Telomerase: A target for cancer therapeutics

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Telomerase: A target for cancer therapeutics Jerry W Shay, Woodring E Wright  Cancer Cell  Volume 2, Issue 4, Pages 257-265 (October 2002) DOI: 10.1016/S1535-6108(02)00159-9

Figure 1 Theoretical approach to managing the care of cancer patients with combinations of conventional and experimental therapies, including telomerase inhibitors. Cancer Cell 2002 2, 257-265DOI: (10.1016/S1535-6108(02)00159-9)

Figure 2 Telomerase promoter-dependent adenoviral therapy. The systemic use of the hTERT proximal promoter in a replication-competent adenoviral should have minimal effects on normal cells that do not express telomerase activity. Cancer cells expressing telomerase activity transcriptionally activate the hTERT promoter, permitting adenoviral replication, lysis, and spread to adjacent cells. Cancer Cell 2002 2, 257-265DOI: (10.1016/S1535-6108(02)00159-9)

Figure 3 Telomerase inhibitors and conventional therapies. A telomerase inhibitor used as a single agent will progressively reduce telomere length, but there is an expected time delay until cell death. Conventional cytoxic therapies will initially reduce tumor burden but not affect telomere length. Combinations of conventional therapies with telomerase inhibitors would be predicted to both reduce tumor burden and shorten telomeres, potentially preventing or delaying tumor recurrences. Cancer Cell 2002 2, 257-265DOI: (10.1016/S1535-6108(02)00159-9)

Figure 4 Telomerase inhibitors and experimental angiogenesis inhibitors. A telomerase inhibitor used as a single agent will progressively reduce telomere length, but there is an expected time delay until cell death. Some angiogenesis inhibitors will maintain a reduced tumor burden but will not eradicate the tumor or affect telomere length. Combinations of angiogenesis inhibitors with telomerase inhibitors would be predicted to maintain a reduced tumor burden while producing progressively shortened telomeres, potentially leading to preventing or delaying tumor recurrences. Cancer Cell 2002 2, 257-265DOI: (10.1016/S1535-6108(02)00159-9)