Invasion colon cancer

Kelly K, Alencar H, Funovics M et al. (2004) Detection of invasive colon cancer using a novel, targeted, library-derived fluorescent peptide. Cancer Res 64 6247-6251. 

Emenaker NJ, Calaf GM, Cox D, Basson MD, Qureshi N. (2001) Short-chain fatty acids inhibit invasive human colon cancer by modulating uPA, TIMP-1, TlMP-2, mntant p53, Bcl-2, BAX, p21 and PCNA protein expression in an in vitro cell cnltnre model. JNutr 131 3041S-3046S. 

Fluorouracil is used in several combination regimens in the treatment of breast cancer. It also has palliative activity in gastrointestinal adenocarcinomas, including those originating in the stomach, pancreas, liver, colon, and rectum. Other tumors in which some antitumor effects have been reported include carcinomas of the ovary, cervix, oropharynx, bladder, and prostate. Topical 5-fluorouracil cream has been useful in the treatment of premalignant keratoses of the skin and superficial basal cell carcinomas, but it should not be used in invasive skin cancer. 

Jiang, W.G., Hiscox, S., Hallett, M.B., Scott, C., Horrobin, D.F., and Puntis, M.C., Inhibition of hepatocyte growth factor-induced motility and in vitro invasion of human colon cancer cells by gamma-lino lenic acid, Br. J. Cancer., 71, 744, 1995. 

Example 3. Butler et al. (2003) conducted a population-based case-control study that evaluated levels of HCAs, meat intake according to doneness and cooking method, and the risk of colon cancer. The study population consisted of participants selected from 33 counties in North Carolina who were part of the North Carolina Colon Cancer Study. Cases included 274 blacks and 346 whites, between the ages of 40 and 84 with invasive adenocarcinoma of the colon diagnosed from 1996 to 2000. Controls, 426 blacks and 611 whites, were randomly selected from the North Carolina Division of Motor Vehicles (under 65) and the Center for Medicare and Medicaid services (over 65). Exposure was assessed using a food-frequency questionnaire. Meat intake frequency data, cooking method, and level of doneness was used to estimate exposure values for three specific HCAs. (Results of this study are discussed in Section 26.2.2b.). Source Butler et al. (2003). 

Kim, W. H., Jun, S. H., Kibbey, M. C., Thompson, E. W. and Kleinman, H. K. (1994). Expression of beta 1 integrin in laminin-adhesion-selected human colon cancer cell lines of varying tumorigenicity. Invasion Metastasis 14, 147-155. 

Vermeulen, S., Bruyneel, E-, Brackc, M., Bmyne, G., fennekens, K-, Vleminckx, K., Berx, G., Roy, EM., and Mareel, M. M. (1995), Transition from the nonin vast ve to the invasive phenotype and loss of a-catenin in human colon cancer cells. Cancer Res. S5,4722-4728,... 

Takeuchi H, Bilchik A, Saha S, et al. c-MET expression level in primary colon cancer a predictor of tumor invasion and lymph node metastases. Cfin Cancer Res 2003 9 1480-88. 

FIGURE 127-1. SEER incidence and mortality rates for invasive colon and rectum cancer, 1975-2000, age-adjusted and age-specific. Rates are per 100,000 and age-adjusted to the 2000 U.S. standard population. (From Ries et al. )... 

Radiographic imaging studies evaluate the extent of disease involvement. A chest x-ray should be performed to rule out the presence of metastatic spread to the lungs. A CT scan of the abdomen and pelvis is often performed to evaluate hepatic and retroperitoneal involvement and occult abdominal and pelvic disease, and to determine the depth of tumor penetration into the bowel wall and/or invasion to adjacent organs. Detection of lymph node involvement with either smdy is limited by the difficulty of distinguishing inflammatory or reactive lymph nodes from those infiltrated with tumor. Because CT scans may not adequately detect peritoneal seeding, small distant lymph node metastasis, or liver metastasis in colon cancer, an occasional patient may... 

FIGURE 14.22 High and low magnification of an invasive cecal adenocarcinoma from a 46-year-old patient with hereditary nonpolyposis colon cancer syndrome (Lynch syndrome). Neoplastic cell nuclei are completely devoid of MLH2 immunoreactivity, whereas cell nuclei of the surrounding stromal cells stain strongly. Only the complete absence of nuclear staining should be interpreted as a marker of a mismatch repair enzyme defect. 

It has been proposed that studying CDIO expression could help to distinguish invasive endometrial cancer from adenocarcinomas that colonize adenomyosis. " Since CDIO expression is characteristic of endometrial stroma and not myometrial smooth muscle, the theory goes that CDIO expression surrounding adenocarcinoma in the myometrium would support adenomyosis over invasive carcinoma. Unfortunately, there are at least two problems with this idea. It turns out that many invasive adenocarcinomas are surrounded by a rim of tissue that expresses CDIO, such that the appearance mimics the endometrial stroma that one expects in adenomyosis. A less common problem involves metaplastic stroma. In occasional endometrial cancers, endometrial stroma supporting endometrial cancer undergoes metaplasia to a smooth muscle or fibroblastic phenotype, similar to the stroma that is characteristic of endometrial polyps. This metaplastic stroma frequently expresses CDIO only weakly or focally. Therefore, absent CDIO staining does not entirely exclude the presence of endometrial stroma and adenomyosis. 

Tumor-Stromal Interaction in Colon Cancer Invasion ... 

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