Connecting chromosomes, crisis, and cancer.
By R. Maser, R. DePinho. Science, 2002
595 citations recorded by the source corpus.
Subfields: Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/fa9434acf68c373a39188715970e597fc9339bc9
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
- T. de Lange
- J. Massagué
- R. DePinho
- N. Bardeesy
- Yosef Shiloh
- Alec C. Kimmelman
- Stephen J. Elledge
- Eric C. Wooten
In Physiology
- T. de Lange
- R. DePinho
- D. Loayza
- Stephen J. Elledge
- N. Bardeesy
- Yosef Shiloh
- Alec C. Kimmelman
- de Lange
Citations in the corpus
- Principles of Cancer Therapy: Oncogene and Non-oncogene Addiction (2009, unknown): “The subsequent fusions of these deprotected ends initiate breakage-fusion-bridge cycles that result in translocations and gene amplification events (Maser and DePinho, 2002).”
- Genetics and biology of pancreatic ductal adenocarcinoma. (2006, background): “This episodic mutational activity could be prompted by key events undermining genomic integrity such as the loss of DNA damage repair and response checkpoints and the erosion of telomeres (Chin et al. 1999a, 2004; Maser and DePinho 2002).”
- Aurora B-mediated abscission checkpoint protects against tetraploidization. (2009, unknown): “, 2007), it could also reduce the risk of cancer in aging tissues, where the incidence of chromosome bridges increases due to telomere attrition (Chin et al., 2004; Maser and DePinho, 2002; Stewenius et al., 2005).”
- Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma. (2003, background): “The basis for this divergence may relate to the cross-species differences in telomere dynamics (Maser and DePinho 2002), the prominent role of p53 (and not ARF) in the telomere checkpoint response of evolving tumors (Chin et al.”
- Tumor aneuploidy correlates with markers of immune evasion and with reduced response to immunotherapy (2017, background): “The different SCNA classes (focal, arm, and chromosome) were considered independently because they arise from biologically distinct mechanisms (31, 32).”
- ATM and related protein kinases: safeguarding genome integrity (2003, background): “Evidence is accumulating that ATM is functionally linked to the maintenance of telomere length and integrity, a process that is crucial to ageing and cance”
- Linking functional decline of telomeres, mitochondria and stem cells during ageing (2010, unknown): “Proliferation beyond this limit drives further telomere erosion, ultimately triggering rampant chromosomal instability driven by chromosome breakage–fusion–breakage event”
- Chromosome aberrations in solid tumors (2003, background): “Most of the cells probably do not survive owing to abnormal and lethal chromosome rearrangement”
- Cancer metastasis: building a framework. (2006, background): “Telomeric crisis may wreak havoc on the genomes of cancer cells, producing a myriad of traits associated with tumor progression (Maser and DePinho, 2002).”
- The genetics and genomics of cancer (2003, background): “Somatic genetic changes in cancer cells A cardinal feature of almost all cancer cells is genomic instability (reviewed in refs”
- POT1 as a terminal transducer of TRF1 telomere length control (2003, background): “jpg" NDATA ITEM> ]> Human telomere maintenance is essential for the protection of chromosome ends, and changes in telomere length have been implicated in ageing and cance”