Priyajeet S. Parekh

Background: Ulcerative colitis (UC) is a subtype of inflammatory bowel disease (IBD), characterized by chronic and recurrent inflammation of the colonic tract. This condition is marked by dysregulated immune responses, leading to sustained intestinal inflammation. Despite the efficacy of current treatments, there remains a critical need for more targeted and effective interventions. Main text: Immunotherapy, which involves modulating the immune system to treat diseases, has emerged as a promising strategy for managing UC. Both innate and adaptive immunotherapies have shown considerable potential in treating colitis. Innate immunotherapies target the body’s first line of defense, offering an appealing option for colitis treatment by addressing components like macrophages and dendritic cells. Conversely, adaptive immunotherapies focus on specific immune cell subsets, such as T-cells, which are crucial in the pathogenesis of colitis. These therapies aim to modulate the abnormal immune response to reduce immuno-inflammation. Various forms of immunotherapies, including monoclonal antibodies, small molecules, and cellular therapies, have been extensively studied for their effectiveness in treating colitis and shown encouraging results. Monoclonal antibodies have been particularly promising, offering targeted action against specific components of the immune response. Small molecule therapies provide another avenue by modulating signaling pathways involved in inflammation. Cellular therapies, including stem cell treatments, represent an innovative approach, potentially offering long-term benefits by repairing damaged tissues and restoring immune balance. Conclusion: This review offers a comprehensive overview of the current landscape of innate and adaptive immunotherapies for the treatment of UC. It details their mechanisms of action, potential benefits, and limitations. Overall, the significant promise of these therapies in combating colitis is underscored, highlighting their continued development and utilization in UC treatment. The potential of combining innate and adaptive immunotherapies could represent a dynamic duo in treating this debilitating condition, ultimately improving patient outcomes and quality of life. Graphical

Colorectal cancer (CRC) ranks among the leading causes of cancer‐related morbidity and mortality worldwide. Despite progress in understanding its molecular intricacies, the management of CRC, especially in advanced stages, remains a significant clinical hurdle. This review delves into the evolving landscape of stem cell‐based therapeutic strategies in CRC, with a specific focus on the interplay between cancer stem cells (CSCs) and CRC pathogenesis and treatment resistance. Highlighting the pivotal roles of CSCs in tumor initiation, progression, metastasis, and recurrence, the review comprehensively examines their involvement in CRC, ranging from normal colonic tissue to cancer initiation. The potential of stem cells for medicinal purposes in CRC management is explored, encompassing diverse modalities such as transplantation, differentiation therapy, immunotherapy, and gene/cell‐based approaches. Challenges and opportunities associated with these strategies are also evaluated, providing insights into their clinical potential and limitations. The review also appraises preclinical investigations contributing to the understanding of CRC and stem cells. Current clinical trials, patient stratification strategies, and regulatory considerations related to stem cell‐based therapies in CRC are scrutinized. Furthermore, the review explores emerging trends and future directions, including developments in stem cell technologies and ethical considerations. It highlights the transformative potential of stem cell‐based therapeutic strategies in CRC.

Background: Lung adenocarcinoma (LUAD) is one of the main forms of carcinomas that contribute towards cancer-related mortality and morbidity. Identification of hub genes through various in silico approaches can lead to the successful prognosis of LUAD and may serve in reducing mortalities rising from it respectively. Method: This research employs an integrated bioinformatics approach to uncover the molecular intricacies of LUAD. Utilizing the Gene Expression Omnibus (GEO) dataset, we identified GSE19188, GSE18842, GSE31210, and GSE19804 specific datasets from 423 LC tissues and 190 healthy tissues (controls). Differential gene expression analysis using GEO2R and Venn diagrams led to the identification of 851 differentially expressed genes (DEGs), comprising 240 overexpressed and 611 under-expressed genes. To elucidate their roles in LUAD etiology, we conducted protein–protein interaction (PPI) analysis utilizing Cytoscape and Cytohubba software’s, revealing densely interconnected gene clusters with potential prognostic significance. Additionally, gene ontology (GO) enrichment and Kyoto Encyclopaedia of Genes and Genomes (KEGG) analyses were able to shed light on the involvement of these DEGs in processes such as cell cycle modulation and apoptosis, which are crucial in LUAD pathogenesis. Moreover, validation of the hub gene expression and their association with overall survival was performed using the University of Alberta Cancer Research Network (UALCAN) and Human Protein Atlas (HPA) databases, supporting our findings. Results: The identified DEGs, including cyclin-dependent kinase-1 (CDK1), cyclin B2 (CCNB2), cell division cycle 20 (CDC20), BUB1 mitotic checkpoint serine/threonine kinase B (BUB1B), cyclin A2 (CCNA2), discs-large associated protein 5 (DLGAP5), abnormal spindle microtubule assembly (ASPM), arrestin beta 1 (ARRB1), and caveolin-1 (CAV1), may serve as potential biomarkers for LUAD pathogenesis and should be explored further. Conclusion: The present bioinformatics analysis enhances our understanding of molecular mechanisms contributing to LUAD and suggests that the hub genes identified could be promising targets for accurate diagnosis and novel therapeutic strategies in LUAD. Further investigations are necessary to validate and translate these findings into real-world clinical applications, paving the way for more effective treatments and improved outcomes in LUAD patients. Graphical

Nano-encapsulated CRISPR-based genome: Next-generation strategies to optimize delivery - IJCAAP- Print ISSN No: - 2581-5555 Online ISSN No:- 2456-9542 Article DOI No:- 10.18231/j.ijcaap.2024.032, IP International Journal of Comprehensive and Advanced Pharmacology-IP Int J Compr Adv Pharmacol

Biogenic metallic nanoparticles (NPs) have garnered significant attention in recent years due to their unique properties and various applications in different fields. NPs, including gold, silver, zinc oxide, copper, titanium, and magnesium oxide NPs, have attracted considerable interest. Green synthesis approaches, utilizing natural products, offer advantages such as sustainability and environmental friendliness. The theranostics applications of these NPs hold immense significance in the fields of medicine and diagnostics. The review explores intricate cellular uptake pathways, internalization dynamics, reactive oxygen species generation, and ensuing inflammatory responses, shedding light on the intricate mechanisms governing their behaviour at a molecular level. Intriguingly, biogenic metallic NPs exhibit a wide array of applications in medicine, including but not limited to anti-inflammatory, anticancer, anti-diabetic, anti-plasmodial, antiviral properties and radical scavenging efficacy. Their potential in personalized medicine stands out, with a focus on tailoring treatments to individual patients based on these NPs’ unique attributes and targeted delivery capabilities. The article culminates in emphasizing the role of biogenic metallic NPs in shaping the landscape of personalized medicine. Harnessing their unique properties for tailored therapeutics, diagnostics and targeted interventions, these NPs pave the way for a paradigm shift in healthcare, promising enhanced efficacy and reduced adverse effects. Graphical Abstract

Stroke, a neurological disorder, is intricately linked to the gut microbiota, influencing microbial composition and elevating the risk of ischemic stroke. The neuroprotective impact of short-chain fatty acids (SCFAs) derived from dietary fiber fermentation contrasts with the neuroinflammatory effects of lipopolysaccharide (LPS) from gut bacteria. The pivotal role of the gut-brain axis, facilitating bidirectional communication between the gut and the brain, is crucial in maintaining gastrointestinal equilibrium and influencing cognitive functions. An in-depth understanding of the interplay among the gut microbiota, immune system, and neurological outcomes in stroke is imperative for devising innovative preventive and therapeutic approaches. Strategies such as dietary adjustments, probiotics, prebiotics, antibiotics, or fecal transplantation offer promise in modulating stroke outcomes. Nevertheless, comprehensive research is essential to unravel the precise mechanisms governing the gut microbiota’s involvement in stroke and to establish effective therapeutic interventions. The initiation of large-scale clinical trials is warranted to assess the safety and efficacy of interventions targeting the gut microbiota in stroke management. Tailored strategies that reinstate eubiosis and foster a healthy gut microbiota hold potential for both stroke prevention and treatment. This review underscores the gut microbiota as a promising therapeutic target in stroke and underscores the need for continued research to delineate its precise role and develop microbiome-based interventions effectively.

Background Disabled 2 (DAB2) is a multifunctional protein that has emerged as a critical component in the regulation of tumor growth. Its dysregulation is implicated in various types of cancer, underscoring its importance in understanding the molecular mechanisms underlying tumor development and progression. This review aims to unravel the intricate molecular mechanisms by which DAB2 exerts its tumor-suppressive functions within cancer signaling pathways. Methods and results We conducted a comprehensive review of the literature focusing on the structure, expression, physiological functions, and tumor-suppressive roles of DAB2. We provide an overview of the structure, expression, and physiological functions of DAB2. Evidence supporting DAB2's role as a tumor suppressor is explored, highlighting its ability to inhibit cell proliferation, induce apoptosis, and modulate key signaling pathways involved in tumor suppression. The interaction between DAB2 and key oncogenes is examined, elucidating the interplay between DAB2 and oncogenic signaling pathways. We discuss the molecular mechanisms underlying DAB2-mediated tumor suppression, including its involvement in DNA damage response and repair, regulation of cell cycle progression and senescence, and modulation of epithelial-mesenchymal transition (EMT). The review explores the regulatory networks involving DAB2, covering post-translational modifications, interactions with other tumor suppressors, and integration within complex signaling networks. We also highlight the prognostic significance of DAB2 and its role in pre-clinical studies of tumor suppression. Conclusion This review provides a comprehensive understanding of the molecular mechanisms by which DAB2 exerts its tumor-suppressive functions. It emphasizes the significance of DAB2 in cancer signaling pathways and its potential as a target for future therapeutic interventions. Graphical Abstract

Theranostics refers to the combination of diagnostic biomarkers with therapeutic agents that share a specific target expressed by diseased cells and tissues. Nuclear medicine is an exciting component explored for its applicability in theranostic concepts in clinical and research investigations. Nuclear theranostics is based on the employment of radioactive compounds delivering ionizing radiation to diagnose and manage certain diseases employing binding with specifically expressed targets. In the realm of personalized medicine, nuclear theranostics stands as a beacon of potential, potentially revolutionizing disease management. Studies exploring the theranostic profile of radioactive compounds have been presented in this review along with a detailed explanation of radioactive compounds and their theranostic applicability in several diseases. It furnishes insights into their applicability across diverse diseases, elucidating the intricate interplay between these compounds and disease pathologies. Light is shed on the important milestones of nuclear theranostics beginning with radioiodine therapy in thyroid carcinomas, MIBG labelled with iodine in neuroblastoma, and several others. Our perspectives have been put forth regarding the most important theranostic agents along with emerging trends and prospects.

Cancer, characterized by the uncontrolled proliferation of aberrant cells, underscores the imperative for innovative therapeutic approaches. Immunotherapy has emerged as a pivotal constituent in cancer treatment, offering improved prognostic outcomes for a substantial patient cohort. Noteworthy for its precision, immunotherapy encompasses strategies such as adoptive cell therapy and checkpoint inhibitors, orchestrating the immune system to recognize and selectively target malignant cells. Exploiting the specificity of the immune response renders immunotherapy efficacious, as it selectively targets the body’s immune milieu. Diverse mechanisms underlie cancer immunotherapies, leading to distinct toxicity profiles compared to conventional treatments. A remarkable clinical stride in the anticancer resources is immunotherapy. Remarkably, certain recalcitrant cancers like skin malignancies exhibit resistance to radiation or chemotherapy, yet respond favorably to immunotherapeutic interventions. Notably, combination therapies involving chemotherapy and immunotherapy have exhibited synergistic effects, enhancing overall therapeutic efficacy. Understanding the pivotal role of immunotherapy elucidates its complementary value, bolstering the therapeutic landscape. In this review, we elucidate the taxonomy of cancer immunotherapy, encompassing adoptive cell therapy and checkpoint inhibitors, while scrutinizing their distinct adverse event profiles. Furthermore, we expound on the unprecedented potential of immunogenic vaccines to bolster the anticancer immune response. This comprehensive analysis underscores the significance of immunotherapy in modern oncology, unveiling novel prospects for tailored therapeutic regimens.