Microbiome dysbiosis in cancer: Exploring therapeutic strategies to counter the disease.

Cancer being a multiplex disease which involves many genomic and physiological alterations that occur consistently in the cancerous tissue, making the treatment and management of the disease even more complicated. The human gut microbiota (GM) harbors collective genomes of microbes comprising of trillions of bacteria along with fungi, archaea, and viruses that have the tendency to affect the development and progression of cancer. Moreover, inter-microbial interactions, diversity and distinct differences among the GM populations could influence the course of disease, making the microbiome an ideal target or to be modulated in such a way so as to improve cancer therapeutics with better efficacy and reduced toxicity. Current review focuses upon exploring the association of gut microbiota with the progression of cancer for which a structured search of bibliographic databases for peer-reviewed research literature has been carried out using focused review questions and inclusion/exclusion criteria. Through this review one could envisage a wide-spectrum role of microbiota in maintaining host metabolism, immune homeostasis paving the way for an anticancer diagnostic and therapeutic solution that has the potential to counter the menace of anti-cancer drug resistance as well.

PI3K/Akt/mTOR Intracellular Pathway and Breast Cancer: Factors, Mechanism and Regulation.

BACKGROUND: The most recurrent and considered second most frequent cause of cancer-related deaths worldwide in women is the breast cancer. The key to diagnosis is early prediction and a curable stage but still treatment remains a great clinical challenge. Origin of the Problem: A number of studies have been carried out for the treatment of breast cancer which includes the targeted therapies and increased survival rates in women. Essential PI3K/mTOR signaling pathway activation has been observed in most breast cancers. The cell growth and tumor development in such cases involve phosphoinositide 3 kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) complex intracellular pathway. HYPOTHESIS: Through preclinical and clinical trials, it has been observed that there are a number of other inhibitors of PI3K/Akt/mTOR pathway, which either alone or in combination with cytotoxic agents can be used for endocrine therapies. CONCLUSION: Structure and regulation/deregulation of mTOR provides a greater insight into the action mechanism. Also, through this review, one could easily scan first and second generation inhibitors for PI3K/Akt/mTOR pathway besides targeted therapies for breast cancer and the precise role of mTOR.