Adenocarcinoma of the gallbladder: Chromosome abnormalities in a genetic form of cancer

Hecht, Frederick; Kuban, Donald J.; Berger, Carol S.; Hecht, Barbara K.; Sandberg, Avery A.

doi:10.1016/0165-4608(83)90133-4

Cited by 12 publications

(6 citation statements)

References 5 publications

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“…Although gallbladder cancer is not a particularly rare malignancy, the number of previously reported short-term cultured epithelial gallbladder tumors with chromosomal aberrations-four-is in sharp contrast to the presently 9,000 published karyotypically abnormal human solid tumors (Mitelman, 1998). Moreover, the karyotypic description of the first aberrant gallbladder adenocarcinoma was incomplete due to suboptimal chromosome quality (Hecht et al, 1983). The current series comprising seven abnormal carcinomas, taken together with our three reported cases (Bardi et al, 1994), thus represents the largest cytogenetic database on this tumor type to date.…”

Section: Discussionmentioning

confidence: 95%

“…As regards other highlevel chromosomal gains attractive for molecular examination, it is noteworthy that the MET and WNT2 oncogenes, both in 7q31, have recently been found to be amplified or overexpressed in other malignancies of the alimentary tract, such as gastric (Nessling et al, 1998) and hepatocellular carcinomas (Ljubimova et al, 1997). It is of importance in this context that the cytogenetic findings of dmin and hsr, the chromosome-level manifestations of gene amplifications, by Hecht et al (1983) and in this series (cases 2 and 3), provide further support for the involvement of activating genomic alterations in gallbladder carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

“…In a further genomewide search for molecular alterations associated with gallbladder cancer, the pattern of chromosomal rearrangements could be an essential guide, as it has proved to be for several human neoplasias (Mitelman et al, 1997b). So far, however, karyotypic abnormalities have been reported only in four short-term cultured epithelial gallbladder tumors (Hecht et al, 1983;Bardi et al, 1994), precluding any firm conclusions as regards disease-related aberrations.…”

Section: Introductionmentioning

confidence: 99%

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Nonrandom chromosomal aberrations and cytogenetic heterogeneity in gallbladder carcinomas

Gorunova

Parada

Limon

et al. 1999

Genes Chromosom. Cancer

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Chromosome banding analysis of 11 short‐term cultured gallbladder carcinomas revealed acquired clonal aberrations in seven tumors (five primary and two metastases). Three of these had one clone, whereas the remaining four were cytogenetically heterogeneous, displaying two to seven aberrant clones. Of a total of 21 abnormal clones, 18 had highly complex karyotypes and three exhibited simple numerical deviations. Double minutes and homogeneously staining regions were observed in one and two carcinomas, respectively. To characterize the karyotypic profile of gallbladder cancer more precisely, we have combined the present findings with our three previously reported cases, thereby providing the largest cytogenetic database on this tumor type to date. A total of 287 chromosomal breakpoints were identified, 251 of which were found in the present study. Chromosome 7 was rearranged most frequently, followed by chromosomes 1, 3, 11, 6, 5, and 8. The bands preferentially involved were 1p32, 1p36, 1q32, 3p21, 6p21, 7p13, 7q11, 7q32, 19p13, 19q13, and 22q13. Nine recurrent abnormalities could, for the first time, be identified in gallbladder carcinoma: del(3)(p13), i(5)(p10), del(6)(q13), del(9)(p13), del(16)(q22), del(17)(p11), i(17)(q10), del(19)(p13), and i(21)(q10). The most common partial or whole‐arm gains involved 3q, 5p, 7p, 7q, 8q, 11q, 13q, and 17q, and the most frequent partial or whole‐arm losses affected 3p, 4q, 5q, 9p, 10p, 10q, 11p, 14p, 14q, 15p, 17p, 19p, 21p, 21q, and Xp. These chromosomal aberrations and imbalances provide some starting points for molecular analyses of genomic regions that may harbor genes of pathogenetic importance in gallbladder carcinogenesis. Genes Chromosomes Cancer 26:312–321, 1999. © 1999 Wiley‐Liss, Inc.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Nonrandom chromosomal aberrations and cytogenetic heterogeneity in gallbladder carcinomas

Gorunova

Parada

Limon

et al. 1999

Genes Chromosom. Cancer

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“…The detection of numerical and structural chromosome aberrations has been extremely difficult in the past using conventional karyotyping methods 24. This perhaps explains the scarce cytogenetic information available for gallbladder carcinomas 6,7. However, the development of FISH has allowed such analysis to be done in stored tissues, including paraffin‐embedded specimens,10 and quantitative analysis of numerical chromosome aberrations in formalin‐fixed tissue sections can now be examined in relation to conventional histologic findings 11,23…”

Section: Methodsmentioning

confidence: 99%

“…Recent studies using molecular and immunohistochemical techniques have identified a variety of genetic alterations in gallbladder carcinomas, such as DNA aneuploidy,2 K‐ ras mutation,3 expression of oncogenes,4 and p53 overexpression 5. Structural or numerical chromosomal abnormalities have also been identified by conventional karyotyping methods 6,7. However, to our knowledge, no study has so far examined aneusomy of gallbladder carcinomas.…”

Section: Introductionmentioning

confidence: 99%

Cytogenetic analysis of gallbladder neoplasms using fluorescence in situ hybridization (FISH)

Nanashima

Yamaguchi

Shibasaki

et al. 1997

J Hep Bil Pancr Surg

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To characterize the numerical chromosome aberrations in gallbladder neoplasms, we examined surgically resected tissues using fluorescence in situ hybridization. The aberrations in 15 specimens of adenocarcinomas and 2 adenomas were compared with those in 4 samples of adenomyomatosis and 17 samples of normal epithelium. We calculated the frequency of aneusomy and determined the chromosome indexes (mean number of chromosomes per nucleus) of chromosomes 17 and 18. The pattern of DNA ploidy was analyzed by flow cytometry. In normal epithelium, adenomyomatosis and adenomas, DNA aneuploidy was not observed, while 13 (87%) carcinomas showed DNA aneuploidy, including 2 specimens with multiploidy. ~qo numerical aberrations were observed in normal epithelium and adenomyomatosis. A numerical gain of chromosome 17 was observed in a single adenoma and in 10 (66%) carcinomas. A numerical gain of chromosome 18 was observed in 6 (40%) carcinomas, but not in other tissues. The chromosome index of chromosome 17 was significantly higher in adenomas and carcinomas (2.45 + 0.60 and 2.29 + 0.14, respectively) compared with normal epithelium. Our cytogenetic findings did not correlate with any histopathologic features of carcinomas. Our results indicated that the gains of chromosome 17 and 18 represented early chromosomal alterations in gallbladder neoplasms and were maintained in advanced carcinomas.

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A human gallbladder adenocarcinoma cell line

Johzaki

Iwasaki

Nishida

et al. 1989

Cancer

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A cell strain (FU-GBC-1) was established from cancerous ascites of a 68-year-old male patient with well-differentiated adenocarcinoma of the gallbladder. By light and electron microscopy, the cultured cells showed the morphologic features of adenocarcinoma characterized by gland-like structures, intracellular microcystic spaces, and mucous production. Immunoperoxidase stains showed that FU-GBC-1 cells expressed several epithelial tumor antigens including CA 19-9, carcinoembryonic antigen (CEA), and epithelial membrane antigen (EMA). The cell strain has been in continuous culture up to passage 44 for 1 1/2 years, with the population doubling time of 120 hours. The cytogenetic analysis by a G-band technique showed a constant loss of chromosome Y in FU-GBC-1 cells. The modal chromosome number at passage 12 was 82 with a range of 77 to 85. Flow cytometry with an ethidium bromide technique additionally confirmed aneuploid DNA content (4C) in the cultured cells at passage 12 and 35. Inoculation of FU-GBC-1 cells into the dermis of BALB/c nude mice produced transplantable adenocarcinoma identical to the original tumor. Because no continuous cell lines of the well-differentiated type of gallbladder adenocarcinoma have been reported in the literature currently, the newly established cell strain we report may yield a useful system for studying the morphologic and biologic characteristics of gallbladder adenocarcinoma.

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Adenocarcinoma of the gallbladder: Chromosome abnormalities in a genetic form of cancer

Cited by 12 publications

References 5 publications

Nonrandom chromosomal aberrations and cytogenetic heterogeneity in gallbladder carcinomas

Nonrandom chromosomal aberrations and cytogenetic heterogeneity in gallbladder carcinomas

Cytogenetic analysis of gallbladder neoplasms using fluorescence in situ hybridization (FISH)

A human gallbladder adenocarcinoma cell line

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