Telomerase, Cell Immortality, and Cancer

  1. C.B. Harley*,
  2. N.W. Kim*,
  3. K.R. Prowse*,
  4. S.L. Weinrich*,
  5. K.S. Hirsch*,
  6. M.D. West*,
  7. S. Bacchetti,
  8. H.W. Hirte,
  9. C.M. Counter,
  10. C.W. Greider,
  11. M.A. Piatyszek§,
  12. W.E. Wright§, and
  13. J.W. Shay§
  1. *Geron Corporation, Menlo Park, California 94025; McMaster University, Hamilton, Ontario, Canada, L8N 3Z5; Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724; §University of Texas, Southwestern Medical Center, Dallas, Texas 75235

This extract was created in the absence of an abstract.

Excerpt

An important hallmark of cancer is aberrant growth control. Genetic changes that confer a growth advantage to the tumor cell are observed on numerous levels. Some of the best understood are mutations in proto-oncogenes and tumor suppressor genes that are linked to signal transduction pathways, cell cycle control, or cell-cell/cell-matrix interactions that regulate growth, movement, differentiation, survival, apoptosis, and genetic stability (Hartwell 1992; Weinberg 1992; Hunter 1993; Runger et al. 1994; Workman 1994). However, in addition to aberrant growth control, many cancer cells possess another important feature which distinguishes them from normal somatic cells: unlimited replicative capacity.

Hayflick first described the limited replicative capacity of normal human fibroblasts more than 30 years ago (for review, see Hayflick 1965; Goldstein 1990). Since then, numerous other somatic cell types, including epithelial cells, endothelial cells, myoblasts, astrocytes, and lymphocytes, have also shown evidence of a mitotic clock which limits their division capacity (Stanulis...

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