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Telomeric lengths and telomerase activity in liposarcomas
Author(s) -
SchneiderStock Regine,
Epplen Joerg T.,
Walter Hajo,
Radig Kathrin,
Rys Janusz,
Epplen Cornelia,
HoangVu Cuong,
Niezabitowski Alexander,
Roessner Albert
Publication year - 1999
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/(sici)1098-2744(199902)24:2<144::aid-mc9>3.0.co;2-7
Subject(s) - telomerase , telomere , biology , telomerase rna component , polymerase chain reaction , cancer research , telomerase reverse transcriptase , microbiology and biotechnology , dna , genetics , gene
To assess the role of telomerase in the development of liposarcomas, we measured telomerase activity in 36 malignant and seven benign lipomatous neoplasias from 34 patients. A sensitive polymerase chain reaction–based telomerase assay (the telomeric repeat amplification protocol) was applied. Shortening or elongation of telomeric repeat fragment lengths, as measured by using hybridization with a telomere‐specific oligonucleotide probe, was correlated with the presence of telomerase activity. The latter was demonstrable in 69% of malignant tumors. Benign tumors can be distinguished from malignant neoplasias on the basis of telomerase activity. However, telomerase expression seems to be characteristic of poorly differentiated liposarcomas. Myxoid/round cell liposarcomas exhibited a higher telomerase activity level than the classical low‐grade variants. Telomerase activity was not correlated with age at the time of diagnosis or with sex. In most cases, telomerase‐positive tumors showed higher proliferation indices than did neoplasias lacking telomerase. All eight recurrences expressed telomerase activity, reflecting a close association of telomerase with the biological behavior of liposarcomas. Our findings suggest that telomerase may play a key role in the establishment and progression of malignant lipomatous tumors. Mol. Carcinog. 24:144–151, 1999. © 1999 Wiley‐Liss, Inc.