Polymorphisms in insulin-related genes predispose to specific KRAS2 and TP53 mutations in colon cancer

Samowitz, Wade S.; Wolff, Roger K.; Ni, Khe; Andersen, Kristen; Caan, Bette J.; Slattery, Martha L.

doi:10.1016/j.mrfmmm.2005.10.014

Cited by 21 publications

(28 citation statements)

References 9 publications

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“…Ren et al (2004) revealed that participants carrying the variant homozygote 32Ala/Ala had a significantly increased risk of breast cancer in Chinese women (adjusted OR = 1.60, 95% CI = 1.1-2.5), compared with the wild-type homozygote 32Gly/Gly, indicating that the variant 32Ala might be a risk allele, which was consistent with our results in GC. In agreement with most previous studies on breast, prostate, colorectal cancers Schernhammer et al, 2003;Wang et al, 2003;Li et al, 2004;Slattery et al, 2004;Wong et al, 2005;Samowitz et al, 2006), however, we did not find a significant association between the A-202C variant and risk of GC. Recently, a nested case-control study of 807 breast cancer patients and 1588 matched control participants from the European Prospective Investigation into Cancer and Nutrition showed that common genetic variation in IGFBP3 does not play a major role in altering breast cancer risk in whites (Canzian et al, 2006).…”

Section: Discussionsupporting

confidence: 93%

The role of IGFBP3 functional polymorphisms in the risk of gastric cancer in a high-risk Chinese population

Chen

Wang²,

Ke³

et al. 2008

European Journal of Cancer Prevention

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Insulin-like growth factors (IGFs) and their receptors play a crucial role in regulating cell proliferation, differentiation, and apoptosis. Insulin-like growth factor-binding protein-3 is the most abundant insulin-like growth factor receptor in the serum and binds the majority of insulin-like growth factors. Studies reported that circulating level of insulin-like growth factor-binding protein-3 was modulated by functional genetic variants of insulin-like growth factor-binding protein-3 and, therefore, maybe associated with the risk of gastric cancer. In this case-control study of 576 gastric cancer cases and 647 cancer-free control participants in a high-risk Chinese population, we tested the hypothesis that functional polymorphisms A-202C and Gly32Ala of insulinlike growth factor-binding protein-3 are associated with risk of gastric cancer. We found that the variant 32Ala allele was associated with a significantly increased risk of gastric cancer (adjusted odds ratio=1.84, 95% confidence interval=1.45-2.33 for 32Gly/Ala and odds ratio=2.39, 95% confidence interval=1.47-3.90 for 32Ala/Ala, respectively), compared with the wild-type homozygote 32Gly/Gly. Although the A-202C variant was not significantly associated with gastric cancer risk in the single locus analysis, we found a significant locus-locus interaction between insulin-like growth factor-binding protein-3 A-202C and Gly32Ala loci on gastric cancer risk (Pint<0.001). These findings suggest that functional variants of insulin-like growth factor-binding protein-3 might be important markers for gastric cancer susceptibility and further studies are warranted to characterize the functional relevance of the locus-locus interaction of this gene.

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Section: Discussionsupporting

confidence: 93%

The role of IGFBP3 functional polymorphisms in the risk of gastric cancer in a high-risk Chinese population

Chen

Wang²,

Ke³

et al. 2008

European Journal of Cancer Prevention

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“…Colorectal carcinomas with B-RAF mutations are associated with early Duke's tumor stages, but this association was not seen with K-RAS mutations (10). Other studies also associated B-RAF mutations with distinct clinical features or outcome (16,19). A recent study using defined genetic alterations found that B-Raf activation alone did not substitute for Ras activation to cause growth transformation of primary human melanocytes (20).…”

Section: Introductionmentioning

confidence: 99%

Context-dependent roles of mutant B-Raf signaling in melanoma and colorectal carcinoma cell growth

Hao

Muñiz-Medina

Mehta

et al. 2007

Molecular Cancer Therapeutics

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Mutational activation of Ras and a key downstream effector of Ras, the B-Raf serine/threonine kinase, has been observed in melanomas and colorectal carcinomas. These observations suggest that inhibition of B-Raf activation of mitogen-activated protein kinase (MAPK)/ extracellular signal-regulated kinase kinase (MEK) and the extracellular signal-regulated kinase MAPK cascade may be an effective approach for the treatment of RAS and B-RAF mutation-positive melanomas and colon carcinomas. Although recent studies with interfering RNA (RNAi) and pharmacologic inhibitors support a critical role for B-Raf signaling in melanoma growth, whether mutant B-Raf has an equivalent role in promoting colorectal carcinoma growth has not been determined. In the present study, we used both RNAi and pharmacologic approaches to further assess the role of B-Raf activation in the growth of human melanomas and additionally determined if a similar role for mutant B-Raf is seen for colorectal carcinoma cell lines. We observed that RNAi suppression of mutant B-Raf (V600E) expression strongly suppressed the anchoragedependent growth of B-RAF mutation-positive melanoma, but not colorectal carcinoma, cells. However, the anchorageindependent and tumorigenic growth of B-RAF mutationpositive colorectal carcinomas was dependent on mutant B-Raf function. Finally, pharmacologic inhibition of MEK and Raf was highly effective at inhibiting the growth of B-RAF mutation-positive melanomas and colorectal carcinoma cells, whereas inhibitors of other protein kinases activated by Ras (AKT, c-Jun NH 2 -terminal kinase, and p38 MAPK) were less effective. Our observations suggest that Raf and MEK inhibitors may be effective for the treatment of B-RAF mutation-positive colorectal carcinomas as well as melanomas. [Mol Cancer Ther 2007;6(8):2220 -9]

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“…Several genetic polymorphisms in the IGFBP-3 gene have been identified for predicting the development, progression, and clinical outcomes of colorectal cancer, but A-202C and C2133G were the most common ones (Poole et al, 2012). Many previous genetic studies have suggested that IGFBP A-202C and C2133G polymorphisms play an important role in colorectal carcinogenesis (Le Marchand et al, 2005;Morimoto et al, 2005;Samowitz et al, 2006;Slattery et al, 2006;Xiang et al, 2009;Feik et al, 2010;Keku et al, 2012;Ollberding et al, 2012), while other studies found no convincing evidence of these polymorphisms in increasing the risk of colorectal cancer (Slattery et al, 2004;Wong et al, 2005;Pechlivanis et al, 2007). This controversy could be explained with several reasons, including the differences in study design, sample size, ethnicity, and statistical method.…”

Section: Discussionmentioning

confidence: 99%

“…Of these articles, 66 were excluded after reviewing their titles and key words; then, abstract and full text were reviewed, and another 68 papers were excluded. Eleven case-control studies met our inclusion criteria (Le Marchand et al, 2005;Morimoto et al, 2005;Wong et al, 2005;Samowitz et al, 2006;Slattery et al, 2004Slattery et al, , 2006Pechlivanis et al, 2007;Xiang et al, 2009;Feik et al, 2010;Keku et al, 2012;Ollberding et al, 2012). The publication years of the involved studies ranged from 2004 to 2012.…”

Section: Baseline Characteristics Of Included Studiesmentioning

confidence: 99%

IGFBP-3 A-202C and C2133G polymorphisms and colorectal cancer risk: a meta-analysis of case-control studies

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Recent evidence suggests that genetic variations in the IGFBP-3 gene may impact susceptibility to colorectal cancer, but individually published results are inconclusive. Our meta-analysis was aimed at providing a more precise estimation of these associations. An extensive literature search was conducted for appropriate articles published before May 1, 2013. This meta-analysis was performed using the STATA 12.0 software. The crude odds ratios (OR) with 95% confidence interval (CI) were calculated. Eleven case-control studies were included with a total of 11,895 colorectal cancer patients and 17,147 healthy controls. Our meta-analysis indicated that the G variant of IGFBP-3 C2133G polymorphism may be associated with increased colorectal cancer risk. However, no statistically significant association was noted between IGFBP-3 A-202C polymorphism and colorectal cancer risk. No publication bias was detected in this metaanalysis. The current meta-analysis suggests that the IGFBP-3 C2133G polymorphism may confer susceptibility to colorectal cancer. The G IGFBP-3 A-202C and C2133G in colorectal cancer risk variant of the IGFBP-3 C2133G polymorphism may serve as a useful biomarker for predicting the risk of colorectal cancer.

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Polymorphisms in insulin-related genes predispose to specific KRAS2 and TP53 mutations in colon cancer

Cited by 21 publications

References 9 publications

The role of IGFBP3 functional polymorphisms in the risk of gastric cancer in a high-risk Chinese population

The role of IGFBP3 functional polymorphisms in the risk of gastric cancer in a high-risk Chinese population

Context-dependent roles of mutant B-Raf signaling in melanoma and colorectal carcinoma cell growth

IGFBP-3 A-202C and C2133G polymorphisms and colorectal cancer risk: a meta-analysis of case-control studies

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