National Cancer Institute®
Last Modified: February 1, 2002
UI - 11515858
AU - Kim HS
TI - Prevention of colon cancer with ursodiol in ulcerative colitis.
SO - Inflamm Bowel Dis 2001 Aug;7(3):279-80
AD - Division of Gastroenterology, University of California-San Diego School of Medicine, La Jolla, USA.
UI - 11794751
AU - Osias GL; Osias KB; Srinivasan R
TI - Colorectal cancer in women: an equal opportunity disease.
SO - J Am Osteopath Assoc 2001 Dec;101(12 Suppl Pt 2):S7-12
AD - Department of Medicine, Section of Gastroenterology, Temple University School of Medicine, Philadelphia, Pa, USA.
Colorectal cancer is the second leading cause of cancer-related deaths in developed countries. For women, it is the third leading cause of cancer-related deaths behind lung and breast cancers. Women have the same risk as men, and the lifetime risk of the development of colorectal cancer is 6%. One in 17 woman will have colorectal cancer diagnosed. There are risk factors unique to women, including gynecologic cancers, and treatment of gynecologic cancers, as well as delayed diagnosis in pregnancy. Fortunately, colorectal cancer is a preventable disease, as almost all colorectal cancers arise from premalignant polyps. Colorectal cancer screening is recommended in asymptomatic women aged 50 years and older who are at average risk. Screening and surveillance for colorectal cancer in women are important to improve the morbidity and mortality rates of this preventable disease.
UI - 11808936
AU - Gwyn K; Sinicrope FA
TI - Chemoprevention of colorectal cancer.
SO - Am J Gastroenterol 2002 Jan;97(1):13-21
AD - Department of Gastrointestinal Medicine and Nutrition, University of Texas M. D. Anderson Cancer Center, Houston 77030, USA.
Colorectal cancer is the third most incident cancer in the United States and is second only to lung cancer as a cause of cancer-related mortality. Colorectal cancer develops through a multistep process characterized by histopathological precursor lesions and molecular genetic alterations. This sequential process of tumorigenesis provides opportunities for the development and testing of both primary and secondary prevention strategies. This review focuses on chemoprevention, which is defined as the use of natural or synthetic agents to reverse the process of carcinogenesis. Epidemiological studies have consistently shown that chronic intake of nonsteroidal anti-inflammatory drugs (NSAIDs), principally aspirin, can reduce the incidence of colorectal adenomas and carcinomas. Evaluation of NSAIDs, including newer selective cyclo-oxygenase-2 inhibitors, in carcinogen-induced and genetically manipulated animal models of colorectal cancer demonstrates that these drugs are effective chemopreventive agents. In humans, the NSAID sulindac has been studied in familial adenomatous polyposis patients and was found to regress colorectal adenomas in a placebo-controlled trial. More recently, the selective cyclo-oxygenase-2 inhibitor Celebrex was also shown to be effective in familial adenomatous polyposis and was approved by the Food and Drug Administration as a adjuct to usual care in these patients. NSAIDs, as well as other chemopreventive agents, are currently being studied in patients at increased risk of colorectal cancer, including those with sporadic adenomas. The outcome of these studies has the potential to impact patient management practices. However, chemopreventive agents cannot be recommeded at present for average-risk individuals or for those with sporadic colorectal neoplasia. In addition to demonstrating efficacy, chemopreventive agents must be safe and well tolerated for chronic administration and should be relatively cost-effective. Although still in its infancy, the field of chemoprevention is an exciting and rapidly advancing area of investigation. Chemopreventive strategies, if effective, offer the promise of producing a paradigm shift in our current approach to colorectal cancer.
UI - 11781283
AU - Suleiman S; Rex DK; Sonnenberg A
TI - Chemoprevention of colorectal cancer by aspirin: a cost-effectiveness analysis.
SO - Gastroenterology 2002 Jan;122(1):78-84
AD - Department of Veterans Affairs Medical Center, Albuquerque, New Mexico 87108, USA.
BACKGROUND & AIMS: The aim of the study is to compare the cost-effectiveness of aspirin and colonoscopy in the prevention of colorectal cancer. METHODS: A Markov process is used to follow a hypothetical cohort of 100,000 subjects aged 50 years until death. Four strategies are compared: (1) no intervention, (2) colonoscopy once per 10 years and every 3 years in subjects with polyps, (3) chemoprevention with 325 mg of daily aspirin, and (4) combination of the second and third strategies. The various strategies are compared calculating incremental cost-effectiveness ratios (ICERs). RESULTS: The expected number of colorectal cancers is 5904 per 100,000 subjects. Colonoscopy prevents 4428 colorectal cancers and saves 7951 life-years at an ICER of $10,983 per life-year saved compared with no intervention. Aspirin prevents 2952 colorectal cancers and saves 5301 life-years at an ICER of $47,249 per life-year saved compared with no intervention. The cost of aspirin therapy plus management of aspirin-related complications was reported to be $172 per year per patient. Varying the annual aspirin-related costs between $50 and $200 results in ICER changes between $4617 and $57,080, with the 2 strategies breaking even at $70. Applying aspirin chemoprevention plus colonoscopy screening concomitantly yields an ICER of $227,607 per life-year saved compared with screening colonoscopy alone. CONCLUSION: As compared with colonoscopy once per 10 years, the use of aspirin to prevent colorectal cancer saves fewer lives at higher costs. The high complication cost and the lower efficacy of aspirin render screening colonoscopy a more cost-effective strategy to prevent colorectal cancer.
UI - 11572568
AU - La Vecchia C
TI - Reducing colorectal cancer through faecal occult blood screening: review of the evidence.
SO - Dig Liver Dis 2001 Aug-Sep;33(6):445-8
AD - Institute for Pharmacological Research Mario Negri, Milano, Italy. email@example.com
UI - 11788554
AU - Zhang ZW; Abdullahi M; Farthing MJ
TI - Effect of physiological concentrations of vitamin C on gastric cancer cells and Helicobacter pylori.
SO - Gut 2002 Feb;50(2):165-9
AD - Digestive Diseases Research Centre, St Bartholomew's and the Royal London School of Medicine and Dentistry, London, UK. firstname.lastname@example.org
BACKGROUND: Gastric juice vitamin C may be protective against gastric carcinogenesis but concentrations are significantly reduced by Helicobacter pylori infection. We investigated the in vitro effects of vitamin C at concentrations comparable with those found in gastric juice on gastric cancer cells and H pylori. METHODS: Gastric cancer cell lines and various H pylori strains were treated with L-ascorbic acid for up to 72 hours. Cell viability, and protein and DNA synthesis were determined. Flow cytometry was used for assessment of H pylori adherence, cell cycle distribution, and apoptosis. H pylori growth and its haemagglutination activity were determined using viability count and microtitration assay. RESULTS: Vitamin C induced a significant dose dependent growth inhibition of gastric AGS and MKN45 cells but this effect was significantly reduced at levels similar to those in gastric juice of H pylori infected patients (<50 microM). Although vitamin C had no obvious effect on H pylori growth, haemagglutination activity, or adherence ability to gastric AGS cells compared with untreated controls, it significantly enhanced H pylori associated apoptosis and induced cell cycle arrest in these cells. CONCLUSION: Vitamin C may inhibit gastric cancer cell growth and alter H pylori induced cell cycle events at concentrations comparable with those in gastric juice, but has no effect on H pylori growth or pathogenicity. However, the inhibitory effect on gastric cancer cells was lost at vitamin C concentrations found in patients with H pylori infection.
UI - 11811216
AU - McGahan L
TI - COX-2 inhibitors: a role in colorectal cancer?
SO - Issues Emerg Health Technol 1999 Dec;(9):1-7
AD - The Canadian Coordinating Office for Health Technology Assessment, Canada. email@example.com
UI - 10856067
AU - Langman MJ; Cheng KK; Gilman EA; Lancashire RJ
TI - Effect of anti-inflammatory drugs on overall risk of common cancer: case-control study in general practice research database.
SO - BMJ 2000 Jun 17;320(7250):1642-6
AD - Department of Medicine University of Birmingham, Birmingham, B15 2TT. firstname.lastname@example.org
OBJECTIVE: To examine whether anti-inflammatory drug treatment protects against the commoner cancers in the United Kingdom. DESIGN: Case-control study using the general practice research database. SETTING: Practices throughout United Kingdom providing data to the database. SUBJECTS: Patients who had a first diagnosis of five gastrointestinal (oesophagus, stomach, colon, rectum, and pancreas) cancers and four non-gastrointestinal (bladder, breast, lung, and prostate) cancers in 1993-5 for whom prescription data were available for the at least the previous 36 months. Each case was matched for age, sex, and general practice with three controls. MAIN OUTCOME MEASURE: Risk of cancer. RESULTS: In 12 174 cancer cases and 34 934 controls overall risk of the nine cancers was not significantly reduced among those who had received at least seven prescriptions in the 13-36 months before cancer diagnosis (odds ratio 0.98, 95% confidence interval 0.89 to 1.07). Findings were nevertheless compatible with protective effects from anti-inflammatory drugs against cancers of the oesophagus (0.64, 0. 41 to 0.98), stomach (0.51, 0.33 to 0.79), colon (0.76, 0.58 to 1. 00), and rectum (0.75, 0.49 to 1.14) with dose related trends. The risk of pancreatic cancer (1.49, 1.02 to 2.18) and prostatic cancer (1.33, 1.07 to1.64) was increased among patients who had received at least seven prescriptions, but the trend was dose related for only pancreatic cancer. CONCLUSIONS: Anti-inflammatory drugs may protect against oesophageal and gastric cancer as well as colon and rectal cancer. The increased risks of pancreatic and prostatic cancer could be due to chance or to undetected biases and warrant further investigation.
UI - 10915728
AU - Ikeda K; Arase Y; Saitoh S; Kobayashi M; Suzuki Y; Suzuki F; Tsubota A;
TI - Chayama K; Murashima N; Kumada H Interferon beta prevents recurrence of hepatocellular carcinoma after complete resection or ablation of the primary tumor-A prospective randomized study of hepatitis C virus-related liver cancer.
SO - Hepatology 2000 Aug;32(2):228-32
AD - Department of Gastroenterology, Toranomon Hospital, Tokyo, Japan, and Okinaka Memorial Institute for Medical Research, Tokyo, Japan. email@example.com
Because hepatocellular carcinoma often recurs after surgical resection or ethanol injection therapy, we conducted a prospective randomized controlled trial of interferon (IFN) in patients with chronic liver disease caused by hepatitis C virus (HCV). Twenty eligible patients with cirrhosis were randomized into two groups: 10 patients treated with 6 million units of natural IFN-beta twice a week for 36 months and 10 patients without IFN therapy. One patient within the treatment group discontinued interferon therapy after 19 months of treatment because of a mild degree of retinopathy. None of the patients in either group lost HCV-RNA until the end of the observation. Although 7 (70.0%) of 10 patients in the nontreatment group showed tumor recurrence, only 1 (10.0%) of 10 patients with IFN therapy developed tumor recurrence during a median observation period of 25.0 months. Cumulative recurrence rates of the treated and untreated groups were 0% and 62.5% at the end of the first year, and 0% and 100% at the second year, respectively (log-rank test, P =.0004). In conclusion, intermittent administration of IFN suppressed tumor recurrence after treatment with surgery or ethanol injection in patients with HCV-related chronic liver disease.
UI - 11805567
AU - Lindberg BU; Broome U; Persson B
TI - Proximal colorectal dysplasia or cancer in ulcerative colitis. The impact of primary sclerosing cholangitis and sulfasalazine: results from a 20-year surveillance study.
SO - Dis Colon Rectum 2001 Jan;44(1):77-85
AD - Department of Diagnostic Radiology, Huddinge University Hospital, Karolinska Institute, Huddinge, Sweden.
PURPOSE: Known risk factors for the development of colorectal dysplasia or cancer in ulcerative colitis are total colonic involvement and long duration of the disease. It has recently been suggested that presence of primary sclerosing cholangitis is another independent risk factor-especially for proximal colorectal dysplasia or cancer-and that treatment with sulfasalazine might reduce the frequency of colorectal cancer in ulcerative colitis; the present study was undertaken to shed light on the validity of these theories. METHODS: A total of 143 patients with ulcerative colitis underwent regular colonoscopies and multiple biopsies in a 20-year surveillance program for studies of long-standing total ulcerative colitis. Fifty-one of the patients developed colorectal dysplasia or cancer. Patient records were scrutinized retrospectively for information of presence of primary sclerosing cholangitis, site of the colorectal malignancy, and results of sulfasalazine treatment. RESULTS: Nineteen of the patients had primary sclerosing cholangitis; these ran a significantly higher risk of developing colorectal dysplasia or cancer than patients with ulcerative colitis only. All colorectal cancers (n = 3) and 75 percent of all colorectal dysplasias or cancers among patients with primary sclerosing cholangitis were located in the proximal part of the colon, whereas 36 percent were found in that same region among the patients with ulcerative colitis without primary sclerosing cholangitis (P = 0.02). Sulfasalazine treatment showed no significant protective effect on the development of colorectal dysplasia or cancer in patients with ulcerative colitis. CONCLUSION: The risk evaluation, as assessed by multivariate analysis, shows that primary sclerosing cholangitis proves to be an additional and independent risk factor for the development of colorectal dysplasia or cancer in patients with ulcerative colitis-particularly in the proximal part of the colon. The findings do not support the theory that sulfasalazine treatment exerts a protective effect against colorectal dysplasia or cancer.
UI - 11817790
AU - Puliyel JM; Taneja V; Jindal K; Thomas N
TI - Hepatitis B leading to hepatocellular carcinoma: calculating the risk.
SO - Indian J Gastroenterol 2001 Nov-Dec;20(6):251-2
UI - 11446930
AU - Castells A
TI - [Prevention of colorectal cancer]
SO - Med Clin (Barc) 2001 Jun 16;117(2):69-75
AD - Servicio de Gastroenterologia, Institut de Malalties Digestives, Hospital Clinic, Barcelona. firstname.lastname@example.org
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