The metabolic syndrome is associated with increased risk of colorectal adenoma development: the Self-Defense Forces health study.

The metabolic syndrome, a cluster of metabolic abnormalities linked to insulin resistance, has attracted much interest as a risk factor for cardiovascular disease and type 2 diabetes. Hyperinsulinemia is also a postulated biological risk factor for colorectal carcinogenesis. We therefore here examined the relation between the metabolic syndrome and colorectal adenoma development. The study subjects were 756 cases of colorectal adenoma and 1751 controls with no polyps who underwent total colonoscopy during the period January 1995 to March 2002 at two Self Defense Forces (SDF) hospitals in Japan. The metabolic syndrome was defined with reference to abdominal obesity in combination with any two of the following conditions: elevated triglycerides (150 mg/dL); lowered HDL cholesterol (<40 mg/dL); elevated blood pressure (systolic blood pressure 130 mmHg and/or diastolic blood pressure 85 mmHg); and raised fasting glucose (110 mg/dL). Abdominal obesity was defined as a waist circumference of 85 cm or more(Japanese criterion) or 90 cm (Asian criterion). Statistical adjustment was made for age, hospital, and rank in the SDF. The metabolic syndrome was found to be associated with a moderately increased risk of colorectal adenomas whether either of the Japanese and Asian criteria was used; adjusted odds ratios with the Japanese and Asian criteria were 1.38 (95% confidence interval [CI] 1.13-1.69) and 1.48 (95% CI 1.13-1.93), respectively. Increased risk was more evident for proximal than distal colon or rectal adenomas, and was almost exclusively observed for large lesions (5 mm in diameter). Thus the metabolic syndrome appears to be an important entity with regard to the prevention of colorectal cancer, as well as cardiovascular disease and type 2 diabetes.

Amplification of 9q34 in childhood adrenocortical tumors: a specific feature unrelated to ethnic origin or living conditions

Adrenocortical tumors (ACT) in children under 15 years of age exhibit some clinical and biological features distinct from ACT in adults. Cell proliferation, hypertrophy and cell death in adrenal cortex during the last months of gestation and the immediate postnatal period seem to be critical for the origin of ACT in children. Studies with large numbers of patients with childhood ACT have indicated a median age at diagnosis of about 4 years. In our institution, the median age was 3 years and 5 months, while the median age for first signs and symptoms was 2 years and 5 months (N = 72). Using the comparative genomic hybridization technique, we have reported a high frequency of 9q34 amplification in adenomas and carcinomas. This finding has been confirmed more recently by investigators in England. The lower socioeconomic status, the distinctive ethnic groups and all the regional differences in Southern Brazil in relation to patients in England indicate that these differences are not important to determine 9q34 amplification. Candidate amplified genes mapped to this locus are currently being investigated and Southern blot results obtained so far have discarded amplification of the abl oncogene. Amplification of 9q34 has not been found to be related to tumor size, staging, or malignant histopathological features, nor does it seem to be responsible for the higher incidence of ACT observed in Southern Brazil, but could be related to an ACT from embryonic origin.