DNA mismatch repair and TP53 defects are early events in uterine carcinosarcoma tumorigenesis

Growing molecular evidence shows that uterine carcinosarcomas are clonal tumors. The carcinoma component has a dominant effect in the aggressive clinical behavior of these tumors. Defective DNA mismatch repair affects up to 30% of endometrial adenocarcinomas. The frequency and importance of defectiv...

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Published in:Modern pathology 2006-10, Vol.19 (10), p.1333-1338
Main Authors: Taylor, Nicholas P, Zighelboim, Israel, Huettner, Phyllis C, Powell, Matthew A, Gibb, Randall K, Rader, Janet S, Mutch, David G, Edmonston, Tina B, Goodfellow, Paul J
Format: Article
Language:English
Subjects:
Adaptor Proteins, Signal Transducing
Aged
Base Pair Mismatch
Cancer
carcinosarcoma
Carcinosarcoma - chemistry
Carcinosarcoma - genetics
Carcinosarcoma - metabolism
Carrier Proteins - analysis
Cell Transformation, Neoplastic - genetics
Cell Transformation, Neoplastic - metabolism
Chromosomal Instability
clonality
Dissection
DNA mismatch repair
DNA Repair
DNA, Neoplasm - genetics
DNA-Binding Proteins - analysis
Female
Humans
Immunohistochemistry
Laboratories
Laboratory Medicine
Loss of Heterozygosity
malignant mixed müllerian tumor
Medicine
Medicine & Public Health
microsatellite instability
Microsatellite Repeats - genetics
MutL Protein Homolog 1
MutS Homolog 2 Protein - analysis
Nuclear Proteins - analysis
Oncology
original-article
Pathology
Retrospective Studies
Sarcoma
TP53
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - metabolism
Tumorigenesis
Tumors
Uterine Neoplasms - chemistry
Uterine Neoplasms - genetics
Uterine Neoplasms - metabolism
Yeast
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description Growing molecular evidence shows that uterine carcinosarcomas are clonal tumors. The carcinoma component has a dominant effect in the aggressive clinical behavior of these tumors. Defective DNA mismatch repair affects up to 30% of endometrial adenocarcinomas. The frequency and importance of defective DNA mismatch repair in the histiogenesis of uterine carcinosarcomas remains controversial. We studied the pattern and frequency of defective DNA mismatch repair and TP53 alterations in the epithelial and mesenchymal components of 28 uterine carcinosarcomas. We found evidence of defective DNA mismatch repair in six cases (21%) with a concordance rate of 83% for carcinoma-sarcoma pairs (κ=0.887, P
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The carcinoma component has a dominant effect in the aggressive clinical behavior of these tumors. Defective DNA mismatch repair affects up to 30% of endometrial adenocarcinomas. The frequency and importance of defective DNA mismatch repair in the histiogenesis of uterine carcinosarcomas remains controversial. We studied the pattern and frequency of defective DNA mismatch repair and TP53 alterations in the epithelial and mesenchymal components of 28 uterine carcinosarcomas. We found evidence of defective DNA mismatch repair in six cases (21%) with a concordance rate of 83% for carcinoma-sarcoma pairs (κ=0.887, P&lt;0.001). Lack of immunostaining for the MLH1 protein was demonstrated in both components in two of these tumors. TP53 defects were evaluated by 17p deletion analysis and p53 immunostaining. Nineteen carcinoma (68%) and 18 sarcoma (64%) components had evidence of either TP53 allelic loss or p53 overexpression. These defects proved clonal in 76% of cases (κ=0.602, P=0.003). 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The carcinoma component has a dominant effect in the aggressive clinical behavior of these tumors. Defective DNA mismatch repair affects up to 30% of endometrial adenocarcinomas. The frequency and importance of defective DNA mismatch repair in the histiogenesis of uterine carcinosarcomas remains controversial. We studied the pattern and frequency of defective DNA mismatch repair and TP53 alterations in the epithelial and mesenchymal components of 28 uterine carcinosarcomas. We found evidence of defective DNA mismatch repair in six cases (21%) with a concordance rate of 83% for carcinoma-sarcoma pairs (κ=0.887, P&lt;0.001). Lack of immunostaining for the MLH1 protein was demonstrated in both components in two of these tumors. TP53 defects were evaluated by 17p deletion analysis and p53 immunostaining. Nineteen carcinoma (68%) and 18 sarcoma (64%) components had evidence of either TP53 allelic loss or p53 overexpression. These defects proved clonal in 76% of cases (κ=0.602, P=0.003). 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The high rate of concordance for these molecular defects between the carcinoma and sarcoma components adds to existing molecular evidence that carcinosarcomas are clonal malignancies.</description><subject>Adaptor Proteins, Signal Transducing</subject><subject>Aged</subject><subject>Base Pair Mismatch</subject><subject>Cancer</subject><subject>carcinosarcoma</subject><subject>Carcinosarcoma - chemistry</subject><subject>Carcinosarcoma - genetics</subject><subject>Carcinosarcoma - metabolism</subject><subject>Carrier Proteins - analysis</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Chromosomal Instability</subject><subject>clonality</subject><subject>Dissection</subject><subject>DNA mismatch repair</subject><subject>DNA Repair</subject><subject>DNA, Neoplasm - genetics</subject><subject>DNA-Binding Proteins - analysis</subject><subject>Female</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Laboratories</subject><subject>Laboratory Medicine</subject><subject>Loss of Heterozygosity</subject><subject>malignant mixed müllerian tumor</subject><subject>Medicine</subject><subject>Medicine &amp; 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subjects Adaptor Proteins, Signal Transducing
Aged
Base Pair Mismatch
Cancer
carcinosarcoma
Carcinosarcoma - chemistry
Carcinosarcoma - genetics
Carcinosarcoma - metabolism
Carrier Proteins - analysis
Cell Transformation, Neoplastic - genetics
Cell Transformation, Neoplastic - metabolism
Chromosomal Instability
clonality
Dissection
DNA mismatch repair
DNA Repair
DNA, Neoplasm - genetics
DNA-Binding Proteins - analysis
Female
Humans
Immunohistochemistry
Laboratories
Laboratory Medicine
Loss of Heterozygosity
malignant mixed müllerian tumor
Medicine
Medicine & Public Health
microsatellite instability
Microsatellite Repeats - genetics
MutL Protein Homolog 1
MutS Homolog 2 Protein - analysis
Nuclear Proteins - analysis
Oncology
original-article
Pathology
Retrospective Studies
Sarcoma
TP53
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - metabolism
Tumorigenesis
Tumors
Uterine Neoplasms - chemistry
Uterine Neoplasms - genetics
Uterine Neoplasms - metabolism
Yeast
title DNA mismatch repair and TP53 defects are early events in uterine carcinosarcoma tumorigenesis
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