Consensus review of the clinical utility of dna cytometry in bladder cancer

Wheeless, Leon L.; Badalament, Robert A.; White, Ralph W. deVere; Fradet, Yves; Tribukait, Bernhard

doi:10.1002/cyto.990140504

Cited by 108 publications

(63 citation statements)

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“…The fact that differences in responsiveness to treatment between hypertetraploid tumors and tumors of lower ploidy were not statistically significant may reflect both the relatively small number of patients represented in the hypertetraploid group, as well as the relatively poor overall responses of tumors with lesser degrees of aneuploidy. High recurrence rates and poor survival among non-tetraploid aneuploid and multiploid tumors have been noted by others (34). It is likely that many of these tumors contained hypertetraploid cells.…”

Section: (34)mentioning

confidence: 84%

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Origins and clinical implications of aneuploidy in early bladder cancer

et al. 1995

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Cytogenetic and flow cytometric studies in a variety of human solid tumors have suggested that gross aneuploidy may arise by a process of abrupt chromosome complement doubling followed by gradual chromosome loss. However, this sequence has not been demonstrated directly in serial studies in individual patients in vivo. The purpose of this study was to search for evidence of chromosome complement doubling and subsequent chromosome loss in flow cytometric ploidy patterns in serial bladder washings and/or biopsies from individual patients with early bladder cancer. Fifty-two patients with noninvasive bladder cancer were followed with serial flow cytometric DNA studies for periods ranging from 5.1 to 42.7 months (median 15.1 months). Serial changes in DNA ploidy and S phase fractions were recorded and correlated with histologic and/or cytologic findings, response to treatment and clinical outcome. The data suggest a series of genetic evolutionary changes in early bladder cancer that include the initial development of peridiploid aneuploidy and repeated rounds of DNA content doubling with chromosome loss in patients with progressive disease. It is likely that gross DNA aneuploidy, and more specifically, DNA multiploidy and DNA hypertetraploidy, all arise by this mechanism. The sequence of DNA diploidy, peridiploid aneuploidy, neartetraploidy, hypotetraploidy and hypertetraploidy is associated with a progressive increase in S phase fraction, and with increasing tumor grade; late steps in this ploidy sequence were often present in tumors that were refractory to local therapeutic measures and tumors that developed deep tumor invasion and/or distant metastases. We conclude that DNA multiploidy and hypertetraploidy are markers of advanced stages of genetic evolution in human bladder cancer. o 1995 Wiley-Liss, Inc.Key terms: Aneuploidy, bladder cancer, prognosis, flow cytometry, tetraploidization Unlike the leukemias, human solid tumors frequently exhibit gross aneuploidy, with chromosome counts often in the range of 60-90 per cell (or a DNA index of 1.3 or greater by flow cytometric DNA analysis). While gross aneuploidy has been implicated in the development and progression of many human solid tumors, its value as a clinical prognostic factor has been controversial. In a recent consensus conference sponsored by the National Cancer Institute, a panel of experts concluded that aneuploidy is a useful prognostic factor in such tumors as ical methods might be helpful in uncovering statistical interactions among various clinical prognostic factors. However, a more fundamental understanding of the biology of the various genetic processes that drive tumor evolution and the mechanisms that underlie the interactions among them may ultimately provide more useful clinical prognostic information.Received for publication June 21, 1994; accepted May 1, 1995. This work was supported by Allegheny-Singer Research Institute grant superficial bladder cancer (34) and in prostate cancer (26), but is not an independent prognostic factor in br...

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Section: (34)mentioning

confidence: 84%

“…This work was supported by Allegheny-Singer Research Institute grant superficial bladder cancer (34) and in prostate cancer (26), but is not an independent prognostic factor in breast cancer (1 1).…”

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confidence: 99%

Origins and clinical implications of aneuploidy in early bladder cancer

et al. 1995

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“…Although urinary cells are readily accessible for cytological examination, the sensitivity (and specificity) of cytology alone is poor in low-grade tumors [12]. Previous studies have suggested that DNA measurement of urinary cells by FCM or image cytometry could be a valuable tool for the diagnosis of bladder cancer recurrences (reviewed in [26]). The results of this study indicate that the sensitivity of FISH for detection of aberrant urinary cells could be even higher than the sensitivity of FCM.…”

Section: Discussionmentioning

confidence: 99%

“…Despite evidence for a diagnostic significance ofDNA aneuploidy [5,6,24,26], DNA measurement has not become a routine examination in bladder cancer patients. This is probably due to the need for expensive equipment and specially trained personel to perform either flow cytometry (FCM) or DNA image cytometry.…”

Section: Introductionmentioning

confidence: 99%

DNA aberrations in urinary bladder cancer detected by flow cytometry and FISH

et al. 1997

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Detection of molecular alterations is of potential significance for diagnosis and prognosis in bladder cancer. Fluorescence in situ hybridization (FISH) allows visualization and quantitation of genes and chromosomes on a cell by cell level and can easily be applied to urinary cells. To evaluate the sensitivity of FISH for detection of DNA aberrations in bladder cancer, formalin-fixed tissues of 293 tumors were examined by FISH and flow cytometry (FCM). Centromere probes for the chromosomes X, Y, 1, 7, 9, and 17 were used for FISH analysis. FISH was more sensitive for detection of quantitative DNA aberrations than FCM. An aberration of at least one chromosome was found in 107 of 108 tumors (99%), which were tetraploid, aneuploid, or multiploid, and in 29 of 49 tumors (59%), which were diploid, by FCM. The frequency of FISH aberrations showed greater differences between pTa (47%) and pT 1 tumors (85 %; P < 0.0001) than between stages pT 1 and pT2-4 (98%). The marked genetic difference between pTa and pT1 tumors argues against the concept of grouping pTa and pTl tumors together as "superficial bladder cancer." The frequency of tumors with chromosomal aberrations detected by FISH increased with the number of chromosomes examined. Aneusomy was seen in 68% of grade 1 tumors examined for >4 chromosomes, suggesting that the cytological diagnosis of bladder cancer recurrences could be substantially improved by FISH.

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“…DNA ploidy analysis of bladder tumor specimens by flow cytometry can provide prognostic and diagnostic information (1,4). As the instrumentation for microscope based measurements has improved, the members of the Marker Network have attempted to extrapolate the flow cytometric results to DNA analysis by image cytometry.…”

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confidence: 99%