Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comment
. 2015 Jul 21:4:e09519.
doi: 10.7554/eLife.09519.

Taking the brakes off telomerase

Kamila Naxerova  1 , Stephen J Elledge  1
Affiliations
Comment

Taking the brakes off telomerase

Kamila Naxerova et al. Elife. .

Abstract

Studies using human embryonic stem cells have revealed how common cancer-associated mutations exert their effect on telomerase after cells differentiate into more specialized cell types.

Keywords: cancer mechanism; chromosomes; developmental biology; genes; genome editing; human; immortalization; ssociated systems 9 CAS9; stem cells; telomerase TERT; tumor spectrum.

PubMed Disclaimer

Conflict of interest statement

Competing interests:The authors declare that no competing interests exist.

Figures

Figure 1.
Figure 1.. How TERT promoter mutations may contribute to cancer.
Chiba et al. report that in human embryonic stem cells (hESCs, top), the promoter (green arrow) of the telomerase gene (TERT) is active, regardless of whether it is wild type (WT, left) or mutated (MUT, right). The telomerase enzyme (blue ellipse) maintains long telomeres at the chromosome ends. When the stem cells differentiate into fibroblasts or nerve cells (bottom), telomerase expression is appropriately down-regulated in cells with a wild type TERT promoter (grey arrow), and telomeres begin to shorten—which leads to senescence. However, this does not occur when cells with telomerase promoter mutations differentiate—which may allow the cells to become immortal.
See this image and copyright information in PMC

Comment on

Similar articles

See all similar articles

Cited by

References

    1. Bell RJ, Rube HT, Kreig A, Mancini A, Fouse SD, Nagarajan RP, Choi S, Hong C, He D, Pekmezci M, Wiencke JK, Wrensch MR, Chang SM, Walsh KM, Myong S, Song JS, Costello JF. Cancer. The transcription factor GABP selectively binds and activates the mutant TERT promoter in cancer. Science. 2015;348:1036–1039. doi: 10.1126/science.aab0015. - DOI - PMC - PubMed
    1. Borah S, Xi L, Zaug AJ, Powell NM, Dancik GM, Cohen SB, Costello JC, Theodorescu D, Cech TR. Cancer. TERT promoter mutations and telomerase reactivation in urothelial cancer. Science. 2015;347:1006–1010. doi: 10.1126/science.1260200. - DOI - PMC - PubMed
    1. Chiba K, Johnson JZ, Vogan JM, Wagner T, Boyle JM, Hockemeyer D. Cancer-associated TERT promoter mutations abrogate telomerase silencing. eLife. 2015;4:e07918. doi: 10.7554/eLife.07918. - DOI - PMC - PubMed
    1. Horn S, Figl A, Rachakonda PS, Fischer C, Sucker A, Gast A, Kadel S, Moll I, Nagore E, Hemminki K, Schadendorf D, Kumar R. TERT promoter mutations in familial and sporadic melanoma. Science. 2013;339:959–961. doi: 10.1126/science.1230062. - DOI - PubMed
    1. Huang FW, Hodis E, Xu MJ, Kryukov GV, Chin L, Garraway LA. Highly recurrent TERT promoter mutations in human melanoma. Science. 2013;339:957–959. doi: 10.1126/science.1229259. - DOI - PMC - PubMed