Trisomy 7: A potential cytogenetic marker of human prostate cancer progression

Bandyk, Mark; Pisters, Louis L.; Eshenbach, Andrew C. Von; Chung, Leland W.K.; Zhao, Lian; Liang, Jan C.; Troncoso, Patricia; Palmer, J. Lynn

doi:10.1002/gcc.2870090105

Cited by 92 publications

(50 citation statements)

References 22 publications

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“…In particular, losses of heterozygosity at chromosomes 8p, 10q, 13q, and 17p are frequent events, and losses of 6q, 7q, 16q, and 18q have also been reported, although they are not as well characterized (Latil et al 1994;Zenklusen et al 1994;Takahashi et al 1995;Cooney et al 1996a;Cunningham et al 1996;Elo et al 1997;Latil et al 1997;Saric et al 1999). In addition, although chromosome gains appear to be less frequent than chromosome losses, gains at 8q and 7 are fairly common (Alcaraz et al 1994;Bandyk et al 1994;Van Den Berg et al 1995).…”

Section: A Pathway For Prostate Cancer Initiation and Progression: Anmentioning

confidence: 99%

Molecular genetics of prostate cancer

Abate‐Shen¹,

Shen²

2000

Genes Dev.

606

521

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Prostate cancer afflicts one man in nine over the age of 65 and represents the most frequently diagnosed cancer in American men (Coffey 1993). Early detection through serum testing for prostate specific antigen (PSA) and improved procedures for surgical intervention and radiation therapy have significantly reduced the number of fatalities; however, there is still no effective cure for men with advanced disease. Therefore, much research has been dedicated to identifying prognostic markers that distinguish indolent versus aggressive forms of prostate cancer. In contrast, significantly less research has been devoted to understanding the molecular mechanisms that underlie normal prostate growth and development or cancer initiation and progression.In this review, we address recent progress toward the central objectives of understanding parameters of normal versus abnormal prostatic development and of elucidating a molecular pathway for prostate cancer progression. We focus on key regulatory molecules that have been implicated by analysis of patterns of allelic loss in human prostate cancers and/or by reverse genetic approaches in the mouse.

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Section: A Pathway For Prostate Cancer Initiation and Progression: Anmentioning

confidence: 99%

Molecular genetics of prostate cancer

Abate‐Shen¹,

Shen²

2000

Genes Dev.

606

521

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“…Trisomy 7, which has been described as a common anomaly in solid malignant tumours (Weaver et al, 1988;Belge et al, 1994), was found in four (14%) cases (Case 3,16,23,27). In a previous study, trisomy 7 was reported to serve as a novel marker for human prostate cancer progression (Bandyk et al, 1994), and several authors (Collard et al, 1987;Trent et al, 1990) (Arps et al, 1993), and that the most common clonal numerical aberration was loss of Y in 5 of 62 (8%) prostatic adenocarcinomas . A previous report (Aly et al, 1994) combining conventional cytogenetic analysis and FISH of short-term culture of benign prostatic hyperplasia showed loss of chromosome Y to be the most common chromosomal change.…”

Section: Discussionmentioning

confidence: 96%

Interphase cytogenetics of prostate cancer: fluorescence in situ hybridisation (FISH) analysis of Japanese cases

Mizunuma

Shiraishi²,

Yatani³

et al. 1996

Br J Cancer

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Summary No numerical aberration of chromosomes that might be specific for prostate cancer has so far been established. We used fluorescence in situ hybridisation (FISH) with centromere-specific probes for chromosomes 7, 8, 17, X and Y to establish the distribution of centromere copy numbers in frozen-stored or freshly prepared samples of benign prostate hypertrophy (BPH) and to detect numerical aberrations of these chromosomes in 28 prostate cancers from Japanese men. There was no significant difference in the data of centromere copy numbers between fresh and frozen-stored tissue. The most common aberration in prostate cancers was a gain of chromosome 8 (57%), with numerical aberration of chromosome 7 being the second most frequent anomaly (50%). Numerical aberration of chromosome 7 is most significantly associated with a higher Gleason score (GS) (P<0.005) or with lymph node metastasis (P<0.001). Numerical aberration of several chromosomes, including chromosomes 7 and/or 8, was common in aggressive prostate cancers. Loss of chromosome Y was detected in only 4% of cases. FISH analysis thus proved to be a useful method for detecting numerical aberrations of individual chromosomes, with application to touch preparations of frozenstored tissue having the advantage of exact sampling of cancer foci. The results suggest that numerical aberration of chromosome 7 is associated with aggressive tumour behaviour and poor prognosis of patients with prostate cancer. The association between genetic change and chromosomal abnormality should be studied in detail.Keywords: interphase cytogenetics; fluorescence in situ hybridization; prostate cancer Fluorescence in situ hybridisation (FISH) has been used to hybridise specific nucleic acid sequences with complemental DNA fragments, revealing their location on chromosomes and their copy numbers (Trask et al., 1990). Compared with conventional metaphase cytogenetics or karyotyping analysis, FISH allows more rapid enumeration of specific chromosomes and detection of chromosomal alterations even in interphase nuclei (interphase cytogenetics) as well as in metaphase nuclei (Cremer et al., 1986;Pinkel et al., 1986). This technique does not always require tissue culturing and can be applied to solid tumours (Persons et al., 1993;Devilee et al., 1988) and even formalin-fixed, paraffin-embedded tissues (Micale et al., 1993;Persons et al., 1994). FISH has been demonstrated to be more sensitive than flow cytometry (FCM) for detecting aneuploidy (Takahashi et al., 1994;Visakorpi et at., 1994), and the methodology can detect numerical aberrations of individual chromosomes at levels impossible with FCM and image cytometry (ICM). FCM also has limitations regarding minor quantitative DNA changes (Hopman et al., 1990). While the application of FISH to studies of the association between DNA aneuploidy and prognosis has attracted attention, no numerical aberration of any chromosome which might be specific for prostate cancer has so far been established. Furthermore, it is unclear whether the numeri...

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“…Trisomy 7 is, however, increased in epithelial tumor cells of colon carcinoma 42 and is considered to correlate with tumor progression in human prostate cancer. 43 Trisomy 7, and a stepwise increase of non-random trisomies, is also a characteristic abnormality in benign thyroid tumors. 44 Loss of the Y chromosome and trisomy 7 were the most common abnormalities noted in benign prostatic hyperplasia, 45 although the authors point out the possibility that the trisomic cells may be infiltrating lymphocytes, which may have trisomy 7.…”

Section: Discussionmentioning

confidence: 99%

Increased frequency of chromosome abnormalities in fibroblasts from hairy cell leukemia patients

et al. 1997

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A hereditary component is implicated in many different cancers, including hairy cell leukemia (HCL), and may involve an instability of the genome. We have previously documented recurrent clonal and non-clonal chromosomal abnormalities in hairy cells. To ascertain whether this instability of the genome is restricted to the malignant cells or if it might also include normal cells we performed cytogenetic investigations on skin fibroblasts and hairy cells from eight HCL patients and skin fibroblasts from eight referents. The frequency of chromosome abnormalities, regardless of clonality, was significantly increased in the fibroblasts from patients compared to referents. Also, five patients compared to one referent showed clonal abnormalities in their fibroblasts. Immunohistochemical investigations excluded the possibility that the fibroblast cultures were contaminated with hairy cells. Two patients had constitutional abnormalities, inv(5)(p13.1q13.3) and t(13;14), and one additional patient, possibly mosaic, showed the same abnormality, inv (9)

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Trisomy 7: A potential cytogenetic marker of human prostate cancer progression

Cited by 92 publications

References 22 publications

Molecular genetics of prostate cancer

Molecular genetics of prostate cancer

Interphase cytogenetics of prostate cancer: fluorescence in situ hybridisation (FISH) analysis of Japanese cases

Increased frequency of chromosome abnormalities in fibroblasts from hairy cell leukemia patients

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