<i>BRAF</i><sup>V600E</sup> mutations occur in ∼10% of colorectal cancer cases, are associated with poor survival, and have limited responses to BRAF/MEK inhibition with or without EGFR inhibition.
<i>BRAF</i><sup>V600E</sup> mutations occur in ∼10% of colorectal cancer cases, are associated with poor survival, and have limited responses to BRAF/MEK inhibition with or without EGFR inhibition.
<i>BRAF</i><sup>V600E</sup> mutations occur in ∼10% of colorectal cancer cases, are associated with poor survival, and have limited responses to BRAF/MEK inhibition with or without EGFR inhibition.
<i>Conclusions.</i> Although the number of patients analysed was limited, we found that the addition of cetuximab significantly improves the outcomes in KRAS wild type patients with unresectable colorectal cancer liver-confined metastases.
<i>In vitro</i> stimulation of macrophages isolated from tumor tissue of colorectal cancer with granulocyte macrophage colony-stimulating factor and lipopolysaccharide did not drive to an inflammatory phenotype.
(-)-Epigallocatechin-3-gallate promotes pro-matrix metalloproteinase-7 production via activation of the JNK1/2 pathway in HT-29 human colorectal cancer cells.
1) Colorectal carcinoma and its resection margin overexpress gastrin and receptors for gastrin (CCK(B)-R), and COX-2; 2) here, we propose that an increased plasma level of gastrin should be considered as suitable biomarker of colorectal cancer, 3) HP infection may contribute to colonic cancerogenesis by enhancing expression of gastrin and COX-2, they may account for stimulation of the tumor growth, angiogenesis and reduction in apoptosis as evidenced an increased ratio of mRNA expression for anti-apoptotic Bcl2 over proapoptotic Bax proteins and 4) HP positive patients who develop colorectal cancer should be subjected to the HP eradication; this is expected to reduce hypergastrinemia and to attenuate COX-2 expression.