Current Cancer Therapy Reviews - Online First

Oral squamous cell carcinoma (OSCC) is the predominant malignant tumour of the oral cavity, constituting more than 90% of oral malignancies. It is linked to elevated morbidity and mortality, often resulting from late-stage diagnosis and restricted therapeutic effectiveness. It is accelerated by a number of risk factors, including genetic predisposition, alcohol use, tobacco use, and human papillomavirus (HPV) infection. In order to promote early detection and improve patient outcomes, this review attempts to provide a comprehensive analysis of the risk factors, diagnostic techniques, and available treatments for OSCC. Using internet databases including PubMed, Scopus, and Google Scholar, a thorough literature analysis was carried out with an emphasis on the differences between previous and current papers published. The selection of studies was based on their scientific quality, relevance, and discussion of risk factors, diagnostic techniques, or therapy approaches linked to OSCC. The results show that prognosis is much improved by early identification. Advanced imaging modalities and molecular biomarkers facilitate early diagnosis. Surgery and adjuvant therapy are two examples of multimodal treatment techniques that increase survival rates. Prompt diagnosis and tailored treatment approaches are essential for improving OSCC management. Additional research is required to formulate innovative medicines and improve early detection methods.

Natural Killer (NK) cells, a subset of innate lymphoid cells, have emerged as a promising avenue in cancer immunotherapy due to their ability to recognize and eliminate malignant and virus-infected cells without prior antigen sensitization. Unlike T cells, NK cells function independently of Major Histocompatibility Complex (MHC) restriction, making them effective against tumors that evade adaptive immune responses. However, several challenges, including limited persistence, poor tumor infiltration, and immune suppression, hinder their clinical efficacy, particularly in solid tumors. Recent advancements in NK cell expansion, activation, and genetic engineering have significantly enhanced their therapeutic potential. Strategies such as cytokine-mediated stimulation, artificial scaffolds, and CRISPR-based modifications have improved NK cell persistence and cytotoxicity. Additionally, Chimeric Antigen Receptor (CAR)-modified NK cells offer targeted tumor recognition while minimizing the risk of Graft-Versus-Host Disease (GVHD) and Cytokine Release Syndrome (CRS), making them a safer alternative to CAR-T therapy. Despite these advancements, immunosuppressive tumor microenvironments and high manufacturing costs remain key obstacles. Emerging approaches, including metabolic reprogramming, synthetic biology, and combinatorial therapies integrating checkpoint inhibitors and bispecific antibodies, hold promise for overcoming these limitations. Furthermore, the development of off-the-shelf, induced Pluripotent Stem Cell (iPSC)-derived NK therapies is expected to enhance scalability and accessibility. This review highlights the latest progress in NK cell-based immunotherapy, addressing both current challenges and future directions in optimizing NK cell expansion, activation, and genetic engineering for clinical applications.

Tripartite Motif Containing 56 (TRIM56) is an important member of the TRIM protein family that has gotten a lot of attention because it plays a big part in how tumours start and grow. Research has shown that TRIM56 promotes the growth of various malignancies, such as Cassibian sarcoma, breast cancer, and glioblastoma, and in some types of cancer with specific predisposing factors, such as ovarian cancer and multiple myeloid. It prevents leukaemia, liver cancer, lung adenocarcinoma, and tumours from growing and proliferating cancer cells. Consequently, TRIM56 may regulate tumour proliferation, metastasis, and other processes in both directions. This study aims to explore the dual role of TRIM56 in tumorigenesis and cancer progression. We have outlined its structure, functional domains, and involvement in key signalling pathways, such as the estragon, NF-κB, and TLR3/TTRIF pathways, which are frequently dysregulated in cancer. Furthermore, we investigate TRIM56's regulatory function in the epithelial-mesenchymal transition (EMT) and its differential impacts on tumour proliferation, metastasis, and suppression across various cancers. This review highlights the potential of TRIM56 as a therapeutic target and prognostic biomarker by synthesizing current evidence, emphasizing the need for additional research into its mechanisms and clinical applications. Although TRIM56's function in tumours has been better understood, research is needed to clarify its precise mechanisms in cancer and explore the possibility of using it as a target for therapeutic interventions.

Globally, lung cancer continues to be the primary cause of cancer-related fatalities. Despite significant advancements in chemotherapy, targeted therapy, and immunotherapy that have improved treatment effectiveness and increased survival rates, the five-year relative survival rate for lung cancer patients remains very low. Most cases receive a diagnosis at an advanced stage, which primarily contributes to this. Drug resistance is still a significant challenge, which is responsible for 90% of cancer-related deaths. Epigenetic alterations, including DNA methylation, RNA modification, and histone modification, play crucial roles in cancer treatment resistance. Among these, the methyltransferase-like 3 (METTL3)-induced N6-methyladenosine (m6A) RNA modification has received a lot of attention because it plays a part in the growth of lung cancer tumors, carcinogenesis, proliferation, and resistance to treatment. Researchers have identified or developed several METTL3 inhibitors that have shown promising therapeutic benefits in both in vivo and in vitro models. This review focuses on the progress that has been made in the research investigating the role of METTL3 in lung cancer treatment resistance. It also elucidates the processes that are at play and investigates prospective therapeutic options that target METTL3 to enhance treatment results and overcome drug resistance.

Globally, breast cancer is still a major health concern because of its complex epidemiology, a wide range of symptoms, and a multitude of causes It is mainly caused by the uncontrolled growth of breast tissue cells and a variety of factors influence breast cancer, including hormones, lifestyle decisions, genetic predispositions, and environmental exposures. Breast cancer is classified based on molecular subtypes and their location. Many current treatments, such as surgery, chemotherapy, radiation therapy, hormone therapy, and targeted therapies, are used to improve the health of patients. However, drug resistance and systemic toxicity may restrict therapeutic efficacy despite advancements in therapy. In pursuit of these unmet challenges, nanotechnology has been employed to serve as drug carriers, aiming to optimize therapeutic efficacy and minimize side effects. These nanoparticulate formulations can be customized for targeted delivery, resulting in accurate drug localization in tumor tissues while protecting healthy cells at the same time. Additionally, they regulate the release of the drug, prolonging its circulation duration and improving its bioavailability. This review addresses various approaches to nano-formulations, such as liposomes, polymeric nanoparticles, solid lipid nanoparticles, carbon nanotubes, dendrimers, polymeric micelles, gold nanoparticles, and quantum dots that can be utilized to overcome treatment obstacles and enhance drug distribution.

Rectal cancer is a significant health concern with substantial morbidity and mortality rates. Magnetic Resonance Imaging (MRI) plays a crucial role in the diagnosis and management of rectal cancer, providing detailed anatomical and functional information. However, traditional MRI techniques have limitations in prognosticating tumor behavior and treatment response. The study emphasizes the importance of emerging techniques such as Diffusion-Weighted Imaging (DWI), mrDEC scoring system, Dynamic Contrast-Enhanced MRI (DCE-MRI), Radiomics, and Machine Learning. By examining recent research and clinical trials, we aim to offer a comprehensive overview of the current landscape, challenges, and future directions associated with the incorporation of these MRI biomarkers in predicting outcomes for rectal cancer patients. This review paper aims to provide an overview of the emerging MRI biomarkers that hold the potential for prognostication of rectal cancer.

MicroRNAs (miRNAs) are small, non-coding RNAs that play a crucial role in post-transcriptional gene regulation by modulating mRNA stability and translation. These evolutionarily conserved molecules undergo processing by ribonucleases Drosha and Dicer, ultimately joining the RNA-induced silencing complex to silence gene expression. Among them, miR-23a, located on chromosome 19, is significant for its roles in cell growth, differentiation, and various diseases, including cancer. Depending on the cancer type, miR-23a can function as both an oncogene and a tumour suppressor. While its overexpression often correlates with aggressive tumours, miR-23a holds promise as a biomarker for early cancer detection and a therapeutic target. Its diverse functions in cancer include promoting tumour growth and hindering immune responses, highlighting its potential for personalized medicine. Beyond cancer, miR-23a is involved in blood sugar regulation, insulin resistance, muscle atrophy, and other diseases. It modulates pathways in type 2 diabetes mellitus, muscle atrophy, leukemia, epilepsy, and osteoarthritis. This paper aims to comprehensively analyze the roles of miR-23a in cancer and other diseases, focusing on its regulatory mechanisms, target genes, and pathways. It also evaluates the potential of miR-23a as a biomarker and therapeutic target. Despite its significance, research gaps remain, particularly in understanding the interactions of miR-23a with other miRNAs and the detailed mechanisms underlying its role in various diseases. More research into miR-23a clustering and how it works with other miRNAs could help us learn more about it and find better ways to use it to diagnose and treat diseases.

Lung cancer is the leading cause of cancer-related deaths globally, necessitating ongoing scientific research to understand its detection, treatment, and prevention. Long non-coding RNAs (lncRNAs) are a diverse group of non-coding RNAs that play crucial roles in regulating tumorigenic processes, such as cell proliferation, invasion, and metastasis in non-small cell lung cancer (NSCLC). Despite not encoding proteins, lncRNAs have significant impacts on the development and progression of NSCLC. Recent evidence suggests that lncRNAs may serve as valuable biomarkers for diagnosing and prognosticating NSCLC through tissue or blood analysis, and as potential therapeutic targets. This review provides a comprehensive overview of recent advancements in lncRNA research for NSCLC, offering new insights into their mechanisms of action and potential therapeutic applications. It also explores promising avenues for therapeutic development. By elucidating the complex roles of lncRNAs in NSCLC, this article aims to contribute to the development of innovative diagnostic and therapeutic strategies that can significantly enhance patient outcomes. Understanding the multifaceted functions of lncRNAs in lung cancer has the potential to lead to substantial progress in early disease detection, targeted treatments, and personalized medicine, ultimately improving the prognosis and quality of life for individuals affected by this devastating disease.

The five-year survival rate for people with colon cancer has increased explosively over the last two decades due to major advances in treatment. Colon cancer survival rates have improved significantly over the past few decades, with some of this success owing to aggressive surgical care and breakthroughs in other complementary treatments. As a new option for Colorectal Cancer (CRC) patients, targeted therapy has been shown to be effective in extending the overall life. A dramatic increase in the number of novel drugs targeting multiple key pathways and immunological checkpoints has been observed after the success of cetuximab (an EGFR inhibitor) and bevacizumab (an anti-angiogenic agent). Neutralizing an already present dysbiosis in the gut microbiome is a novel strategy for combating colorectal cancer and its metastases. Several methods have been employed to date, such as prebiotics, postbiotics, antibiotics, and the transplantation of faecal microbiota. An overview of the epidemiological study and possible mechanisms of colon cancer is presented in this review. We have covered a wide range of targeted treatments for CRC in addition to diagnostic biomarkers as therapeutic targets.

Platelets are small anucleated blood cells that play a vital role in preserving the integrity of tissue because of their hemostatic properties. However, through their interactions with leukocytes, they also have important functions in immunological responses and inflammation. Platelets have an impact on the tumor's development and metastasis at different stages of cancer. They promote angiogenesis and metastasis by modifying endothelial activation, improving leukocyte migration to tumor locations, and changing inflammatory conditions. Patients with cancer frequently have aberrant platelet activity, which accelerates the progression of the illness. Tumor cells that penetrate the bloodstream stimulate platelets, which causes the tumor cells to take on a mesenchymal-like phenotype and widen the permeability of the endothelium. As a result, tumor cell-platelet emboli are created. In addition, platelets draw in myeloid cells, shield tumor cells from immunological reactions and shear stress, and aid in their extravasation into distant organs. Ultimately, growth factors derived from platelets help create micrometastatic foci. With an emphasis on current advancements in the area, this review clarifies the intricate mechanisms of platelet activation and their interactions with cancer cells.