Biomedical subjects

P Senesse

Publications and source records attributed to P Senesse.

24 records · Page 2Linked to original sources

PubMed1997

Environmental and familial risk factors in relation to the colorectal adenoma--carcinoma sequence: results of a case-control study in Burgundy (France).

A case-control study in the Cote-d'Or area (Burgundy, France) investigated the relationship between environmental and familial risk factors and the different steps of the adenoma-carcinoma sequence. Two adenoma groups (< 10 mm and > or = 10 mm), a polyp-free control group, a colorectal cancer group and a general population control group were recruited. Tobacco was associated with the risk of adenomas, and alcohol with the risk of large adenomas. They proved to be independently related to large adenoma formation when compared with controls. There was no association with cancer risk. Refined cereals, delicatessen, offal and fats appear to be risk factors along the adenoma-carcinoma sequence. This data does not support an increased risk with high consumption of fresh meat, or a protective effect of dairy products and calcium. A high consumption of vegetables was a protective factor for cancer, mainly in men. Excess weight and body mass index influenced the earlier step of the adenoma carcinoma sequence and excess calorie intake was risk factor for cancer. The decision to study precancerous lesions as well as cancer appears fruitful. Results suggest that the three stages of large bowel carcinogenesis are partly related to diet in different ways. They are concordant with risk factors recorded for colorectal cancer, but suggest some local specificities.

Adenoma↗

PubMed1996

Calcium, phosphorus, vitamin D, dairy products and colorectal carcinogenesis: a French case--control study.

A protective effect of calcium against colorectal cancer has been described in Anglo-Saxon but not in Latin communities, and no such effect has been observed regarding adenomas. We investigated the relationship between calcium, dairy products and the adenoma-carcinoma sequence in a French region by comparing small adenoma ( < 10 mm, n = 154), large adenoma (n = 208) and polyp-free (n = 426) subjects, and cancer cases (n = 171) with population controls (n = 309). There was no protective effect of calcium against colorectal tumours except for low fat calcium and large adenomas in men (OR for highest quintile = 0.3, P for trend = 0.06). There was even a trend towards an increased risk of cancer with dairy calcium in men and non-dairy calcium in women. Vitamin D was inversely related to the risk of small adenomas in women (OR for highest quintile = 0.4, P for trend = 0.04). Regarding dairy products, only consumption of yoghurt displayed an inverse relationship with risk of large adenomas, in both men and women. These data failed to demonstrate a protective effect of calcium against colorectal carcinogenesis. They suggest that the type of dairy product might be the important factor with regard to prevention of colorectal tumours.

Adenoma↗

PubMed1996

Folate and alcohol intakes: related or independent roles in the adenoma-carcinoma sequence?

Epidemiologic studies have suggested that high alcohol and low folate intakes might be jointly associated with colorectal tumors via DNA metabolism. We investigated this hypothesis in a case-control study comparing small adenoma (< 10 mm, n = 154), large adenoma (n = 208), and polyp-free (n = 426) subjects, recruited after colonoscopy, and cancer cases (n = 171) with population controls (n = 309). Odds ratios for the fifth vs. the first quintile of intake (OR5) were as follows: Folate intake was related to the risk of small and large adenomas compared with polyp-free subjects [OR5 = 0.5, 95% confidence interval (CI) 0.3-1.0; OR5 = 0.5, 95% CI 0.3-1.0, respectively], whereas alcohol was related to risk of large adenomas (OR5 = 4.1, 95% CI 2.1-8.1), but not of small adenomas (OR5 = 1.2, 95% CI 0.7-2.2). In large adenomas, there was some interaction between alcohol and folate, with a stronger protective effect of folate with high alcohol intake and a stronger risk with alcohol with low folate intake. For cancer patients compared with general population controls, neither alcohol (OR5 = 1.6, 95% CI 0.8-3.0) nor folates (OR5 = 1.0, 95% CI 0.5-2.0) were related to risk. Our data support the hypothesis that folate intake might be mostly beneficial to prevent adenoma formation but might have an additional protective effect against adenoma growth associated with alcohol.

Adenoma↗

PubMed1995

Tobacco, alcohol, and colorectal tumors: a multistep process.

A case-control study in the Côte d'Or area of France used the multistep concept of colorectal carcinogenesis to compare lifetime tobacco consumption and present alcohol consumption in patients with small adenomas (less than 1 cm, n = 154) or large adenomas (n = 208) and in polyp-free controls (n = 427). Cancer patients (n = 171) were compared with population controls (n = 309). In men, smoking was associated with the risk of adenomas (odds ratio = 3.6 over 20 pack-years vs. nonsmokers, p < 0.001). Alcohol was a risk factor for large adenomas only, with relative risks of 4.2 (p < 0.01), 3.0 (p < 0.05), and 4.4 (p < 0.01) for consumptions of 20-39, 40-59, and 60 g/day compared with less than 10 g/day. When patients with large adenomas were compared with polyp-free controls, both alcohol and tobacco were independently related to the risk of tumor. There was no association between tobacco or alcohol intakes and cancer risk. In women, consumption was much lower in all groups, and no significant association with either risk factor was observed. These data suggest for the first time that there is an independent effect of alcohol and tobacco in men at different early steps of the adenoma-carcinoma sequence. They demonstrate the usefulness of such a model for etiologic studies on cancer.

Adenoma↗

PubMed1995

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

Family history of colorectal cancer is a risk factor for sporadic colorectal cancer, but it is not known which step of the adenoma-carcinoma pathway it influences. This case control study investigated the relation between family history of cancer and colorectal adenomas and cancers. Family history of colorectal cancer (FHCRC) was as frequent in small (< 10 mm) adenoma patients (11.7%, n = 154) as in polyp free patients (10.6%, n = 426), whereas it was more frequent in patients with large adenoma(s) (18.8%, n = 208; p < 0.01). Odds ratios for FHCRC were 1.2 (p > 0.10) for small adenomas and 2.1 (p < 0.01) for large adenomas. Family history of other (non-colorectal) cancers (FHOC) was similar in the three groups. Patients with a colorectal cancer (n = 171) had more frequently a family history of cancer, both colorectal (15.8%; p < 0.01) and other cancers (35.7%; p < 0.001) than general population controls (n = 309; FHCRC: 8.1%; FHOC: 21.7%). In a logistic model, both factors were independently related to colorectal cancers (odds ratios: 1.9 (p < 0.05) for FHCRC and 2.1 (p < 0.001) for FHOC). These data suggest that family history of colorectal cancer influences only the growth of adenomas or their malignant transformation. The finding of a further predisposition to any type of cancer needs to be confirmed.

Adenoma↗

PubMedDate not supplied

Efficacy of prophylactic anti-diarrhoeal treatment in patients receiving Campto for advanced colorectal cancer.

This study assessed the efficacy of combined prophylactic and curative anti-diarrhoeal medication in advanced colorectal patients treated by irinotecan. Thirty-four pre-treated eligible patients were evaluated. There were 44% women, the median age was 65 and 38% of the patients had a 0 performance status. The patients received sucralfate(4g/d) and nifuroxazide(600 mg/d) prophylactic treatment on days 0-7. In the case of severe diarrhoea, preventive treatment was replaced by loperamide(12 mg/d) and diosmectite (9 g/d). Grade 3 delayed diarrhoea occurred in 18% of patients (90% CI: [9.5-28.9]) and 4.6% of cycles. No grade 4 delayed diarrhoea was observed. Twenty-nine patients (85%) received the preventive treatment at cycle 1, while 14% (90% CI: [6.2-25.7]) experienced grade 3 delayed diarrhoea in 3.7% of cycles for a median 4.5 days. The objective response rate was 8% (90% CI [1.4-23.1]) among the 25 assessable patients. Preventive combined treatment is effective in reducing the incidence of severe delayed diarrhoea, and it should be proposed to patients treated with mono-therapy Campto(r) and evaluated in poly-chemotherapy protocols.

Adenocarcinoma↗