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The global pandemic caused by COVID-19 has caused more than 1 million deaths worldwide. Some vaccines in clinical trials have reached stage 3. In the meantime, the understanding of the biological and pathophysiological mechanisms of Sars-CoV2 infection is still unclear, such as the role that ACE-2 and DPP-IV may play in patients with diabetes related to COVID-19. The individual with diabetes is a known COVID-19 risk patient. Probably the pharmacological regulation of the RAS system and of ACE-2 on the one hand, and of the incretin system and DPP-IV on the other, could represent a therapeutic route of fundamental importance to reduce the risk of Sars-CoV-2 infection or of serious complications caused by infection.

Cancer patients are more susceptible to COVID-19; however, the prevalence of COVID-19 in different types of cancer is still inconsistent and inconclusive. Here, we delineate the intricate relationship between breast cancer and COVID-19. Breast cancer and COVID-19 share the involvement of common comorbidities, hormonal signalling pathways, gender differences, rennin- angiotensin system (RAS), angiotensin-converting enzyme-2 (ACE-2), transmembrane protease serine 2 (TMPRSS2) and dipeptidyl peptidase-IV (DPP-IV). We also shed light on the possible effects of therapeutic modalities of COVID-19 on breast cancer outcomes. Briefly, we conclude that breast cancer patients are more susceptible to COVID-19 in comparison with their normal counterparts. Women are more resistant to the occurrence and severity of COVID-19. Increased expressions of ACE2 and TMPRSS2 are correlated with occurrence and severity of COVID-19, but higher expression of ACE2 and lower expression of TMPRSS2 are prognostic markers for overall disease free survival in breast cancer. The ACE2 inhibitors and ibuprofen therapies for COVID-19 treatment may aggravate the clinical condition of breast cancer patients through chemo-resistance and metastasis. Most of the available therapeutic modalities for COVID-19 were also found to exert positive effects on breast cancer outcomes. Besides drugs in clinical trend, TMPRSS2 inhibitors, estrogen supplementation, androgen deprivation and DPP-IV inhibitors may also be used to treat breast cancer patients infected with SARS-CoV-2. However, drug-drug interactions suggest that some of the drugs used for the treatment of COVID-19 may modulate the drug metabolism of anticancer therapies which may lead to adverse drug reaction events., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Female breast cancer recently surpassed lung cancer and became the most commonly diagnosed cancer worldwide. As per the recent data from WHO, breast cancer accounts for one out of every 8 cancer cases diagnosed among an estimated 2.3 million new cancer cases. Breast cancer is the most prevailing cancer type among women causing the highest number of cancer-related mortality. It has been estimated that in 2020, 68,5000 women died due to this disease. Breast cancers have varying degrees of molecular heterogeneity; therefore, they are divided into various molecular clinical sub types. Recent reports suggest that type 2 diabetes (one of the common chronic diseases worldwide) is linked to the higher incidence, accelerated progression, and aggressiveness of different cancers; especially breast cancer. Breast cancer is hormone-dependent in nature and has a cross-talk with metabolism. A number of antidiabetic therapies are known to exert beneficial effects on various types of cancers, including breast cancer. However, only a few reports are available on the role of incretin-based antidiabetic therapies in cancer as a whole and in breast cancer in particular. The present review sheds light on the potential of incretin based therapies on breast cancer and explores the plausible underlying mechanisms. Additionally, we have also discussed the sub types of breast cancer as well as the intricate relationship between diabetes and breast cancer., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)