Molecular Aspects of Medicine最新文献

Over the past two decades, advances in cancer therapy have significantly improved survival rates, particularly in childhood cancers. Still, many treatments pose a substantial risk for diminishing future fertility potential due to the gonadotoxic nature of many cancer regimens, justifying fertility preservation programs for both childhood and adult cancer patients. To assure a balance between offering fertility preservation and actual chance of infertility post-treatment, guidelines are in place. However, assessing the actual risk of infertility after treatment remains challenging, given the multi-faceted approach of many cancer treatment plans, which are continuously evolving. This review discusses the evolution of cancer therapy over the past 20 years and attempts to assess their impact on fertility after treatment. Overall, cancer regimens have shifted from broadly killing fast dividing cells to more targeting therapies, reducing collateral damage in general. Although progress has been made to reduce overall toxicity, unfortunately this does not automatically translate to reduced gonadotoxicity. Therefore, current fertility preservation programs continue to be an important part of cancer care.

Cancer cachexia is the prototypical example of comorbidity, occurring in most of cancer patients. It is a direct consequence of tumor growth and of the associated inflammatory/immune response. Cachexia can be exacerbated by anti-cancer therapies, frequently resulting in dose limitation and/or treatment delay or discontinuation. The pathogenesis of cancer cachexia is still unclear and includes nutritional, metabolic, hormonal and immunological components.

Tumor ability to shape the immune response to its own advantage is now well accepted, while the possibility that such an altered immune response could play a role in the onset of cachexia is still an undefined issue. Indeed, most of the immune-related research on cachexia mainly focused on pro-inflammatory mediators, almost totally disregarding the interactions among immune cells and the homeostasis of peripheral tissues. The present review provides an overview of the immune system dysregulations occurring in cancer cachexia, focusing on the possibility that immunomodulating strategies, mainly developed to stimulate the anti-cancer immune response, could be useful to counteract cachexia as well.

Cancer and cachexia are frequent comorbidities of aging. Along this line, cancer- and aging-associated muscle wasting likely coexist in the same patients. Since both conditions share some of the underlying mechanisms, the potential effectiveness of immunomodulation on sarcopenia of aging is discussed.

The vaginal microbiome is an important aspect of women's health that changes dynamically with various stages of the woman's life. Just like the gut microbiome, the vaginal microbiome can also be affected by pathologies that dramatically change the typical composition of native vaginal microorganisms. However, the mechanism as to how both vaginal endemic and gut endemic opportunistic microbes can express pathogenicity in vaginal polymicrobial biofilms is poorly understood. Quorum sensing is the cellular density-dependent bacterial and fungal communication process in which chemical signaling molecules, known as autoinducers, activate expression for genes responsible for virulence and pathogenicity, such as biofilm formation and virulence factor production. Quorum sensing inhibition, or quorum quenching, has been explored as a potential therapeutic route for both bacterial and fungal infections. By applying these quorum quenchers, one can reduce biofilm formation of opportunistic vaginal microbes and combine them with antibiotics for a synergistic effect. This review aims to display the relationship between the vaginal and gut microbiome, the role of quorum sensing in polymicrobial biofilm formation which cause pathology in the vaginal microbiome, and how quorum quenchers can be utilized to attenuate the severity of bacterial and fungal infections.