NDLI: Tumorigenesis in colorectal tumors from patients with hereditary non-polyposis colorectal cancer

Content Provider	Springer Nature Link
Author	Tannergård, P. Liu, T. Weger, Adolf rdenskjöld, Magnus Lindblom, A.
Copyright Year	1997
Abstract	Tumorigenesis of colorectal cancer in patients with hereditary non-polyposis colorectal cancer (HNPCC) has been postulated to follow a different pathway from that of sporadic colorectal tumors. A characteristic of HNPCC-associated tumors is the replication error phenotype. We studied tumorigenesis in 8 fresh-frozen and 67 paraffin-embedded colorectal tumors derived from 29 families with HNPCC or a familial aggregation of colorectal cancer. By using intragenic markers, inactivation of the wild-type allele of hMLH1 was shown to occur through loss of heterozygosity and not through a somatic point mutation. Microsatellite instability is very common and occurs early in almost all colorectal tumors from HNPCC patients. Transforming growth factor β type II receptor (TβRII) mutations occur in these tumors at a high frequency. Of colorectal cancers from families with HNPCC, 63% have frameshift mutations in TβRII, compared with 10% of sporadic colorectal cancers. APC and K-RAS mutations appear to be as frequent in the HNPCC tumors as in the sporadic counterpart.
Starting Page	51
Ending Page	55
Page Count	5
File Format	PDF
ISSN	03406717
Journal	Human Genetics
Volume Number	101
Issue Number	1
e-ISSN	14321203
Language	English
Publisher	Springer-Verlag
Publisher Date	1997-10-08
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Content Type	Text
Resource Type	Article
Subject	Genetics Genetics (clinical)

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