This study comprises the largest series of GCT cytogenetics attempted so far. Notably, it includes data on a series of primary mediastinal tumors, a group which previously has not been studied in any detail.

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“…In contrast to immunohistochemically undetectable levels in normal testes and morphologically normal tissue areas in the tumourbearing testes, the accumulation of the p53 protein was clearly identified in a high proportion (59% of cases) of the pre-invasive lesions with positive atypical intratubular germ cells often found in the tissue adjacent to invasive tumours. Altered expression of the p53 protein is therefore a unifying feature of the majority of invasive male germ-cell tumours and the change resulting in high levels of p53 appears to be a relatively early step in the human testicular cancer pathogenesis.Testicular germ-cell tumours are the most common malignancy in males between 15 and 34 years of age and represent a major cause of death due to cancer in this age category (Silverberg, 1982). The histogenesis and relationship of various histological types of testicular germ-cell tumours are complex and not fully understood at present, a fact also reflected by the existence of several classification schemes for this biologically extremely interesting group of neoplasms (Mostofi et al, 1986).…”

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confidence: 99%

p53 Protein alterations in human testicular cancer including pre‐invasive intratubular germ‐cell neoplasia

Bártková

Bartek

Lukáš

et al. 1991

Intl Journal of Cancer

123

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Expression of the p53 oncoprotein was examined in a wide range of primary human testicular germ-cell tumours using a new mouse monoclonal antibody (MAb) BP53-11 raised and characterized in this study, in parallel with a polyclonal rabbit antiserum CM-1. Immunohistochemistry on paraffin sections showed positive nuclear reaction in at least a fraction of malignant cells in 90 (84%) out of 107 cases studied. Aberrant accumulation of the p53 protein was found among testicular tumours of all major histological types, although generally a higher percentage of positive cases and a higher proportion of p53 over-expressing nuclei within individual lesions was observed in embryonal carcinomas when compared with seminomas. The typical heterogeneous staining pattern characteristic of histological specimens was also found in a cultured cell line derived from a human embryonal carcinoma. In contrast to immunohistochemically undetectable levels in normal testes and morphologically normal tissue areas in the tumour-bearing testes, the accumulation of the p53 protein was clearly identified in a high proportion (59% of cases) of the pre-invasive lesions with positive atypical intratubular germ cells often found in the tissue adjacent to invasive tumours. Altered expression of the p53 protein is therefore a unifying feature of the majority of invasive male germ-cell tumours and the change resulting in high levels of p53 appears to be a relatively early step in the human testicular cancer pathogenesis.

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Cancer in Young Adutts (Ages 15 to 34)

Cited by 43 publications

References 0 publications

Gene Expression Profiling of Early- and Late-Relapse Nonseminomatous Germ Cell Tumor and Primitive Neuroectodermal Tumor of the Testis

Gene Expression Profiling of Early- and Late-Relapse Nonseminomatous Germ Cell Tumor and Primitive Neuroectodermal Tumor of the Testis

Cytogenetic and molecular analysis of human male germ cell tumors: Chromosome 12 abnormalities and gene amplification

p53 Protein alterations in human testicular cancer including pre‐invasive intratubular germ‐cell neoplasia

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