SwePub - search: WFRF:(Dimberg Jan)

Enumeration	Reference	Cover	Find
1.	Fransén, Karin, 1973-, et al. (author) Mutation analysis of the BRAF, ARAF and RAF-1 genes in human colorectal adenocarcinomas. 2004 In: Carcinogenesis. - : Oxford University Press. - 0143-3334 .- 1460-2180. ; 25:4, s. 527-533 Journal article (other academic/artistic)
2.	Monstein, Hans-Jürg, et al. (author) K-ras and B-raf gene mutations are not associated with gastrin- and CCK2-receptor mRNA expression in human colorectal tumour tissues 2004 In: European Journal of Clinical Investigation. - : Wiley. - 0014-2972 .- 1365-2362. ; 34:2, s. 100-106 Journal article (peer-reviewed)abstract Background: Colorectal cancer is a multistep process caused by genetic alterations in cell growth regulatory genes such as K-ras and B-raf. It has been assumed that mutations in the K-ras gene induce gastrin gene expression and that gastrin stimulates the growth of colorectal cancer in an autocrine fashion by coexpressing gastrin and cholecystokinin (CCK)2 receptors. The aim of this study was to examine a possible association of K-ras and B-raf gene mutations with gastrin and CCK2 receptor mRNA expression in human colon and rectum tumour biopsy specimens. Methods: K-ras and B-raf gene mutations as well as gastrin and CCK2 receptor mRNA expression in 50 colon and 46 rectum biopsies, respectively, were determined using molecular biology methods. Results: K-ras mutations occurred in 44% colon and 30% rectum and B-raf mutations in 16% colon and 4% rectum tumours, respectively. Gastrin mRNA was expressed in 64% colon and 61% rectum tumours, whereas CCK2 receptor mRNAs was expressed in 32% colon and 13% rectum tumours. K-ras or B-raf gene mutations and simultaneous gastrin mRNA expression was observed in 40% colon and 17% rectum tumours, respectively. Coexpression of gastrin and CCK2 receptor mRNA occurred in 20% colon and 9% rectal tumours. Conclusions: The results do not support the hypothesis that K-ras and B-raf gene mutations have an impact on gastrin- and CCK-receptor mRNA expression in colorectal tumour tissues.

Monstein, Hans-Jürg, et al. (author)
K-ras and B-raf gene mutations are not associated with gastrin- and CCK2-receptor mRNA expression in human colorectal tumour tissues
2004
In: European Journal of Clinical Investigation. - : Wiley. - 0014-2972 .- 1365-2362. ; 34:2, s. 100-106
Journal article (peer-reviewed)abstract
- Background: Colorectal cancer is a multistep process caused by genetic alterations in cell growth regulatory genes such as K-ras and B-raf. It has been assumed that mutations in the K-ras gene induce gastrin gene expression and that gastrin stimulates the growth of colorectal cancer in an autocrine fashion by coexpressing gastrin and cholecystokinin (CCK)2 receptors. The aim of this study was to examine a possible association of K-ras and B-raf gene mutations with gastrin and CCK2 receptor mRNA expression in human colon and rectum tumour biopsy specimens. Methods: K-ras and B-raf gene mutations as well as gastrin and CCK2 receptor mRNA expression in 50 colon and 46 rectum biopsies, respectively, were determined using molecular biology methods. Results: K-ras mutations occurred in 44% colon and 30% rectum and B-raf mutations in 16% colon and 4% rectum tumours, respectively. Gastrin mRNA was expressed in 64% colon and 61% rectum tumours, whereas CCK2 receptor mRNAs was expressed in 32% colon and 13% rectum tumours. K-ras or B-raf gene mutations and simultaneous gastrin mRNA expression was observed in 40% colon and 17% rectum tumours, respectively. Coexpression of gastrin and CCK2 receptor mRNA occurred in 20% colon and 9% rectal tumours. Conclusions: The results do not support the hypothesis that K-ras and B-raf gene mutations have an impact on gastrin- and CCK-receptor mRNA expression in colorectal tumour tissues.

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