Colorectal and extracolonic cancer variations in MLH1/MSH2 hereditary nonpolyposis colorectal cancer kindreds and the general population

1998 ◽  
Vol 41 (4) ◽  
pp. 428-433 ◽  
Author(s):  
Kevin M. Lin ◽  
M. Shashidharan ◽  
Charles A. Ternent ◽  
Alan G. Thorson ◽  
Garnet J. Blatchford ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
General Population ◽  
Hereditary Nonpolyposis Colorectal Cancer ◽  
Extracolonic Cancer ◽  
Hereditary Nonpolyposis

Histologic comparison of hereditary nonpolyposis colorectal cancer associated with MSH2 and MLH1 and colorectal cancer from the general population

1999 ◽  
Vol 42 (6) ◽  
pp. 722-726 ◽  
Author(s):  
Maniamparmpil Shashidharan ◽  
Thomas Smyrk ◽  
Kevin M. Lin ◽  
Charles A. Ternent ◽  
Alan G. Thorson ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
General Population ◽  
Hereditary Nonpolyposis Colorectal Cancer ◽  
Hereditary Nonpolyposis

scholarly journals Molecular diagnosis of hereditary nonpolyposis colorectal cancer (Lynch syndrome)

2016 ◽  
Vol 64 (3) ◽  
pp. 537
Author(s):  
David Serrano ◽  
Clara Eugenia Arteaga
Keyword(s):  
Colorectal Cancer ◽  
Lynch Syndrome ◽  
Molecular Diagnosis ◽  
Hereditary Nonpolyposis Colorectal Cancer ◽  
State Of The Art ◽  
Clinical Criteria ◽  
Extracolonic Cancer ◽  
Pubmed Database ◽  
Hereditary Nonpolyposis ◽  
Repair Genes

Lynch syndrome is the most common cause of inherited colorectal cancer, totaling 5 to 8% of all the cases with high susceptibility to this type of cancer and extracolonic cancer. It is related to germinal mutations taking place at mismatch repair genes. The diagnosis of Lynch syndrome is essential for both monitoring patients with this disease and detecting asymptomatic carriers, in order to establish appropriate clinical monitoring, preventive management and genetic counselingAlthough clinical criteria have been standardized by implementing Amsterdam I and II, as well as Bethesda guidelines, the detection rate of mutations in these genes only varies between 20% and 60%.The objective of this research was to review the state of the art regarding molecular diagnosis of Lynch syndrome; thus, a review of the literature published from 1995 to 2015 in PubMed database was performed by using the criteria “lynch syndrome molecular screening”. 19 articles were selected and reviewed, and the relevant bibliography related to such articles was also reviewed.This paper presents different approaches proposed by several researchers on molecular algorithms to improve the efficiency of Lynch syndrome diagnosis.

Exploring the potential chemopreventative effect of aspirin and rofecoxib on hereditary nonpolyposis colorectal cancer–like endometrial cancer cells in vitro through mechanisms involving apoptosis, the cell cycle, and mismatch repair gene expression

2007 ◽  
Vol 17 (2) ◽  
pp. 447-454 ◽  
Author(s):  
N. J. Wood ◽  
N. A. Quinton ◽  
S. Burdall ◽  
E. Sheridan ◽  
S. R. Duffy
Keyword(s):  
Gene Expression ◽  
Colorectal Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Endometrial Cancer ◽  
General Population ◽  
Hereditary Nonpolyposis Colorectal Cancer ◽  
Mismatch Repair Gene ◽  
Repair Gene ◽  
Hereditary Nonpolyposis

Women in hereditary nonpolyposis colorectal cancer (HNPCC) families have up to a 71% lifetime risk for developing endometrial cancer (EC). This compares to the female lifetime risk for colorectal cancer (CRC) in HNPCC of 60%. The basis of HNPCC is an inherited mutation in a mismatch repair gene (MMR). Aspirin and COX2 inhibitors seem to have a chemoprotective effect on CRC in the general population and are the subject of prospective clinical studies in patients at high risk for CRC including HNPCC. There is no evidence that these agents have any protective effect against EC in the general population. This study investigated the effect of aspirin and a COX2 inhibitor (rofecoxib) on an HNPCC EC cell line model (Ishikawa) by assessing the effect on proliferation, apoptosis, the cell cycle, and MMR gene expression. Aspirin inhibits EC cell proliferation by inducing apoptosis and changes in the cell cycle. This effect is not mediated by changes in MMR gene (hMSH2) expression as assessed by quantitative reverse transcription–polymerase chain reaction. Rofecoxib inhibits EC cell proliferation; this did not appear to be mediated by induction of apoptosis, by alterations of the cell cycle, or by changes in MMR gene expression

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