© 1999 by Oxford University Press
Journal of the National Cancer Institute, Vol. 91, No. 1, 4-6,
January 6, 1999
© 1999 Oxford University Press
EDITORIALS |
Toward Identifying a Cellular Determinant of Telomerase Repression
Correspondence to: Jerry W. Shay, Ph.D., Department of Cell Biology and Neuroscience, The University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd., Dallas, TX 75235-9039 (e-mail: Shay@UTSW.SWMED.EDU).
Normal human cells undergo an irreversible growth arrest after a
limited number of cell divisions (1,2). In contrast, a
hallmark of most cancer cells is their ability to divide an unlimited
number of times. Lately, the importance of counteracting the
limitations of normal cell growth as a cellular requirement for cancer
progression has become appreciated (3-5). There is evidence
for a genetic basis of cellular aging. Thus, somatic cell hybrids
between immortal cancer cells and normal cells are mortal,
demonstrating that cellular aging/senescence is dominant over
immortality (6). These findings have been pursued in an
attempt to identify specific genes regulating these processes.
Microcell-mediated chromosome transfer has provided mounting evidence
that there are several senescence-specific genetic pathways
(7). In some instances, the introduction of specific
chromosomes or genes into proliferating cells results in a rapid growth
arrest, suggesting
Reduction of Telomeres and Cellular Growth Arrest
Telomerase: a Cellular Reverse Transcriptase That Bypasses Telomere-Based Cell Growth Limitations
Inhibiting Telomerase as a Therapy for Treating Cancer
Evidence for a Chromosome 3 Telomerase Repressor
NOTES
REFERENCES
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