EGF, TGF-a, and EGF-R in Human Colorectal Adenocarcinoma

Messa, Caterina; Russo, Francesco; Caruso, Maria Gabriella; Leo, Alfredo Di

doi:10.1080/028418698429595

Cited by 229 publications

(127 citation statements)

References 22 publications

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“…In this regard, many methods were developed to detect commonly known mutations and to screen new mutations of the EGFR in CRC but mainly in non-small cell lung cancer [28]. Epidermal growth factor EGF is frequently found co-expressed with EGFR in various types of cancer including colorectal adenocarcinoma [29]. In addition, significant regional differences in EGFR expression in the normal human colon mucosa was previously found.…”

Section: Product Of Pcr-rflp Analysis Of Egf A61g (Left) and P53 Arg7mentioning

confidence: 99%

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Association of EGF and p53 gene polymorphisms and colorectal cancer risk in the Slovak population

et al. 2014

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AbstractDuring the transformation process single nucleotide polymorphisms (SNPs) of key genes, such as p53 Arg72Pro or EGF A61G, may mediate various cellular processes. These variants may be associated with colorectal cancer risk (CRC), but conflicting findings have been reported. The purpose of this study was to determine the association of the SNPs in 5′ UTR of EGF A61G and p53 Arg72Pro and CRC in the Slovak population. The present case-control study was carried out in 173 confirmed CRC patients and 303 healthy subjects. Genotyping was performed by PCR-RFLP methods. Significant association was observed between age and CRC risk (p=0.001). Lower CRC risk was seen in younger patients carrying genotype p53 Arg72Pro (0.14; 95% CI 0.02–0.99, p=0.049). Gender-stratified analysis showed a significant inverse association of the polymorphism EGF G61G with CRC risk (0.48; 95% CI 0.2–0.9, p=0.04) only in male patients. Tumour site genotype distribution revealed that female patients with localized colon cancer were significantly associated with p53 Pro72Pro genotype (4.0; 95% CI 1.27–12.7, p=0.04) whereas the cancer of rectosigmoid junction was associated with the EGF G61G genotype (4.5; 95% CI 1.2–16.97, p=0.02). Combination of p53 Arg72Pro or EGF A61G polymorphisms were not associated with CRC risk by using logistic regression.

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Section: Product Of Pcr-rflp Analysis Of Egf A61g (Left) and P53 Arg7mentioning

confidence: 99%

“…These networks activate or deactivate some transcription factors regulating some proteins responsible for the death or survival of cell. Expression of both EGF and EGFR have been described to be significantly increased in a various human tumours including breast [26], lung [27][28] and colorectal adenocarcinoma [29].…”

Section: Introductionmentioning

confidence: 99%

Association of EGF and p53 gene polymorphisms and colorectal cancer risk in the Slovak population

et al. 2014

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“…8 A large body of evidence suggests that EGF-receptor (EGFR) and/or its family members, specifically ErbB-2/HER-2 and ErbB-3/HER-3 [collectively referred to as EGFRs], play a crucial role in regulating several pathways that affect tumor cell survival, angiogenesis, motility and invasiveness. [9][10][11] Recent data have also implicated IGF/IGF-1R system in the development and progression of colorectal cancer. 12,13 Therefore, agent(s) that would target EGFRs and IGF-1R are likely to affect multiple aspects of tumor progression.…”

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confidence: 99%

Curcumin enhances the effects of 5‐fluorouracil and oxaliplatin in mediating growth inhibition of colon cancer cells by modulating EGFR and IGF‐1R

Patel

Sengupta

Qazi

et al. 2007

Intl Journal of Cancer

194

133

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Curcumin (diferuloylmethane), which has been shown to inhibit growth of transformed cells, has no discernible toxicity and achieves high levels in colonic mucosa. 5-fluorouracil (5-FU) or 5-FU plus oxaliplatin (FOLFOX) remains the backbone of colorectal cancer chemotherapeutics, but with limited success. The present investigation was, therefore, undertaken to examine whether curcumin in combination with conventional chemotherapeutic agent(s)/regimen will be a superior therapeutic strategy for colorectal cancer. Indeed, results of our in vitro studies demonstrated that curcumin together with FOLFOX produced a significantly greater inhibition (p < 0.01) of growth and stimulated apoptosis (p < 0.001) of colon cancer HCT-116 and HT-29 cells than that caused by curcumin, 5-FU, curcumin 1 5-FU or FOLFOX. These changes were associated with decreased expression and activation (tyrosine phosphorylation) of EGFR, HER-2, HER-3 (72-100%) and IGF-1R (67%) as well as their downstream effectors such as Akt and cycloxygenase-2 (51-97%). Furthermore, while these agents produced a 2-3-fold increase in the expression of IGF-binding protein-3 (IGFBP-3), curcumin together with FOLFOX caused a 5-fold increase in the same, when compared to controls. This in turn led to increased sequestration of IGF by IGFBP-3 rendering IGF-1 unavailable for binding to and activation of IGF-1R. We conclude that the superior effects of the combination therapy of curcumin and FOLFOX are due to attenuation of EGFRs and IGF-1R signaling pathways. We also suggest that inclusion of curcumin to the conventional chemotherapeutic agent(s)/regimen could be an effective therapeutic strategy for colorectal cancer. ' 2007 Wiley-Liss, Inc.Key words: colorectal cancer; EGFR; IGF-1R; curcumin; chemotherapy; IGFBP3There will be an estimated 148,610 new cases and 55,170 deaths due to colorectal caner (CRC) in 2006 in the USA. 1 CRC is estimated to be the second and third leading cause of cancerrelated deaths in men and women, respectively, in 2006. 1 Surgery and subsequent chemotherapy can cure over 75% colon cancer patients, but more than 30% of these patients develop new neoplastic polyps, and 10% progress to frank second malignancy. [2][3][4] The risk of second malignancy is higher for microsatellite instable tumor (MSI). 5 Metastatic colorectal cancer has poor a prognosis with 5-year survival of less than 10%. 6 As a result of great efforts are being spent on improving chemotherapeutic interventions for metastatic colon cancer, and the median survival has improved to over 20 months of this group of patients. 7 However, this comes at a cost of additional toxicities, some of which are even fatal. 7 The validation of a nontoxic agent that could improve upon the current chemotherapeutic regimen would therefore be highly desirable.Accumulating evidence suggests that the development and progression of many malignancies, including colorectal cancer, are associated with constitutive activation of multiple signaling pathways that promote proliferation, inhibit apoptosis an...

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“…The differences, in FN3K activity and mRNA, between proximal and distal colon tumor underline the biochemical regional variability of colon neoplastic transformation. A biological difference between proximal and distal colon tumors has been observed also for other enzymes, growth factors and multiple genetic alterations [7,13,14,18]. We have previously already observed that different biochemical pathways linking proliferation and tumor progression are modified in a different manner in the large bowel, suggesting a different susceptibility of colon regions to neoplastic transformation [7,18].…”

Section: Discussionmentioning

confidence: 96%

Reduced fructosamine-3-kinase activity and its mRNA in human distal colorectal carcinoma

Notarnicola¹,

Caruso²,

Tutino³

et al. 2010

Genes Nutr

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Fructosamine-3-Kinase (FN3K) is an enzyme phosphorilating fructoselysine (FL) residues on glycated proteins, resulting in the production of protein-bound FL-3-phosphate. The pathological role of the non-enzymatic modification of proteins by reducing sugars has become increasingly evident in various types of disorders, including the cancer. In this study, our aim was to study FN3K enzyme activity, as well as its mRNA in human colorectal cancer (CRC). Thirty consecutive CRC patients undergoing surgery of the colon were enrolled in the study. FN3K enzymatic activity and gene expression were analyzed using a radiometric assay and quantitative RT-PCR, respectively. FN3K is a functionally active enzyme in human colon tissue, without significant differences between normal mucosa and cancer. The mean level of FN3K mRNA was significantly lower in cancer than in the corresponding normal colorectal mucosa The colorectal tumors located on the left side showed lower levels of both enzymatic activity and mRNA FN3K than tumors located in the right side of colon. This paper is the first studying FN3K enzyme activity in human CRC, showing a significant relationship between enzymatic activity, its mRNA and tumor side.

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EGF, TGF-a, and EGF-R in Human Colorectal Adenocarcinoma

Cited by 229 publications

References 22 publications

Association of EGF and p53 gene polymorphisms and colorectal cancer risk in the Slovak population

Association of EGF and p53 gene polymorphisms and colorectal cancer risk in the Slovak population

Curcumin enhances the effects of 5‐fluorouracil and oxaliplatin in mediating growth inhibition of colon cancer cells by modulating EGFR and IGF‐1R

Reduced fructosamine-3-kinase activity and its mRNA in human distal colorectal carcinoma

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