National Cancer Institute®
Last Modified: September 1, 2002
1
UI - 12019505
AU - Immanuel A; Lamb PJ; Wayman J; Preston S; Griffin SM
TI -
Prevention of the neoplastic progression of Barrett's oesophagus by
argon beam plasma ablation (Br J Surg 2001;88:1357-62).
SO - Br J Surg 2002 May;89(5):626; discussion 626
2
UI - 11885965
AU - Okamoto T; Kajino K; Hino O
TI -
Hepatoprotective drugs for the treatment of virus-induced chronic
hepatitis: from hypercarcinogenic state to hypocarcinogenic state.
SO - Jpn J Pharmacol 2001 Nov;87(3):177-80
AD - Research Laboratories, Nippon Chemiphar Co, Ltd, Saitama, Japan.
Interferon (IFN)-based therapy is a standard treatment for chronic
hepatitis caused by hepatitis C virus (HCV) infection. This treatment is
effective in approximately 30-40% of the patients and using ribavirin in
combination with IFN increases the rate of sustained virologic
clearance. For the remaining patients, glycyrrhizin is often used.
Glycyrrhizin is known to prevent the development of hepatocellular
carcinoma (HCC), but glycyrrhizin is usually administered intravenously.
Drugs that are effective by oral administration are convenient for
patients for long-term administration, and development of more effective
drugs than glycyrrhizin is preferable. However, studies on drugs for the
treatment of hepatitis are not actively conducted, and promotion of the
study of drugs in this area is encouraging. For that reason, we show our
approach to study drugs for the treatment of hepatitis. We analyzed the
effect of glycyrrhizin on hepatitis as a standard chemical using the
mouse liver injury model. Based on this, we screened drugs and found
that a coumarin derivative seems to be one of model chemicals for the
treatment of hepatitis.
3
UI - 11948369
AU - Saha D; Roman C; Beauchamp RD
TI -
New strategies for colorectal cancer prevention and treatment.
SO - World J Surg 2002 Jul;26(7):762-6
AD - Department of Surgery, Vanderbilt University Medical Center and the
Vanderbilt-Ingram Cancer Center, D5230 MCN, 21st Avenue South,
Nashville, Tennessee 37232-2730, USA.
Colorectal cancer (CRC) is the second most common fatal malignancy in
the Western world, with more than 150,000 new cases accounting for
55,000 deaths in the United States every year. Surgical resection is an
effective treatment for localized disease, achieving a 5-year survival
rate of 90%; but chemotherapy and other novel treatments for metastatic
disease remain ineffective. There have been significant efforts to
identify risk factors associated with the development of CRC and to
explore potential preventive therapies. Both genetic and epigenetic
factors contribute to the development of colorectal cancer. Specific
genetic changes in proto-oncogenes, tumor suppressor genes, and DNA
mismatch repair genes have led to a genetic model of CRC. Cooperative
genetic aberrations involving APC (adenomatous polyposis coli),
beta-catenine, K-ras, and p53 are involved in the multistep
adenoma-carcinoma sequence of CRC. Emerging data have implicated
cyclooxygenase-2 (COX-2) and prostanoid production in the pathogenesis
of colorectal carcinoma. Several reports indicate a close relation
between the intake of nonsteroidal antiinflammatory drugs (NSAIDs) and a
decreased risk for developing colorectal cancer. Epidemiologic studies
indicate a 40% to 50% reduction in mortality due to colorectal cancer in
individuals taking NSAIDs (e.g., aspirin). Epigenetic factors including
age, diet, angiogenesis, and immune responses also appear to contribute
to the development of CRC. Combining knowledge of the genetic and
epigenetic events implicated in this disease may allow a broader
understanding of the pathogenesis of CRC. These developments may yield
benefits in earlier detection and in the design of better antitumor
interventions.
4
UI - 11895870
AU - Fuchs CS; Willett WC; Colditz GA; Hunter DJ; Stampfer MJ; Speizer FE;
TI -
Giovannucci EL
The influence of folate and multivitamin use on the familial risk of
colon cancer in women.
SO - Cancer Epidemiol Biomarkers Prev 2002 Mar;11(3):227-34
AD - Channing Laboratory, Department of Medicine, Brigham and Women's
Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
Charles_Fuch@dfci.harvard.edu
Low intake of folate and methionine and heavy alcohol consumption have
been associated with an increased overall risk of colon cancer, possibly
related to their role in methylation pathways. We estimated the relative
risk (RR) of colon cancer according to a history of colorectal cancer in
a first-degree relative and categories of folate, methionine, and
alcohol intake in a prospective cohort study of 88,758 women who
completed family history and detailed food frequency questionnaires.
During 16 years of follow-up, colon cancer was diagnosed in 535 women.
The inverse association of folic acid with colon cancer risk was greater
in women with a family history. Compared with women who consumed 200
microg or less of folic acid/day, the age-adjusted RR of colon cancer
for those who consumed >400 microg/day was 0.81 (95% confidence
interval, 0.62-1.07) in women without a family history of colorectal
cancer and 0.48 (95% confidence interval, 0.28-0.83) in women with a
family history (P for interaction = 0.02). The influence of family
history was markedly diminished by use of multivitamins containing folic
acid (P for interaction = 0.04). High levels of dietary methionine also
reduced the effect of family history (P for interaction = 0.05), whereas
moderate to heavy alcohol consumption increased the risk associated with
family history (P for interaction = 0.004). Other risk factors for
colorectal cancer did not significantly modify the influence of family
history. Our results suggest that higher intake of folate and
methionine, regular use of multivitamins containing folate, and
avoidance of moderate to heavy alcohol consumption may diminish the
excess risk of colon cancer associated with a family history of the
disease.
5
UI - 11895877
AU - Sample D; Wargovich M; Fischer SM; Inamdar N; Schwartz P; Wang X; Do KA;
TI -
Sinicrope FA
A dose-finding study of aspirin for chemoprevention utilizing rectal
mucosal prostaglandin E(2) levels as a biomarker.
SO - Cancer Epidemiol Biomarkers Prev 2002 Mar;11(3):275-9
AD - Department of Gastrointestinal Medical Oncology, The University of Texas
M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
Epidemiological and experimental evidence indicates that aspirin can
protect against colorectal cancer. Aspirin inhibits cyclooxygenase
enzymes and blocks prostaglandin (PG) biosynthesis. Using rectal PGE(2)
levels as a mucosal biomarker, we sought to determine the optimal
aspirin dose that would significantly suppress PGE(2) levels for
chemoprevention trials. We conducted a randomized, double-blinded study
in 60 subjects with prior sporadic colorectal adenoma(s) and evaluated
three aspirin doses (81, 325, and 650 mg) or placebo taken daily for 4
weeks. PGE(2) levels in rectal biopsies performed at baseline and week 4
were analyzed by competitive immunoassay. Plasma salicylate levels, pill
counts, and subject calendars were used to assess compliance. The 81-mg
aspirin dose significantly suppressed PGE(2) levels relative to placebo
(P = 0.005) and did so to an equivalent extent as did higher doses (P >
0.4) in evaluable subjects (n = 55) over a 4-week treatment period.
Serum salicylate levels were associated with aspirin dose (P = 0.0002).
Pill counts and calendars indicated that >98% of doses were taken by all
subjects. No adverse events occurred in this short-term study. The 81-mg
daily aspirin dose suppressed PGE(2) levels to an equivalent extent as
did the 650-mg dose and supports the use of this dose for
chemoprevention trials.
6
UI - 11895878
AU - Sample DA; Sinicrope PS; Wargovich MJ; Sinicrope FA
TI -
Post-study aspirin intake and factors motivating participation in a
colorectal cancer chemoprevention trial.
SO - Cancer Epidemiol Biomarkers Prev 2002 Mar;11(3):281-5
AD - Department of Gastrointestinal Medicine and Nutrition, The University of
Texas M. D. Anderson Cancer Center, and The University of Texas Health
Science Center at Houston, School of Public Health, Houston, Texas
77030, USA.
We conducted an exploratory, cross-sectional study examining motivators
for study participation and post-study aspirin intake in a
chemoprevention trial. The parent clinical trial aimed to determine the
optimal aspirin dose for colorectal cancer chemoprevention using
prostaglandin E(2) as a mucosal biomarker. This trial was randomized and
double-blinded in 60 subjects with prior sporadic colorectal adenoma(s)
and evaluated three aspirin doses or placebo taken once daily for 4
weeks. A cross-section of 55 evaluable participants who completed the
chemoprevention trial were mailed a 16-item, self-administered
questionnaire evaluating subject demographics, motivational factors, and
health-related behaviors within the framework of Pender's Health
Promotion Model (HPM). Forty-three (78%) of 55 participants returned the
questionnaire. The most important motivators for study participation
were altruistic, i.e., a desire to help future generations at risk of
colorectal cancer and personal factors including a desire to reduce
one's own risk. Nineteen (44%) of 43 respondents reported that they
chose to take daily aspirin post-study without knowledge of study
results. At a mean follow-up of 17.3 months, 18 of these 19 subjects
continued to take aspirin regularly. Regular use of vitamin supplements
pre-study was found to correlate with post-study aspirin use
(Mann-Whitney U test, U = 154.0; P = 0.04). We demonstrate, for the
first time, that participation in a chemoprevention study can influence
the decision to continue the study drug, if available, to reduce
perceived cancer risk. Continued post-study aspirin intake indicates an
impact of study participation on a health-related behavior and
underscores the importance of patient education to guide such
decision-making.
7
UI - 12101116
AU - Keller JJ; Offerhaus GJ; Hylind LM; Giardiello FM
TI -
Rectal epithelial apoptosis does not predict response to sulindac
treatment or polyp development in presymptomatic familial adenomatous
polyposis patients.
SO - Cancer Epidemiol Biomarkers Prev 2002 Jul;11(7):670-1
AD - Department of Pathology, Academic Medical Center, 1105 AZ Amsterdam, The
Netherlands. j.j.keller@amc.uva.nl
8
UI - 8416152
AU - Selby JV; Friedman GD; Quesenberry CP Jr; Weiss NS
TI -
Effect of fecal occult blood testing on mortality from colorectal
cancer. A case-control study.
SO - Ann Intern Med 1993 Jan 1;118(1):1-6
AD - Kaiser Permanente Medical Care Program, Oakland, California.
OBJECTIVE: To estimate by case-control methods the effect of screening
using the fecal occult blood test (FOBT) on mortality from colorectal
cancer and to examine the relation of that effect to the interval since
the most recent screening test. DESIGN: A case-control study. SETTING:
The Kaiser Permanente Medical Care Program of Northern California.
PATIENTS: A total of 485 persons who developed fatal colorectal cancer
after 50 years of age and 727 age- and sex-matched controls.
MEASUREMENTS: History of screening FOBTs during the 5 years before case
diagnosis. RESULTS: After adjustment for potentially confounding
factors, an odds ratio of 0.69 (95% Cl, 0.52 to 0.91) was observed for
exposure to at least one screening FOBT during the 5-year interval. The
odds ratio was lowest for the first year after the most recent FOBT and
rose to 1.00 three years after the last screening examination.
False-negative results among cases in the 1 to 2 years before diagnosis
contributed substantially to lowering the estimate of efficacy.
CONCLUSIONS: These data suggest that a program of annual or biennial
screening using FOBTs might lower population risk for mortality from
colorectal cancer sufficiently to have important public health
implications. However, the confidence intervals around our odds ratio
estimates were wide. We therefore believe that additional data will be
needed before making recommendations that FOBT screening be expanded.
9
UI - 8416162
AU - Simon JB
TI -
Colonic polyps, cancer, and fecal occult blood.
SO - Ann Intern Med 1993 Jan 1;118(1):71-2
10
UI - 8037405
AU - Giovannucci E; Rimm EB; Stampfer MJ; Colditz GA; Ascherio A; Willett WC
TI -
Aspirin use and the risk for colorectal cancer and adenoma in male
health professionals.
SO - Ann Intern Med 1994 Aug 15;121(4):241-6
AD - Harvard Medical School, Brigham and Women's Hospital, Boston,
Massachusetts.
OBJECTIVE: To determine whether regular use of aspirin decreases the
risk for colorectal cancer. DESIGN: Prospective cohort study. SETTING:
Male health professionals throughout the United States. PATIENTS: 47,900
male respondents to a mailed questionnaire in 1986, who were 40 to 75
years of age. MEASUREMENTS: Questionnaires in 1986, 1988, and 1990 about
use of aspirin and other variables including occurrence of cancer.
RESULTS: 251 new patients were diagnosed with colorectal cancer during
the study period. Regular users of aspirin (> or = 2 times per week) in
1986 had a lower risk for total colorectal cancer (relative risk [RR] =
0.68; 95% CI, 0.52 to 0.92) and advanced (metastatic and fatal)
colorectal cancer (RR = 0.51; CI, 0.32 to 0.84) after controlling for
age; history of polyp; previous endoscopy; parental history of
colorectal cancer; smoking; body mass; physical activity; and intakes of
red meat, vitamin E, and alcohol. The incremental association was
greater among men who reported regular use of aspirin consistently on
subsequent questionnaires. The total number of colorectal adenomas
discovered among aspirin users was lower with or without overt or occult
fecal blood. Thus, earlier diagnosis and treatment of adenomas did not
account for the inverse association between aspirin and cancer.
CONCLUSIONS: These results support laboratory, clinical, and other
epidemiologic evidence that regular use of aspirin is associated with a
decreased risk for colorectal cancer.
11
UI - 8037413
AU - Garewal HS
TI -
Aspirin in the prevention of colorectal cancer.
SO - Ann Intern Med 1994 Aug 15;121(4):303-4
12
UI - 12060040
AU - Urosevic P; Kiroff GK
TI -
Ablation of Barrett's epithelium: the promise and the problems.
SO - Dis Esophagus 2002;15(1):30-8
AD - The University of Melbourne, Department of Clinical and Biomedical
Sciences, The Geelong Hospital, Victoria, Australia.
The incidence of adenocarcinoma of the esophagus has increased
dramatically over recent years. Because Barrett's epithelium is
recognized as a risk factor for adenocarcinoma there is an interest in
reversing this metaplasia. A number of endoscopic methods of destruction
of esophageal columnar epithelium have been described. The purpose of
this article is to review the currently available methods of managing
Barrett's epithelium with particular reference to the role of ablative
therapy in reducing the risk of adenocarcinoma.
13
UI - 12060041
AU - Lin OS; Mannava S; Hwang KL; Triadafilopoulos G
TI -
Reasons for current practices in managing Barrett's esophagus.
SO - Dis Esophagus 2002;15(1):39-45
AD - Division of Gastroenterology, Stanford University Medical Center,
California, USA. otto.lin@vmmc.org
We evaluated the reasons for current practices in managing Barrett's
esophagus. Using a questionnaire, we assessed the practices and beliefs
of 162 Californian gastroenterologists in managing Barrett's esophagus,
using descriptive statistics as well as multivariate logistic
regression. Out of the 103 respondents, 87% screened for Barrett's
esophagus in patients with > 12 months of reflux symptoms, but only 72%
believed that screening would improve survival, and 48% believed it to
be cost-effective. In total, 98% surveyed patients with long-segment
Barrett's esophagus at least biennially (76% thought this would improve
survival and 49% believed it to be cost-effective) and 82% surveyed
short-segment Barrett's esophagus at least biennially (57% thought this
would improve survival and 30% believed it to be cost-effective).
Finally, 44% surveyed microscopic intestinal metaplasia at least
biennially (26% thought this would improve survival and 11% believed it
to be cost-effective). In total, 18% performed endoscopic ablation,
whereas 3% referred patients with low-grade dysplasia and 85% referred
patients with high-grade dysplasia for esophagectomy. Finally, 81%
treated asymptomatic Barrett's esophagus patients with proton pump
inhibitors, but only 56% believed that this would reduce the risk of
cancer. Logistic regression showed that the only independent factor
predictive of surveillance practices was belief in efficacy. Practice
patterns tend to be more aggressive than those recommended by recent
guidelines and those reported by previous surveys. Medico-legal
considerations affect practice substantially.
14
UI - 11501466
AU - Canadian Task Force on Preventive Health Care
TI -
Colorectal cancer screening. Recommendation statement from the Canadian
Task Force on Preventive Health Care.
SO - CMAJ 2001 Jul 24;165(2):206-8
15
UI - 11578292
AU - Morris CD; Byrne JP; Armstrong GR; Attwood SE
TI -
Prevention of the neoplastic progression of Barrett's oesophagus by
endoscopic argon beam plasma ablation.
SO - Br J Surg 2001 Oct;88(10):1357-62
AD - Department of Upper Gastrointestinal Surgery, Hope Hospital, Stott Lane,
Salford, Manchester M6 8HD, UK.
BACKGROUND: Patients with Barrett's oesophagus have a risk of
approximately 1 per 100 patient-years for the development of oesophageal
adenocarcinoma. Endoscopic ablation of Barrett's oesophagus has been
shown to lead to the regrowth of a 'neo' squamous epithelium if
gastro-oesophageal reflux is controlled, but the incidence of subsequent
tumour formation is unknown. METHODS: The follow-up of 55 patients who
underwent endoscopic ablation of Barrett's oesophagus by argon beam
plasma coagulation (ABPC) is reported. Of the 55 patients, nine had
low-grade dysplasia, nine had high-grade dysplasia and the remainder had
non-dysplastic Barrett's metaplasia. Twelve patients had reflux control
by antireflux surgery and the remainder received proton pump inhibitor
therapy. Barrett's metaplasia was ablated by ABPC to within 2 cm of the
gastro-oesophageal junction. RESULTS: To date, one patient has died and
one patient was unable to complete treatment. The remaining patients
were followed by regular endoscopic surveillance for a mean of 38.5
months to give a total follow-up of 173.5 patient-years. No malignancy
has developed in any patient during follow-up. CONCLUSION: The absence
of malignant complications in this study of prophylactic ablation of
long-segment Barrett's oesophagus strengthens the argument for
endoscopic ablation in the prevention of oesophageal adenocarcinoma.
16
UI - 11917202
AU - Hill MJ
TI -
Vegetables, fruits, fibre and colorectal cancer.
SO - Eur J Cancer Prev 2002 Feb;11(1):1-2
17
UI - 11932472
AU - Giardiello FM; Yang VW; Hylind LM; Krush AJ; Petersen GM; Trimbath JD;
TI -
Piantadosi S; Garrett E; Geiman DE; Hubbard W; Offerhaus GJ; Hamilton SR
Primary chemoprevention of familial adenomatous polyposis with sulindac.
SO - N Engl J Med 2002 Apr 4;346(14):1054-9
AD - Department of Medicine, Johns Hopkins University School of Medicine,
Baltimore, USA.
BACKGROUND: Familial adenomatous polyposis is caused by a germ-line
mutation in the adenomatous polyposis coli gene and is characterized by
the development of hundreds of colorectal adenomas and, eventually,
colorectal cancer. Nonsteroidal antiinflammatory drugs can cause
regression of adenomas, but whether they can prevent adenomas is
unknown. METHODS: We conducted a randomized, double-blind,
placebo-controlled study of 41 young subjects (age range, 8 to 25 years)
who were genotypically affected with familial adenomatous polyposis but
phenotypically unaffected. The subjects received either 75 or 150 mg of
sulindac orally twice a day or identical-appearing placebo tablets for
48 months. The number and size of new adenomas and side effects of
therapy were evaluated every four months for four years, and the levels
of five major prostaglandins were serially measured in biopsy specimens
of normal-appearing colorectal mucosa. RESULTS: After four years of
treatment, the average rate of compliance exceeded 76 percent in the
sulindac group, and mucosal prostaglandin levels were lower in this
group than in the placebo group. During the course of the study,
adenomas developed in 9 of 21 subjects (43 percent) in the sulindac
group and 11 of 20 subjects in the placebo group (55 percent) (P=0.54).
There were no significant differences in the mean number (P=0.69) or
size (P=0.17) of polyps between the groups. Sulindac did not slow the
development of adenomas, according to an evaluation involving linear
longitudinal methods. CONCLUSIONS: Standard doses of sulindac did not
prevent the development of adenomas in subjects with familial
adenomatous polyposis.
18
UI - 11932478
AU - Chau I; Cunningham D
TI -
Cyclooxygenase inhibition in cancer--a blind alley or a new therapeutic
reality?
SO - N Engl J Med 2002 Apr 4;346(14):1085-7
19
UI - 12117879
AU - Khosraviani K; Weir HP; Hamilton P; Moorehead J; Williamson K
TI -
Effect of folate supplementation on mucosal cell proliferation in high
risk patients for colon cancer.
SO - Gut 2002 Aug;51(2):195-9
AD - Department of Surgery, Queen's University of Belfast, UK.
AIMS: Intracellular folate deficiency has been implicated in colonic
carcinogenesis in epidemiological studies and animal and human cancer
models. Our aim was to determine the effect of folate supplementation on
patients with recurrent adenomatous polyps using rectal mucosal cell
proliferation as a biomarker. PATIENTS AND METHODS: Eleven patients with
recurrent adenomatous polyps of the colon were randomised into a
treatment group (n=6) receiving a dietary supplement of 2 mg folic acid
per day for three months and a control group (n=5) receiving a placebo.
Rectal biopsies where taken at 10 cm from the anal verge prior to
supplementation and repeated at four, 12, and 18 weeks from the start of
the supplementation. Each biopsy was immediately incubated in culture
medium enriched with bromodeoxyuridine (BrdU). The S phase cells which
incorporated BrdU into their DNA were identified following
immunohistochemical staining. Twenty five orientated crypts were
identified for each time point and the number and position of BrdU
positive and BrdU negative cells were counted. BrdU labelling indices
(LIs) were calculated for the entire crypt and for each of five equal
compartments running consequently from the base to the luminal surface.
RESULTS: The LI of the treatment group (9.1 (6.7, 12.3)) and the control
group (9.3 (7.8, 10.3)) were comparable at the start. Over the duration
of the supplementation period, LI in the control group did not alter
significantly (9.3 (7.8, 10.3) v 9.6 (8.9, 10.4)). However, LI of the
folate treated group was lowered after 12 weeks of supplementation (9.1
(6.7, 12.3) v 7.4 (5.3, 9.6)). Analysis of the LI for compartments
within the crypt showed that the most significant drop in number of
proliferating cells was in the upper most regions of the crypt.
CONCLUSION: These data indicate that (a) folate supplementation
decreases colonic mucosal cell proliferation in a high risk group for
colon cancer and (b) the most significant reduction takes place at the
luminal aspect of the crypt.
20
UI - 11956579
AU - Rigas B; Williams JL
TI -
NO-releasing NSAIDs and colon cancer chemoprevention: a promising novel
approach (Review).
SO - Int J Oncol 2002 May;20(5):885-90
AD - American Health Foundation, New York Medical College, Valhalla, NY
10595, USA. brigas@ahf.org
The chemoprevention of colon cancer, the second leading cause of
cancer-related deaths in the United States, has been pursued actively
during the last two decades. Methodological problems and those stemming
from the available agents per se have constrained this difficult task;
to some extent, these problems persist to date. That NSAIDs decrease the
incidence of and mortality from colon cancer has been a major advance in
chemoprevention. These compounds are, however, limited by their
significant side effects. NO-releasing NSAIDs (NO-NSAIDs) are a novel
class of compounds, synthesized to overcome the limitations of NSAIDs.
In general, they appear safer and much more effective than their
traditional counterparts. We review their structural features,
metabolism and pharmacological actions. In vitro and in vivo studies
indicate that they are much more effective than traditional NSAIDs in
modulating colonocyte kinetics and the formation of premalignant colon
lesions. Their mechanism of action is complex and not fully understood,
including modulation of NO synthesis, signaling mediated via NF-kappaB
and likely other pathways. Current early findings indicate that
NO-NSAIDs may play a highly promising role in the chemoprevention of
colon cancer.
21
UI - 12093420
AU - Zapka JG; Puleo E; Vickers-Lahti M; Luckmann R
TI -
Healthcare system factors and colorectal cancer screening.
SO - Am J Prev Med 2002 Jul;23(1):28-35
AD - Medical School, University of Massachusetts, Worcester 01655, USA.
Jane.Zapka@umassmed.edu
BACKGROUND: Developing effective programs to promote colorectal cancer
(CRC) screening requires understanding of the effect of healthcare
system factors on access to screening and adherence to guidelines.
METHODS: This study assessed the role of insurance status, type of plan,
the frequency of preventive health visits, and provider recommendation
on utilization of CRC screening tests using a cross-sectional,
random-digit-dial survey of 1002 Massachusetts residents aged > or =50.
RESULTS: A broad definition of CRC screening status included colonoscopy
or barium enema (screening or diagnostic) within 10 years, flexible
sigmoidoscopy (FSIG) within 5 years, and fecal occult blood testing
(FOBT) in the past year as options; 51.7% of subjects aged 50 to 64 and
61.5% of older subjects were current. The uninsured had the lowest
current testing rate. Among insured participants, type of insurance had
little impact on CRC testing; older subjects enrolled in HMOs had
marginally higher rates, although not statistically significant.
Increased frequency of preventive health visits and ever receiving a
physician's recommendation for FSIG or ever receiving FOBT cards were
associated with higher rates of CRC screening among both age groups.
CONCLUSIONS: Even when broad criteria are used to define current CRC
screening status, a substantial proportion of the age-eligible
population remains underscreened. Obtaining regular preventive care and
receiving a physician's recommendation for screening appear to be potent
facilitators of screening that should be considered in designing
promotional efforts.
22
UI - 12182097
AU - Chiaverini L; Fulton JP; Darcy DM
TI -
Progress in the control of colorectal cancer in Rhode Island, 1987-2000.
SO - Med Health R I 2002 Jul;85(7):226-8
23
UI - 12108042
AU - Jedrychowski W; Tobiasz-Adamczyk B; Steindorf K; Popiela T; Penar A;
TI -
Matyja A; Wahrendorf J
[Protective effects of physical activity in the occurrence of colon
cancer]
SO - Przegl Lek 2002;59(1):21-5
AD - Katedra Epidemiologii i Medycyny Zapobiegawczej Collegium Medicum
Uniwersytetu Jagiellonskiego, 31-034 Krakow. myjedryc@cyf-kr.edu.pl
The purpose of the study was to assess the role of occupational and
leisure physical activity on the risk pattern of colon cancer
considering the possible confounding effects of dietary habits.
Case-control study has been carried out in 180 incident cases of colon
cancer hospitalized in Chair of Surgery CMUJ in Krakow. The equal number
of controls individually matched by gender and age were chosen amongst
patients with no history of cancer from the university hospital. Food
frequency questionnaire combined with quantity of foods eaten was used
to assess the usual dietary patterns for 148 food items. The
occupational physical activity of the interviewed subjects before the
occurrence of the disease was assessed by self-rating. Leisure time
activity was measured by the number of hours watching TV. The adjusted
risk of colon cancer was reduced by half in those being active in
leisure time (OR = 0.56, 95% CI: 0.32-0.98). The effect of occupational
physical activity had the same order of magnitude in terms of risk
reduction (OR = 0.56; 95% CI: 0.28-1.10). The protective effect of
healthy nutrition appeared to be independent from that attributed to
physical effort.
24
UI - 12183926
AU - Santavirta J
TI -
[Is screening of colorectal cancer by endoscopy economically
profitable?]
SO - Duodecim 2001;117(12):1240-4
AD - Satakunnan keskussairaala, kirurgian klinikka 28500 Pori.
25
UI - 12149048
AU - Miller K; Waye JD
TI -
Colorectal polyps in the elderly: what should be done?
SO - Drugs Aging 2002;19(6):393-404
AD - Division of Gastroenterology, Department of Medicine, Mount Sinai
Hospital, New York, USA.
Colorectal cancer is an important cause of morbidity and mortality among
Western nations, and is more common in the elderly than in younger
individuals. With the general acceptance of the adenoma-carcinoma
sequence, the current consideration is that colorectal cancer is
preventable if all adenomas are removed before they have the chance to
progress to cancer. To that end, physicians should now advocate
screening for colorectal cancer and through this effort a large number
of patients with adenomatous polyps will be discovered. It is important
to understand the strategy in dealing with this growing population of
patients with adenomas. After an initial polypectomy, patients with
adenomas should be entered into a surveillance program to detect and
remove recurrent adenomas. Recommended surveillance intervals are
shorter for patients with a family history of colorectal cancer, those
with multiple adenomas (>2), large adenomas (> or = 1cm), or those whose
adenomas have high-grade dysplasia, villous architecture, or that are
cancerous. Effective chemoprevention would be a potential method of
lengthening colonoscopic surveillance intervals. Unfortunately, no
treatment has been found to be effective enough to alter our current
surveillance practice. The only recommendation that can be made at this
time for those patients with a history of colonic adenomas is to add 3
g/day of calcium carbonate to their diet, though its effect on adenoma
recurrence is modest.
26
UI - 12296364
AU - Rollins G
TI -
Alert urges doctors to improve colorectal cancer screening rates.
SO - Rep Med Guidel Outcomes Res 2001 Aug 23;12(17):5-7
27
UI - 12217773
AU - Hitt E
TI -
Aspirin may lower risk of pancreatic cancer.
SO - Lancet Oncol 2002 Sep;3(9):518
28
UI - 10498414
AU - Barber MD
TI -
Diet and prevention of cancer. Consumption of oily fish should be
encouraged.
SO - BMJ 1999 Jul 17;319(7203):187; discussion 187-8
29
UI - 12116042
AU - Montesano R
TI -
Hepatitis B immunization and hepatocellular carcinoma: The Gambia
Hepatitis Intervention Study.
SO - J Med Virol 2002 Jul;67(3):444-6
AD - International Agency for Research on Cancer, Lyon, France.
montesano@iarc.fr
The Gambia Hepatitis Intervention Study (GHIS) was initiated by the
International Agency for Research on Cancer (IARC) in 1986. It consisted
of a randomized trial in the Gambian population, aiming to evaluate the
protection provided by HBV vaccination administered during the first
year of life against primary infection, the development of chronic
carriage, and primary liver cancer. The results, reported at 9 years
from the introduction of the vaccine as conferring a high degree of
protection (83% against primary infection and 95% against chronic
carriage), are briefly discussed. It is expected that HBV vaccination
will result in a reduction of mortality from hepatocellular carcinoma,
the most frequent cancer in males in sub-Sahara Africa. Copyright 2002
Wiley-Liss, Inc.
30
UI - 12154470
AU - Vetter C
TI -
[Colon carcinoma. Can it be prevented by diet?]
SO - MMW Fortschr Med 2002 Jun 27;144(26):10-2
31
UI - 12195161
AU - Fabiani R; De Bartolomeo A; Rosignoli P; Servili M; Montedoro GF;
TI -
Morozzi G
Cancer chemoprevention by hydroxytyrosol isolated from virgin olive oil
through G1 cell cycle arrest and apoptosis.
SO - Eur J Cancer Prev 2002 Aug;11(4):351-8
AD - Dipartimento di Scienze Biochimiche e Biotecnologie Molecolari, Sezione
di Scienze Igienistiche e Ambientali, Universita di Perugia, Via del
Giochetto, 06126 Perugia, Italy.
Recent epidemiological evidence and animal studies suggest a
relationship between the intake of olive oil and a reduced risk of
several malignancies. The present study assesses the effect of
hydroxytyrosol, a major antioxidant compound of virgin olive oil, on
proliferation, apoptosis and cell cycle of tumour cells. Hydroxytyrosol
inhibited proliferation of both human promyelocytic leukaemia cells HL60
and colon adenocarcinoma cells HT29 and HT29 clone 19A. The
con-centrations of hydroxytyrosol which inhibited 50% of cell
proliferation were approximately 50 and approximately 750 micromol/l for
HL60 and both HT29 and HT29 clone 19A cells, respectively. At
concentrations ranging from 50 to 100 micromol/l, hydroxytyrosol induced
an appreciable apoptosis in HL60 cells after 24 h of incubation as
evidenced by flow cytometry, fluorescence microscopy and
internucleosomal DNA fragmentation. Interestingly, no effect on
apoptosis was observed after similar treatment of freshly isolated human
lymphocytes and polymorphonuclear cells. The DNA cell cycle analysis,
quantified by flow cytometry, showed that the treatment of HL60 cells
with hydroxytyrosol 50-100 micromol/l arrested the cells in the G0/G1
phase with a concomitant decrease in the cell percentage in the S and
G2/M phases. These results support the hypothesis that hydroxytyrosol
may exert a protective activity against cancer by arresting the cell
cycle and inducing apoptosis in tumour cells, and suggest that
hydroxytyrosol, an important component of virgin olive oil, may be
responsible for its anticancer activity.
32
UI - 12195164
AU - Deneo-Pellegrini H; Boffetta P; De Stefani E; Ronco A; Brennan P;
TI -
Mendilaharsu M
Plant foods and differences between colon and rectal cancers.
SO - Eur J Cancer Prev 2002 Aug;11(4):369-75
AD - Registro Nacional de Cancer, Avda. Brasil 3080 dep. 402, Montevideo,
Uruguay.
A case-control study on plant food intake and its role in the risk of
colon and rectal cancers was carried out in Montevideo, Uruguay. Four
hundred and eighty-four (484) cases of colorectal cancer and 1452
controls were frequency matched on age, sex, residence and urban/rural
status. Among cases, 260 patients had colon cancer whereas 224 had
rectal tumours. Controls had non-neoplastic conditions. Both cases and
controls were interviewed in the four major hospitals in Montevideo
shortly after admittance for diagnosis or treatment. The questionnaire
included a section on frequency of foods, which included 64 items, in
particular, queries on 18 vegetables, 10 fruits and 6 cereal dishes were
included. Thus, the amount of plant foods consumed was complete and
included the main plant foods in the Uruguayan diet. The analysis showed
that rectal cancer displayed inverse associations with total plant
foods, total vegetables, cooked vegetables, potatoes and legumes. When
data were stratified by tumour site and sex, only men showed a
protective effect of plant foods (odds ratio (OR) of rectal cancer for
men 0.4, 95% confidence interval (CI) 0.2-0.7). In contrast, women with
rectal carcinoma were not associated with plant food intake. It can be
concluded that plant foods are protective factors for men afflicted with
colorectal cancer but that plant food intake is not associated with risk
in women. This is, at least in part, due to the high risk associated
with bread intake in this gender.
33
UI - 12023992
AU - Kauff ND; Satagopan JM; Robson ME; Scheuer L; Hensley M; Hudis CA; Ellis
TI -
NA; Boyd J; Borgen PI; Barakat RR; Norton L; Castiel M; Nafa K; Offit K
Risk-reducing salpingo-oophorectomy in women with a BRCA1 or BRCA2
mutation.
SO - N Engl J Med 2002 May 23;346(21):1609-15
AD - Clinical Genetics Service, Memorial Sloan-Kettering Cancer Center, New
York 10021, USA.
BACKGROUND: Risk-reducing salpingo-oophorectomy is often considered by
carriers of BRCA mutations who have completed childbearing. However,
there are limited data supporting the efficacy of this approach. We
prospectively compared the effect of risk-reducing salpingo-oophorectomy
with that of surveillance for ovarian cancer on the incidence of
subsequent breast cancer and BRCA-related gynecologic cancers in women
with BRCA mutations. METHODS: All women with BRCA1 or BRCA2 mutations
identified during a six-year period were offered enrollment in a
prospective follow-up study. A total of 170 women 35 years of age or
older who had not undergone bilateral oophorectomy chose to undergo
either surveillance for ovarian cancer or risk-reducing
salpingo-oophorectomy. Follow-up involved an annual questionnaire,
telephone contact, and reviews of medical records. The time to cancer in
the two groups was compared by Kaplan-Meier analysis and a Cox
proportional-hazards model. RESULTS: During a mean follow-up of 24.2
months, breast cancer was diagnosed in 3 of the 98 women who chose
risk-reducing salpingo-oophorectomy and peritoneal cancer was diagnosed
in 1 woman in this group. Among the 72 women who chose surveillance,
breast cancer was diagnosed in 8, ovarian cancer in 4, and peritoneal
cancer in 1. The time to breast cancer or BRCA-related gynecologic
cancer was longer in the salpingo-oophorectomy group, with a hazard
ratio for subsequent breast cancer or BRCA-related gynecologic cancer of
0.25 (95 percent confidence interval, 0.08 to 0.74). CONCLUSIONS:
Salpingo-oophorectomy in carriers of BRCA mutations can decrease the
risk of breast cancer and BRCA-related gynecologic cancer.
34
UI - 12023993
AU - Rebbeck TR; Lynch HT; Neuhausen SL; Narod SA; Van't Veer L; Garber JE;
TI -
Evans G; Isaacs C; Daly MB; Matloff E; Olopade OI; Weber BL; The
Prevention and Observation of Surgical End Points Study Group
Prophylactic oophorectomy in carriers of BRCA1 or BRCA2 mutations.
SO - N Engl J Med 2002 May 23;346(21):1616-22
AD - Center for Clinical Epidemiology and Biostatistics, University of
Pennsylvania School of Medicine, Philadelphia 19104-6021, USA.
trebbeck@cceb.med.upenn.edu
BACKGROUND: Data concerning the efficacy of bilateral prophylactic
oophorectomy for reducing the risk of gynecologic cancer in women with
BRCA1 or BRCA2 mutations are limited. We investigated whether this
procedure reduces the risk of cancers of the coelomic epithelium and
breast in women who carry such mutations. METHODS: A total of 551 women
with disease-associated germ-line BRCA1 or BRCA2 mutations were
identified from registries and studied for the occurrence of ovarian and
breast cancer. We determined the incidence of ovarian cancer in 259
women who had undergone bilateral prophylactic oophorectomy and in 292
matched controls who had not undergone the procedure. In a subgroup of
241 women with no history of breast cancer or prophylactic mastectomy,
the incidence of breast cancer was determined in 99 women who had
undergone bilateral prophylactic oophorectomy and in 142 matched
controls. The length of postoperative follow-up for both groups was at
least eight years. RESULTS: Six women who underwent prophylactic
oophorectomy (2.3 percent) received a diagnosis of stage I ovarian
cancer at the time of the procedure; two women (0.8 percent) received a
diagnosis of papillary serous peritoneal carcinoma 3.8 and 8.6 years
after bilateral prophylactic oophorectomy. Among the controls, 58 women
(19.9 percent) received a diagnosis of ovarian cancer, after a mean
follow-up of 8.8 years. With the exclusion of the six women whose cancer
was diagnosed at surgery, prophylactic oophorectomy significantly
reduced the risk of coelomic epithelial cancer (hazard ratio, 0.04; 95
percent confidence interval, 0.01 to 0.16). Of 99 women who underwent
bilateral prophylactic oophorectomy and who were studied to determine
the risk of breast cancer, breast cancer developed in 21 (21.2 percent),
as compared with 60 (42.3 percent) in the control group (hazard ratio,
0.47; 95 percent confidence interval, 0.29 to 0.77). CONCLUSIONS:
Bilateral prophylactic oophorectomy reduces the risk of coelomic
epithelial cancer and breast cancer in women with BRCA1 or BRCA2
mutations.
35
UI - 12145419
AU - Campbell S; Ghosh S
TI -
Ulcerative colitis and colon cancer: strategies for cancer prevention.
SO - Dig Dis 2002;20(1):38-48
AD - Milton Keynes General Hospital, Eaglestone, Milton Keynes, London, UK.
The risk of development of colon cancer in patients with ulcerative
colitis is an emotive issue with patients and a potential medico-legal
problem for physicians caring for such patients. The exact magnitude of
the risk is not clearly defined. Current surveillance programmes use
dysplasia as a marker for the risk of invasive carcinoma development,
but this strategy has inherent limitations. A number of new molecular
markers have been investigated but none are currently considered robust
enough for routine clinical use. Recommendations for patient selection
and interval for colonoscopic surveillance are currently pragmatic, and
not entirely evidence-based. Nevertheless, optimal medical management
and adherence to a surveillance programme geared to detect dysplasia
might still be the best risk reduction strategy. Copyright 2002 S.
Karger AG, Basel
36
UI - 12145421
AU - Reinacher-Schick A; Schmiegel W
TI -
Surveillance strategies in patients after polypectomy.
SO - Dig Dis 2002;20(1):61-9
AD - Ruhr-Universitat Bochum, Medizinische Universitatsklinik,
Knappschaftskrankenhaus, Bochum, Deutschland.
Colorectal cancer (CRC) is a major cause of cancer death in the Western
world. It develops slowly over several years from premalignant lesions
(most prominently adenomatous polyps) to invasive cancer. The molecular
basis of CRC pathogenesis has been well characterized. The most
effective method to prevent CRC is endoscopic polypectomy. However,
adenomatous polyps are known to recur at significant rates. The aim of
surveillance programs after polypectomy is to further reduce the
incidence of CRC in individuals where precancerous lesions have been
identified and treated. However, the medical risks and the costs of
repeated examinations must be kept as low as possible. Therefore, the
identification of patient subgroups with a particular low cancer risk
who may be followed-up less frequently seems important. There is recent
evidence that other colorectal lesions, namely flat and depressed type
adenomas (F&D adenoma) and possibly some hyperplastic polyps and
serrated adenomas may also carry a malignant potential which could
influence our screening, treatment and surveillance strategies for the
colorectum in the future. General surveillance guidelines regarding
these entities have not been issued to date. This article will first
discuss the biology, natural history, present surveillance
recommendations and future issues for sporadic adenomatous polyps. Then,
recent literature on F&D type adenomas, hyperplastic polyps and serrated
adenomas will be reviewed with respect to their malignant potential and
the potential necessity for treatment and surveillance of these lesions.
Copyright 2002 S. Karger AG, Basel
37
UI - 12145422
AU - Ricciardiello L; Roda E; Bazzoli F
TI -
Chemoprevention in colorectal neoplasias: what is practical and
feasible?
SO - Dig Dis 2002;20(1):70-2
AD - Dipartimento di Medicina Interna e Gastroenterologia, Universita di
Bologna, Italy.
Chemoprevention strategies for colorectal cancer have gained increasing
attention. Despite contradictory data regarding the use of
micronutrients and antioxidant vitamins as chemopreventive tools, the
identification of cyclooxygenase 2 (COX-2) upregulation in colorectal
adenomas has led to the development of new drugs, named COX-2
inhibitors, that directly target the molecular mechanism of
carcinogenesis. Celecoxib, one of the two COX-2 inhibitors available on
the market, has been approved for chemoprevention of familial
adenomatous polyposis. In the future, we might expect these drugs to be
used in the prevention of colon cancer in patients at increased risk,
such as those with a positive family history. Copyright 2002 S. Karger
AG, Basel
38
UI - 12145424
AU - Blum HE
TI -
Molecular targets for prevention of hepatocellular carcinoma.
SO - Dig Dis 2002;20(1):81-90
AD - Department of Medicine II, University Hospital Freiburg, Germany.
heblum@ukl.uni-freiburg.de
Hepatocellular carcinoma (HCC) is one of the most common malignant
tumors in some areas of the world with an extremely poor prognosis. The
major etiologic risk factors for HCC development include toxins
(alcohol, aflatoxin B1), androgens and estrogens, hepatitis B virus
(HBV) and hepatitis C virus (HCV) infection as well as various inherited
metabolic disorders, such as alpha-1-antitrypsin deficiency and
hemochromatosis. The molecular pathogenesis of HCC development is very
complex and involves alterations in the structure or expression of
several tumor suppressor genes, oncogenes and, possi