Pleomorphic adenoma cells vary in their susceptibility to SV40 transformation depending on the initial karyotype

Kazmierczak, Bernd; Thode, Brita; Bartnitzke, Sabine; Bullerdiek, Jörn; Schloot, W.

doi:10.1002/gcc.2870050106

Cited by 9 publications

(5 citation statements)

References 11 publications

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“…The lack of apparent association between LOH on 8q in tumors with malignant conversion in PA suggests that this is an early event in the progression of these tumors. This finding correlates well with the study of Kazmierczak et al, 15 which showed that all primary cultures of PA with a 12q13‐15 arrangement were susceptible to SV40 transformation (7 of 7), whereas those specimens with 8q12 abnormalities were less likely to undergo transformation (4 of 13). Our specimen with CXPA showed LOH at both 8q and 12q loci.…”

Section: Discussionsupporting

confidence: 91%

Microsatellite Alterations at Chromosome 8q Loci in Pleomorphic Adenoma

Gillenwater

Hurr

Wolf

et al. 1997

Otolaryngol.--head neck surg.

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OBJECTIVE: To determine the extent, localization, and clinical significance of microsatellite loci alterations at sites of reported cytogenetic abnormalities in pleomorphic adenomas. BACKGROUND: Pleomorphic adenoma is a benign salivary gland tumor with a propensity for recurrence and potential for malignant conversion. Although its cause remains unclear, clonal cytogenetic abnormalities have been reported consistently. DESIGN: DNA extracted from paired normal and tumor tissue specimens from 1 patient with carcinoma ex pleomorphic adenoma and 17 patients with pleomorphic adenoma (3 contained foci of carcinoma ex pleomorphic adenoma) was evaluated for loss of heterozygosity at microsatellite loci with a multiplex polymerase chain reaction-based analysis. Correlation with clinical and pathologic features was performed. RESULTS: Overall 10 (56%) of 18 cases manifested loss of heterozygosity at the loci tested. The frequency of loss of heterozygosity noted on 3p, 6q, 8p, 8q, and 12q microsatellite loci was 17%, 12%, 8%, 47%, and 27% of informative cases, respectively. Specimens from patients with carcinoma ex pleomorphic adenoma showed a similar loss of heterozygosity incidence at these loci. No apparent association between molecular abnormalities and clinical-pathologic features was observed in this cohort. CONCLUSIONS: Loss of heterozygosity at microsatellite loci on 8q, a breakpoint at which translocations have been previously documented in pleomorphic adenoma, is a frequent event in this tumor. The incidence is not increased in patients with focal carcinoma ex pleomorphic adenoma, suggesting that loss of heterozygosity at 8q is an early event in tumorigenesis. Further evaluation at these loci is needed to identify potential tumor suppressor genes that may be associated with the initiation and progression of pleomorphic adenomas.

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Section: Discussionsupporting

confidence: 91%

Microsatellite Alterations at Chromosome 8q Loci in Pleomorphic Adenoma

Gillenwater

Hurr

Wolf

et al. 1997

Otolaryngol.--head neck surg.

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“…Intensive efforts have been made in the past to establish salivary gland tumor cell lines, but they have achieved only a low rate of success (Fujioka et al ., 1996; Kazmierczak et al ., 1992). Here, we have described the establishment and characterization of 9 cell lines derived from 9 salivary gland tumor cell cultures by infection with the HPV16 E6 and E7 genes.…”

Section: Discussionmentioning

confidence: 99%

“…In cases where structural changes have been observed, they frequently are reciprocal translocations in benign tumors or 6q deletions in malignant tumors (Sandros et al ., 1990). By contrast, the few salivary gland tumor cell lines established to date have complex karyotypic abnormalities (Bullerdiek et al ., 1990; Fujioka et al ., 1996; Kazmierczak et al ., 1992). The high frequency of normal karyotypes seen in salivary gland tumors raises the question of whether these cells represent bona fide tumor cells without gross chromosomal deviations or are actually contaminating stromal cells or normal salivary gland epithelial cells (Sandros et al ., 1990).…”

Section: Discussionmentioning

confidence: 99%

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In vitro transformation of cell lines from human salivary gland tumors

Queimado

Lopes

et al. 1999

Int. J. Cancer

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Explanted cells from salivary gland tumors are particularly difficult to propagate in vitro and not efficiently immortalized by agents such as simian virus 40. Human papillomavirus 16 (HPV16) has been widely used to transform cells of epithelial origin, but its use for salivary gland cell transformation has not been described. In this study, we employed viral constructs containing the E6/E7 genes of HPV16 to infect and stably transform 9 salivary gland tumor cell cultures. Four of the tumor cell cultures were derived from benign tumors and 5 from malignant tumors. All of the original cell cultures were diploid; however, 6 contained subpopulations of cells with structural abnormalities. All 9 cell cultures were successfully transformed, and 8 were immortalized. The resulting cell lines have decreased serum requirements, exhibit a high proliferation rate, are E6/E7‐positive and form colonies in soft agar. Immuno‐histochemical and molecular studies confirmed that the transformed cells were indeed epithelial/myoepithelial in origin. All of the transformed cell lines had a diploid or near‐diploid karyotype, and 2 contained the original translocated chromosomes in all cells. Our report represents a new application of the E6/E7 system in immortalizing salivary gland cell cultures, resulting in retention of the cellular features found in the native tissue without a general destabilization of the karyotype. These types of tissue culture resources should prove useful for positional cloning and functional studies of genes involved in salivary gland oncogenesis. Int. J. Cancer 81:793–798, 1999. © 1999 Wiley‐Liss, Inc.

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“…This event has to some extent been mitigated, albeit not completely eliminated, by the use of hTERT as a cotransforming gene [137,[183][184][185][186]. Because there are numerous genetic changes that need to occur to result in immortalization [41, 66,183,[187][188][189][190], it is important that the cells are grown for extended periods (generally >150-200 generations) to ascertain whether they are in fact immortalized. Once the cells have gone through a crisis event, it will be important to reevaluate them in the context of the desired phenotypic endpoints.…”

Section: Discussionmentioning

confidence: 99%

Immortalization Strategies for Epithelial Cells in Primary Culture

Frappart¹,

Maurisse²,

Vock³

et al.

Drug Absorption Studies

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The development of immortalized cell culture systems has been a tremendous asset to basic research as well as to the pharmaceutical and biotechnology industries. These cell culture systems have facilitated advances in our knowledge of the biochemical and metabolic mechanisms underlying cell function and disease pathology. The immortalization of epithelial cells has been particularly important for elucidating specialized cell function and/or neoplastic progression. The strategies required for the generation of epithelial cell systems, in particular, human airway epithelial cells, can serve a paradigm for other specialized cell systems such as endothelial cells. Numerous airway epithelial cell systems have been generated from tumor tissue and primary cells. The methodologies for establishing these transformed and immortalized cultures have relied primarily on oncogenic viruses and expression vectors carrying oncogenes and/or telomerase. Because of the extensive work that has already been carried out over the last two decades, these human epithelial cell systems provide an ideal model for defining the parameters that lead to cell transformation and immortalization as well as those that result in cells with differentiated functions similar to those of primary epithelial cells. With this in mind, the strategies and techniques employed to develop transformed and immortalized cells that can be used to study neoplastic progression or differentiated function can be readily extrapolated to other cell systems.

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Pleomorphic adenoma cells vary in their susceptibility to SV40 transformation depending on the initial karyotype

Cited by 9 publications

References 11 publications

Microsatellite Alterations at Chromosome 8q Loci in Pleomorphic Adenoma

Microsatellite Alterations at Chromosome 8q Loci in Pleomorphic Adenoma

In vitro transformation of cell lines from human salivary gland tumors

Immortalization Strategies for Epithelial Cells in Primary Culture

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