International review of cell and molecular biology最新文献

Solid tumors are the most prevalent form of cancer. Considerable technological and medical advancements had been achieved for the diagnosis of the disease. However, detection of the disease in an early stage is of utmost importance, still far from reality. On the contrary, the treatment and therapeutic area to combat solid tumors are still in its infancy. Conventional treatments like chemotherapy and radiation therapy pose challenges due to their indiscriminate impact on healthy and cancerous cells. Contextually, efficient drug targeting is a pivotal approach in solid tumor treatment. This involves the precise delivery of drugs to cancer cells while minimizing harm to healthy cells. Targeted drugs exhibit superior efficacy in eradicating cancer cells while impeding tumor growth and mitigate side effects by optimizing absorption which further diminishes the risk of resistance. Furthermore, tailoring targeted therapies to a patient's tumor-specific molecular profile augments treatment efficacy and reduces the likelihood of relapse. This chapter discuss about the distinctive characteristics of solid tumors, the possibility of early detection of the disease and potential therapeutic angle beyond the conventional approaches. Additionally, the chapter delves into a hitherto unknown attribute of magnetic field effect to target cancer cells which exploit the relatively less susceptibility of normal cells compared to cancer cells to magnetic fields, suggesting a future potential of magnetic nanoparticles for selective cancer cell destruction. Lastly, bioinformatics tools and other unconventional methodologies such as AI-assisted codon bias analysis have a crucial role in comprehending tumor biology, aiding in the identification of futuristic targeted therapies.

Cancers are diseases caused by genetic and non-genetic environmental factors. Epigenetic alterations, some attributed to non-genetic factors, can lead to cancer development. Epigenetic changes can occur in tumor suppressors or oncogenes, or they may contribute to global cell state changes, making cells abnormal. Recent advances in gene editing technology show potential for cancer treatment. Herein, we will discuss our current knowledge of epigenetic alterations occurring in cancer and epigenetic editing technologies that can be applied to developing therapeutic options.

Acute myeloid leukemia (AML) results in disruption of the hematopoietic differentiation process. Crucial progress has been made, and new therapeutic strategies for AML have been developed. Induction chemotherapy, however, remains the main option for the majority of AML patients. Epigenetic dysregulation plays a central role in AML pathogenesis, supporting leukemogenesis and maintenance of leukemic stem cells. Here, we provide an overview of the intricate interplay of altered epigenetic mechanisms, including DNA methylation, histone modifications, and chromatin remodeling, in AML development. We explore the role of epigenetic regulators, such as DNMTs, HMTs, KDMs, and HDACs, in mediating gene expression patterns pushing towards leukemic cell transformation. Additionally, we discuss the impact of cytogenetic lesions on epigenomic remodeling and the potential of targeting epigenetic vulnerabilities as a therapeutic strategy. Understanding the epigenetic landscape of AML offers insights into novel therapeutic avenues, including epigenetic modifiers and particularly their use in combination therapies, to improve treatment outcomes and overcome drug resistance.

Inflammatory breast cancer (IBC) is a diagnosis based on a constellation of clinical features of edema (peau d'orange) of a third or more of the skin of the breast with a palpable border and a rapid onset of breast erythema. Incidence of IBC has increased over time, although it still makes up only 1-4% of all breast cancer diagnoses. Despite recent encouraging data on clinical outcomes, the published local-regional control rates remain consistently lower than the rates for non-IBC. In this review, we focus on radiotherapy, provide a framework for multi-disciplinary care for IBC, describe local-regional treatment techniques for IBC; highlight new directions in the management of patients with metastatic IBC and offer an introduction to future directions regarding the optimal treatment and management of IBC.

Chemoradiation (CRT) is a conventional therapy used in local cancers, especially when they are locally advanced. Studies have shown that CRT induces strong anti-tumor responses involving several immune effects in pre-clinical models and humans. In this review, we have described the various immune effects involved in CRT efficacy. Indeed, effects such as immunological cell death, activation and maturation of antigen-presenting cells, and activation of an adaptive anti-tumor immune response are attributed to CRT. As often described in other therapies, various immunosuppressive mechanisms mediated, in particular, by Treg and myeloid populations may reduce the CRT efficacy. We have therefore discussed the relevance of combining CRT with other therapies to potentiate the CRT-induced anti-tumor effects.

Sarcomas are heterogeneous and aggressive malignant tumors with variable responses to current standard treatments being usually incurable for those patients with metastatic and unresectable diseases. The lack of curative strategies has led to develop new therapies in the treatment of sarcomas where the role of immune system is an evolving field. Most sarcomas often exhibit an immunosuppressive microenvironment, which reduces their capacity to trigger an immune response. Therefore, sarcomas are broadly considered as an "immune cold" tumor, although some studies have described a great immune heterogeneity across sarcoma subtypes. Sarcoma cells, like other tumors, evade their immune destruction through a variety of mechanisms, including expansion and recruitment of myeloid derived suppressor cells (MDSCs). MDSCs are immature myeloid cells that have been correlated with a reduction of the therapeutic efficacy, including immunotherapy, tumor progression and worst prognosis. Consequently, different strategies have been developed in recent years to target MDSCs in cancer treatments. This chapter discusses the role of MDSCs in sarcomas and their current potential as a therapeutic target in these malignancies.

Myeloid-derived suppressor cells (MDSCs), which originated from hematopoietic stem cells, are heterogeneous population of cells that have different differentiation patterns and widely presented in tumor microenvironment. For tumor research, myeloid suppressor cells have received extensive attention since their discovery due to their specific immunosuppressive properties, and the mechanisms of immunosuppression and therapeutic approaches for MDSCs have been investigated in a variety of different types of malignancies. To improve the efficacy of treatment for head and neck squamous cell carcinoma (HNSCC), a disease with a high occurrence, immunotherapy has gradually emerged in after traditional surgery and subsequent radiotherapy and chemotherapy, and has made some progress. In this review, we introduced the mechanisms on the development, differentiation, and elimination of MDSCs and provided a detailed overview of the mechanisms behind the immunosuppressive properties of MDSCs. We summarized the recent researches on MDSCs in HNSCC, especially for targeting-MDSCs therapy and combination with other types of therapy such as immune checkpoint blockade (ICB). Furthermore, we looked at drug delivery patterns and collected the current diverse drug delivery systems for the improvement that contributed to therapy against MDSCs in HNSCC. Most importantly, we made possible outlooks for the future research priorities, which provide a basis for further study on the clinical significance and therapeutic value of MDSCs in HNSCC.

Cutaneous T-cell lymphoma (CTCL) is a type of cancer that affects skin, and is characterized by abnormal T-cells in the skin. Epigenetic changes have been found to play a significant role in the development and progression of CTCL. Recently, non-coding RNAs (ncRNAs), such as microRNAs and long non-coding RNAs, have been identified as key players in the regulation of gene expression in CTCL. These ncRNAs can alter the expression of genes involved in cell growth, differentiation, and apoptosis, leading to the development and progression of CTCL. In this review, we summarize the current understanding of the role of ncRNAs in CTCL, including their involvement in DNA methylation, and other biological processes. We also discuss the types of ncRNAs, their role as oncogenic or tumor suppressive, and their putative use as diagnostic and prognostic biomarkers, based on the emerging evidence from laboratory-based as well as patients-based studies. Moreover, we also present the potential targets and pathways affected by ncRNAs. A better understanding of the complex epigenetic landscape of CTCL, including the role of ncRNAs, has the potential to lead to the development of novel targeted therapies for this disease.

Oncolytic virus therapy (OVT) is a promising modality that leverages the propensity of natural or engineered viruses to selectively replicate in and kill cancer cells. Over the past decade, (pre)clinical studies have focused on the development and testing of adenovirus, herpes simplex virus, and vaccinia virus-based vectors. These studies have identified barriers to success confronting the field. Here, we propose a set of selection criteria or ideal properties of a successful oncolytic virus, which include lack of pathogenicity, low seroprevalence, selectivity (infection and replication), transgene carrying capacity, and genome stability. We use these requirements to analyze the oncolytic virus landscape, and then identify a potentially optimal species for platform development - vesicular stomatitis virus.

Immunotherapy has shifted the paradigm of cancer treatment. However, the majority of cancer patients display de novo or acquired resistance to immunotherapy. One of the main mechanisms of immunotherapy resistance is the immunosuppressive microenvironment dominated by the myeloid-derived suppressor cells (MDSCs). Emerging evidence demonstrates that genetic or epigenetic aberrations in cancer cells shape the accumulation and activation of MDSCs. Understanding this genotype-immunophenotype relationship is critical to the rational design of combination immunotherapy. Here, we review the mechanisms of how molecular changes in cancer cells induce recruitment and reprogram the function of tumor-infiltrating myeloid cells, particularly MDSCs. Tumor-infiltrating MDSCs elicit various pro-tumor functions to promote tumor cell fitness, immune evasion, angiogenesis, tissue remodeling, and metastasis. Through understanding the genotype-immunophenotype relationship between neoplastic cells and MDSCs, new approaches can be developed to tailor current immunotherapy strategies to improve cancer patient outcomes.