Document Detail


Improved survival with an intact DNA mismatch repair system in endometrial cancer.
MedLine Citation:
PMID:  17077244     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: To correlate survival and surgical-pathologic factors with DNA mismatch repair status in patients with endometrial cancer. METHODS: Specimens from 336 patients with endometrial cancer were used to create a tissue microarray. Immunohistochemistry with antibodies against the mismatch repair genes MLH1, MSH2, MSH6, and PMS2 were used to stain the tissue microarray. Clinical, pathologic, and survival data were collected and correlated with the immunohistochemistry results. RESULTS: Mismatch repair deficiency was seen in 29% (84 of 294) of cases. Correlation was noted between lack of expression of MLH1 and an increased risk for lymphvascular space involvement (32% versus 21%, P=.05) and cervical involvement (26% versus 14%, P=.02). Lack of expression of either MLH1 or MSH2 was associated with thinner patients (85% had a body mass index less than 40 versus 73% of patients with normal expression, P=.02), as well as with the absence of a history of previous primary malignancy (0 verus 13 cases [4%], P=.023). The estimated disease-free survival is 88%; despite a small number of recurrences, there was a nonsignificant improvement in disease-free survival in tumors with an intact mismatch repair system (P=.1). Significantly improved disease-free survival was seen in patients with normal MLH1 and MSH2 expression compared with those with abnormal expression (92% versus 81%, P=.035). CONCLUSION: Defects in DNA mismatch repair in endometrial cancer is correlated with negative prognostic factors and worse progression-free survival (without a difference in overall survival) compared with tumors with an intact mismatch repair system. LEVEL OF EVIDENCE: II-3.
Authors:
David E Cohn; Wendy L Frankel; Kimberly E Resnick; Vanna L Zanagnolo; Larry J Copeland; Heather Hampel; Nicole Kelbick; Carl D Morrison; Jeffrey M Fowler
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Obstetrics and gynecology     Volume:  108     ISSN:  0029-7844     ISO Abbreviation:  Obstet Gynecol     Publication Date:  2006 Nov 
Date Detail:
Created Date:  2006-11-01     Completed Date:  2006-12-05     Revised Date:  2009-10-26    
Medline Journal Info:
Nlm Unique ID:  0401101     Medline TA:  Obstet Gynecol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1208-15     Citation Subset:  AIM; IM    
Affiliation:
Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, the Ohio State University College of Medicine and Comprehensive Cancer Center, Columbus, Ohio 43210, USA. David.Cohn@osumc.edu
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MeSH Terms
Descriptor/Qualifier:
Adaptor Proteins, Signal Transducing
Adenosine Triphosphatases / genetics,  metabolism
Adolescent
Adult
Aged
Aged, 80 and over
Body Mass Index
Carrier Proteins / genetics*,  metabolism
DNA Mismatch Repair*
DNA Repair Enzymes / genetics,  metabolism
DNA-Binding Proteins / genetics,  metabolism
Disease-Free Survival
Endometrial Neoplasms / genetics*,  mortality,  surgery
Female
Gene Expression*
Humans
Middle Aged
MutS Homolog 2 Protein / genetics*,  metabolism
Nuclear Proteins / genetics*,  metabolism
Oligonucleotide Array Sequence Analysis
Prognosis
Chemical
Reg. No./Substance:
0/Adaptor Proteins, Signal Transducing; 0/Carrier Proteins; 0/DNA-Binding Proteins; 0/G-T mismatch-binding protein; 0/MLH1 protein, human; 0/Nuclear Proteins; EC 3.6.1.-/Adenosine Triphosphatases; EC 3.6.1.-/PMS2 protein, human; EC 3.6.1.3/MSH2 protein, human; EC 3.6.1.3/MutS Homolog 2 Protein; EC 6.5.1.-/DNA Repair Enzymes

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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