scholarly journals Systemic Inflammatory Markers of Resectable Colorectal Cancer Patients with Different Mismatch Repair Gene Status

2021 ◽  
Vol Volume 13 ◽  
pp. 2925-2935
Author(s):  
Jingjing Li ◽  
Yiwen Zhang ◽  
Qi Xu ◽  
Gang Wang ◽  
Lai Jiang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Patients ◽  
Mismatch Repair ◽  
Inflammatory Markers ◽  
Mismatch Repair Gene ◽  
Repair Gene ◽  
Gene Status ◽  
Colorectal Cancer Patients

scholarly journals Inflammatory Markers and MicroRNAs: The Backstage Actors Influencing Prognosis in Colorectal Cancer Patients

2018 ◽  
Vol 19 (7) ◽  
pp. 1867 ◽  
Author(s):  
Rihab Nasr ◽  
Miza Salim Hammoud ◽  
Farah Nassar ◽  
Deborah Mukherji ◽  
Ali Shamseddine ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Patients ◽  
Inflammatory Markers ◽  
Colorectal Cancer Patients

T2042 Mismatch Repair Gene Product Expression and Colorectal Cancer in Hispanics

2008 ◽  
Vol 134 (4) ◽  
pp. A-606-A-607 ◽  
Author(s):  
Wilfredo E. De Jesus-Monge ◽  
Ronghua Zhao ◽  
Carmen Gonzalez-Keelan ◽  
Stanley R. Hamilton ◽  
Miguel Rodriguez-Bigas ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Mismatch Repair ◽  
Gene Product ◽  
Mismatch Repair Gene ◽  
Repair Gene ◽  
Product Expression

Immunohistochemistry Identifies Carriers of Mismatch Repair Gene Defects Causing Hereditary Nonpolyposis Colorectal Cancer

2005 ◽  
Vol 23 (21) ◽  
pp. 4705-4712 ◽  
Author(s):  
Astrid T. Stormorken ◽  
Inger Marie Bowitz-Lothe ◽  
Tove Norèn ◽  
Elin Kure ◽  
Steinar Aase ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Mismatch Repair ◽  
Hereditary Nonpolyposis Colorectal Cancer ◽  
Mismatch Repair Gene ◽  
Repair Gene ◽  
Predictive Values ◽  
Blood Samples ◽  
Bethesda Criteria ◽  
Amsterdam Criteria ◽  
Hereditary Nonpolyposis

Purpose Hereditary nonpolyposis colorectal cancer (HNPCC) may be caused by mutations in mismatch repair (MMR) genes. The aim of this study was to validate immunohistochemistry and family history as prescreening tools to predict germline mutations in MLH1, MSH2, and MSH6. Patients and Methods Pedigrees from 250 families were extended, cancer diagnoses were verified, and families were classified according to the Amsterdam and the Bethesda criteria. Tumor specimens were examined with immunohistochemistry for the presence of MLH1, MSH2, and MSH6 proteins. Mutation analyses were performed in blood samples from the same patients. Results Blood samples from affected index persons in 181 families and tumor specimens from 127 of the affected index persons were obtained. Thirty tumors lacked one or more gene products. Sensitivity of immunohistochemistry to detect mutation carriers was 100%, specificity was 82%, and positive predictive value was 85%. Sensitivities, specificities, and positive predictive values for the Amsterdam criteria were 82%, 8%, and 45%, respectively, and for the Bethesda criteria were 100%, 0%, and 48%, respectively. Distribution of mutations was MLH1 = 4, MSH2 = 11, and MSH6 = 4. Conclusion Wide clinical criteria to select HNPCC kindreds, followed by immunohistochemistry of tumor material from one affected person in each family, had high sensitivity and specificity to predict MMR mutations.

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