Objective: Cyclin D1 is an essential protein that acts as a mitogenic sensor. In this manuscript, we discuss the importance of cyclin D1 in oncology and cardio-oncology, and we challenge the prognostic and therapeutic response values of cyclin D1 to figure out if it can be a beneficial marker. We also discuss the agents and microRNAs that can be used as a potential therapeutic approach via regulating cyclin D1 expression in oncology and cardio-oncology. Discussion: Clinical significance of cyclin D1 is defined not only in several cancers such as breast cancer, melanoma, and glioblastoma but also in cardiomyocyte regeneration and cardiac hypertrophic growth. Several studies have indicated that the injection of cardiotoxic agents such as doxorubicin (DOX) induces damage to the cardiac system and increases cyclin D expression at single injection, which might be related to DXO-mediated damage in the adult heart. However, cyclin D1 overexpression leads to hypertrophic growth of cardiomyocytes, and cyclin-dependent kinase (CDK)) inhibitors such as p16 do not inhibit the hypertrophic growth of cardiomyocytes. Thus, the reaction is CDK-independent. Conclusions: Cyclin D1 overexpression is positively correlated with tumor progression, treatment response, cardiotoxicity, and poor prognosis. Cyclin D1 expression has an important role in cardiac hypertrophy, and it can be a promising marker in monitoring cardiomyocyte treatment responses, cardioprotection, and cardiotoxicity. Finally, cyclin D1 plays an important role in hypertrophic growth of cardiomyocytes via a novel mechanism. Given all these pieces of evidence, cyclin D1 can be introduced as a favorable biomarker in future cardiology and cardio-oncology.

Inflammatory cytokines exert different effects on hematopoietic stem cells (HSCs), lead to the development of various cell lineages in bone marrow (BM) and are thus a differentiation axis for HSCs. The content used in this article has been obtained by searching PubMed database and Google Scholar search engine of English‐language articles (1995–2020) using “Hematopoietic stem cell,” “Inflammatory cytokine,” “Homeostasis,” and “Myelopoiesis.” Inflammatory cytokines are involved in the differentiation and proliferation of hematopoietic progenitors to compensate for cellular death due to inflammation. Since each of these cytokines differentiates HSCs into a specific cell line, the difference in the effect of these cytokines on the fate of HSC progenitors can be predicted. Inhibitors of these cytokines can also control the inflammatory process as well as the cells involved in leukemic conditions. In general, inflammatory signaling can specify the dominant cell line in BM to counteract inflammation and leukemic condition via stimulating or inhibiting hematopoietic progenitors. Therefore, detection of the effects of inflammatory cytokines on the differentiation of HSCs can be an appropriate approach to check inflammatory and leukemic conditions and the suppression of these cytokines by their inhibitors allows for control of homeostasis in stressful conditions.

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