Cytogenetic heterogeneity and histologic tumor growth patterns in prostatic cancer

Alers, Janneke C.; Krijtenburg, Pieter Jaap; Vissers, C. J.; Bosman, Fred T.; Kwast, Theodorus H. van der; Dekken, Herman van

doi:10.1002/cyto.990210116

Cited by 26 publications

(12 citation statements)

References 37 publications

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“…Using interphase cytogenetics, we and others found that numerical chromosomal aberrations are unevenly distributed among different tumour foci within the prostatic gland. 7,15 Marked intra-tumour heterogeneity was also found in a case of metastatic carcinoma by comparative genomic hybridisation. 54 With microsatellite analysis, different patterns of allelic loss at 8p and 17q were observed among different tumour foci and PIN areas.…”

Section: Allelic Losses In Prostatic Cancermentioning

confidence: 93%

Allelic losses at 8p, 10q, 11p, 13q, 16q, 17p, and 18q in prostatic carcinomas: The impact of zonal location, Gleason grade, and tumour multifocality

Erbersdobler

Graefen

Wullbrand

et al. 1999

Prostate Cancer Prostatic Dis

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Molecular genetic investigations have made it clear that the development and progression of prostate cancer is associated with losses of genetic material in certain chromosomal arms. However, there are only few data about the question of whether the zonal location, a higher Gleason grade, or multifocality of the tumour have any in¯uence on the pattern of allelic losses.In the present study, 48 tumour foci from 32 radical prostatectomy specimens were investigated for allelic losses at chromosomes 8p, 10q, 11p, 13q, 16q, 17p, and 18q with a set of 20 microsatellite markers. The results were analysed for the zonal location of the tumour foci and the presence of a Gleason grade 4 differentiation.Overall, focal allelic losses at 8p, 10q, 11p, 13q, 16q, 17p, and 18q were observed in 62.5%, 17.2%,. 3.2%, 18.8%, 40%, 9.7%, and 22.6% of the 32 cases, respectively. Comparing the frequencies of allelic losses with the zonal location or the Gleason grade, no highly signi®cant correlations were found at any chromosomal locus investigated. However, the observation of different patterns of allelic losses in 12 of 14 cases containing more than one tumour focus indicates a high rate of genetic heterogeneity.We conclude that allelic losses at the chromosomal loci investigated are not strongly associated with a speci®c zonal location or a higher Gleason grade of prostatic carcinoma. Genetic heterogeneity of multiple tumour foci within one gland might contribute to the dif®culties in predicting the prognosis for this common malignancy.

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Section: Allelic Losses In Prostatic Cancermentioning

confidence: 93%

Allelic losses at 8p, 10q, 11p, 13q, 16q, 17p, and 18q in prostatic carcinomas: The impact of zonal location, Gleason grade, and tumour multifocality

Erbersdobler

Graefen

Wullbrand

et al. 1999

Prostate Cancer Prostatic Dis

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“…Likewise, Macoska et al (1994) showed loss of 8p22 sequences in frozen tissue sections of prostatic tumors by FISH. Further, intratumoral heterogeneity for both ploidy and chromosomal aberrations appeared a prominent feature of prostatic adenocarcinomas (Alers et al 1995b). Another study by our group described aneuploidy and loss of the Y chromosome in prostatic intraepithelial neoplastic lesions adjacent to adenocarcinoma (Alers et al 1995a).…”

Section: Esophageal Cancermentioning

confidence: 94%

Interphase cytogenetics and comparative genomic hybridization of human epithelial cancers and precursor lesions

Dekken

Rosenberg

Krijtenburg

et al. 1997

Histochemistry and Cell Biology

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The accuracy of cytogenetic analyses of human solid cancers has improved enormously over the past decade by the introduction and refinement of DNA in situ hybridization (ISH) techniques. This methodology can be applied to cells in the interphase state, thereby making it an excellent tool for the delineation of chromosomal aberrations in solid tumors. The use of non-isotopic ISH to intact and disaggregated cancer specimens will be discussed, as well as comparative genomic hybridization (CGH) with tumor-derived DNAs. In this review we will focus on hybridocytochemical interphase approaches for the detection of chromosomal changes in frequently occurring human epithelial malignancies, e.g., breast, lung, and prostate carcinomas. We will further discuss the use of ISH procedures for the genetic analysis of precursor conditions leading to invasive carcinomas. Knowledge concerning these precancerous conditions is increasing, and its importance in cancer prevention has been recognized. Interphase cytogenetics by ISH, as well as CGH, with DNAs derived from microdissected, precancerous, dysplastic tissue areas will increase our understanding of these lesions, both at the investigative and diagnostic levels.

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“…[9][10][11][12][13][14] A large amount of data has been generated about alterations, aberrations, rearrangements, gain, or loss of Y-chromosome materials in prostate cancer using different techniques of molecular cytogenetics. [15][16][17][18][19][20] The simple fact that the Y chromosome and prostate cancer have male-specificity in common lead many researchers to investigate if there is Y involvement in such a male-specific cancer, however, yet there is no clear conclusions. [21][22][23] Except for the pseudoautosomal region, all other Y-linked loci on the nonrecombining part of the Y chromosome are haploid and paternally inherited.…”

Section: Introductionmentioning

confidence: 99%

Prostate cancer incidence varies among males from different Y-chromosome lineages

Ewis

Lee

Naroda

et al. 2006

Prostate Cancer Prostatic Dis

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The incidence rate of prostate cancer in African-American males is two times higher than Caucasian men and ten times higher than Japanese men. The geographical specificity of Y haplogroups implies that males from different ethnic groups undoubtedly have various Y lineages with different Y-chromosomal characteristics that may affect their susceptibility or resistance to such a malespecific cancer. To confirm this hypothesis we studied the Y-chromosomal haplogroups of 92 Japanese prostate cancer patients comparing them with randomly selected 109 unrelated healthy Japanese male controls who were confirmed to be residents of the same geographical area. Males could be classified using three binary Y-chromosome markers (sex-determining region Y (SRY), YAP, 47z) into four haplogroups DE, O2b*, O2b1, and untagged group. Our results confirmed that prostate cancer incidence varies among males from different Y-chromosome lineages. Males from DE and the untagged haplogroups are at a significantly higher risk to develop prostate cancer than O2b* and O2b1 haplogroups (P ¼ 0.01), odds ratio 2.17 and 95% confidence interval (1.16-4.07). Males from haplogroup DE are over-represented in the patient group showing a percentage of 41.3%. The underlying possible causes of susceptibility variations of different Y lineages for such a male-specific cancer tumorigenesis are discussed. These findings explain the lower incidence of prostate cancer in Japanese and other South East Asian males than other populations. To our knowledge, this is the first reliable study examining the association between prostate cancer and Y-chromosomal haplogroups, comparing prostate cancer patients with carefully selected matched controls.

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Cytogenetic heterogeneity and histologic tumor growth patterns in prostatic cancer

Cited by 26 publications

References 37 publications

Allelic losses at 8p, 10q, 11p, 13q, 16q, 17p, and 18q in prostatic carcinomas: The impact of zonal location, Gleason grade, and tumour multifocality

Allelic losses at 8p, 10q, 11p, 13q, 16q, 17p, and 18q in prostatic carcinomas: The impact of zonal location, Gleason grade, and tumour multifocality

Interphase cytogenetics and comparative genomic hybridization of human epithelial cancers and precursor lesions

Prostate cancer incidence varies among males from different Y-chromosome lineages

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