Cancer Science & Therapy

This comprehensive overview explores the recent advancements in targeted cancer therapies, a groundbreaking approach in the fight against cancer. Targeted therapies have revolutionized cancer treatment by specifically targeting cancer cells, minimizing damage to healthy tissues and reducing side effects. The article covers various types of targeted therapies, including small molecule drugs, monoclonal antibodies, and immunotherapies, highlighting their mechanisms of action and clinical applications. Challenges, such as resistance and accessibility, are discussed, along with the role of precision medicine, biomarkers, and combination therapies. The article also delves into the evolving regulatory landscape, patient-centric approaches, and future directions in the field. As cancer research continues to progress, this comprehensive overview provides insights into the transformative potential of targeted cancer therapies.

Cancer remains one of the most formidable challenges in the field of medicine, affecting millions of lives globally. Traditional cancer treatments such as surgery, chemotherapy, and radiation therapy have made significant strides, but the quest for more effective and targeted therapies continues. In recent years, cancer vaccines have emerged as a promising avenue in the battle against cancer, leveraging the body's immune system to prevent and treat this complex disease. This article delves into the fascinating world of cancer vaccines, exploring their mechanisms, current developments, challenges, and the potential they hold for revolutionizing cancer care.

Breast Cancer (BC) is the most common cancer in women accounting for about 30% of all female cancers. The average age of incidence varies among countries. While it is 62 years in the US, it is 48 years in the Arab countries. According to a recent statistics done on well studied charts of consecutive one thousand operations on breast cancer patients done by me in Syria, 20% of cases occurred below the age of 40 (vs. 8% in the US). This has an important implication.

Objective: Malignant Pleural Mesothelioma (MPM), a locally invasive tumor, is treated with a combination of surgical, radiation, and medical therapies, but the treatment efficacy remains insufficient. Gene therapy for MPM has been attempted to improve the prognosis of the disease, but has not yet reached a practical level. One of the barriers to MPM gene therapy is the resistance of MPM cells to transgene expression. Therefore, the purpose of this study was to find techniques to achieve high-level transgene expression in MPM cells resistant to transgene expression.

Methods: We evaluated two MPM cell lines, NCI-H28 (H28) and NCI-H2052 (H2052), for their resistance to transgene expression, and then examined whether transgene expression in the resistant H2052 cells was enhanced by treating the cells with D-glucose, an extracellular signalregulated kinase 1/2 inhibitor LY3214996 (LY), and a histone deacetylase inhibitor trichostatin A (TSA), which have been reported to increase transgene expression. Cellular transgene expression was evaluated by a reporter gene assay in which a human cytomegalovirus immediate early (CMV) promoter-controlled Enhanced Green Fluorescent Protein (EGFP) gene was inserted into the cells using a human adenovirus (ADV) vector. The extent of EGFP gene expression was examined by fluorometric assay, fluorescence microscopy, and EGFP quantification by ELISA.

Results: The fluorescence intensity in H2052 cells was only 13.9% of that in H28 cells. D-glucose treatment of H2052 cells after transduction (posttreatment) increased the fluorescence intensity in H2052 cells by only 1.9-fold. LY treatment of H2052 cells before transduction (pretreatment) increased the fluorescence intensity in the cells by only 1.7-fold. TSA pretreatment increased the fluorescence intensity in H2052 cells by as much as 6.9-fold, to almost the same level as that in H28 cells. When the TSA-pretreated H2052 cells were posttreated with D-glucose, the fluorescence intensity in H2052 cells was enhanced to 400% of that in H28 cells. The elevated EGFP gene expression by the joint effect of TSA and D-glucose was also confirmed by fluorescence microscopy and EGFP quantification by ELISA.

Conclusion: It was suggested that TSA pretreatment could remove the resistance to transgene expression of MPM cells and the joint effect of TSA and D-glucose could highly enhance transgene expression in the resistant MPM cells.