Review to Understand the Crosstalk between Immunotherapy and Tumor Metabolism.

Immune checkpoint inhibitors have ushered in a new era of cancer treatment by increasing the likelihood of long-term survival for patients with metastatic disease and by introducing fresh therapeutic indications in cases where the disease is still in its early stages. Immune checkpoint inhibitors that target the proteins cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) or programmed death-1/programmed death ligand-1 have significantly improved overall survival in patients with certain cancers and are expected to help patients achieve complete long-lasting remissions and cures. Some patients who receive immune checkpoint inhibitors, however, either experience therapeutic failure or eventually develop immunotherapy resistance. Such individuals are common, which necessitates a deeper understanding of how cancer progresses, particularly with regard to nutritional regulation in the tumor microenvironment (TME), which comprises metabolic cross-talk between metabolites and tumor cells as well as intracellular metabolism in immune and cancer cells. Combination of immunotherapy with targeted metabolic regulation might be a focus of future cancer research despite a lack of existing clinical evidence. Here, we reviewed the significance of the tumor microenvironment and discussed the most significant immunological checkpoints that have recently been identified. In addition, metabolic regulation of tumor immunity and immunological checkpoints in the TME, including glycolysis, amino acid metabolism, lipid metabolism, and other metabolic pathways were also incorporated to discuss the possible metabolism-based treatment methods being researched in preclinical and clinical settings. This review will contribute to the identification of a relationship or crosstalk between tumor metabolism and immunotherapy, which will shed significant light on cancer treatment and cancer research.

Deciphering the Correlation between the Emergence of Lung Carcinoma Associated with Tuberculosis-related Inflammation.

Lung cancer and tuberculosis (TB) are classified as the second-most life-threatening diseases globally. They both are exclusively represented as major public health risks and might exhibit similar symptoms, occasionally diagnosed simultaneously. Several epidemiological studies suggest that TB is a significant risk factor for the progression of lung cancer. The staggering mortality rates of pulmonary disorders are intrinsically connected to lung cancer and TB. Numerous factors play a pivotal role in the development of TB and may promote lung carcinogenesis, particularly among the geriatric population. Understanding the intricacies involved in the association between lung carcinogenesis and TB has become a crucial demand of current research. Consequently, this study aims to comprehensively review current knowledge on the relationship between tuberculosis-related inflammation and the emergence of lung carcinoma, highlighting the impact of persistent inflammation on lung tissue, immune modulation, fibrosis, aspects of reactive oxygen species, and an altered microenvironment that are linked to the progression of tuberculosis and subsequently trigger lung carcinoma.

Current Perspectives on Nanoparticle-based Targeted Drug Delivery Approaches in Breast Cancer Treatment.

Breast cancer is avertible yet one of the most widespread carcinomas globally. Though periodic screening and monitoring have resulted in reduced incidences, the malignancy claims increased death rates across the globe. Due to the non-specific and aggressive nature of available conventional cancer therapeutics, there is a crucial need for better treatment paradigms. Recent advancements in nanotechnology have aided in this by utilizing nanocarriers in targeted drug delivery approaches. Optimized nanoparticles have been used to enhance the circulation time and target the efficacy of conventional therapeutic drugs. Passive targeting comprises surface modulation to avoid drug elimination via a standard body defense system. Active targeting includes chemical interaction with various genes, receptors, and antigens overexpressed during cancer progression. Therefore, the present review recapitulates drug delivery approaches and nanoparticle-based targeting that can potentially overcome the limitations of conventional drug therapies.

Insights on the Correlation between Mitochondrial Dysfunction and the Progression of Parkinson's Disease.

The aetiology of a progressive neuronal Parkinson's disease has been discussed in several studies. However, due to the multiple risk factors involved in its development, such as environmental toxicity, parental inheritance, misfolding of protein, ageing, generation of reactive oxygen species, degradation of dopaminergic neurons, formation of neurotoxins, mitochondria dysfunction, and genetic mutations, its mechanism of involvement is still discernible. Therefore, this study aimed to review the processes or systems that are crucially implicated in the conversion of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) into its lethal form, which directly blockades the performance of mitochondria, leading to the formation of oxidative stress in the dopaminergic neurons of substantia nigra pars compacta (SNpc) and resulting in the progression of an incurable Parkinson's disease. This review also comprises an overview of the mutated genes that are frequently associated with mitochondrial dysfunction and the progression of Parkinson's disease. Altogether, this review would help future researchers to develop an efficient therapeutic approach for the management of Parkinson's disease via identifying potent prognostic and diagnostic biomarkers.