Abstract:
:Recent progress in the field of molecular biology has allowed us to identify at least two different molecular mechanisms implicated in colorectal carcinogenesis (CRC): chromosomal instability (CIN) and genetic instability. Even though the two molecular mechanisms differ, their signalling pathways, implicated in malignant transformation of colonic epithelial cells, appear to be similar. The most frequent group of CRC, which represents 80% of sporadic CRC, is characterized by allelic losses on the short arm of chromosome 17 and 8 and on the long arm of chromosome 5, 18 and 22. These allelic losses are associated with mutations in TP53, APC, SMAD2 and SMAD4 genes. All of these alterations are grouped under the phenotype CIN. A genetic instability termed MSI (microsatellite instability), which results from a mismatch repair (MMR) deficiency, appears in 12-15% of CRC cases. The presence of MMR deficiency leads to the accumulation of mutations in genes controlling cell cycle and apoptosis (TGFBRII, BAX or CASPASE5). More recently, the existence of a third phenotype was suggested. The main alteration associated with this group of tumors is the hypermethylation of the promoter region of numerous genes, leading to their inactivation. An activating mutation of BRAF is frequently associated with this phenotype. As described above, CRC shows genetic heterogeneity, however the consequences in terms of signalling pathway alterations are similar. For example, the activation of Wnt signalling pathways can result from the inactivation of the APC gene in the CIN phenotype or from an activating mutation in the β-catenin gene in MSI tumors. The inactivation of TGFβ pathways is also present in both tumor types and is driven by SMAD4, and more rarely by a SMAD2 inactivating mutation in CIN tumors, or by the existence of a frame-shift mutation occurring in a polyG coding track of the TGFβ (transforming growth factor) receptor type II in MSI tumors. The RAS-MAP kinase pathway is activated by KRAS mutations in CIN tumors or by BRAF mutations in MSI tumors. The p53 pathway is inactivated by TP53 inactivation in CIN tumors or by BAX inactivating mutations in MSI tumors.
journal_name
Bull Cancerjournal_title
Bulletin du cancerauthors
Laurent-Puig P,Agostini J,Maley Kdoi
10.1684/bdc.2010.1216subject
Has Abstractpub_date
2010-11-01 00:00:00pages
1311-21issue
11eissn
0007-4551issn
1769-6917pii
S0007-4551(15)30753-0journal_volume
97pub_type
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journal_title:Bulletin du cancer
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journal_title:Bulletin du cancer
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journal_title:Bulletin du cancer
pub_type: 杂志文章
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journal_title:Bulletin du cancer
pub_type: 杂志文章,评审
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更新日期:1995-12-01 00:00:00
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journal_title:Bulletin du cancer
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journal_title:Bulletin du cancer
pub_type: 杂志文章
doi:
更新日期:2006-09-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章
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更新日期:2005-12-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章
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更新日期:1986-01-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章
doi:
更新日期:2004-01-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章
doi:
更新日期:1982-01-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章,评审
doi:
更新日期:1996-03-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章
doi:10.1684/bdc.2013.1787
更新日期:2013-07-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章,评审
doi:10.1684/bdc.2014.1984
更新日期:2014-06-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章
doi:10.1016/j.bulcan.2018.04.008
更新日期:2019-01-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章
doi:
更新日期:1989-01-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章,评审
doi:10.1684/bdc.2008.0599
更新日期:2008-03-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章
doi:10.1016/j.bulcan.2014.12.001
更新日期:2015-01-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章,评审
doi:10.1684/bdc.2011.1477
更新日期:2012-03-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章,评审
doi:
更新日期:1989-01-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章
doi:
更新日期:1989-01-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章
doi:10.1016/j.bulcan.2017.11.011
更新日期:2018-03-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章
doi:
更新日期:2003-11-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章
doi:
更新日期:1995-01-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章,评审
doi:10.1016/j.bulcan.2015.10.017
更新日期:2016-01-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章
doi:
更新日期:2007-01-01 00:00:00
abstract::In recent studies, the economic criteria has begun to be integrated to the appraisal in cancerology. The question asked by the economist can be framed as follows: what incremental cost should the collectivity or the health insurance system consent, in order to improve the care of cancer patients? This involves first t...
journal_title:Bulletin du cancer
pub_type: 杂志文章
doi:
更新日期:1997-05-01 00:00:00
abstract::Cell signalling represents the network of cell communication pathways. Reception of a message by a cell results in the implementation of various direct and indirect actions, especially through the transcription of the genes required for carrying out the orders received. The signals exchanged by cells may concern proli...
journal_title:Bulletin du cancer
pub_type: 杂志文章,评审
doi:10.1684/bdc.2010.1199
更新日期:2010-11-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章
doi:
更新日期:1995-01-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章
doi:10.1684/bdc.2009.0895
更新日期:2009-09-01 00:00:00
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journal_title:Bulletin du cancer
pub_type: 杂志文章,评审
doi:
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