Differential gene expression signatures between colorectal cancers with and without KRAS mutations: Crosstalk between the KRAS pathway and other signalling pathways

Watanabe, Toshiaki; Kobunai, Takashi; Yamamoto, Yasutake; Matsuda, Keiji; Ishihara, Soichiro; Nozawa, Keijiro; Iinuma, Hisae; Ikeuchi, Hiroki; Eshima, Kiyoshi

doi:10.1016/j.ejca.2011.03.029

Cited by 54 publications

(50 citation statements)

References 34 publications

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“…7 Moreover, in HT-29 and LS-174T cells SPRY2 increases the level of c-MET and HGF-stimulated ERK and AKT phosphorylation, promoting cell migration and invasion. 8 Further supporting a tumorigenic role, SPRY2 is upregulated in KRAS mutant colorectal cancer, 9 and in melanoma cells harbouring N-RAS or B-RAF mutations. 10,11 RNA expression repository databases show upregulation of SPRY2 expression in colorectal tumors versus others neoplasias.…”

Section: Introductionmentioning

confidence: 99%

SPROUTY-2 represses the epithelial phenotype of colon carcinoma cells via upregulation of ZEB1 mediated by ETS1 and miR-200/miR-150

et al. 2015

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Section: Introductionmentioning

confidence: 99%

SPROUTY-2 represses the epithelial phenotype of colon carcinoma cells via upregulation of ZEB1 mediated by ETS1 and miR-200/miR-150

et al. 2015

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“…15,16 Moreover, several reports have shown that more genes were methylated in primary colorectal tumors than in corresponding metastatic lesions and metastases can exhibit substantial differences in gene expression patterns compared with primary tumors. [17][18][19] In view of these data, the heterogeneity between primary tumors and metastases emerged as an additional reason for the failure of targeted therapies in colorectal cancer; thus, the current study was conducted in order to determine the degree of discordance between potential predictive and/or prognostic molecular markers in primary tumors and corresponding metastases, and to investigate the possible associations between these biomarkers in primary tumors, as well as in metastases.…”

mentioning

confidence: 99%

Combined analysis of KRAS and PIK3CA mutations, MET and PTEN expression in primary tumors and corresponding metastases in colorectal cancer

et al. 2013

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Metastasis is the main cause of mortality in patients with colorectal cancer. However, most of the targeted therapies and predictive molecular biomarkers were developed based mainly on primary tumors. The current study was conducted to determine the degree of discordance between potential predictive and/or prognostic molecular markers in primary colorectal tumors and corresponding metastases, as this could have an impact on the efficacy of targeted therapies in the advanced colorectal cancer. KRAS, PIK3CA and BRAF mutations were determined by Sanger sequencing and mutant-enriched polymerase chain reaction (PCR) assays in 83 paired samples, MET gene copy number by quantitative PCR in 59, MET expression by immunohistochemistry in 73 and nuclear and cytoplasmic expression of PTEN by immunohistochemistry in 78 and 71 pairs, respectively. A certain degree of discordance between primary tumors and corresponding metastases was demonstrated for all examined biomarkers except BRAF mutations. PIK3CA exon 9 mutations in primary tumors and loss of PTEN nuclear expression in metastases correlated with KRAS mutations. KRAS wild-type status in primary tumors was associated with loss of PTEN cytoplasmic expression and high gene copy number of MET. Survival and clinical data were available for 68 patients. The multiple regression analysis revealed that the right-sided tumor localization and overexpression of MET were associated with shorter overall survival.

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“…However, radiation sensitivity is only one of the variables that determines whether a tumor will be curable by radiation. Furthermore, the value of radiation sensitivity tests in vitro and their correlation with the clinical outcome are controversial, possibly because of a host response or other interactions of various signaling pathways that cannot be reconstituted in cell lines [42,43]. Therefore, the translation of the results of in vitro studies into clinical practice remains a challenge for the future.…”

Section: Microarray Analysis Using Colorectal Cancer Cell Linesmentioning

confidence: 95%

Predicting the response to preoperative radiation or chemoradiation by a microarray analysis of the gene expression profiles in rectal cancer

2012

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Preoperative radiotherapy or chemoradiotherapy (CRT) has become a standard treatment for patients with locally advanced rectal cancer. However, there is a wide spectrum of responses to preoperative CRT, ranging from none to complete. There has been intense interest in the identification of molecular biomarkers to predict the response to preoperative CRT, in order to spare potentially non-responsive patients from unnecessary treatment. However, no specific molecular biomarkers have yet been definitively proven to be predictive of the response to CRT. Instead of focusing on specific factors, microarray-based gene expression profiling technology enables the simultaneous analysis of large numbers of genes, and might therefore have immense potential for predicting the response to preoperative CRT. We herein review published studies using a microarray-based analysis to identify gene expression profiles associated with the response of rectal cancer to radiation or CRT. Although some studies have reported gene expression signatures capable of high predictive accuracy, the compositions of these signatures have differed considerably, with little gene overlap. However, considering the promising data regarding gene profiling in breast cancer, the microarray analysis could still have potential to improve the management of locally advanced rectal cancer. Increasing the number of patients analyzed for more accurate prediction and the extensive validation of predictive classifiers in prospective clinical trials are necessary before such profiling can be incorporated into future clinical practice.

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Differential gene expression signatures between colorectal cancers with and without KRAS mutations: Crosstalk between the KRAS pathway and other signalling pathways

Cited by 54 publications

References 34 publications

SPROUTY-2 represses the epithelial phenotype of colon carcinoma cells via upregulation of ZEB1 mediated by ETS1 and miR-200/miR-150

SPROUTY-2 represses the epithelial phenotype of colon carcinoma cells via upregulation of ZEB1 mediated by ETS1 and miR-200/miR-150

Combined analysis of KRAS and PIK3CA mutations, MET and PTEN expression in primary tumors and corresponding metastases in colorectal cancer

Predicting the response to preoperative radiation or chemoradiation by a microarray analysis of the gene expression profiles in rectal cancer

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