During the interaction between a virus and its host, a complex interplay arises between the host's defence mechanisms and the viral survival strategies. This interaction impacts not only viral replication and the viral lifecycle but also affects the host's homeostasis, including cellular genetics and immune responses. The outcomes of host-virus interactions can vary widely, ranging from successful pathogen clearance to severe disease or even death, influenced by factors such as host genetics, age, comorbidities, and environmental conditions. Viruses adeptly manipulate cellular machinery and metabolism, reprogram signalling pathways, and undermine immune responses to enhance their survival. A key strategy employed by viruses is immune evasion, utilising various techniques to bypass the host's immunovigilance. These strategies not only encourage persistent infections but also raise concerns about oncogenic potential, particularly in hematologic malignancies like acute lymphoblastic leukaemia (ALL). Such mechanisms may play a pivotal role in the alterations induced by viral contributions that disrupt immune surveillance and foster malignancy. This review seeks to elucidate the potential role of human cytomegalovirus (HCMV) as a risk factor and etiological contributor to the development of ALL in children. Although HCMV has not been officially recognized as an oncogenic virus, emerging evidence suggests that early-life infection may predispose to malignant transformation by promoting oncogenic pathways and immune dysregulation.

Gynecological cancers (GCs), which primarily encompass cervical cancer (CESC), ovarian cancer (OC), and endometrial cancer (EC), represent a group of malignancies that pose a severe threat to women's health. The advancement of precision medicine holds profound significance for enhancing the diagnosis and treatment of gynecological cancers. The application of molecular-targeted drugs, coupled with progress in surgical concepts and techniques, has substantially improved the survival outcomes of patients with ovarian cancer. Neuropilin-1 (NRP1) was initially identified as a neuronal guidance protein. Recent studies have revealed multifaceted roles of NRP1 in cancers, including its regulatory effects on tumor cell proliferation, growth, metastasis, and angiogenesis. NRP1 functions as a potent modulator of immune cells in the tumor microenvironment. Suppressing NRP1 results in antitumor immune responses and affects the efficacy of cancer immunotherapy. Alterations in NRP1 expression are associated with poor prognosis across a spectrum of malignancies, indicating its potential as a biomarker for evaluating the prognosis of cancer patients. In the present review, we first aim to summarize the expression characteristics and clinical associations of NRP1 in gynecological cancers; second, we elaborate on the role and molecular mechanisms of NRP1 in the progression of these cancers. Therapeutic strategies targeting NRP1 to prevent the development of gynecological cancers will also be discussed. In conclusion, this review highlights the pivotal role of NRP1 in the progression of gynecological cancers and the development of targeted therapeutic strategies, suggesting that NRP1 is a key target for personalized treatment.

Cholangiocarcinoma (CCA) is a highly aggressive malignancy of the biliary tract with limited therapeutic options and a dismal prognosis. Although immune checkpoint inhibitors (ICIs) have transformed treatment paradigms for several solid tumors, their impact on CCA remains minimal. The unique immunobiology of CCA, including its immune excluded phenotype, low tumor mutational burden, and paucity of actionable biomarkers, has constrained meaningful immunotherapy responses. This review outlines the key immunologic barriers that define the tumor microenvironment in CCA, including the abundance of myeloid-derived suppressor cells, tumor-associated macrophages, regulatory T cells, metabolic reprogramming, and immune checkpoint overexpression. Given the modest clinical outcomes of ICI monotherapy in CCA, we highlight the rationale for combination strategies incorporating chemotherapy, anti-angiogenic agents, epigenetic modulators, and metabolic inhibitors. Additionally, we assessed the emerging roles of adoptive cell therapy, tumor vaccines, and gut microbiome modulation as novel immunologic interventions. We also discussed how adaptive trial designs and real-time circulating tumor DNA monitoring support dynamic therapy optimization. Although the immunologic silence of CCA has historically limited the efficacy of immunotherapy, growing insights into the tumor microenvironment (TME) and advances in biomarker-guided, personalized strategies offer a compelling roadmap forward. Overcoming immune resistance in CCA will require multidimensional innovation combining biology, technology, and trial design to shift this malignancy from immune evasion to immune engagement.

Lipids are a broad group of hydrophobic macromolecules that play critical roles in cell physiology, specifically in metabolism, membrane synthesis and signaling, which also includes the physiology of cancer cells. Due to the metabolic changes in cancer cells, lipids are used as an important energy source and signaling intermediates, which support the progression and survival of the transformed cells. Cholesterol is also an important part of these mechanisms, since it is an essential component of lipid rafts, which act as membrane platforms for signal transduction. Apart from the metabolism and signaling implication of lipids in cancer cells, these molecules may also affect histone modifications and the tumor microenvironment, modifying gene expression, cytokines secretion and the infiltration of white blood cells in the tumor, impeding tumor detections and clearance by the immune system. Due to the preponderant role of lipids in malignant cells, enzyme lipid uptake and synthesis represent potential therapeutic targets that are being studied to provide a complete treatment that focuses on different mechanisms to kill malignant cells. This review aims to provide a metabolic explanation about the influence of lipids in the survival of cancer cells, the immune response evasion, as well as some potential therapeutic targets that regulate these processes.

Glioblastoma multiforme (GBM) is a highly aggressive and invasive type of primary brain tumor. Despite maximal safe surgical resection followed by concurrent adjuvant chemotherapy and radiotherapy, the clinical prognosis is grim, with only marginal prolongation of survival and poor quality of life. Median survival time is 15 months. This review will discuss the pathogenesis of GBM, diagnostic challenges, clinical evaluation, imaging, genomics and current therapeutic options. The intrinsic immunosuppressive properties of GBM and additional adverse changes in immune surveillance and the systemic immune environment brought about by chemoradiotherapy will be addressed. GBM stem cell properties and their role in local recurrence and preclusion of cure will be covered. We will discuss the limited penetration of the blood-brain barrier by therapeutics as a major obstacle in treatment. Advances in novel therapeutic strategies using personalized approaches, cell-based therapies, tumor vaccines and targeted drug delivery will be considered.

Background: Glioblastoma multiforme (GBM) is one of the deadliest and most heterogeneous forms of brain cancer, characterized by its resistance to conventional therapies. Within GBM, a subpopulation of slow-cycling cells, often linked to quiescence and stemness, plays a crucial role in treatment resistance and tumor recurrence. This study aimed to identify novel biomarkers associated with these slow-cycling GBM cells.

Methods: We utilized The Cancer Genome Atlas (TCGA)-GBM dataset and presented the reproducible bioinformatics analysis for our results.

Results: Our analysis highlighted Membrane-Associated Protein 17 (MAP17) as strongly associated with the slow-cycling phenotype. We found that the protein cargo MAP17 expression is related to mesenchymal signatures and stem cell-related pathways. Also, MAP17 was linked to a distinct metabolic profile, characterized by significant enrichment in pathways related to folate, zinc, and fatty acids. Moreover, the immune cell distribution analysis revealed that MAP17 correlates with key molecular immune processes, including interferon-gamma (IFN-γ) signaling and antigen presentation, as well as immunosuppressive cells like myeloid-derived suppressor cells (MDSCs) and macrophages. MAP17-high tumors also showed elevated expression of several immune checkpoint inhibitors, indicating an immunosuppressive microenvironment.

Conclusion: These findings provide insight into the role of MAP17 in quiescence, stemness, and immune evasion, positioning it as a promising therapeutic target.