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Colonic Neoplasms (colonic + neoplasm)

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Medical Sciences	100%

Selected Abstracts

Flat adenoma in colon: Two decades of debate

JOURNAL OF DIGESTIVE DISEASES, Issue 4 2010
Patrick CP LAU
The existence of flat adenomas in the colon is well recognized. Whether they represent a distinct disease with a pathogenetic pathway different from that of the classical adenoma-carcinoma sequence in colorectal tumorigenesis and have higher malignant potential remains a matter of debate. To review the epidemiology, clinical features, detection and management of flat and depressed (non-polypoid) colonic neoplasm, we performed a thorough literature review on studies focusing on the prevalence, histological features, genetics, detection and treatment of flat and depressed (non-polypoid) colonic neoplasm. A high percentage of severe dysplasia in flat colonic adenomas has not been consistently demonstrated. Their malignant potential appears to be size-dependent. Flat adenomas are found to have a lower incidence of major genetic abnormalities involved in the classical adenoma-carcinoma sequence and that has raised suspicions that they may have a different pathogenesis. The depressed type of colorectal carcinoma is uncommon but shows more aggressive behavior. More advanced colonoscopic techniques, such as chromoendoscopy, may enhance the detection of small and inconspicuous colonic neoplastic lesions that lack a protruding configuration. It is essential for endoscopists to appreciate the existence and clinical significance of flat and depressed colonic lesions as an important variant of colonic neoplasms so that the goal of reducing colorectal carcinoma incidence by polypectomy can be better achieved. [source]

Incidence and odds ratio of appendicitis as first manifestation of colon cancer: A retrospective analysis of 1873 patients

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 11 2006
Hung-Wen Lai
Abstract Background and Aim:, Obstruction of the lumen of the appendix is the major cause of appendicitis. Tumors could obstruct this lumen and cause appendicitis in the elderly. The association between appendicitis and colon cancer has not been sufficiently investigated, and this study was designed to clarify this association. Methods:, This was a retrospective study. Patients diagnosed with acute appendicitis from January 1998 to December 2003 at the Taipei Veterans General Hospital were surveyed. Patients found to have colon cancers immediately or subsequently after appendectomy were included and analyzed. Results:, A total of 1873 patients were diagnosed as having appendicitis of whom 16 were found to have colon cancer. The incidence of appendicitis associated with colon cancer was 0.85%. The time from appendectomy to the recognition of colonic cancer was at a median delay of 5.8 months. From the Taiwan Cancer Research Annual Report, the incidence of colon cancer was 31.91/100 000 in the year 2000. The odds ratio of colon cancer incidence had a 38.5-fold increase among patients older than 40 with acute appendicitis. Conclusions:, In patients over 40 years who present with symptoms of acute appendicitis the possibility of a coexistent colonic neoplasm should always be kept in mind. These patients should undergo colonoscopy 6 weeks after surgery to exclude the possibility of a coexistent colorectal cancer. [source]

Aggressive chronic platelet inhibition with prasugrel and increased cancer risks: revising oral antiplatelet regimens?

FUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 4 2009
Victor L. Serebruany
Abstract The TRITON-TIMI 38 was a head-to-head trial to assess the efficacy and safety of the experimental antiplatelet agent prasugrel vs. standard care with clopidogrel on top of aspirin. Besides some ischemic protection at expense of overwhelming bleeding disadvantage, prasugrel treated patients experienced three times higher rate of colonic neoplasms then after clopidogrel, and this difference was significant. Importantly, known gastrointestinal bleeding preceded the diagnosis of colonic neoplasms only in half of the patients. Three potential mechanisms responsible for such harmful association are reviewed, namely: (i) direct hazard of the experimental drug on cancer occurrence and progression; (ii) indirect modulation of tumor growth; and (iii) enhanced metastatic dissemination due to instability of platelet-tumor cell aggregates, or/and inability to keep the disease locally due by much more potent long-term platelet inhibition should be considered. Significant excess of cancer after prasugrel is alarming, and can be reasonably explained, with critical clinical implications not only for prasugrel further development, but also for existing and future chronic antiplatelet strategies. If the hypothesis that oral aggressive platelet inhibition cause higher cancer risks will turn out to be true, then intensity of platelet inhibition, and especially duration of chronic antiplatelet therapy should be reconsidered. More delicate platelet inhibition, and shorter exposure to oral antiplatelet agents will prevail. [source]

A specific inducible nitric oxide inhibitor, ONO-1714 attenuates inflammation-related large bowel carcinogenesis in male ApcMin/+ mice

INTERNATIONAL JOURNAL OF CANCER, Issue 3 2007
Hiroyuki Kohno
Abstract It is generally assumed that inflammation influences carcinogenesis. We previously reported that dextran sodium sulfate (DSS) strongly enhances colon carcinogenesis in the ApcMin/+ mice and the over-expression of inducible nitric oxide synthase (iNOS) contributes to this enhancement. In the current study, we investigated the effect of a selective iNOS inhibitor, ONO-1714 on colitis-related colon carcinogenesis in the ApcMin/+ mouse treated with DSS. Male C57BL/6J ApcMin/+ and Apc+/+ mice were exposed to 1% DSS in their drinking water for 7 days. ONO-1714 was given to the mice at a dose level of 50 or 100 ppm in diet for 5 weeks (during the administration of DSS). The tumor inhibitory effects by ONO-1714 were assessed at week 5 by counting the incidence and multiplicity of colonic neoplasms. Additionally, we assessed serum lipid levels and colonic mRNA expression for cyclooxygenase (COX)-2, iNOS, tumor necrosis factor (TNF)-, and interleukin (IL)-1,. Feeding with ONO-1714 significantly inhibited the occurrence of colonic adenocarcinoma in a dose-dependent manner in the ApcMin/+ mice. In addition, the treatment with ONO-1714 significantly lowered the serum triglyceride levels and mRNA expression levels of COX-2, TNF, and IL-1, of colonic mucosa in the DSS-treated ApcMin/+ mice. Neither ONO-1714 nor DSS affected the colonic pathology in the Apc+/+ mice. Our findings may suggest that ONO-1714 could therefore serve as an effective agent for suppression of colitis-related colon cancer development in the ApcMin/+ mice. © 2007 Wiley-Liss, Inc. [source]

Dextran sodium sulfate strongly promotes colorectal carcinogenesis in ApcMin/+ mice: Inflammatory stimuli by dextran sodium sulfate results in development of multiple colonic neoplasms

INTERNATIONAL JOURNAL OF CANCER, Issue 1 2006
Takuji Tanaka
Abstract The mouse model for familial adenomatous polyposis, ApcMin/+ mouse, contains a truncating mutation in the Apc gene and spontaneously develops numerous adenomas in the small intestine but few in the large bowel. Our study investigated whether dextran sodium sulfate (DSS) treatment promotes the development of colonic neoplasms in ApcMin/+ mice. ApcMin/+ and Apc+/+ mice of both sexes were exposed to 2% dextran sodium sulfate in drinking water for 7 days, followed by no further treatment for 4 weeks. Immunohistochemistry for cyclooxygenase-2, inducible nitric oxide synthase, ,-catenin, p53, and nitrotyrosine, and mutations of ,- catenin and K- ras and loss of wild-type allele of the Apc gene in the colonic lesions were examined. Sequential observation of female ApcMin/+ mice that received DSS was also performed up to week 5. At week 5, numerous colonic neoplasms developed in male and female ApcMin/+ mice but did not develop in Apc+/+ mice. Adenocarcinomas developed in ApcMin/+ mice that received DSS showed loss of heterozygosity of Apc and no mutations in the ,- catenin and K- ras genes. The treatment also significantly increased the number of small intestinal polyps. Sequential observation revealed increase in the incidences of colonic neoplasms and dysplastic crypts in female ApcMin/+ mice given DSS. DSS treatment increased inflammation scores, associated with high intensity staining of ,-catenin, cyclooxygenase-2, inducible nitric oxide synthase and nitrotyrosine. Interestingly, strong nuclear staining of p53 was specifically observed in colonic lesions of ApcMin/+ mice treated with DSS. Our results suggest a strong promotion effect of DSS in the intestinal carcinogenesis of ApcMin/+ mice. The findings also suggest that strong oxidative/nitrosative stress caused by DSS-induced inflammation may contribute to the colonic neoplasms development. © 2005 Wiley-Liss, Inc. [source]

Dietary seed oil rich in conjugated linolenic acid from bitter melon inhibits azoxymethane-induced rat colon carcinogenesis through elevation of colonic PPAR, expression and alteration of lipid composition

INTERNATIONAL JOURNAL OF CANCER, Issue 6 2004
Hiroyuki Kohno
Abstract Our previous short-term experiment demonstrated that seed oil from bitter melon (Momordica charantia) (BMO), which is rich in cis(c)9, trans(t)11, t13 -conjugated linolenic acid (CLN), inhibited the development of azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF). In our study, the possible inhibitory effect of dietary administration of BMO on the development of colonic neoplasms was investigated using an animal colon carcinogenesis model initiated with a colon carcinogen AOM. Male F344 rats were given subcutaneous injections of AOM (20 mg/kg body weight) once a week for 2 weeks to induce colon neoplasms. They also received diets containing 0.01%, 0.1% or 1% BMO for 32 weeks, starting 1 week before the first dosing of AOM. At the termination of the study (32 weeks), AOM induced 83% incidence (15/18 rats) of colonic adenocarcinoma. Dietary supplementation with 0.01% and 0.1% BMO caused significant reduction in the incidence (47% inhibition by 0.01% BMO, p<0.02; 40% inhibition by 0.1% BMO, p<0.05; and 17% inhibition by 1% BMO) and the multiplicity (64% inhibition by 0.01% BMO, p<0.005; 58% inhibition by 0.1% BMO, p<0.02; and 48% inhibition by 1% BMO, p<0.05) of colonic adenocarcinoma, though a clear dose response was not observed. Such inhibition was associated with the increased content of CLA (c9,t11-18:2) in the lipid composition in colonic mucosa and liver. Also, BMO administration in diet enhanced expression of peroxisome proliferator-activated receptor (PPAR) , protein in the nonlesional colonic mucosa. These findings suggest that BMO rich in CLN can suppress AOM-induced colon carcinogenesis and the inhibition might be caused, in part, by modification of lipid composition in the colon and liver and/or increased expression of PPAR, protein level in the colon mucosa. © 2004 Wiley-Liss, Inc. [source]

Flat adenoma in colon: Two decades of debate

,-Amino-butyric acid immunoreactivity in intramucosal colonic tumors

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 9 2003
KENTARO MAEMURA
Abstract Background and Aim:, The level of ,-amino-butyric acid (GABA) is reported to be increased in colon cancer. Moreover, data suggests that GABA plays a role in the proliferation or maturation of some types of cells. We examined the expression of GABA in intramucosal colonic tumors to clarify the relation between GABA and the degree of atypia. Methods:, Paraffin sections were prepared from 56 protruded-type colonic neoplasms, which were classified as intramucosal adenocarcinoma (AC), adenoma with severe atypia (ASA), or adenoma with mild to moderate atypia (AMA). Expression of GABA was investigated immunohistochemically, and GABA immunoreactivity was compared to the staining patterns of carcinoembryonic antigen (CEA) and cancer-associated antigen (CA19-9) which were classified into three categories. Results:, Intense GABA immunoreactivity was observed in 73.7%, 54.6%, 13.3%, and 5.4% of AC, ASA, AMA, and normal mucosa specimens, respectively. Kendall's correlation coefficient between GABA immunoreactivity and the degree of atypia was 0.447. Strong, positive CEA staining (pattern 3) was observed in 57.9%, 36.3%, and 13.3% of AC, ASA, and AMA specimens, respectively. Strong, positive CA19-9 staining was observed: 26.3%, 9.1% and 0%, respectively. In AC and ASA, the proportion of glands with strong GABA immunoreactivity was greater than the proportion of glands that were strongly positive for CA19-9. Conclusion:, GABA may be useful as a tumor marker in combination with other tumor markers such as CEA and CA19-9. [source]

CR10 LAPAROSCOPIC RIGHT HEMICOLECTOMY PERFORMED DURING THE ,LEARNING CURVE PHASE' DOES NOT IMPACT ON ONCOLOGICAL RESECTION

ANZ JOURNAL OF SURGERY, Issue 2007
E. Mignanelli
Purpose Laparoscopic colectomy for the management of colonic neoplasia is technically feasible and increasingly popular. It is expected that the laparoscopic operation deliver similar oncological clearance to open operation. The ,learning curve' for laparoscopic right hemicolectomy has been estimated to be 20 cases and is now set as a guideline by ASCRS. This study was performed to compare histopathology specimens following laparoscopic right hemicolectomy (LRH) performed during the ,learning curve' phase with those following open right hemicolectomy (ORH) to evaluate oncological clearance of colonic neoplasms. Methods 125 patients were identified as having undergone right hemicolectomy by two surgeons for colonic neoplasia from January 2001. Data regarding patient details and tumour pathology were obtained by retrospective case note review. Thirty-five patients underwent LRH compared to 90 who had ORH during the same period. Histopathology from the two groups were compared for length of specimen resected, proximal and distal resection margins, size of tumour resected or number of lymph nodes harvested. Analysis was performed using Student's T-test. Results The two groups were matched with respect to age, sex and tumour characteristics. There was no significant difference between the groups in terms of length of specimen resected (p = 0.37), proximal (p = 0.29) and distal (p = 0.40) resection margins, size of tumour resected (p = 0.37) or number of lymph nodes harvested (p = 0.58). Conclusions ,Learning curve' laparoscopic right hemicolectomy allows similar lymphovascular clearance to traditional open surgery. [source]