ABSTRACT
Single nucleotide polymorphism of brain derived neurotropic factor gene, also known as Val66Met or rs6562, wasfound to be linked to obesity. However, reports on the link between this gene variant and obesity in Caucasian andAsian populations are inconsistent. A meta-analysis was, therefore, performed to determine the association betweenVal66Met polymorphism and the risk of obesity. Electronic databases, including Embase, CINAHL, and PubMed,were searched for relevant studies published before November 2018. Random effects model was used to calculatethe pooled estimate based on the heterogeneity test results. Data were obtained from 11 studies involving 13,153individuals with obesity and 18,689 non-obese individuals. The overall estimated odds ratio did not support theproposed association (OR 0.9, 95% CI 0.793–1.136). Stratified analysis, however, showed that Val/Val genotype isassociated with increased risk of obesity among adults (OR 1.135, 95% CI 1.001–1.286) but associated with a reducedrisk among adolescents (OR 0.61, 95% CI = 0.376, 0.984). The results highlight the role of confounding factors thatneed to be addressed when making inference
ABSTRACT
Cancer is fundamentally a cellular genetic disease capable of transferring the "disease" to the next generation of mutated cells. Similar proliferative and information transferring capacity exists in the stem cells of various organ systems in the human body. Understanding the bio-mechanism of stem cell metabolism and its regulation by signaling molecules and extracellular micro-environment is an important step toward successful prevention and treatment of cancer. According to the cancer stem cell hypothesis, both hereditary and sporadic cancers can arise from deregulation of these cancer stem cells (CSCs), triggered by genetic and environmental factors. It is shown that deregulation of normal self-renewal pathways in undifferentiated breast stem cells or progenitor cells had altered mammary system or progenitor cells, resulting in abnormally differentiated cells in human and rodent breast cancer cell lines. Breakthroughs in molecular pathways have important therapeutic implications. Hence, significant stress is laid on targeting signaling molecules and their micromilieu in breast cancer therapy.