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[Cancer Research 56, 4836-4840, November 1, 1996]
© 1996 American Association for Cancer Research
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Altered Expression of hMSH2 and hMLH1 in Tumors with Microsatellite Instability and Genetic Alterations in Mismatch Repair Genes1

Stephen N. Thibodeau2, Amy J. French, Patrick C. Roche, Julie M. Cunningham, David J. Tester, Noralane M. Lindor, Gabriela Moslein3, Sean M. Baker, R. Michael Liskay, Lawrence J. Burgart, Ronald Honchel4 and Kevin C. Halling5

Department of Laboratory Medicine and Pathology [S. N. T., A. J. F., P. C. R., J. M. C., D. J. T., L. J. B., R. H., K. C. H.] and Department of Medical Genetics [N. M. L.], Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905; University of Dusseldorf, Dusseldorf, Germany [G. M.]; and Department of Molecular and Medical Genetics, Oregon Health Science University, Portland, Oregon 97207 [S. M. B., R. M. L.]

To date, at least four genes involved in DNA mismatch repair (MMR) have been demonstrated to be altered in the germline of patients with hereditary nonpolyposis colon cancer: hMSH2, hMLH1, hPMS1, and hPMS2. Additionally, loss of MMR function has been demonstrated to lead to the phenomenon of microsatellite instability (MIN) in tumors from these patients. In this study, we have examined the protein expression pattern of hMSH2 and hMLH1 by immunohistochemistry in paraffin-embedded tumors from 7 patients with MIN+ sporadic cancer, 13 patients with familial colorectal cancer, and 12 patients meeting the strict Amsterdam criteria for hereditary nonpolyposis colon cancer. The relationship between the expression of these two gene products, the presence of germline or somatic mutations, and the presence of tumor MIN was examined. Nineteen of the 28 tumors studied demonstrated MIN, whereas mutations in hMLH1 and hMSH2 were detected in 6 and 2 patients, respectively. Of the eight MIN+/mutation+ cases, the absence of protein expression was observed for the corresponding gene product in all but one case (missense mutation in hMLH1). However, seven MIN+/mutation- cases also showed no expression of either hMLH1 (n = 5), hMSH2 (n = 1), or both (n = 1), whereas four MIN+/mutation- cases demonstrated normal expression for both. None of the MIN-/mutation- cases (n = 9) demonstrated an altered expression pattern for either protein. These data suggest that examination of protein expression by immunohistochemistry may be a rapid method for prescreening tumors for mutations in the MMR genes.

1 This work was supported by NIH Grant CA 68535-2.

2 To whom requests for reprints should be addressed, at Laboratory Genetics/HI 970, Mayo Clinic, 200 First Street SW, Rochester, MN 55905. Phone: (507) 284-4696.

3 G. M. was funded by Deutsche Forschungsgemeinschaft.

4 Current affiliation: Indiana University, Indianapolis, IN 46236.

5 Current affiliation: R. L. Roudebush Veterans Affairs Medical Center, Indianapolis, IN 46236.

Received 7/26/96. Accepted 9/18/96.




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Methylation of CpG in a Small Region of the hMLH1 Promoter Invariably Correlates with the Absence of Gene Expression
Cancer Res., May 1, 1999; 59(9): 2029 - 2023.
[Abstract] [Full Text] [PDF]

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 Cancer Res.Home page
A. S. Fleisher, M. Esteller, S. Wang, G. Tamura, H. Suzuki, J. Yin, T.-T. Zou, J. M. Abraham, D. Kong, K. N. Smolinski, et al.
Hypermethylation of the hMLH1 Gene Promoter in Human Gastric Cancers with Microsatellite Instability
Cancer Res., March 1, 1999; 59(5): 1090 - 1095.
[Abstract] [Full Text] [PDF]

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 Cancer Res.Home page
S. Y. Leung, S. T. Yuen, L. P. Chung, K. M. Chu, A. S. Y. Chan, and J. C. I. Ho
hMLH1 Promoter Methylation and Lack of hMLH1 Expression in Sporadic Gastric Carcinomas with High-Frequency Microsatellite Instability
Cancer Res., January 1, 1999; 59(1): 159 - 164.
[Abstract] [Full Text] [PDF]

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 Am. J. Pathol.Home page
T. Fujiwara, J. M. Stolker, T. Watanabe, A. Rashid, P. Longo, J. R. Eshleman, S. Booker, H. T. Lynch, J. R. Jass, J. S. Green, et al.
Accumulated Clonal Genetic Alterations in Familial and Sporadic Colorectal Carcinomas with Widespread Instability in Microsatellite Sequences
Am. J. Pathol., October 1, 1998; 153(4): 1063 - 1078.
[Abstract] [Full Text] [PDF]

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 BloodHome page
L. M. Larocca, D. Capello, A. Rinelli, S. Nori, A. Antinori, A. Gloghini, A. Cingolani, A. Migliazza, G. Saglio, S. Cammilleri-Broet, et al.
The Molecular and Phenotypic Profile of Primary Central Nervous System Lymphoma Identifies Distinct Categories of the Disease and Is Consistent With Histogenetic Derivation From Germinal Center-Related B Cells
Blood, August 1, 1998; 92(3): 1011 - 1019.
[Abstract] [Full Text] [PDF]

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 Proc. Natl. Acad. Sci. USAHome page
J. G. Herman, A. Umar, K. Polyak, J. R. Graff, N. Ahuja, J.-P. J. Issa, S. Markowitz, J. K. V. Willson, S. R. Hamilton, K. W. Kinzler, et al.
Incidence and functional consequences of hMLH1 promoter hypermethylation in colorectal carcinoma
PNAS, June 9, 1998; 95(12): 6870 - 6875.
[Abstract] [Full Text] [PDF]

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 FASEB J.Home page
M. De las Alas, R. A. M. de bruin, L. T. Eyck, G. Los, and S. B. Howell
Prediction-based threading of the hMSH2 DNA mismatch repair protein
FASEB J, June 1, 1998; 12(9): 653 - 663.
[Abstract] [Full Text]


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