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Immunoassay for wild-type protein in lymphocytes predicts germline mutations in patients at risk for hereditary colorectal cancer.

作者信息

Fields Jeremy Z, Gao Zhiping, Gao Zhenqiang, Lewis Marcia, Maimonis Peter, Harvey Jean, Lynch Henry T, Boman Bruce M

机构信息

CA*TX Inc, Gladwyne, Pennsylvania, USA,

出版信息

J Lab Clin Med. 2004 Jan;143(1):59-66. doi: 10.1016/j.lab.2003.10.001.

DOI:10.1016/j.lab.2003.10.001
PMID:14749686
Abstract

Using colorectal cancer (CRC) as an example, we present the hypothesis that quantitative immunoassays for wild-type (full-length) proteins can be used to identify carriers of traits for hereditary diseases. In the case of hereditary CRC, this involves identifying individuals with germline mutations in a mismatch-repair (MMR) gene (mainly hMSH2 or hMLH1) or in the adenomatous polyposis coli (APC) gene. Because expression of wild-type protein should reflect wild-type gene dosage, we predicted that individuals harboring a germline mutation will have a reduction of approximately 50% in expression in lymphocytes of the corresponding full-length protein. In this pilot study, we tested lymphoblastoid cell lines that had been established from controls and individuals with, or at high risk for, hereditary CRC: 9 lines from healthy, unaffected individuals; 4 from affected members in familial adenomatous polyposis families (with known germ-line APC mutation); 42 from CRC patients in our Familial CRC Registry (increased risk of hereditary nonpolyposis colon cancer as assessed by family history, age at adenoma or carcinoma diagnosis, and other clinical criteria). For MSH2 and MLH1 we used western blots; for APC we used immunoprecipitation. All familial adenomatous polyposis lines had about 50% less immunoprecipitable full-length APC protein. Some cell lines (7 of 42) from Familial CRC Registry patients showed on western blots a reduction (mean 46%) in either MSH2 or MLH1 (relative to the other protein). All 7 subsequently were proved to contain a germline MMR mutation. We conclude that (1) because most of the expected CRC-causing germ line mutations are truncation-causing, immunoassays for wild-type protein should be able to identify most individuals with hereditary CRC-causing traits; (2) these assays, which are more practical and inexpensive than current mutation-detecting tests for hereditary CRC traits, have the potential for commercial development into broad-based population screens of high-risk patients and their families and the potential to save both lives and health-care dollars; (3) this strategy may be useful for other hereditary cancers and even other hereditary diseases; (4) our approach has the potential to greatly benefit public-health programs for cancer control.

摘要

相似文献

1
Immunoassay for wild-type protein in lymphocytes predicts germline mutations in patients at risk for hereditary colorectal cancer.
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2
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引用本文的文献

1
Detection of DNA mismatch repair proteins in fresh human blood lymphocytes--towards a novel method for hereditary non-polyposis colorectal cancer (Lynch syndrome) screening.检测新鲜人血淋巴细胞中的 DNA 错配修复蛋白--一种新的遗传性非息肉病性结直肠癌(林奇综合征)筛查方法。
J Exp Clin Cancer Res. 2011 Oct 21;30(1):100. doi: 10.1186/1756-9966-30-100.