Telomerase is an attractive cancer target since 85% - 90% of tumors express telomerase (while normal cells express little to no telomerase). One paradigm in this model is the “cancer stem cell” hypothesis. Cancer stem cells (or tumor-initiating cells with stem-cell like properties) can self-renew, as well as give rise to heterogeneous tumor cell populations (essentially, they are believed to be responsible for the formation and maintenance of the tumor). If these cells are indeed “stem-like” they also divide more slowly, and presumably express telomerase (like normal stem cells). Do you think a treatment strategy that inhibits telomerase would be effective in treating cancer? How does the cancer stem cell hypothesis complicate or compliment these strategies? Justify your answer.
Telomerase is an attractive cancer target since 85% - 90% of tumors express telomerase (while normal cells express little to no telomerase). One paradigm in this model is the “cancer stem cell” hypothesis. Cancer stem cells (or tumor-initiating cells with stem-cell like properties) can self-renew, as well as give rise to heterogeneous tumor cell populations (essentially, they are believed to be responsible for the formation and maintenance of the tumor). If these cells are indeed “stem-like” they also divide more slowly, and presumably express telomerase (like normal stem cells).
Do you think a treatment strategy that inhibits telomerase would be effective in treating cancer? How does the cancer stem cell hypothesis complicate or compliment these strategies? Justify your answer.
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