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Colorectal cancer adenocarcinoma

It has been postulated that wood dust carcinoma results from a multistep process Exposure causes loss of cilia and hyperplasia of the goblet cells and initiation of cuboidal cell metaplasia, followed (after a quiescent period) by squamous cell metaplasia. Decades later, cellular aplasia leads to nasal adenocarcinoma. The time between first occupational exposure to wood dust and the development of nasal cavity adenocarcinoma averages 40 years. Other cancers, including lung cancer, Hodgkin disease, multiple myeloma, stomach cancer, and colorectal cancer and lymphosarcoma, have been mentioned in relation to wood... [Pg.743]

Anti-tumor activity of bevacizumab has been reported in various preclinical animal models (primary and metastatic) with a broad array of tumor types [106, 107]. Clinical studies have further validated the focal role of VEGF in cancer. A single infusion of bevacizumab at 5 mg/kg in patients with primary and locally advanced adenocarcinoma of the rectum demonstrated direct and rapid antivascular effect in human tumors, with decreases in tumor perfusion, vascular volume, microvascular density, and interstitial pressure [108]. Clinical efficacy of bevacizumab in combination with 5-FU- and irinotecan-based regimens has been demonstrated in patients with metastatic colorectal cancer a significant improvement in overall survival time was observed compared with chemotherapy alone (20.3 versus 15.6 months for chemotherapy plus bevacizumab versus chemotherapy alone) [109]. [Pg.319]

In cases of inflammatory bowel disease, no overall increased incidence of cancer was noted after a median of 9 years follow-up in 755 patients who had taken less than 2 mg/kg/day of azathioprine over a median period of 12.5 years (69). Only colorectal cancers (mostly adenocarcinoma) were more frequent, but their incidence was also increased in chronic inflammatory bowel diseases. More specifically, there was no excess of non-Hodgkin s lymphoma, but the power of the study to detect an increased risk of this disorder was low. [Pg.382]

Witek, M.E., Nielsen, K., Walters, R., Hyslop, T., Palazzo, J., Schulz, S. and Waldman, S.A. (2005) The putative tumor suppressor Cdx2 is overexpressed by human colorectal adenocarcinomas. Clinical Cancer Research, 11 (24 Pt 1), 8549-8556. [Pg.272]

However, the impact of Cryptosporidium species in human health could be still more important. Actually, we have reported recently that C. parvum is able to induce intestinal adenocarcinoma in SCID mice (Certad et al. 2007). This is the first demonstration of the ability of an Apicomplexan parasite to induce neoplastic lesions in an epithelinm. We do not know if C. parvum is able to cause intestinal neoplasia in hnmans, but a recent survey reported a high frequency of Cryptosporidium infection in patients with colorectal cancer (Sulzyc-Bielicka et al. 2007). [Pg.312]

Interestingly, Cryptosporidium infection has been related to carcinogenesis. The association of cryptosporidiosis and colonic adenocarcinoma was speculated in the case of a Spanish patient carrying both, who died rapidly after the onset of symptoms (Izquierdo et al. 1988). More recently, an epidemiological study in Poland reported a high frequency of cryptosporidiosis in patients with colorectal cancer (Sulzyc-Bielicka et al. 2007). However, in these reports it was unclear if Cryptosporidium sp. behaved as a carcinogenesis factor or simply as an opportunistic agent whose development was enhanced by host immunosuppression. [Pg.385]

COLORECTAL ADENOCARCINOMA EGFR is a tyrosiue kinase receptor. Humanized monoclonal antibody chemotherapy to EGFR blocks its functional activation. Immuno-histochemical documentation of EGFR reactivity within colorectal cancers was once necessary to initiate anti-EGFR therapy. Currently, the initiation of therapy relies on documentation of a normal (wild-type) KRAS gene... [Pg.529]

Inamtrra K, Satoh Y, Okumura S, et al. Pulmonary adenocarcinomas with enteric differentiation histologic and immunohistochemical characteristics compared with metastatic colorectal cancers and usual pulmonary adenocarcinomas. Am J Surg Pathol. 2005 29 660-665. [Pg.535]

Cancers with a high frequency of CpG transitions include colorectal cancer (45%), adenocarcinoma of the esophagus (48%) and stomach (34%), tumors of the brain (35%) and uterus (35%), and some hematopoietic malignancies (e.g., Burkitt s lymphoma (32%) (Fig. 3B). In colorectal carcinogenesis, p53 mutation is typically a relatively late event that correlates with the acquisition of an invasive potential (Fearon and Vogelstein, 1990). Acquisition of a CpG mutation in this context may be a consequence of deregulated cell proliferation, DNA instability, or altered nitric oxide metabolism. In the development of adenocarcinoma of the esophagus, however, mutations are often detectable in the preneoplastic lesion, Barrett s mucosa (Montesano et al., 1996). In the latter case, it has been speculated that... [Pg.109]

Similarly, Survivin levels were increased in 34 (out of 34) tumor samples (adenocarcinoma and squamous cell carcinoma) when compared with nontumor controls. Survivin expression is frequently observed in tumors from breast cancer patients. One study reported that 71% of breast carcinomas (stages I to IH) were positive for Survivin whereas no expression of Survivin was detected in adjacent normal tissues. In colorectal cancers the expression of Survivin is inversely correlated with the apoptotic index of transformed cells and is significantly related to an increased disease-free survival rate and to a reduced risk for distant metastases. [Pg.464]

Bandres et al. examined the expression of 156 mature miRNA in colorectal cancer by real-time PCR and the results suggested that miRNA expression profile could be relevant to the biological and clinical behavior of colorectal neoplasia [58]. Michael et al. identified 28 different miRNAs in a colonic adenocarcinoma and normal mucosa by using miRNA cloning and northern blotting. They also indicated that miR-143 and miR-145 are downregulated in cells derived from breast, prostate, cervical, and lymphoid cancers as well as colorectal tumors [59]. [Pg.451]

Little has been published on the results of hepatic-directed therapy in the setting of liver metastases from gastrointestinal adenocarcinomas other than those of colorectal primary. The distinctive natural histories and the lower chemoresponsiveness of these tumors turns into a shorter projected survival for advanced disease than for colorectal cancer. There-... [Pg.129]

Meng L, Romano A, Smith E, Macik G, Grosh WW. Disseminated intravascular coagulation and immune hemolytic anemia, possibly evans syndrome, after oxahplatin and bevacizumab infusion for metastatic colon adenocarcinoma a case report and hterature review. Clinical Colorectal Cancer. 2015 14(l) el-e3. [Pg.37]

Tumorigenicity A 47-year-old patient with long-standing Crohn s disease, without a family history of colorectal cancer, who had previously had low-grade dysplasia that was not confirmed in subsequent studies, developed an adenocarcinoma of the colon with peritoneal invasion after a fourth infusion of infliximab [64 ]. [Pg.585]


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See also in sourсe #XX -- [ Pg.1343 ]




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