Matthias Jungck
Overview
Explore the profile of Matthias Jungck including associated specialties, affiliations and a list of published articles.
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Articles
6
Citations
70
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0
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Recent Articles
1.
Grunhage F, Jungck M, Lamberti C, Keppeler H, Becker U, Schulte-Witte H, et al.
BMC Med Genet
. 2008 Jul;
9:70.
PMID: 18644122
Background: The genetics of sporadic and non-syndromic familial colorectal cancer (CRC) is not well defined. However, genetic factors that promote the development of precursor lesions, i.e. adenomas, might also predispose...
2.
Grunhage F, Jungck M, Lamberti C, Schulte-Witte H, Plassmann D, Becker U, et al.
Cancer Biomark
. 2008 May;
4(2):55-61.
PMID: 18503156
Unlabelled: Mutations of the base excision repair gene MUTYH have been reported as underlying genetic defects in autosomal-recessive familial adenomatous polyposis (FAP). Our aim was to determine the frequency of...
3.
Grunhage F, Jungck M, Lamberti C, Berg C, Becker U, Schulte-Witte H, et al.
Int J Colorectal Dis
. 2007 Oct;
23(2):147-54.
PMID: 17960397
Introduction: About 20% of colorectal cancer (CRC) patients show some kind of familiarity, which might be caused by yet unknown combinations of low penetrance susceptibility genes. We aimed to identify...
4.
Wang Y, Friedl W, Lamberti C, Jungck M, Mathiak M, Pagenstecher C, et al.
Int J Cancer
. 2002 Dec;
103(5):636-41.
PMID: 12494471
Hereditary nonpolyposis colorectal cancer (HNPCC) is often caused by a deficiency in DNA mismatch repair. By using conventional methods of mutation analysis, point mutations in the DNA mismatch repair genes...
5.
Wang Y, Friedl W, Sengteller M, Jungck M, Filges I, Propping P, et al.
Hum Mutat
. 2002 Feb;
19(3):279-86.
PMID: 11857745
A method for detection of large genomic deletions in the MSH2 and MLH1 genes based on multiplex PCR and quantitative evaluation of PCR products is presented. All 35 exons of...
6.
Lamberti C, Jungck M, Laarmann M, Knapp M, Caspari R, Friedl W, et al.
Pharmacogenetics
. 2002 Jan;
12(1):49-54.
PMID: 11773864
Familial adenomatous polyposis (FAP) exhibits a variable phenotype even in carriers of the same adenomatous polyposis coli germline mutation. Xenobiotic-metabolizing enzymes such as N-acetyltransferases (NATs) and glutathione S-transferases (GSTs) were...