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Abramson Cancer CenterNCI CANCERLIT® Search: Screening and Prevention of Digestive Cancers - February 2002
National Cancer Institute®
Last Modified: February 1, 2002
Table of Contents
1
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.
2
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.
3
UI - 11802353
AU - Anonymous
TI -
Continue colonoscopy screening in stable patients, regardless of age.
SO - Geriatrics 2002 Jan;57(1):23
4
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.
5
UI - 11808948
AU - Levin TR
TI -
Could screening for colorectal cancer be harmful?
SO - Am J Gastroenterol 2002 Jan;97(1):198
AD - University of California, San Francisco, USA.
6
UI - 11781299
AU - Provenzale D
TI -
The cost-effectiveness of aspirin for chemoprevention of colorectal
cancer.
SO - Gastroenterology 2002 Jan;122(1):230-3
7
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.
8
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.
epidemiology@marionegri.it
9
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.
z.w.zhang@bristol.ac.uk
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.
10
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. lyndam@ccohta.ca
11
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.
m.j.langman@bham.ac.uk
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.
12
UI - 11141162
AU - Brown PJ
TI -
Avoidance of ingestion of anti-inflammatory drugs in dyspepsia is
confounding variable.
SO - BMJ 2001 Jan 6;322(7277):46
13
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.
ikedakenji@tora.email.ne.jp
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.
14
UI - 10915756
AU - Everson GT
TI -
Maintenance interferon for chronic hepatitis C: more issues than
answers?
SO - Hepatology 2000 Aug;32(2):436-8
15
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.
16
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
17
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. acastell@medicina.ub.es
The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.
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