Telomeres and human disease: ageing, cancer and beyond

By M. Blasco. Nature reviews genetics, 2005

1,722 citations recorded by the source corpus.

Subfields: Aging, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/cc5cf52a969bf0814ec307129135a17bec14f1aa

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Aging

1. Michael Fenech
2. Anthony Rhoads
3. Kin Fai Au
4. Jesús Gil
5. M. Blasco

In Molecular Biology

1. Michael Fenech
2. Anthony Rhoads
3. Kin Fai Au
4. José C. R. Silva
5. Jesús Gil
6. M. Blasco
7. L. Vallier
8. Martin Zenke

In Physiology

1. Michael Fenech
2. Anthony Rhoads
3. Kin Fai Au
4. Jesús Gil
5. M. Blasco

Citations in the corpus

• Cellular senescence in cancer and aging. (2007, neutral): “Due to the intrinsic inability of the replication machinery to copy the ends of linear molecules, telomeres become progressively shorter with every round of cell division (Blasco, 2005).”
• Senescence impairs successful reprogramming to pluripotent stem cells. (2009, background): “Embryonic stem cells exhibit telomerase activity As mentioned before most human cancers contain high levels of telomerase activity underscoring the importance of telomere maintenance in cellular immortality (Blasco, 2005).”
• Aging of blood can be tracked by DNA methylation changes at just three CpG sites (2014, background): “Leukocyte telomere length has been suggested as a marker for biological age [3].”
• The epigenetic regulation of mammalian telomeres (2007, background): “, pointing to a higher-order structure at telomeres that is epigenetically regulated and is important for length contro”
• Side population in human lung cancer cell lines and tumors is enriched with stem-like cancer cells. (2007, background): “Furthermore, telomerase is a crucial marker of cellular immortalization in cancers ( 17 ).”
• NAD+/NADH and NADP+/NADPH in Cellular Functions and Cell Death: Regulation and Biological Consequences (2008, neutral): “Telomere and telomerases have been indicated as mediators of cellular aging (36).”
• PacBio Sequencing and Its Applications (2015, background): “In humans, the loss of telomeres has been associated with diseases, including premature aging syndromes and cancer [38].”
• Hallmarks of cancer: the next generation. (2011, neutral): “Multiple lines of evidence indicate that telomeres protecting the ends of chromosomes are centrally involved in the capability for unlimited proliferation (Blasco, 2005; Shay and Wright, 2000).”
• Cytokinesis-block micronucleus cytome assay (2007, background): “An alternative mechanism for dicentric chromosome and NPB formation is telomere end fusion caused by telomere shortening, loss of telomere capping proteins or defects in telomere cohesio”