Colorectal cancer biology

Kondo, Y, Shen, L. and Issa, J.P. (2003) Critical role of histone methylation in tumor suppressor gene silencing in colorectal cancer. Molecular and Cellular Biology, 23, 206-215. 

Epidemiology and Biology of Colorectal Cancer Adjuvant Therapy of Colon Carcinoma Adjuvant Therapy of Rectal Carcinoma Future Trends in Combined Modality Therapy for Colorectal Carcinoma References... 

Molecular Biology of 5-FU Metabolism Current Standard of Care for Metastatic Colorectal Cancer Pharmacogenomics and Prognostic AND Predictive Markers Thymidylate Synthase Polymorphisms TS Polymorphisms as Prognostic AND Predictive Factors Other Polymorphisms of the 5-FU Metabolism Conclusion References... 

Kufer, P., Mack, M., and Gruber, R., 1996. Construction and biological activity of a recombinant bi-specific single-chain antibody designed for therapy of minimal residual colorectal cancer. Cancer Immunol. Immunother. 45 193-197. 

Bevacizumab, a humanized IgG and cetuximab, a chimeric IgGx, are currently marketed in the US for treatment of metastatic colorectal cancer [92, 93]. Bevacizumab neutralizes the biological activity of vascular endothelial growth factor (VEGF), while cetuximab binds specifically to the extracellular domain of the human epidermal growth factor receptor (EGFR). Bevacizumab, in combination with IV 5-fluorouracil (5-FU) -based chemotherapy, is indicated for first-line treatment of metastatic colorectal cancer, whereas cetuximab is used in patients refractory to or intolerant to irinotecan-based chemotherapy. The clinical pharmacokinetics of cetuximab are discussed in detail in Chapter 14. 

Damgaard, A. M., Heegard, P. M., Hansen,J. E., and B0g-Hansen, T. G. (1986) The microheterogeneity of the acute phase reactant alpha-1-antichymotiypsin in testicular and colorectal cancer, in Protides of the Biological Fluids, 34th Colloquium, 1986 (Peeters, H., ed.), Elsevier, Amsterdam, pp. 449-452. 

IL-2 has been approved for the heatment of renal cell carcinoma and also has shown good activity in malignant melanoma. Both of these tumors are refractory to chemotherapy. IL-2 has also been used invesdgationally, both alone and in combinadon with LAK cells, with chemotherapy and with other biological response modifier s (BRM s) to d eat a variety of different cancers (e.g., head and neck carcinoma, colorectal cancer, cend al nervous system cancer etc). In addidon to cancer therapy, IL-2 has been used to d eat padents infected with human immunodeficiency virus and it has been used ex vivo to generate antiviral T cells which were reinfused into padents (Lewko and Oldham, 2003 Dorr, 1993). 

Mason, J. B., Dickstein, A., Jacques, P. F., Haggarty, R, Selhub, J., Dallal, G., and Rosenberg, I. H. (2007). A temporal association between foUc acid fortification and an increase in colorectal cancer rates may be illuminating important biological principles A hypothesis. Cancer Epidemiol Biomarkers Prev 16, 1325-1329. 

The tumors may arise sporadically or in patients with the hereditary nonpolyposis colorectal cancer (HNPCC) syndrome.Current experience is too limited to determine their biologic behavior and prognosis however, in one study, the patients were found to have an improved survival rate relative to those with DAs. ° Immunohistochemically, the epithelioid cells are labeled by antibodies to cytokeratins whereas trypsin, chymotrypsin, lipase, chromogranin, and synaptophysin are usually negative. CD3 antibody highlights the presence of numerous intratumoral T lymphocytes. Rare examples also contain Epstein-Barr virus RNA. ... 

In order to improve the response of solid tumors to RIT, recent trials have focused on combining RIT with cytotoxic agents that radiosensitize tumors or biologic agents that up-regulate the target epitope. In one study, 21 patients with metastatic colorectal cancer were treated with 0.61 GBq m ... 

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