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Cutaneous Squamous Cell Carcinoma (cSCC) is a common and potentially fatal type of skin cancer that poses a significant threat to public health and has a high prevalence rate. Exposure to ultraviolet radiation on the skin surface increases the risk of cSCC, especially in those with genetic syndromes like xerodermapigmentosum and epidermolysis bullosa. Therefore, understanding the molecular pathogenesis of cSCC is critical for developing personalized treatment approaches that are effective in cSCC. This article provides a comprehensive overview of current knowledge of cSCC pathogenesis, emphasizing dysregulated signaling pathways and the significance of molecular profiling. Several limitations and challenges associated with conventional therapies, however, are identified, stressing the need for novel therapeutic strategies. The article further discusses molecular targets and therapeutic approaches, i.e., epidermal growth factor receptor inhibitors, hedgehog pathway inhibitors, and PI3K/AKT/mTOR pathway inhibitors, as well as emerging molecular targets and therapeutic agents. The manuscript explores resistance mechanisms to molecularly targeted therapies and proposes methods to overcome them, including combination strategies, rational design, and optimization. The clinical implications and patient outcomes of molecular-targeted treatments are assessed, including response rates and survival outcomes. The management of adverse events and toxicities in molecular-targeted therapies is crucial and requires careful monitoring and control. The paper further discusses future directions for therapeutic advancement and research in this area, as well as the difficulties and constraints associated with conventional therapies., Competing Interests: The authors declare no conflict of interest., (Copyright © 2024 Singh et al.)

Amyloidosis is a protein deposition disorder in which insoluble fibril structures accumulate in the bodily tissues damaging the organ function. Cardiac amyloidosis is a severe but under-reported medical condition characterized by the accumulation of amyloid in the extracellular area of the myocardium, which results in thickening and stiffening of ventricular walls. Cardiac amyloidosis has recently gained much attention with its slowly surging incidence. With this study, we seek to comprehensively compile the pathophysiology and clinical picture of cardiac amyloidosis subtypes, extending a clinically oriented, up-to-date clinical approach to diagnosis and therapy. Cardiac amyloidosis can be caused by rare genetic mutations which may be inherited or acquired. The growing incidence can be attributed to advancements in imaging methods and other diagnostic modalities. Most occurrences of cardiac amyloidosis result from two forms of precursor protein: transthyretin [TTR] amyloid and immunoglobulin-derived light-chain amyloid. Prompt identification of cardiac amyloidosis can facilitate the implementation of evolving therapeutic interventions to enhance the outcomes. The modalities for the management of CA have evolved significantly in the last ten years. Apart from therapies for modifying disease and heart failure, a myriad of novel therapeutic approaches that target specific aspects of the disease, including gene therapies, are being researched. These aim at impeding its progression and improving clinical outcomes. See also Figure 1(Fig. 1)., Competing Interests: The authors declare no conflict of interest. There are no relevant financial or non-financial competing interests to report., (Copyright © 2023 Medarametla et al.)

The severe acute respiratory syndrome (SARS-CoV, now SARS-CoV-1), middle east respiratory syndrome (MERS-CoV), Neo-CoV, and 2019 novel coronavirus (SARS-CoV-2/COVID-19) are the most notable coronaviruses, infecting the number of people worldwide by targeting the respiratory system. All these viruses are of zoonotic origin, predominantly from bats which are one of the natural reservoir hosts for coronaviruses. Thus, the major goal of our review article is to compare and contrast the characteristics and attributes of these coronaviruses. The SARS-CoV-1, MERS-CoV, and COVID-19 have many viral similarities due to their classification, they are not genetically related. COVID-19 shares approximately 79 % of its genome with SARS-CoV-1 and about 50 % with MERS-CoV. The shared receptor protein, ACE2 exhibit the most striking genetic similarities between SARS-CoV-1 and SARS-CoV-2. SARS-CoV primarily replicates in the epithelial cells of the respiratory system, but it may also affect macrophages, monocytes, activated T cells, and dendritic cells. MERS-CoV not only infects and replicates inside the epithelial and immune cells, but it may lyse them too, which is one of the common reasons for MERS's higher mortality rate. The details of infections caused by SARS-CoV-2 and lytic replication mechanisms in host cells are currently mysterious. In this review article, we will discuss the comparative highlights of SARS-CoV-1, MERS-CoV, SARS-CoV-2, and Neo-CoV, concerning their structural features, morphological characteristics, sources of virus origin and their evolutionary transitions, infection mechanism, computational study approaches, pathogenesis and their severity towards several diseases, possible therapeutic approaches, and preventive measures., (Copyright © 2022 Goyal et al.)