Abstract
Access to cDNA encoding the catalytic subunit of telomerase and the consequent ability to immortalize human cells in culture has enabled researchers to 'transform' normal cells into malignant clones. However, there is a continuing debate over the number of genetic alterations required and clear differences in the way that mouse and human cells respond to these alterations.
MeSH terms
-
Aging
-
Animals
-
Catalytic Domain
-
Cell Survival
-
Cell Transformation, Neoplastic / genetics*
-
Cyclin-Dependent Kinase Inhibitor p16 / physiology
-
DNA-Binding Proteins
-
Humans
-
Mice
-
Oncogenes / physiology
-
Retinoblastoma Protein / physiology
-
Telomerase / physiology
-
Telomere / genetics
-
Telomere / physiology
-
Tumor Suppressor Protein p14ARF / physiology
-
Tumor Suppressor Protein p53 / physiology
Substances
-
Cdkn2a protein, mouse
-
Cyclin-Dependent Kinase Inhibitor p16
-
DNA-Binding Proteins
-
Retinoblastoma Protein
-
Tumor Suppressor Protein p14ARF
-
Tumor Suppressor Protein p53
-
Telomerase