Cytogenetic Analysis of 39 Prostate Carcinomas and Evaluation of Short Term Tissue Culture Techniques

König, Josée J.; Teubel, Wilma; Kamst, Eric; Romijn, Johannes C.; Schröder, Fritz H.; Hagemeijer, Anne

doi:10.1016/s0165-4608(97)00224-0

Cited by 19 publications

(10 citation statements)

References 21 publications

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“…The technical aspects of these analyses are not perfected, and the field looks optimistically at new technologies as they are developed to help answer questions and provide new clues to the chromosomal basis of this disease. Cell culturing methods and in vitro conditions clearly are not yet ideal to grow prostate tumor cells, and several groups have shown that variations in specific components of growth medium and methods used appear to improve the outgrowth of the correct cells [10,11,15,72].…”

Section: Discussionmentioning

confidence: 99%

“…It is apparent from that summary that there is clearly clustering of ''activity'' at certain chromosomal sites. Genetic instability, showing rearrangements, gains, and losses at the same re- [8,10,11,. Small circles represent sites at which any structural abnormalities were reported in 2-10 different tumors; large circles represent sites at which any structural abnormalities were reported in >10 different tumors.…”

Section: Datamentioning

confidence: 99%

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Chromosomal clues to the development of prostate tumors

et al. 1999

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BACKGROUND Cytogenetic, molecular cytogenetic, and molecular studies of prostate cancer have revealed an enormous amount of data regarding chromosomal loci that are aberrant in prostate tumors. METHODS These data have been compared and condensed in this review to determine which chromosomes and chromosome sites have been most frequently reported. RESULTS Loss of the Y chromosome, gain of 7, 8, and X, and interstitial deletions on 6q, 7q, 8p, 10q, 13q, 16q, 17q, and 18q are the most prevalent. CONCLUSIONS A potential model for genetic control of tumor progression is presented, as are data regarding the evaluation of a new series of tumors. Prostate 38:303–312, 1999. © 1999 Wiley‐Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

Section: Datamentioning

confidence: 99%

Chromosomal clues to the development of prostate tumors

et al. 1999

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“…In contrast, primary cultures derived from adenocarcinomas are often diploid, especially when analyzed by standard karyotyping methods [Micale et al, 1992;Konig et al, 1993a;Ketter et al, 1996]. However, clonal chromosomal aberrations are found in a subset of primary cultures of cancer cells [Brothman et al, 1990[Brothman et al, , 1991Limon et al, 1990;Arps et al, 1993;Jones et al, 1994;Webb et al, 1996;Chopra et al, 1997;Konig et al, 1998]. When sensitive methods such as fluorescence in situ hybridization (FISH) are employed, up to 80% of primary cultures derived from cancers have been reported to have clonal abnormalities [Brothman et al, 1992;Szucs et al, 1994].…”

Section: Chromosomal Aberrationsmentioning

confidence: 99%

Are primary cultures realistic models of prostate cancer?

Peehl

2003

J of Cellular Biochemistry

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Primary cultures fill a unique niche among the repertoire of in vitro model systems available to investigate the biology of the normal and malignant human prostate. This review summarizes some of the properties of primary cultures, with special emphasis on two questions: are primary cultures from adenocarcinomas really comprised of cancer rather than normal cells, and do primary cultures faithfully retain characteristics of cells of origin?

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“…While the molecular pathogenesis of the disease is largely unknown, it has been suggested to involve a series of genetic alterations affecting both tumor suppressor genes and oncogenes (Sandberg, 1992;Isaacs, 1995;Kallioniemi and Visakorpi, 1996). Identification of structural chromosome abnormalities in prostate cancer has traditionally relied on karyotyping by banding techniques (Sandberg, 1992;Konig et al, 1998;Brothman et al, 1999). Numerical and structural alterations of several different chromosomes have been found without preferential involvement of any single chromosome.…”

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confidence: 99%

Characterization of chromosomal abnormalities in prostate cancer cell lines by spectral karyotyping

Pan¹,

Kytölä²,

Farnebo³

et al. 1999

Cytogenet Genome Res

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Human prostate cancer is characterized by multiple gross chromosome alterations involving several chromosome regions. However, the specific genes involved in the development of prostate tumors are still largely unknown. Here we have studied the chromosome composition of the three established prostate cancer cell lines, LNCaP, PC-3, and DU145, by spectral karyotyping (SKY). SKY analysis showed complex karyotypes for all three cell lines, with 87, 58/113, and 62 chromosomes, respectively. All cell lines were shown to carry structural alterations of chromosomes 1, 2, 4, 6, 10, 15, and 16; however, no recurrent breakpoints were detected. Compared to previously published findings on these cell lines using comparative genomic hybridization, SKY revealed several balanced translocations and pinpointed rearrangement breakpoints. The SKY analysis was validated by fluorescence in situ hybridization using chromosome-specific, as well as locus-specific, probes. Identification of chromosome alterations in these cell lines by SKY may prove to be helpful in attempts to clone the genes involved in prostate cancer tumorigenesis.

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Cytogenetic Analysis of 39 Prostate Carcinomas and Evaluation of Short Term Tissue Culture Techniques

Cited by 19 publications

References 21 publications

Chromosomal clues to the development of prostate tumors

Chromosomal clues to the development of prostate tumors

Are primary cultures realistic models of prostate cancer?

Characterization of chromosomal abnormalities in prostate cancer cell lines by spectral karyotyping

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