The molecular genetics of colorectal cancer
By I. Ewing, J. Hurley, E. Josephides, A. Millar. Frontline Gastroenterology, 2013
1,167 citations recorded by the source corpus.
Colorectal cancer is a common but heterogeneous disease, which arises through the accumulation of genetic mutations. Knowledge of the molecular basis of colorectal cancer has advanced at a rapid pace in recent years, reflecting progress made in the field of genomic medicine. Targeted therapies have come into mainstream use, and the exciting prospect of treatment regimens tailored to the mutation profile of individual tumours is beginning to emerge. In order to understand the development and application of the next generation of colorectal cancer treatments, it is important that gastroenterologists have a working knowledge of the pathological mechanisms that drive the disease. This review examines our current understanding of the molecular genetics of colorectal carcinogenesis.
Subfields: Oncology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/4a55d0a52edecee8745f9d9b74f0c25ec2aa97f4
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In Oncology
- Hans Clevers
- Nick Barker
- Alexander van Oudenaarden
- Michael R. Stratton
- Prashanth Rawla
- Gad Getz
- F. Greten
- Adam Barsouk
In Pathology and Forensic Medicine
Citations in the corpus
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- The Tumor Suppressor p53 Limits Ferroptosis by Blocking DPP4 Activity. (2017, neutral): “TP53 Inhibits Ferroptosis in Human CRC Cells K-RAS mutations can be found in 30%–50% of advanced-stage human CRC (Fearon, 2011).”
- Prospective derivation of a Living Organoid Biobank of colorectal cancer patients (2015, background): “Seminal studies have revealed a series of molecular pathways that are critical to the pathogenesis of CRC, including WNT, RAS-MAPK, PI3K, P53, TGF-b, and DNA mismatch repair (Fearon, 2011; Fearon and Vogelstein, 1990).”
- Epidemiology of colorectal cancer: incidence, mortality, survival, and risk factors (2019, background): “The cancer arises when certain cells of the epithelium acquire a series of genetic or epigenetic mutations that confer on them a selective advantage [1].”
- Intestinal tumorigenesis initiated by dedifferentiation and acquisition of stem-cell-like properties. (2013, background): “The transition of an intestinal epithelial cell (IEC) into a fully transformed metastatic intestinal cancer cell follows a series of activating and inactivating mutations in various oncogenes and tumor suppressors, respectively (Fearon, 2011).”