AIM: To investigate the genotype frequencies of MLH1 promoter polymorphism -93G>A and to determine whether it could play any role in modulating familial and sporadic CRC susceptibility risk.
METHODS: A case-control study comprising of 104 histopathologically confirmed CRC patients as cases (52 sporadic CRC and 52 Lynch syndrome patients) and 104 normal healthy individuals as controls was undertaken. DNA was extracted from peripheral blood and the polymorphism was genotyped employing PCR-RFLP methods. The genotypes were categorized into homozygous wild type, heterozygous and homozygous variants. The risk association between these polymorphisms and CRC susceptibility risk was calculated using binary logistic regression analysis and deriving odds ratios (ORs).
RESULTS: When risk association was investigated for all CRC patients as a single group, the heterozygous (G/A) genotype showed a significantly higher risk for CRC susceptibility with an OR of 2.273, (95%CI: 1.133-4.558 and p-value=0.021). When analyzed specifically for the 2 types of CRC, the heterozygous (G/A) genotype showed significantly higher risk for sporadic CRC susceptibility with and OR of 3.714, (95%CI: 1.416-9.740 and p-value=0.008). Despite high OR value was observed for Lynch syndrome (OR: 1.600, 95%CI: 0.715-3.581), the risk was not statistically significant (P=0.253).
CONCLUSION: Our results suggest an influence of MLH1 promoter polymorphism -93G>A in modulating susceptibility risk in Malaysian CRC patients, especially those with sporadic disease.
METHOD: Between October 2009 and April 2010, a survey was prospectively conducted among women admitted to clinics of Penang General Hospital for examination and/or treatment by using a questionnaire. Therefore, characteristics of patients diagnosed with breast cancer (n=150) were compared with control cases (n=150) admitted to hospital for non-neoplastic, non-hormone related diseases.
RESULTS: Family history of a distant relative with breast cancer (OR=2.84), history of first-degree relatives with breast cancer (OR=2.95), history of benign breast disease (OR=2.43), menstrual irregularity (OR=4.24), and use of oral contraceptive pills (OCP) (OR=2.15) were found to be significant risk factors for breast cancer in our population. Furthermore, education more than 11 years (OR=0.40), breastfeeding (OR=0.50), being employed (OR=0.45) and practicing low fat diet (OR=0.53) were strongly protective against breast cancer development.
CONCLUSION: The results emphasize the importance of conducting a series of awareness campaigns that highlights the protective role of longer breastfeeding period against breast cancer and the negative relationships between OCP use and high fat diet with this disease.
OBJECTIVE: This study aimed to determine the relationship between dietary intake (macronutrients, fruits, vegetables and lycopene), lifetime physical activity and oxidative DNA damage with prostate cancer.
DESIGN: A case control study was carried out among 105 subjects (case n=35, control n=70), matched for age and ethnicity. Data on sociodemographic, medical, dietary intake, consumption of lycopene rich food and lifetime physical activity were obtained through an interview based questionnaire. Anthropometric measurements including weight, height and waist hip circumferences were also carried out on subjects. A total of 3 mL fasting venous blood was drawn to assess lymphocyte oxidative DNA damage using the alkaline comet assay.
RESULTS: Cases had a significantly higher intake of fat (27.7 ± 5.5%) as compared to controls (25.1 ± 5.9%) (p < 0.05). Mean intakes of fruits and vegetables (3.11 ± 1.01 servings/d)(p < 0.05), fruits (1.23 ± 0.59 servings/d) (p<0.05) and vegetables (1.97 ± 0.94 servings/d) were higher in controls than cases (2.53 ± 1.01, 0.91 ∓ 0.69, 1.62 ± 0.82 servings/d). A total of 71% of cases did not met the recommendation of a minimum of three servings of fruits and vegetables daily, as compared to 34% of controls (p < 0.05) (adjusted OR 6.52 (95% CI 2.3-17.8)) (p < 0.05). Estimated lycopene intake among cases (2,339 ∓ 1,312 mcg/d) were lower than controls (3881 ∓ 3120 mcg/d) (p< 0.01). Estimated lycopene intake of less than 2,498 mcg/day (50th percentile) increased risk of prostate cancer by double [Adjusted OR 2.5 (95%CI 0.99-6.31)]. Intake of tomatoes, watermelon, guava, pomelo, papaya, mango, oranges, dragon fruit, carrot, tomato sauce and barbeque sauce were higher in controls compared to cases. Intake of tomato sauce of more than 2.24 g/d (25th percentile), papaya more than 22.7 g/d (50th percentile) and oranges more than 19.1g/h (50th percentile) reduced prostate cancer risk by 7.4 (Adjusted OR 7.4 (95% CI 1.17-46.8)), 2.7 (adjusted OR 2.75 (95% CI 1.03-7.39)) and 2.6 times (adjusted OR = 2.6 (95% CI=1.01-6.67)), respectively (p < 0.05 for all parameters). No oxidative damage was observed among subjects. Past history of not engaging with any physical activities at the age of 45 to 54 years old increased risk of prostate cancer by approximately three folds (Adjusted OR 2.9(95% CI = 0.8-10.8)) (p < 0.05). In conclusion, low fat diet, high intake of fruits, vegetables and lycopene rich foods and being physical active at middle age were found to be protective. Thus, it is essential for Malaysian men to consume adequate fruits and vegetables, reduce fat intake and engage in physical activity in order to reduce prostate cancer risk.
OBJECTIVE: To assess the association of premenopausal and postmenopausal breast cancer risk with fat and fat subtypes intake.
METHODOLOGY: This is a population based case-control study conducted in Kuala Lumpur, Malaysia from January 2006 to December 2007. Food intake pattern was collected from 382 breast cancer patients and 382 control group via an interviewer-administered food frequency questionnaire. Logistic regression was used to compute odds ratios (OR) with 95% confidence intervals (CI) and a broad range of potential confounders was included in analysis.
RESULTS: This study showed that both premenopausal and postmenopausal breast cancer risk did not increase significantly with greater intake of total fat [quartile (Q) 4 versus Q1 OR=0.76, 95% CI, 0.23-2.45 and OR=1.36, 95% CI, 0.30-3.12], saturated fat (ORQ4 to Q1=1.43, 95% CI, 0.51-3.98 and ORQ4 to Q1=1.75, 95% CI, 0.62-3.40), monounsaturated fat (ORQ4 to Q1=0.96, 95% CI, 0.34-1.72 and ORQ4 to Q1=1.74, 95% CI, 0.22-2.79), polyunsaturated fat (ORQ4 to Q1=0.64, 95% CI, 0.23-1.73 and ORQ4 to Q1=0.74, 95% CI, 0.39-1.81), n-3 polyunsaturated fat (ORQ4 to Q1=1.10, 95% CI, 0.49-2.48 and ORQ4 to Q1=0.78, 95% CI, 0.28-2.18), n-6 polyunsaturated fat (ORQ4 to Q1=0.67, 95% CI, 0.24-1.84 and ORQ4 to Q1=0.71, 95% CI, 0.29-1.04) or energy intake (ORQ4 to Q1=1.52, 95% CI, 0.68-3.38 and ORQ4 to Q1=2.21, 95% CI, 0.93-3.36).
CONCLUSION: Total fat and fat subtypes were not associated with pre- and postmenopausal breast cancer risk after controlling for age, other breast cancer risk factors and energy intake. Despite the lack of association, the effects of total fat and fat subtypes intake during premenopausal years towards postmenopausal breast cancer risk still warrant investigation.
OBJECTIVE: This study investigated the relationship between adiposity, lifetime physical activities and serum adiponectin as breast cancer risk factors among Malaysian women in Klang Valley, Malaysia.
DESIGN: A case-control study was carried out among 70 newly diagnosed breast cancer patients and 138 controls aged 29 to 65 years old in Klang Valley.
SUBJECTS: The inclusion criteria for both groups were not having menstruation for premenopausal women, no evidence of pregnancy, not lactating and no chronic diseases such as hypertension and diabetes at the time of data collection. In addition, the cases must be pathologically newly diagnosed with breast cancer (stage I to III) and not on any therapy for cancer, with the exception of surgery. The controls were matched with cases for age +/- 5 years and menopausal status.
MEASUREMENTS: Subjects were interviewed to obtain information on socio-demography, health and reproductive history using a pretested questionnaire. Subjects were also asked on their engagement of physical activity since secondary school. Anthropometric parameters included height, weight, waist and hips were also measured. A total of 6 ml of fasting venous blood was drawn for analysis of serum adiponectin in duplicate using Linko Adiponectin ELISA Kit. Fasting blood glucose (FBG) and blood pressure were also measured.
RESULTS: Mean body mass index (BMI) among cases and controls were not significantly different (p> 0.05) at 26.1 -/+ 4.8 kg/m2 and 25.3 -/+ 4.5 kg/m2, respectively. FBG among cases (6.3 -/+ 1.8 mmol/L) was higher than controls (5.6 -/+ 1.1 mmol/L) (p<0.05). Waist hip ratio (WHR) of cases (0.85 -/+ 0.07) was also higher than controls (0.80 -/+ 0.06) (p<0.05). Abdominal obesity (WHR > 0.85) increased risk of breast cancer by three folds [Adjusted OR 3.3 (95%CI 1.8-6.2)] (p<0.05). Adiponectin level was inversely related to waist circumference (r=-0.510, p=0.000), BMI (r=-0.448, p=0.000) and FBG (r=-0.290, p=0.026). Adiponectin level in cases (11.9 -/+ 4.8 microg/ml) were lower than controls (15.2 -/+ 7.3 microg/ml) (p<0.05). A greater reduction of breast cancer risk was observed with the increasing level of serum adiponectin level according to percentiles (p<0.05). Subjects with mean serum adiponectin level at the highest quintile (> 75th)( >or= 16.7 microg/ml) had 80% reduced risk of breast cancer [Adjusted OR 0.2 (0.0-0.6)](p<0.05). A higher percentage of cases (47%) had not engaged in any physical activity throughout life as compared to controls (19%)[Adjusted OR 3.7 (1.7-7.7)](p<0.001).
CONCLUSIONS: Abdominal obesity and physical inactivity throughout life were associated with low serum adiponectin and breast cancer risk among subjects. Thus, it is essential for Malaysian women to be physically active and achieve a healthy waistline in order to increase serum adiponectin level and reduce breast cancer risk.