Telomere reduction in endometrial adenocarcinoma

Smith, Julie K.; Yeh, G. T.

doi:10.1016/0002-9378(92)91791-8

Cited by 31 publications

(16 citation statements)

References 15 publications

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“…To determine whether this was the case for fresh tumor cells, lengths of TRFs were measured by Southern analysis of DNA from unfractionated ascites cells, using a (CCCTAA)3 telomeric probe. Consistent with results from studies of other tumors (7,(21)(22)(23)(24)(25)(26), the average TRF in these cells was short (4.7 + 0.7 kbp; Table 2). The TRF size distribution, however, was quite heterogeneous, ranging from 2 to >12 kbp (Fig.…”

Section: Resultssupporting

confidence: 87%

“…We reasoned that tumor metastases or recurrent tumors, arising from repeated clonal expansion, should contain immortal cells with stable telomeres and telomerase activity and that if telomerase activation were a late event, telomeres would be short. Indeed, in some cancers it appears as though telomere length decreases with increasing tumor grade (21,22), and tumors with very short telomeres have been detected in a variety of cancers (7,(21)(22)(23)(24)(25)(26)35 F12 supplemented with epidermal growth factor (5 ng/ml), insulin (5 pg/ml), transferrin (10 ug/ml), phosphoethanolamine (50 ,AM), ethanolamine (50 ,uM), and 3% fetal bovine serum]. The nonmalignant fraction of ascites cells were maintained in a minimal essential medium (aMEM) supplemented with 10%6 fetal bovine serum, whereas the tumor fraction and lines derived from them were cultured in E3 medium.…”

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confidence: 99%

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Telomerase activity in human ovarian carcinoma.

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Hirte

Bacchetti

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

593

292

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Telomeres fulfill the dual function of protecting eukaryotic chromosomes from illegitimate recombination and degradation and may aid In chromosome attachment to the nuclear membrane. We have previously shown that telomerase, the enzyme which synthesizes telomeric DNA, is not detected in normal somatic cells and that telomeres shorten with replicative age. In cells immortalized in vitro, activation of telomerase apparently stabilizes telomere length, preventing a critical destabilization of chromosomes, and cell proliferation continues even when telomeres are short. In vivo, telomeres of most tumors are shorter than telomeres of control tissues, suggesting an analogous role for the enzyme. To assess the relevance of telomerase and telomere stability in the development and progression of tumors, we have measured enzyme activity and telomere length in metastatic cells of epithelial ovarian carcinoma. We report that extremely short telomeres are maintaine in these cells and that tumor cells, but not isogenic nonmalignant cells, express telomerase. Our findilgs suggest that progression of malignancy is ultimately dependent upon activation of telomerase and that telomerase inhibitors may be effective antitumor drugs.Telomeres contain both DNA and protein that together appear to stabilize the ends ofeukaryotic DNA (reviewed in refs.

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Section: Resultssupporting

confidence: 87%

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confidence: 99%

Telomerase activity in human ovarian carcinoma.

Counter

Hirte

Bacchetti

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

593

292

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“…It has been suggested that telomeric fusion may be involved in the development of the chromosome rearrangements which are frequently observed in human neoplasia. Although two types of leukemia with chromosomal telomeric associations have been reported (9,10), descriptions of telomeric DNA changes have only been provided for Wilms' tumor ( 11), colorectal carcinoma ( 12), endometrial adenocarcinoma (13), and ovarian carcinoma (14). We recently found that prominent DNA changes were present in two leukemic cell lines (15).…”

Section: Introductionmentioning

confidence: 99%

Telomeric DNA in normal and leukemic blood cells.

Yamada¹,

Oshimi²,

Motoji³

et al. 1995

J. Clin. Invest.

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We studied telomeric DNA in leukemic cells as well as in normal T cells, B cells, monocytes, polymorphonuclear leukocytes, and bone marrow hematopoietic progenitor cells. No marked differences were observed in the sizes of the telomeric repeats in the various populations of normal blood cells obtained from donors in their twenties to sixties, and the telomere length ranged between 8.5 and 9.0 kb. The leukemic cells of 12 patients with acute leukemia (seven with myeloid and five with lymphoid leukemia) showed a variable reduction in the length of telomeric DNA, ranging from 2.7 to 6.4 kb. The average telomere length was 4.8 and 4.7 kb in myeloid and lymphoid leukemia, respectively, while the telomere length in peripheral blood mononuclear cells obtained from the same patients during complete remission was 8.5 and 7.9 kb, respectively. When the same Southern blots were hybridized with Alu or alphoid sequences, no marked changes in the sizes of the repetitive DNA sequences were observed, indicating that the DNA abnormality in the leukemic cells was specific to the telomere region. Investigation of telomeric DNA changes may be helpful in determining the biological properties of leukemic cells.

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“…For example, human embryonic kidney cells that have been immortalized by simian virus 40 or adenovirus have short but stabilized telomeres, suggesting that telomerase is functioning in these cells (7). Although many cancer cells have shortened telomeres (8,19,46) (24,25). The FEP-EIL cell line was made by transfection of human foreskin keratinocytes with the HPV 16 genome (26).…”

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confidence: 99%

“…The telomeric TTAGGG repeat probe (50) was kindly provided by T. de Lange (University of California, San Francisco). This probe has been used previously by others to measure telomere length (1,8,18,19,46 (Fig. 4).…”

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confidence: 99%