 | ANTICANCER MOLECULES: STRUCTURE, FUNCTION, AND DESIGN
Copyright © 1999 by the New York Academy of Sciences
description
Annals of the New York Academy of Sciences 886:1-11 (1999)
© 1999 New York Academy of Sciences
Telomerase: A Target for Anticancer Therapy
SERGE P. LICHTSTEINERa,
JANE S. LEBKOWSKI AND
ALAIN P. VASSEROT
Geron Corporation, 230 Constitution Drive, Menlo Park, California 94025, USA
aFor telecommunication: phone, 650/473-7715; fax, 650/473-7750.
e-mail, slichtsteiner{at}geron.com
Telomerase is absent in most normal tissues, but is abnormally reactivated in all major cancer types. Telomerase enables tumor cells to maintain telomere length, allowing indefinite replicative capacity. Albeit not sufficient in itself to induce neoplasia, telomerase is believed to be necessary for cancer cells to grow without limit. The presence of telomerase has been detected in virtually all cancer types including the most prevalent cancers of the prostate, breast, lung, colon, bladder, uterus, ovary, and pancreas as well as in lymphomas, leukemias, and melanomas. In addition, data from cancer patients indicate that telomerase levels correlate with clinical outcome in neuroblastomas, leukemias, and prostate, gastric, and breast cancers. Studies using an anti-sense to the human telomerase RNA component demonstrate that telomerase in human tumor lines can be blocked ex vivo. In these experiments, telomerase inhibition led to telomere shortening and cancer cell death, validating telomerase as a target for anticancer therapy. Telomerase is a uniquely appealing target for drug discovery because its dichotomic expression in normal versus cancer cells suggests that no serious side effects would result from a treatment abrogating telomerase activity. A variety of approaches to telomerase inhibition are being investigated and are discussed.
This article has been cited by other articles:
|
|
|
|
 
U. Moehren, M. Papaioannou, C. A. Reeb, A. Grasselli, S. Nanni, M. Asim, D. Roell, I. Prade, A. Farsetti, and A. Baniahmad
Wild-type but not mutant androgen receptor inhibits expression of the hTERT telomerase subunit: a novel role of AR mutation for prostate cancer development
FASEB J,
April 1, 2008;
22(4):
1258 - 1267.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
W. C. Hines, A. M. Fajardo, N. E. Joste, M. Bisoffi, and J. K. Griffith
Quantitative and Spatial Measurements of Telomerase Reverse Transcriptase Expression within Normal and Malignant Human Breast Tissues
Mol. Cancer Res.,
September 1, 2005;
3(9):
503 - 509.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. Patry, L. Bouchard, P. Labrecque, D. Gendron, B. Lemieux, J. Toutant, E. Lapointe, R. Wellinger, and B. Chabot
Small Interfering RNA-Mediated Reduction in Heterogeneous Nuclear Ribonucleoparticule A1/A2 Proteins Induces Apoptosis in Human Cancer Cells but not in Normal Mortal Cell Lines
Cancer Res.,
November 15, 2003;
63(22):
7679 - 7688.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S.-Q. Xu, M. He, H.-P. Yu, X.-Y. Wang, X.-L. Tan, B. Lu, X. Sun, Y.-K. Zhou, Q.-F. Yao, Y.-J. Xu, et al.
Bioluminescent Method for Detecting Telomerase Activity
Clin. Chem.,
July 1, 2002;
48(7):
1016 - 1020.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. Komata, Y. Kondo, T. Kanzawa, S. Hirohata, S. Koga, H. Sumiyoshi, S. M. Srinivasula, B. P. Barna, I. M. Germano, M. Takakura, et al.
Treatment of Malignant Glioma Cells with the Transfer of Constitutively Active Caspase-6 Using the Human Telomerase Catalytic Subunit (Human Telomerase Reverse Transcriptase) Gene Promoter
Cancer Res.,
August 1, 2001;
61(15):
5796 - 5802.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
