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Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway is a common signaling pathway used to transduce signals from the extracellular to the intracellular (nucleus) upon the binding of cytokines and growth factors to the extracellular domain of specific cell surface receptors. This signaling pathway is tightly regulated and has a multitude of biological functions such as cell proliferation, differentiation, and apoptosis. Besides, the regulated JAK2/STAT3 signaling plays a crucial role in embryonic development, hemopoiesis, and controlling the immune system. Conversely, aberrantly activated JAK2/STAT3 is frequently detected in varieties of tumors and involved in oncogenesis, angiogenesis, and metastasis of many cancer diseases that are usually refractory to the standard chemotherapy. However, the JAK3/STAT3 pathway recently emerged interestingly as a new site for the development of novel anti-tumor agents and becomes a promising therapeutic target in the treatment of many solid malignancies. Herein, this review aimed to provide insight into the JAK2/STAT3 pathway, in the hope to gain an understanding of its potential role in the pathogenesis, progression, chemotherapy resistance, and cancer therapy of solid tumors.

Since the emergence of COVID 19, the authentic SARS-CoV-2 has evolved into a range of novel variants that are of more global concern. In late November 2021, the Omicron (lineage B.1.1.529) variant was identified as a new variant and considered as the fifth variant of concern. Omicron harbors a genetic profile that is exceedingly unusual, with a huge number of mutations. Above thirty mutations are localized in the S protein, while some are found in other structural and non-structural proteins. Half of the mutations in the S protein are in the RBD, which is a major target of antibodies, showing that Omicron mutations may affect antibody binding affinity to the S protein. The Omicron variant has been found to result in immune escape, therapeutic or vaccine escape, as well as increased transmissibility and reinfection risk, explaining its rapid international spread that sparks a global alarm even more serious than the previously reported variants. Omicron has the capability to bypass at least some of the multi-faceted immune responses induced by prior infection or vaccination. It is shown to extensively escape neutralizing antibodies while evading cell mediated immune defense to a lesser extent. The efficacy of COVID 19 vaccines against Omicron variant is decreased with primary vaccination, showing that the vaccine is less efficient in preventing Omicron infections. However, after receiving a booster vaccine dose, the immunological response to Omicron significantly improved and hold promising results. Despite the mild nature of the disease in most vaccinated people, the rapid spread of Omicron, as well as the increased risk of re-infection, poses yet another major public health concern. Therefore, effort should be devoted to maintaining the existing COVID 19 preventive measures as well as developing new vaccination strategies in order to control the fast dissemination of Omicron.

Fetuin-A is a heterodimeric plasma glycoprotein containing an A-chain of 282 amino acids and a B-chain of 27 amino acid residues linked by a single inter-disulfide bond. It is predominantly expressed in embryonic cells and adult hepatocytes, and to a lesser extent in adipocytes and monocytes. Fetuin-A binds with a plethora of receptors and exhibits multifaceted physiological and pathological functions. It is involved in the regulation of calcium metabolism, osteogenesis, and the insulin signaling pathway. It also acts as an ectopic calcification inhibitor, protease inhibitor, inflammatory mediator, anti-inflammatory partner, atherogenic factor, and adipogenic factor, among other several moonlighting functions. Fetuin-A has also been demonstrated to play a crucial role in the pathogenesis of several disorders. This review mainly focuses on the structure, synthesis, and biological roles of fetuin-A. Information was gathered manually from various journals via electronic searches using PubMed, Google Scholar, HINARI, and Cochrane Library from inception to 2022. Studies written in English and cohort, case-control, cross-sectional, or experimental studies were considered in the review, otherwise excluded.

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