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PubMed2000

Nonprotruding colorectal neoplasms: epidemiologic viewpoint.

Histologic sections from 781 nonprotruding colorectal neoplasias (adenomas and early carcinomas) recorded in Sweden and in Japan were reviewed by the same observer, using strict histologic criteria. Low grade dysplasia (LGD) was present in 82.8% (299/361) of the nonprotruding neoplasms recorded in Sweden but in only 42.6% (179/420) of those recorded in Japan. On the other hand, high grade dysplasia (HGD) was found in 42.4% (178/420) of the nonprotruding colorectal neoplasias in Japanese patients but in only 14.1% (51/361) of those in Swedish patients. Whereas 15.0% (63/420) of the nonprotruding neoplasms in Japan were intramucosal carcinomas (IMCs) or submucosal carcinomas (SMCs), only 3.0% (11/361) of those reviewed in Sweden were IMCs or SMCs. Thus in Japan the lesions were histologically more "advanced" (significantly more lesions had HGD) and more "aggressive" (significantly more lesions were IMC or SMC) than in Sweden. The cause(s) of that phenomenon remains elusive. The term nonpolypoid adenoma connotes a group of dysplastic lesions with different histologic phenotypes. Interestingly, similar phenotypes were recently found in overt colorectal carcinomas in both Sweden and Japan. Experimental and clinical findings indicate that nonprotruding colorectal adenomas are closely associated with colonic lymphoid nodules, suggesting that the lymphoid-associated colorectal mucosa might be the birthplace of many nonprotruding adenomas (and consequently of nonprotruding early colorectal carcinomas).

Adenoma↗
PubMed2003

Distinct chromosomal imbalances in nonpolypoid and polypoid colorectal adenomas indicate different genetic pathways in the development of colorectal neoplasms.

Cytogenetic changes are widely unknown for nonpolypoid (synonymously termed as "flat" or "depressed") colorectal adenomas. A comparison with polypoid adenomas will contribute to the discussion whether different genetic pathways for colorectal tumorigenesis depending on its origin from nonpolypoid or polypoid adenomas exist. Tissue samples of nonpolypoid (n = 22), polypoid (n = 28) adenomas, carcinomas ex-nonpolypoid adenomas (n = 9), carcinomas ex-polypoid adenomas (n = 14), and normal colonic mucosa (n = 9) were investigated by comparative genomic hybridization of whole genomic DNA. Chromosomal imbalances were detected from average comparative genomic hybridization profiles for each entity. Nonpolypoid adenomas show recurrent chromosomal losses on chromosomes 16, 17p, 18, 20, and 22 and gains on chromosomes 2q, 4q, 5, 6, 8q, 12q, and 13q. In polypoid adenomas losses of whole chromosomes 16, 18, and 22 and gains of chromosomes 7q and 13 were detected. The frequency of copy number changes was higher in nonpolypoid compared to polypoid adenomas and early onset of chromosomal changes became apparent in low-grade dysplasias of nonpolypoid adenomas. Gains on chromosomes 2q, 5, 6, 8q, and 12q and losses on chromosomes 17p and 20 occurred exclusively in nonpolypoid adenomas, whereas 16p deletions are significantly more frequent in nonpolypoid than in polypoid adenomas. Carcinomas ex-nonpolypoid adenomas are characterized by more complex aberration patterns compared to nonpolypoid adenomas exhibiting frequent losses on chromosomes 8p, 12q, 14, 15q, 16, 17p, 18, and 22 and gains on 3q, 5, 6, 7, 8q, 12q, and 13, respectively. Normal colonic mucosa showed no chromosomal imbalances. Distinct differences of chromosomal imbalances between nonpolypoid and polypoid colorectal adenomas have been characterized that support the hypothesis that different genetic pathways may exist in the development of colorectal adenomas exhibiting nonpolypoid and polypoid phenotype.

Adenoma↗
PubMed1999

Angiogenic factor VEGF is decreased in human colorectal neoplasms showing DNA microsatellite instability.

Vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) are two important determinants of angiogenesis in human cancers. Expression of VEGF and bFGF was examined by immunohistochemistry in 120 colorectal cancers. Neoplasms were classified according to the presence or absence of microsatellite instability determined at six microsatellite loci and labelled as a high microsatellite instability (MSI-H), low microsatellite instability (MSI-L) or microsatellite stable (MSS). Only 4/30 MSI-H cancers expressed VEGF (13 per cent), compared with 24/64 MSS cancers (38 per cent; p< 0.01). Fewer MSI-H cancers showed bFGF expression (38 per cent) than MSS cancers (53 per cent; p< 0.09). MSI-L cancers showed the same pattern as MSS cancers. Western blotting and immunohistochemistry showed that the tumour suppressor gene p53 was mutated infrequently in MSI-H cancers (8 per cent; p< 0. 001). Microvessel density counts using CD31 and UEA-1 demonstrated no difference in the number of blood vessels in MSI-H and MSS cancers. Although these results are consistent with the known role of wild-type p53 in down-regulating VEGF, no association was found between a mutation in p53 and VEGF or bFGF levels in all colonic neoplasms. This is the first evidence that MSI-H cancers may follow a different pathway to angiogenesis. The low frequency of VEGF expression amongst MSI-H cancers may partially explain why these cancers are less aggressive, with a better overall prognosis.

Adenocarcinoma↗
PubMed1998

[Diagnostic and prognostic significance of biochemical indicators in colorectal neoplasms].

Activities of some enzymes and content of medium-weight molecules in patients with colorectal cancer were studied in order to assess the diagnostic value of these parameters for detection of tumors in the large intestine and development of endogenous intoxication after surgery and for prediction of remote results of treatment. Increased activities of creatine phosphokinase and hexokinase is typical of tumor growth, whereas increased activities of alkaline phosphatase and gamma-glutamyl transpeptidase are observed only in metastases to the liver. The role of medium-weight molecules in the diagnosis of endogenous intoxication during the early postoperative period is shown. The content of these molecules in the sera increases 3 days before clinical manifestation of endotoxicosis, when the traditional parameters are virtually normal.

Adenocarcinoma↗
PubMed1990

Evaluation of the occult blood test in screening for colorectal neoplasms. A prospective study using flexible endoscopy.

Survival rates from colorectal cancer will rise only when polyps and cancers are found at an earlier, curable stage. Consequently, the purpose of the present study was to compare the yield of colonic neoplasms from flexible sigmoidoscopy and colonoscopy with that from occult blood testing. Results from 474 flexible sigmoidoscopies and 1,115 colonoscopies were prospectively recorded during a four-year study period. Colorectal polyps were found in 111 (23.4%) patients undergoing flexible sigmoidoscopy and 325 (29.1%) patients undergoing colonoscopy. Among the 436 patients with polyps, the occult blood test was negative in 282 (64.7%). Among the 51 patients with colorectal cancers, the occult blood test was negative in 20 (39.1%). Thus, testing for occult blood missed the majority of polyps and a large percentage of the carcinomas. These data indicate that lower gastrointestinal endoscopy is superior to occult blood testing as a screening test for detecting colorectal polyps or cancers. Furthermore, given the high incidence of neoplasia in this patient population, the authors suggest that colonoscopy become the screening test of choice for colorectal cancer.

Colonic Polyps↗
PubMed2004

Trend of incidence, subsite distribution and staging of colorectal neoplasms in the 15-year experience of a specialised cancer registry.

BACKGROUND: Two-thirds of colorectal malignancies are localised in the left colon and rectum. Recent studies suggest a trend towards an increase of right-sided tumours which might have important implications for screening and surveillance. A colorectal cancer registry was set up in Modena, northern Italy, with the purpose of examining incidence, subsite distribution and staging of colorectal malignancies over a 15-year period. PATIENTS AND METHODS: From 1984 to 1998, 2517 tumours in 2462 patients were detected and staged with the tumour node metastasis (TNM) system. The 'right colon' was considered from caecum to splenic flexure; the 'left colon' included descending and sigmoid colon; and the 'rectum' included rectosigmoid junction, ampulla and anus. RESULTS: Cancer incidence showed an overall increase. Considering the various subsites, an increase of 33.7% in all colonic segments was shown whereas rectal tumours tended to decline. TNM staging showed a gradual increase of localised lesions (41.2% in 1984 versus 53.3% in 1998), with a proportional reduction of advanced tumours. CONCLUSIONS: Our study indicates an increase of tumour incidence in all colonic segments more than a shift to the right colon. TNM staging tended to improve with an appreciable increase of localised lesions. These findings could be consequent to a more extensive use of colonoscopy.

Aged↗
PubMed1989

[Prognosis of surgically treated colorectal neoplasms. Contribution of multivariate analysis].

Dukes' classification is the most usually used method of staging in colorectal carcinoma. However the pitfalls of this classification may be attested by the multitude of modifications of Dukes' staging during the last sixty years. The aim of our study was to evaluate the influence of 25 variables on survival in colorectal carcinoma using the Cox model. This study was performed in 321 patients operated on for colorectal carcinoma. In the 252 patients who had had a curative resection univariate analysis showed that survival was related to 6 variables: age, juxtatumoral lymph node involvement, an abdominal mass, complicated carcinoma, duration of symptoms, and depth of tumor penetration. Stepwise analysis showed the independent influence of 7 variables on survival: age, lymph node involvement, depth of tumor penetration, duration of symptoms, direct spread, preexisting deficiencies, and sex. A byproduct of the regression coefficient of Cox' model was a numerical value for each of these predictive factors. A single composite score was obtained by adding the individual scores of factors from which a prediction of outcome can be made. Applying this model to each of the 252 patients resected for cure, we established three prognostic groups. They predict survival more accurately than the Dukes' system. Our scoring system based on multivariate analysis must successfully defined prognostic groups of patients in other series. Then, it should be recommended for staging in curative resection for colorectal carcinoma.

Aged↗
PubMed1999

MUC1 expression in intramucosal colorectal neoplasms. Possible involvement in histogenesis and progression.

PURPOSE: The mucin core peptide MUC1 often is detectable in colorectal carcinoma (CRC) tissue and cell lines. However, whether MUC1 in CRC correlates with tumor histogenesis and progression is unclear. We studied the relationship between MUC1 expression in intramucosal CRC and clinicopathologic features, expression of Ki-67, and p53 protein, and apoptosis. METHODS: The intramucosal CRC we studied included 140 endoscopically or surgically resected lesions, including 106 low-grade carcinomas and 34 high-grade carcinomas. De novo carcinoma, defined as carcinoma with no adenomatous component, represented 9 of 140 tumors. Three macroscopic types were identified: 57 lesions were polypoid, 55 were superficial and flat, and 28 were granular-type laterally spreading tumors (G-LST). MUC1, Ki-67, and p53 expression were examined immunohistochemically. Apoptotic cells were identified by in situ DNA nick end labeling. RESULTS: MUC1 expression in high-grade carcinomas was significantly more frequent (p < 0.01) than in low-grade carcinomas; expression in adenomas was almost nil. MUC1 expression in polypoid carcinomas was significantly more frequent (p < 0.05) than in superficial carcinomas or G-LST. MUC1 expression in carcinomas with p53 expression was significantly more frequent (p < 0.01) than in carcinomas not expressing p53. No significant correlation was found between expression of MUC1 and Ki-67 labeling index. MUC1 was expressed more frequently in carcinomas with relatively high apoptotic index (p < 0.01). MUC1 expression did not differ between de novo carcinomas and those developing from adenomas. CONCLUSIONS: The results suggest that MUC1 is likely to be expressed in the course of colorectal carcinoma development when p53 protein is overexpressed and apoptosis is prominent.

Apoptosis↗
PubMed2004

Correlation of N-myc downstream-regulated gene 1 overexpression with progressive growth of colorectal neoplasm.

AIM: To study the function of N-myc downstream-regulated gene 1 (NDRG1) in colorectal carcinogenesis and its correlation with tumor lymph node metastasis. METHODS: NDRG1 was detected at its protein level by immunohistochemistry (IHC) and image analysis (IA), and NDRG1 mRNA was detected by in situ hybridization (ISH) in formalin-fixed and paraffin-embedded sections with a total of 190 specimens including 38 normal colorectal mucosae, 31 colorectal adenomas, 45 non-metastatic colorectal carcinomas (CRCs), 38 metastatic primary CRC and subsequently regional lymph nodes respectively. At the same time, the correlations of NDRG1 with sex, age of patients and histological types of colorectal carcinomas were observed. RESULTS: NDRG1 proteins were gradually increased in colorectal carcinogenesis (P<0.05 or P<0.01). There was a significant difference in the expression of NDRG1 between non-metastatic and metastatic CRCs (P<0.05), and the correlation was positive (P<0.01, r(s)=0.329). However, there was no obvious difference in the expression of NDRG1 between the primary sites of CRCs and that in the metastatic sites of corresponding regional lymph nodes, nor was there an apparent difference in sex, age, and histological types. The expression of NDRG1 mRNA was generally in concordance with that of NDRG1 protein. CONCLUSION: NDRG1 gene may play an important role in colorectal carcinogenesis. In addition, NDRG1 may be a putative tumor metastasis promoter gene and is regarded as one of the molecular biological markers that can forecast early metastasis of CRCs. NDRG1 gene in the metastatic sites of regional lymph nodes may preserve its expression characteristics in the primary sites of CRCs to some extent. The expression of NDRG1 is not affected by sex, age and histological types. The role of NDRG1 in tumor metastatic process can be demonstrated by in vivo and in vitro.

Adenoma↗
PubMedDate not supplied

[The immunohistochemical demonstration of intracytoplasmic estradiol in colorectal neoplasms].

Intracytoplasmic estradiol content was studied retrospectively using immunohistochemical procedures in tissue samples from subjects suffering from colorectal cancer. The results obtained reveal the presence of intracytoplasmic estradiol in cancer tissue. In precancerous lesions this presence is rarer and inconstant. Estradiol was not detected in the healthy tissue examined. These data suggest that such tumours may depend to some degree on endocrine factors.

Adenoma↗