Numeric Alterations in Chromosomes 7 and 8 Detected by Fluorescent in situ Hybridization Correlate with High-Grade Localized Prostate Cancer

Barranco, Miguel Angel Molinero; Alcaraz, Antonio; Corral, Juan Manuel; Sole, M.; Mallofré, Carmen; Llopis, Juan; Rodríguez, Alfredo Nodarse; Ribal, María J.; Álvarez-Vijande, R.; Carretero, P

doi:10.1159/000019776

Cited by 10 publications

(4 citation statements)

References 16 publications

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“…The frequency of trisomy 7 was statistically higher in pT3 stage (64%) and in bony metastatic tumors (33%) showing the association of trisomy 7 with aggressive tumor and poor prognosis. Aneusomy of chromosome 7 was reported to be associated with higher histological grade, advanced pathological stage, and early PC death in other studies (12,14,(30)(31)(32). Trisomy 7 was described as a common anomaly in prostate carcinoma (22,(33)(34)(35) and was associated with aggressive tumor behavior and poor prognosis (13,15,36).…”

Section: Discussionmentioning

confidence: 94%

Chromosomal changes in prostate cancer: A fluorescence in situ hybridization study

Das¹,

Lau²,

Sivaswaren³

et al. 2005

Clinical Genetics

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The incidence of prostate cancer (PC) is increasing steadily with the aging population in Singapore. As the pattern of chromosomal aberrations in Asian men with PC is poorly understood, we investigated the numerical aberrations for chromosomes 7, 8, 11, and 17 by fluorescence in situ hybridization (FISH). FISH was performed on standard sections and tissue microarrays of 54 PC and 33 benign prostatic hyperplasia (BPH) specimens. Among the 54 PC specimens, FISH detected 44 cases as aneusomy and two as disomy and was unsuccessful for eight cases. Cytogenetic alterations of two or more chromosomes per tumor were detected in 33/46 (72%) PCs. The most frequent alteration was aneusomy of chromosome 8 detected in 34/46 (74%) cases followed by numerical aberrations in chromosome 7 (61%). Gain of 8q24, loss of chromosome 7, and gain of 11q13 were associated with higher Gleason score and were statistically significant. Gain of chromosome 7 was more common in locally advanced disease, while gain of chromosome 11q13 and chromosome 7 was more common in metastatic disease.

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Section: Discussionmentioning

confidence: 94%

Chromosomal changes in prostate cancer: A fluorescence in situ hybridization study

Das¹,

Lau²,

Sivaswaren³

et al. 2005

Clinical Genetics

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“…(22); TSU-Prl, 80 (14), and DuPro-1, about 96 (8). It may be worth noting that aneusomy of chromosomes 7 and 8 has been associated with prostate cancer (1,5,15,20). were subsequently injected with cells from this tumor.…”

Section: Resultsmentioning

confidence: 99%

A new human prostate carcinoma cell line, 22Rv1

Sramkoski

Pretlow

Giaconia

et al. 1999

In Vitro Cell.Dev.Biol.-Animal

499

442

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A cell line has been derived from a human prostatic carcinoma xenograft, CWR22R. This represents one of very few available cell lines representative of this disease. The cell line is derived from a xenograft that was serially propagated in mice after castration-induced regression and relapse of the parental, androgen-dependent CWR22 xenograft. Flow cytometric and cytogenetic analysis showed that this cell line represents one hyper DNA-diploid stem line with two clonal, evolved cytogenetic sublines. The basic karyotype is close to that of the grandparent xenograft, CWR22, and is relatively simple with 50 chromosomes. In nude mice, the line forms tumors with morphology similar to that of the xenografts, and like the parental CWR22 and CWR22R xenografts, this cell line expresses prostate specific antigen. Growth is weakly stimulated by dihydroxytestosterone and lysates are immunoreactive with androgen receptor antibody by Western blot analysis. Growth is stimulated by epidermal growth factor but is not inhibited by transforming growth factor-beta1.

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“…Monosomy 8 has been described in conjunction with other genetic abnormalities in prostatic adenocarcinoma (12, 25). Trisomy 7 has also been reported in peritumoural, non‐neoplastic tissues and cell cultures from normal brain (2, 11, 39), and it has been suggested that gain of chromosome 7 in neoplastic and non‐neoplastic tissues may be an aging phenomenon (3, 17).…”

Section: Discussionmentioning

confidence: 99%

Genome‐Wide Analysis of Subependymomas Shows Underlying Chromosomal Copy Number Changes Involving Chromosomes 6, 7, 8 and 14 in a Proportion of Cases

et al. 2008

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Subependymomas (SE) are slow-growing brain tumors that tend to occur within the ventricles of middle-aged and elderly adults. The World Health Organization classifies these tumors within the ependymoma group. Previous limited analysis of this tumor type had not revealed significant underlying cytogenetic abnormalities.We have used microarray comparative genomic hybridization to study a series of SE (n = 12). A whole-genome array at 0.97-Mb resolution showed copy number abnormalities in five of 12 cases (42%). Two cases (17%) showed regions of loss on chromosome 6. More detailed analysis of all cases using a chromosome 6 tile-path array confirmed the presence of overlapping regions of loss in only these two cases. One of these cases also showed trisomy chromosome 7. Monosomy of chromosome 8 was seen in a further two cases (17%), and a partial loss on chromosome 14 was observed in one additional case. This is the first array-based, genome-wide study of SE. The observation that five of 12 cases examined (42%) at 0.97-Mb resolution showed chromosomal copy number abnormalities is a novel finding in this tumor type.

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Numeric Alterations in Chromosomes 7 and 8 Detected by Fluorescent in situ Hybridization Correlate with High-Grade Localized Prostate Cancer

Cited by 10 publications

References 16 publications

Chromosomal changes in prostate cancer: A fluorescence in situ hybridization study

Chromosomal changes in prostate cancer: A fluorescence in situ hybridization study

A new human prostate carcinoma cell line, 22Rv1

Genome‐Wide Analysis of Subependymomas Shows Underlying Chromosomal Copy Number Changes Involving Chromosomes 6, 7, 8 and 14 in a Proportion of Cases

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