In-Silico CLEC5A mRNA expression analysis to predict Dengue susceptibility in cancer patients.

Dengue fever is the fastest-growing infectious disease in the world. It is the leading vector-borne viral neglected tropical disease. The most acute immune response to dengue virus infection is dengue shock syndrome and hemorrhagic fever, which is due to the activation of CLEC5A C-type lectin domain family 5, member A (CLEC5A). It is a cell surface receptor, and its well-known ligand is the dengue virus. It gets activated by the attachment of dengue virion, which, as a result, phosphorylates its adaptor protein DAP12 leading to the induction of various pro-inflammatory cytokines. Clinical data suggested that the kidneys and lungs are among the major hit organs in the case of severe dengue infection. Here we predict kidney and lung cancer patients are vulnerable to dengue virus infection as CLEC5A mRNA expression in tumor samples using publicly available software such as TIMER and GEPIA database. We also identified the immunomodulatory role CLEC5A gene therefore targeting it could be a vital tool to cure dengue.

Prognostic value of circulating mitochondrial DNA in prostate cancer and underlying mechanism.

Circulating DNAs are considered as degraded DNA fragments of approximately 50-200 bp, found in blood plasma, consisting of cell-free mitochondrial and nuclear DNA. Such cell-free DNAs in the blood are found to be altered in different pathological conditions including lupus, heart disease, and malignancies. While nuclear DNAs are being used and being developed as a powerful clinical biomarker in liquid biopsies, mitochondrial DNAs (mtDNAs) are associated with inflammatory conditions including cancer progression. Patients with cancer including prostate cancer are found to have measurable concentrations of mitochondrial DNA in circulation in comparison with healthy controls. The plasma content of mitochondrial DNA is dramatically elevated in both prostate cancer patients and mouse models treated with the chemotherapeutic drug. Cell-free mtDNA, in its oxidized form, induced a pro-inflammatory condition and activates NLRP3-mediated inflammasome formation which causes IL-1ß-mediated activation of growth factors. On the other hand, interacting with TLR9, mtDNAs trigger NF-κB-mediated complement C3a positive feedback paracrine loop and activate pro-proliferating signaling through upregulating AKT, ERK, and Bcl2 in the prostate tumor microenvironment. In this review, we discuss the growing evidence supporting cell-free mitochondrial DNA copy number, size, and mutations in mtDNA genes as potential prognostic biomarkers in different cancers and targetable prostate cancer therapeutic candidates impacting stromal-epithelial interactions essential for chemotherapy response.

In silico prediction of COVID-19 cytokine storm in lung cancer types.

Lung cancer is one of the most frequently diagnosed malignant tumors and the leading cause of cancer-related death worldwide. Mainly, Non-small-cell lung cancer (NSCLC), which accounts for more than eighty-five percent of all lung cancers, consists of two major subtypes: lung adenocarcinoma (LUAD) and squamous cell carcinoma (LUSC). Novel coronavirus disease (COVID-19) affected millions of people caused by acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) around the globe. Lung cancer patients and COVID-19 present unique and unfortunate lethal combinations because the lungs are the primary target organ of SARS-CoV-2 infection. Clinical studies have demonstrated that an over-activated inflammatory response associated with severe COVID-19 cases is characterized by excessive auto-amplifying cytokine release, which is defined as a "cytokine storm." ACE2 and TMPRSS2 receptors play an essential role in SARS-CoV-2 infection; therefore, using in silico analysis, we did correlation analysis with immune infiltration markers in LUAD and LUSC patient groups. Our study identified a promising correlation between immune-modulators and receptor proteins (ACE-2 and TMPRSS2), creating a domain that requires further laboratory studies for clinical authentication.

Harnessing the role of epigenetic histone modification in targeting head and neck squamous cell carcinoma.

Head and neck squamous cell carcinoma (HNSCC) is the sixth most prevalent form of cancer worldwide. Despite advancements made in treatment strategies, the fatality rate of HNSCC is very high. An accumulating body of evidence suggests that epigenetic modification of histones plays an influential role in the development and progression of the disease. In this review we discuss the role of epigenetic modifications in HNSCC and the inter-relationships of human papillomavirus oncoproteins and histone-modifying agents. Further, we explore the possibility of identifying these modifications as biomarkers for their use as drugs in treatment strategies.

Head and neck squamous cell carcinoma (HNSCC) is the most common kind of head and neck cancer. HNSCC can develop therapeutic resistance, making therapy more difficult. Many studies have found that epigenetic events play a key role in HNSCC. Better understanding epigenetic regulation could help discovery of biomarkers that help detect and diagnose HNSCC. This review will present recent studies, showing the importance of epigenetic regulation targeting histone modifications in the development of HNSCC.

Cancer Nanotechnology in Medicine: A Promising Approach for Cancer Detection and Diagnosis.

Despite extraordinary advances that have been made in cancer therapy, the number of cancer cases continue to surge, making it the leading cause of death across the world. As a result, early detection is one of the key aspects in the battle against the disease. Screening and early diagnosis play a pivotal role for effective treatment and to lower the cancer mortality rate. Cancer nanotechnology is a new branch in biology that provides a link between nanotechnology and clinical cancer research. Moreover, it also aims to integrate the advancements made in the manufacture of nanoscale devices with cellular and molecular components associated with cancer diagnosis and therapy. Understanding these new technologies is crucial to integrating these practices into clinical settings. This novel approach has facilitated the conjugation of nanoscale devices with agents such as tumor-specific li-gands, antibodies, and imaging probes. This review summarizes the advancements made in nanotechnology based approaches in diagnosing cancer. Coupling of nanoparticles with targeting molecules enables an efficient interaction between biological systems with extraordinary accuracy. The progress associated with nanoscale devices such as metal based nanomaterials, exosomes, magnetic nanoparticles, in addition to quantum dots and lab on chip devices with regard to diagnostic applications has been discussed. We summarize how nanoparticles take advantage of the tumor microenvironment for targeting cancer cells. Further, the review outlines the drawbacks, challenges, and future prospects associated with these techniques as effective strategies to replace current clinical trends.

Epigenetic changes in fibroblasts drive cancer metabolism and differentiation.

Genomic changes that drive cancer initiation and progression contribute to the co-evolution of the adjacent stroma. The nature of the stromal reprogramming involves differential DNA methylation patterns and levels that change in response to the tumor and systemic therapeutic intervention. Epigenetic reprogramming in carcinoma-associated fibroblasts are robust biomarkers for cancer progression and have a transcriptional impact that support cancer epithelial progression in a paracrine manner. For prostate cancer, promoter hypermethylation and silencing of the RasGAP, RASAL3 that resulted in the activation of Ras signaling in carcinoma-associated fibroblasts. Stromal Ras activity initiated a process of macropinocytosis that provided prostate cancer epithelia with abundant glutamine for metabolic conversion to fuel its proliferation and a signal to transdifferentiate into a neuroendocrine phenotype. This epigenetic oncogenic metabolic/signaling axis seemed to be further potentiated by androgen receptor signaling antagonists and contributed to therapeutic resistance. Intervention of stromal signaling may complement conventional therapies targeting the cancer cell.