Family history of colorectal tumours and implications for the adenoma-carcinoma sequence: a case control study.

Boutron, M C; Faivre, Jean; Quipourt, Valérie; Sénesse, Pierre; Michiels, C.

doi:10.1136/gut.37.6.830

Cited by 56 publications

(38 citation statements)

References 19 publications

(1 reference statement)

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“…The reason for this may be that in patients with a prevailing genetic disposition for CRC, the carcinogenic factors may prevail in spite of inhibitory environmental factors. This may partly be supported by the recently reported relationship between large adenomas and a family history of cancer [65]. However, one cannot rule out the possibility that higher doses of calcium or vitamins are necessary to counteract an increased genetic tendency to polyp growth.…”

Section: Discussionsupporting

confidence: 53%

Growth and Recurrence of Colorectal Polyps: A Double-Blind 3-Year Intervention with Calcium and Antioxidants

et al. 1998

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Background: Dietary calcium and antioxidants have been suggested as protective agents against colorectal cancer. This has been supported by animal experimental studies, case control and cohort studies. Materials and Methods: In a prospective intervention study of colorectal adenomas, and intermediary stage in colorectal carcinogenesis, 116 polyp-bearing patients received a placebo-controlled daily mixture of β-carotene 15 mg, vitamin C 150 mg, vitamin E 75 mg, selenium 101 µg, and calcium (1.6 g daily) as carbonate for a period of 3 years with annual colonoscopic follow-up to test if the mixture was able to reduce polyp growth or recurrence. All polyps of <10 mm at enrolment or follow-up were left unresected until the end of the study. Results: 87–91% of the patients attended the annual endoscopic follow-up investigations, and 19% of the patients dropped out of the medical intervention. The rest consumed 85% of the total amount of tablets over the 3 years. The fecal calcium concentration was 2.3–2.7 times higher in patients taking active medication compared to the placebo group. Diet registration showed that, when adding the intake of antioxidants and calcium from diet and intervention, there was a significant difference between the intake of these substances in the active and the placebo group. No difference was detected in the growth of adenomas between the active and the placebo group from year to year and for the total study period. Moreover, there was no effect on polyps of <5 or 5–9 mm, or on polyps in the different colonic segments analyzed separately. A reduced growth of adenomas was found in patients <60 years of age taking active medication (n = 8) compared to those taking placebo (n = 6; mean difference 2.3 mm; 95% CI 0.26–4.36). There was a significantly lower number of patients free of new adenomas in the placebo group compared to those taking active medication as tested by logistic regression and Kaplan-Meier analysis (log-rank test p value 0.035). Subgroup analysis showed that only the group of patients with no family history of colorectal cancer, those with only one adenoma at inclusion, and those <65 years benefitted from the intervention medication. Conclusion: The study did not find an overall effect on polyp growth. Our data, however, may support a protective role of calcium and antioxidants on new adenoma formation.

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Section: Discussionsupporting

confidence: 53%

Growth and Recurrence of Colorectal Polyps: A Double-Blind 3-Year Intervention with Calcium and Antioxidants

et al. 1998

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“…Estimates of the relative risk of colorectal cancer for a first-degree relative of an affected individual vary from 1.9-7.5. 24,25 About 5-10% of colorectal cancers are thought to arise in individuals with a monogenic colon cancer predisposition syndrome (Table 6). …”

Section: Colorectal Cancermentioning

confidence: 99%

Genetic predisposition to cancer

Turnbull

Hodgson

2005

Clinical Medicine

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-Over recent decades a number of genes causing predisposition to cancer have been identified. Some of these cause rare autosomal dominant monogenic cancer predisposition syndromes. In the majority of families, the increased incidence of cancers is due to a multifactorial aetiology with a number of lower penetrance cancer predisposition genes interacting with environmental factors. Identification of those at increased risk of cancer on account of their family history is important, as genetic testing, enhanced surveillance, prophylactic surgery and chemoprophylaxis may be indicated. In this article the issues surrounding genetic predisposition to cancer are considered by examining two common cancers: colorectal and breast cancer.KEY WORDS: breast, cancer, colorectal, genes, genetic, hereditary, inherited, monogenic, predisposition, surveillanceThe hereditary nature of cancer has been well recognised for over 100 years, but the inherited aspects of cancer susceptibility have become more clearly characterised only in the last few decades. Almost half the referrals to genetics centres are now for assessment of cancer susceptibility compared with only a small minority twenty years ago. Studies of familial aspects of cancer have focused on families with:• several individuals affected with a rare cancer, possibly accompanied by other phenotypic abnormalities • characteristic familial constellations of different cancers, or• an excess of specific 'common cancers' , particularly occurring at young ages.Epidemiological studies have shown that the occurrence of a cancer in one family member confers an increased empirical risk of the same or related cancers to relatives, the degree of risk depending on the age at diagnosis and the number of affected relatives on the same side of the family. Linkage studies in families with several close relatives affected with the same cancer type have led to the identification of the genes underlying a number of monogenic syndromes of cancer predisposition. Some of these are predisposition syndromes which confer susceptibility to cancer alone; in other rare inherited multisystem disorders, cancer predisposition is accompanied by a characteristic phenotype, including facial dysmorphism, neurological pathology or other features.Single gene cancer predisposition syndromes are rare and account for only a small proportion of familial clusters of common cancers. More commonly, familial predisposition may be due to the effects of several less penetrant genes interacting with environmental factors. The search is on for these higher frequency, lower penetrance candidate genes for common cancers. As the members of the orchestra of interacting predisposition and protective genetic factors are characterised, the distinction between inherited and sporadic cancers will become a spectrum rather than dichotomous. The evolution and widespread availability of affordable microarray technology may in the future offer the general population accessible individualised risk profiling for many cancer types...

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“…As for colorectal cancers, this increase in risk appears to be more pronounced if the index case is younger than 60 or 65. 6 Although our data need to be confirmed, we suggest that first degree relatives of index cases with colorectal cancer or large adenomas should be considered similarly. In these groups, screening should start at age 50, using a strategy which has yet to be defined.…”

Section: Discussionmentioning

confidence: 95%

“…In a case control study in the Burgundy area, we investigated the relation between family history of colorectal cancer among first degree relatives of both colorectal cancers and adenomas. 6 Patients eligible for the study were residents of the Côte d'Or area, aged 30 to 79. Between April 1985 and April 1990, 171 patients with a histologically confirmed colon or rectal carcinoma were recruited from all public and private gastroenterologists of the Côte d'Or area, as were 208 patients with at least one adenoma 10 mm or more in diameter, 154 patients with only small adenomas, 426 polyp free controls, and 309 general population controls.…”

Section: Cumulative Riskmentioning

confidence: 99%

Family history and risk of colorectal cancer: implications for screening programmes

et al. 2000

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Objective-To estimate the lifetime risk of colorectal cancer in the general population and in first degree relatives of patients with sporadic colorectal cancer or adenoma. Main outcomes measures-The cumulative risk of colorectal cancer (0-74) in the general population combined with the relative risk of colorectal cancer and the prevalence of diVerent groups of subjects with family history of colorectal tumour allows the calculation of cumulative risks in these groups. Results-The lifetime risk of colorectal cancer was 1 in 23 in men and 1 in 40 in women. In males, 0.5% in the 55-59 age group and 4.5% in the 70-74 age group will develop a colorectal cancer. The corresponding values in females were 0.4% and 2.5%. The cumulative risk at age 74 varied between 7.7% (one family member affected) and 25.6% (two aVected) in males, and 4.3% and 14.3% respectively in females. The risk in the 40-44 year age group for individuals with one first degree relative aVected before 45 years of age was 0.5%, similar to that of those aged 45-49 with one first degree relative aVected with a colorectal cancer or a large adenoma (> 1 cm). Conclusions-These results suggest that screening in the general population should start at 50 or 55. The lifetime risk is high enough (over 10%) among individuals with one aVected first degree relative before age 45, or with at least two aVected first degree relatives, to warrant colonoscopic screening. The data provide a basis for recommendations that relatives of these patients should enter screening programmes at age 40 to 44. (J Med Screen 2000;7:136-140)

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Family history of colorectal tumours and implications for the adenoma-carcinoma sequence: a case control study.

Cited by 56 publications

References 19 publications

Growth and Recurrence of Colorectal Polyps: A Double-Blind 3-Year Intervention with Calcium and Antioxidants

Growth and Recurrence of Colorectal Polyps: A Double-Blind 3-Year Intervention with Calcium and Antioxidants

Genetic predisposition to cancer

Family history and risk of colorectal cancer: implications for screening programmes

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