Epigenetic and genetic alterations in Netrin-1 receptors UNC5C and DCC in human colon cancer.
Sung Kwan Shin,Takeshi Nagasaka,Barbara H. Jung,Nagahide Matsubara,Won Ho Kim,John M. Carethers,C. Richard Boland,Ajay Goel +7 more
TLDR
The majority of CRCs harbor defects in Netrin-1 receptors, emphasizing the importance of this growth regulatory pathway in cancer, and the timing of the molecular alterations in the Netrin -1 receptors is not random.About:
This article is published in Gastroenterology.The article was published on 2007-12-01 and is currently open access. It has received 103 citations till now. The article focuses on the topics: Deleted in Colorectal Cancer & Intestinal mucosa.read more
Citations
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Netrins: versatile extracellular cues with diverse functions.
TL;DR: The mechanisms involved in netrin signalling in vertebrate and invertebrate systems are reviewed and the functions ofNetrin signalling during the development of neural and non-neural tissues are discussed.
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DNA methylation markers in colorectal cancer.
TL;DR: The aim of this review is to understand DNA methylation as a driving force in colorectal neoplasia and its emerging value as a molecular marker in the clinic.
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Epigenetics of Colorectal Cancer
Ajay Goel,C. Richard Boland +1 more
TL;DR: This review focuses on the epigenetics of colorectal cancer and illustrates the impact epigenetics has had on this field.
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Genetics, Cytogenetics, and Epigenetics of Colorectal Cancer
TL;DR: The loss of heterozygosity that occur in the first phases of the CRC cancerogenesis as well as the alteration of methylation pattern of multiple key genes can drive the development of colorectal cancer by facilitating the acquisition of multiple tumor-associated mutations and the instability phenotype.
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Novel roles for Slits and netrins: axon guidance cues as anticancer targets?
TL;DR: Netrin 1 and members of the Slit family are secreted extracellular matrix proteins that bind to deleted in colorectal cancer (DCC) and UNC5 receptors, and roundabout receptors (Robos), respectively, suggesting that they could be tumour suppressor genes or oncogenes.
References
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Methylation-specific PCR: a novel PCR assay for methylation status of CpG islands
TL;DR: The use of MSP is demonstrated to identify promoter region hypermethylation changes associated with transcriptional inactivation in four important tumor suppressor genes (p16, p15, E-cadherin and von Hippel-Lindau) in human cancer.
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5' CpG island methylation is associated with transcriptional silencing of the tumour suppressor p16/CDKN2/MTS1 in human cancers.
Adrian Merlo,James G. Herman,Li Mao,Daniel J. Lee,Edward Gabrielson,Peter C. Burger,Stephen B. Baylin,David Sidransky +7 more
TL;DR: De novo methylation of the 5′ CpG island of p16 was found in approximately 20% of different primary neoplasms, but not in normal tissues, potentially representing a common pathway of tumour suppressor gene inactivation in human cancers.
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Genetic instability in colorectal cancers
TL;DR: It is shown that colorectal tumours without microsatellite instability exhibit a striking defect in chromosome segregation, resulting in gains or losses in excess of 10 –2 per chromosome per generation, and that such instability can arise through two distinct pathways.
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Incidence and functional consequences of hMLH1 promoter hypermethylation in colorectal carcinoma
James G. Herman,Asad Umar,Kornelia Polyak,Jeremy R. Graff,Nita Ahuja,Jean Pierre J. Issa,Sanford Markowitz,Sanford Markowitz,James K V Willson,Stanley R. Hamilton,Kenneth W. Kinzler,Michael F. Kane,Richard D. Kolodner,Bert Vogelstein,Thomas A. Kunkel,Stephen B. Baylin +15 more
TL;DR: The results suggest that microsatellite instability in sporadic colorectal cancer often results from epigenetic inactivation of hMLH1 in association with DNA methylation.
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Identification of a chromosome 18q gene that is altered in colorectal cancers
Eric R. Fearon,Kathleen R. Cho,Janice M. Nigro,Scott E. Kern,Jonathan W. Simons,J. Michael Ruppert,Stanley R. Hamilton,Antonette C. Preisinger,Giles Thomas,Kenneth W. Kinzler,Bert Vogelstein +10 more
TL;DR: A contiguous stretch of DNA comprising 370 kilobase pairs has now been cloned from a region of chromosome 18q suspected to reside near the DCC gene, which may play a role in the pathogenesis of human colorectal neoplasia, perhaps through alteration of the normal cell-cell interactions controlling growth.