Colon cancer tissue

Keshavarzian, A., Zapeda, D., List, T. and Mobarhan, S. (1992d). High levels of reactive oxygen metabolites in colon cancer tissues analysis by chemiluminescence probe. Nutr. Cancer 17, 243-249. 

Hernandez-Blazquez, F. J., Habib, M., Dumollard, J.-M., Barthelemy, C., Benchaib, M., de Capoa, A., and Niveleau, A. 2000. Evaluation of global DNA hypomethylation in human colon cancer tissues by immunohistochemistry and image analysis. Gwi47 689-693. 

CEA is a marker for colorectal, gastrointestinal, lung, and breast carcinoma. CEA was discovered by Gold and Freeman in 1965. Rabbits were immunized with extracts of human colon cancer tissue, and the resultant antisera were absorbed with extracts of normal human colon. Some antisera reacted with the tumor extracts but not with the extracts... 

Park JG, Choe GY, Helman LJ, et al. Chromogranin-A expression in gastric and colon cancer tissues. Int J Cancer. 1992 51 189-194. 

The mRNA of C3/33GnT6 is expressed at high levels in the foveolar epithelium of the stomach, in colon, and small intestine, but at low levels in other tissues. In colon cancer tissues, the activity is greatly reduced compared to normal colon, which favors the synthesis of core 1, and might explain the prevalence of the T antigen (core 1) in colon cancer. The mRNA expression of C3/33GnT6 is also reduced in gastric cancer. Consistent with the loss of the enzyme in cancer tissue, the activity is not detectable in many cultured colon... 

SIP lyase expression is significantly down-regulated in human colon cancer tissues (as are SIP phosphatases), which should increase the stability of SIP that might contribute to carcinogenesis (B. Oskouian, 2006). 

Figure 3.41 shows the result of imaging mass spectrometry-principal component analysis (IMS-PCA) for the colon cancer tissue. In this case, this unsupervised analysis revealed that the largest spectral difference (i.e., the largest difference in metabolite composition) was observed between the normal and the other tissue areas (i.e., normal vs. stroma/cancer area), and the second largest difference was observed between the stroma and normal/cancer area. The overall interpretation of PCA was shown in Table 3.6. 

K. (2013) Immunohistochemistry, histopathology and infrared spectral histopathology of colon cancer tissue sections. /. Biophotonics, 6, 88-100. 

A recent smdy examined the level of DiAcSpm in colorectal cancer and intraepithelial neoplasia tissues (Kuwata et al. 2013). DiAcSpm was very scant in normal tissues but was markedly increased in resected stage II, HI, and IV colon cancer tissues. The level of DiAcSpm was also maikedly elevated in metastatic liver lesions in individuals with stage IV colon cancer compared to adjacent normal tissue. HPLC analysis indicated that the levels of Af-acetylspermidine and Af-acetylspermine are also increased in cancer tissues. This is the first report that definitively identifies the presence of DiAcSpm in human tissues. Importantly, DiAcSpm is markedly increased in tumor tissue compared to normal tissue. The levels of A/ -acetylspermidine and Af, V -diacetylspermidine were very low or undetectable in normal tissues and were not significantly increased in cancer tissues. 

Breast Cancer Resistance Protein (BCRP, also known as MXR or ABCP), first cloned from mitoxantrone and anthracycline-resistant breast and colon cancer cells [188, 189] is a half-transporter efflux pump believed to function as a homo-or hetero-dimer. Following its identification, BCRP-mediated drug resistance was observed for topoisomerase inhibitors including camptothecins [190, 191] and in-dolocarbazoles [192]. In normal tissues, BCRP was detected in placental syncytio-trophoblasts, hepatocyte canalicular membrane, apical intestinal epithelia and vascular endothelial cells [193]. These findings support the important role BCRP plays in modulating topotecan bioavailability, fetal exposure and hepatic elimination [194]. Considering that the substrates and tissue distributions for BCRP overlap somewhat with MDR1 and MRPs [195], additional studies will be required to define the relative contribution of each of these transporters in the overall and tis-... 

By virtue of rendering iron catalytically inactive, dietary phytate may also suppress the incidence of colonic cancer (J2j>). Intestinal aerobic bacteria and/or minor inflammatory events generate substantial amounts of O27 leading to OH formation and lipid peroxidation. These two processes are thought to be important elements in tissue injury which occurs during inflammation. This argument is compatible with the observation that colonic cancer is frequently preceded, or accompanied, by pigmentation of the colonic epithelium lipofuscin, a byproduct of lipid... 

Colon [biopsies from colonic mucosa (nontumour tissue) of patients with colon cancer] Increased resistance to DOC-induced apoptosis of colonic epithelial cells of cancer patients or increased expression of anti-apoptotic protein Bc1-xl. 1,27,28,52,127... 

Fig. 1. Microenvironmental factors and the invasive process. The primary tumor is a heterogeneous mix of cell populations, further diversified by gradients of blood-borne nutrients, oxygen, and drugs. Hypoxia contributes to treatment resistance, upregulates pro-angiogenic and pro-invasive molecules, and helps to maintain cancer stem-like cell populations. Tumor cells may undergo epithelial-to-mesenchymal transition (EMT), enter blood vessels, and disseminate to distant sites where they extravasate, invade, and colonize the tissues. Once established, the cells may undergo the reverse program (mesen-chymal-to-epithelial transition, MET) and proliferate to form metastases, the major reason for treatment failure.

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