TNF-α and -β, the multi-functional pro-inflammatory cytokines, are known to play important roles in both tumor progression and destruction based on their concentrations. Growth factors and various stimuli such as cytokines regulate proliferation of the breast epithelial cells. Therefore, the polymorphisms in the genes encoding these signaling molecules could affect the risk of breast cancer. We have investigated selected genetic polymorphisms in TNF-α promoter (rs1800629, -308 G>A and rs361525, -238 G>A) and TNF-β intron 1 (rs909253, +252 A>G) in ethnically two different case-control groups from India. The study included 200 cases and 200 controls from an Indo-European (North Indian) group, and 265 cases and 237 controls from a Dravidian (South Indian) group. Genotyping of a total of 902 individuals was done by direct DNA sequencing. None of the polymorphisms showed significant association with breast cancer in the Indo-European group; however, all the three polymorphisms showed strong association with breast cancer in the Dravidian group. Further, sub-group analysis in the Indo-European group showed no significant difference between pre-menopausal cases and controls or between post-menopausal cases and controls at any of the loci analyzed. However, all the polymorphisms in the Dravidian group were significantly associated with pre-menopausal but not with post-menopausal breast cancer. In conclusion, TNF-α and -β polymorphisms are strongly associated with breast cancer in the Dravidian but not in the Indo-European group.

Interleukins and cytokines are important regulator of the aetio-pathogenesis of the majority of cancers. Mechanistic role of IL-1RN and IL-4, particularly in breast carcinogenesis, is well documented. However, the role of polymorphisms of IL-1RN and IL-4 combinations associated with risk of breast cancer is not reported. The IL-1RN and IL-4 gene polymorphisms were genotyped with VNTR-PCR in 100 patients (benign tumor n = 32 and breast cancer n = 68) and 200 normal healthy control subjects with normal mammogram. Genotype distribution and allelic frequencies between patients and controls were compared and odds ratios (OR) with 95% confidence intervals (CI) were calculated using SPSS software (version 12.0). There were no significant differences in the genotype distributions of both IL-1RN and IL-4 polymorphisms between cases and controls. Similarly, subgroup analysis showed that there is no significant association for pre- and postmenopausal women. However, BB genotype of IL-1RN significantly differs among benign and malignant stages of breast cancer. IL-1RN and IL-4 polymorphisms alone or in combination are not associated with risk of breast cancer in Indian patients. The association of IL-1RN with malignant stages may indicate its possible role in progression of breast cancer. Further studies in other population are needed to confirm our findings and to elucidate the role of IL-1RN in progression of breast cancer.

Metabolic disorder refers to a cluster of metabolic abnormalities (i.e., insulin resistance, hypertension, dyslipidemia, obesity, high cholesterol and high blood pressure). The metabolic disorder is fast becoming a global emergency. Drugs presently available in the market help in curing the disorder only up to some extent and providing symptomatic relief, in lieu of an array of side effects, hence it is the need of the hour to look for alternative strategy for prevention and treatment of metabolic syndrome. Marine natural products are a source of antihypertensive, antihyperglycemic, antioxidative, and anticancer agents possibly useful in the treatment or in the prevention of metabolic disorders. Through this review we have made an effort to throw some light on potential uses of the marine sea weed, a genus of brown algae Turbinaria (Phaeophyceae) as a potential agent for the treatment and amelioration of metabolic syndrome and related disorder, we have briefed about various chemical constituents found in the different species of Turbinaria and the role they can play in achieving the above said goal.