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Cover: The cover image is based on the Review Article MicroRNAs in cancer drug resistance: Basic evidence and clinical applications by Mehri Ghasabi et al., DOI: 10.1002/jcp.26810. [ABSTRACT FROM AUTHOR]

Cytokines bind to specific receptors on target cells to activate intracellular signaling pathways that control diverse cellular functions, such as proliferation, differentiation, migration, and death. They are essential for the growth, activation, and operation of immune cells and the control of immunological reactions to pathogens, cancer cells, and other dangers. Based on their structural and functional properties, cytokines can be roughly categorized into different families, such as the tumor necrosis factor (TNF) family, interleukins, interferons, and chemokines. Leukocytes produce interleukins, a class of cytokines that have essential functions in coordinating and communicating with immune cells. Cancer, inflammation, and autoimmunity are immune-related disorders brought on by dysregulation of cytokine production or signaling. Understanding cytokines' biology to create novel diagnostic, prognostic, and therapeutic methods for various immune-related illnesses is crucial. Different immune cells, including T cells, B cells, macrophages, and dendritic cells, and other cells in the body, including epithelial cells and fibroblasts, generate and secrete interleukins. The present study's main aim is to fully understand interleukins' roles in cancer development and identify new therapeutic targets and strategies for cancer treatment., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier GmbH.)

In the past fifteen years, it has been clear that tumor-associated p53 mutations can cause behaviors distinct from those brought on by a simple loss of p53's tumor-suppressive function in its wild-type form. Many of these mutant p53 proteins develop oncogenic characteristics that allow them to encourage cell survival, invasion, and metastasis. But it is now understood that the immune response is also significantly influenced by the cancer cell's p53 status. The recruitment and activity of myeloid and T cells can be impacted by p53 loss or mutation in malignancies, allowing immune evasion and accelerating cancer growth. Additionally, p53 can work in immune cells, which can have various effects that either hinder or assist the growth of tumors. In this review article, we examined different mutations of P53 in some significant cancers, such as liver, colorectal, and prostate, and reviewed some new therapeutic approaches., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Neoplasms are a worldwide recognized non-contagious disease which has the most mortality rate after cardiovascular diseases. For decades, there has been a vast amount of study on treatment methods of cancer which has led to conventional therapies such as chemotherapy, radiation therapy, surgery and so on. Clinicians and researchers believed that there is an urgent need, considering the high rate of incidence and prevalence, for an alternative treatment option which is more efficacious and has less adverse effects than the above-mentioned treatments. Immunotherapy has emerged as a potential treatment alternative in a few years and became one of the fastest developing therapeutic approaches. Different kinds of immunotherapies are FDA approved and available for treatment of various cancer types. In this review, we have summarized the major immunotherapy methods including checkpoint inhibitors, CAR T cell therapies and cancer vaccines. Furthermore, application of combination therapy, precision medicine, biomarker discovery, overcoming resistance and reduction of adverse effects are discussed in this study., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

One of the most prevalent cancers impacting women worldwide is breast cancer. Although there are several risk factors for breast cancer, the p53 gene's function has recently received much attention. The "gatekeeper" gene, or p53, is sometimes referred to as such since it is crucial in controlling cell proliferation and preventing the development of malignant cells. By identifying DNA damage and initiating cellular repair processes, p53 usually functions as a tumor-suppressor. But p53 gene alterations can result in a lack of function, allowing cells to divide out of control and perhaps triggering the onset of cancer. Various factors, such as mutation genes, signaling pathways, and hormones, can dysregulate P53 proteins and cause breast cancer. A promising strategy for individualized cancer treatment involves focusing on p53 mutations in breast cancer. While numerous techniques, including gene therapy and small compounds, have shown promise, further study is required to create safe and efficient treatments to target p53 mutations in breast cancer successfully., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Sericin protein is a type of protein derived from silk cocoons. Sericin hydrogen bonds cause adhesion to the silk cocoon. This substance contains a large amount of serine amino acids in its structure. At first, the medicinal properties of this substance were unknown, but today many properties have been discovered for this substance. The unique properties of this substance have made it widely used in the pharmaceutical and cosmetic industries. The applications of Sericin in pharmacy are as follows. Sericin is used to repair wounds by producing collagen. Other uses for the drug include anti-diabetic, anti-cholesterol, metabolic modulator, anti-tumor, heart protection, antioxidant, antibacterial, wound healing, cell proliferation, UV protection, freezing, and skin moisturizing. The physicochemical properties of Sericin have attracted the attention of pharmacists and their widespread use in the production of drugs and treatment of diseases. One of the critical and unique properties of Sericin is its anti-inflammatory property. In this article, this property of Sericin is discussed in detail, and according to the experiments performed by pharmacists, this substance has shown a significant effect in eliminating inflammation. This study aimed to evaluate the impact of Sericin protein in relieving inflammation., Competing Interests: Conflict of interest None., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Blood disorders include a wide spectrum of blood-associated malignancies resulting from inherited or acquired defects. The ineffectiveness of existing therapies against blood disorders arises from different reasons, one of which is drug resistance, so different types of leukemia may show different responses to treatment. Leukemia occurs for a variety of genetic and acquired reasons, leading to uncontrolled proliferation in one or more cell lines. Regarding the genetic defects, oncogene signal transducer and activator of transcription (STAT) family transcription factor, especially STAT3, play an essential role in hematological disorders onset and progress upon mutations, dysfunction, or hyperactivity. Besides, microRNAs, as biological molecules, has been shown to play a dual role in either tumorigenesis and tumor suppression in various cancers. Besides, a strong association between STAT3 and miRNA has been reported. For example, miRNAs can regulate STAT3 via targeting its upstream mediators such as IL6, IL9, and JAKs or directly binding to the STAT3 gene. On the other hand, STAT3 can regulate miRNAs. In this review study, we aimed to determine the role of either microRNAs and STAT3 along with their effect on one another's activity and function in hematological malignancies., Competing Interests: Authors declare no conflict of interests., (© 2021 Chongqing Medical University. Production and hosting by Elsevier B.V.)

microRNAs (miRs) are short noncoding RNAs that post-transcriptionally suppress gene expression. miR-146a acts as an oncogene or a tumor suppressor in various cancers, including gastric cancer, but it is unclear what determines whether miR-146a is oncogenic or tumor suppressive and the molecular mechanisms are still largely unknown. The aim of this study was to investigate the role of miR-146a in gastric cancer, by focusing on its expression in patients who were negative for Helicobacter pylori and its reduced and increased expression effect in vitro. Twenty gastric cancer patients who were negative for H. pylori infection were selected and the expression levels of miRNA-146a in these gastric tumors, in their matched normal gastric tissues and in gastric cancer cell lines with varying tumorigenic potential was measured. Further, the impact of increased and decreased miR-146a expression levels on the expression of predicted target genes, cell migration, viability, proliferation, and apoptosis was examined, respectively. Our results for the first time indicated that miR-146a is downregulated in H. pylori-negative gastric cancers and suggests that H. pylori infection determines whether miR-146a acts as an oncogene or tumor suppressor. The level of miR-146a expression inversely correlates with the tumorigenicity of three gastric cancer cell lines and low miR-146a expression predicts poor recurrence-free survival. It was also found that miR-146a reduces the expression levels of the prometastatic genes and suppresses MKN-45 cell migration. Functional studies showed that miR-146a acts as a tumor suppressor miR and identifies miR-146a as a candidate for antimetastatic miRNA replacement therapy for gastric cancer patients., (© 2018 Wiley Periodicals, Inc.)

Development of drug resistance has considerably limited the efficacy of cancer treatments, including chemotherapy and targeted therapies. Hence, understanding the molecular mechanisms underpinning the innate or the acquired resistance to these therapies is critical to improve drug efficiency and clinical outcomes. Several studies have implicated microRNAs (miRNA) in this process. MiRNAs repress gene expression by specific binding to complementary sequences in the 3' region of target messenger RNAs (mRNAs), followed by target mRNA degradation or blocked translation. By targeting molecules specific to a particular pathway within tumor cells, the new generation of cancer treatment strategies has shown significant advantages over conventional chemotherapy. However, the long-term efficacy of targeted therapies often remains poor, because tumor cells develop resistance to such therapeutics. Targeted therapies often involve monoclonal antibodies (mAbs), such as those blocking the ErB/HER tyrosine kinases, epidermal growth factor receptor (cetuximab) and HER2 (trastuzumab), and those inhibiting vascular endothelial growth factor receptor signaling (e.g., bevacizumab). Even though these are among the most used agents in tumor medicine, clinical response to these drugs is reduced due to the emergence of drug resistance as a result of toxic effects in the tumor microenvironment. Research on different types of human cancers has revealed that aberrant expression of miRNAs promotes resistance to the aforementioned drugs. In this study, we review the mechanisms of tumor cell resistance to mAb therapies and the role of miRNAs therein. Emerging treatment strategies combine therapies using innovative miRNA mimics or antagonizers with conventional approaches to maximize outcomes of patients with cancer., (© 2018 Wiley Periodicals, Inc.)