Medical Oncology最新文献

Colorectal cancer (CRC), breast cancer (BC), and lung cancer (LC) are among the most common and deadly malignancies worldwide. In recent years, the role of tumor-associated microbiota in the initiation and progression of cancer has attracted increasing attention. However, studies examining different cancer types together with their clinical stages remain limited. The aim of this study was to compare the composition of tumor tissue microbiota across three cancer types and different disease stages. For this purpose, DNA was isolated from formalin-fixed paraffin-embedded (FFPE) tumor samples, and sequencing of the 16 S rRNA gene region was performed. Microbial profiles were analyzed at the phylum and genus levels, and diversity indices were compared between groups. In stage III LC samples, the phylum Cyanobacteria was found to be markedly more abundant compared to other stages. In CRC, the phylum Firmicutes was most abundant in stage III tumors, showing higher levels than in early stages. In metastatic cases (advanced stages), both the operational taxonomic unit (OTU) count and Shannon diversity index were found to be highly similar to those of LC control tissues but markedly lower than those of the CRC control group. Across all cancer types, Actinobacteria, Cyanobacteria, Proteobacteria, and Firmicutes were identified as the dominant phyla, though their relative abundances varied by cancer type and stage. The findings suggest that tumor-associated microbiota composition exhibits distinct signatures depending on tumor type and progression stage. Similarities observed between certain cancer types and stages may indicate the presence of shared microbial patterns within the tumor microenvironment. Such microbial signatures may serve as potential biomarkers for diagnosis, prognosis, or therapeutic targeting.

Melanoma is a type of skin cancer that starts in melanocytes. It is estimated to increase by 2050 based on prediction studies. Exosomes have been identified as crucial intracellular mediators by carrying the donor-derived cargoes from stromal cells, immune cells, and even tumor cells, thereby affecting the function of recipient cells in a context-dependent manner. Although EVs can transport biologically active compounds like proteins, lipids, RNA, and DNA, their exact role remains unclear. The past few years have seen a surge in studies on tumor-associated cargo in exosomes, particularly concerning ncRNAs. The function of exosomal non-coding RNAs in melanoma's immunopathogenesis has been reviewed in detail in the current narrative review article. Exosomal ncRNAs have the potential to develop novel diagnostic and therapeutic targets in melanoma.

Endocrine tumors are hormone-secreting tumors that pose significant challenges for diagnosis and treatment due to their complex biological processes, delayed detection, and poor response to existing therapies. Despite advancements in imaging, surgery, and medicine, tumor heterogeneity, substantial barriers, and systemic toxicity hinder therapeutic success. A novel approach utilizing nanotechnology presents theranostics capabilities for various applications, enhances bioavailability, and ensures precise drug delivery. Engineered nanoparticles (NPs), including lipid-based, polymeric, and inorganic nanocarriers, enable targeted therapy through active targeting (ligand-receptor interactions) or passive accumulation (increased permeability and retention). These nanotechnologies address drug resistance and rapid clearance, delivering treatments directly to tumors while minimizing adverse effects on healthy cells. NPs that mimic biological processes or respond to external stimuli can adapt to the evolving tumor microenvironment. This review focuses on NP-based therapy for endocrine cancer, discussing their mechanisms of action, targeted approaches, and diagnostic and therapeutic applications. The limitations of current therapies and the future prospects of NP-based therapies are explored.

Fungi are a vital component of the gastrointestinal microbiota and are increasingly recognized for their critical roles in the initiation, progression, and therapeutic response of digestive tract cancers. Accumulating evidence indicates that specific fungal species contribute to the pathogenesis of various gastrointestinal malignancies-including oral, esophageal, gastric, and colorectal cancers-by promoting chronic inflammation, inducing host DNA damage, and modulating immune responses. Moreover, fungal-bacterial interactions can indirectly influence tumorigenesis by disrupting microbial community homeostasis and altering the functional landscape of the gut microbiome. In this review, we systematically synthesize current evidence from human cohort studies, preclinical models, and multi-omics analyses to delineate mycobiome-cancer associations, elucidate underlying mechanisms, and evaluate emerging diagnostic and therapeutic strategies. Together, these insights position the mycobiome not merely as a bystander but as an active contributor to gastrointestinal carcinogenesis-offering novel opportunities for early detection, risk stratification, and microbiome-targeted interventions in cancer prevention and therapy.

This letter commends the recent study by Abdelkarim et al. on the pro-apoptotic effects of an Allium sativum (garlic) extract in acute myeloid leukemia (AML). While acknowledging the significance of their ex vivo findings on primary patient cells, we propose several key considerations to strengthen the translational potential of this research. Firstly, we emphasize the need for standardized phytochemical characterization of the complex extract to ensure reproducibility. Additionally, we suggest expanding the mechanistic investigation to include the extrinsic apoptosis pathway and direct measurement of reactive oxygen species. Furthermore, we discuss strategies to enhance the targeting of resistant leukemia stem cell populations, such as prolonged exposure or combination therapy with venetoclax. Finally, we advocate for in vivo validation using patient-derived xenograft models to evaluate efficacy within a physiologically relevant microenvironment. Addressing these points will be crucial for harnessing the full potential of Allium sativum as a complementary therapy in AML.

Exosomes are among the various secreted vesicles which play a pivotal role in tumor growth and progression. In fact, tumor-derived exosomes are considered to be an excellent reservoir of oncogenic factors which govern the metastatic potential of cancer cells. Previously, we observed systemic damage within the lymphoma-bearing host and established the immunomodulatory effect of lymphoma-derived factors/ascites on macrophages. However, whether this host-tumor interaction involves exosomes or not remains unclear. In view of this, we aimed to explore the proteomics landscape of tumor-derived exosomes to unravel their possible involvement in governing lymphoma-induced pathogenicity. Interestingly, we observed significant increase in exosome abundance in blood and tissues of lymphoma-bearing hosts. Comprehensive proteome profile of exosomes revealed a distinct set of tumor-associated proteins, such as metalloproteinases (MMPs) and myeloperoxidase, which might be mediating tissue degradation within the host. Various exosomal proteins overlapped with known markers of epithelial to mesenchymal transition (EMT) and lymphoma. Functional enrichment analysis of exosomal cargoes revealed their immunomodulatory potential which could alter the activation state of macrophages. In vitro assay confirmed active uptake of these exosomes by macrophages resulting in morphological alterations, increased reactive oxygen species (ROS) production and reduction in LPS-induced nitrite release by inhibiting NOS2 expression. Conclusively, exosome abundance in blood and tissues highlight their possible involvement in mediating systemic alterations in lymphoma-bearing hosts. This study gives the first evidence of MMP-8 within the exosomes suggesting a novel pathway for its contribution to tissue damage in cancer condition. The study underscores the possible link for exosome-macrophage crosstalk to promote systemic immunomodulation in lymphoma. Our results give key insight into exosome profiling and illustrate the presence of invasive and immunomodulatory proteins which might be used as diagnostic or prognostic markers and could serve as an important target in therapeutic intervention in cancer.

Tumor hypoxia poses a major challenge in tumor therapy. Many strategies have been explored to alleviate tumor hypoxic microenvironment to improve the efficacy of tumor therapy. Ultrasound-stimulated microbubbles cavitation (USMC) was proved to improve tumor perfusion, and thus to alleviate tumor hypoxia. The synergistic role of USMC in tumor therapy has been identified by several preclinical and clinical studies. The effect of USMC on improving tumor perfusion is influenced by many factors, and the stability and reproducibility of this effect in long-term tumor treatment remain to be explored. In this study, we established rabbit VX2 tumor model. Fifteen tumor-bearing rabbits were enrolled to compare the effects of USMC with two different mechanical indexes (MIs). The results of contrast-enhanced ultrasound (CEUS) imaging showed that USMC with MI of 0.25 could improve the tumor perfusion better compared with MI 0.40. Then we conducted repeated USMC treatments on tumor-bearing rabbits once a week for six weeks. The results of CEUS showed that USMC with appropriate parameters could always enhance the tumor perfusion although the tumor had developed. Transmission electron microscopy revealed that tumors received multiple USMC treatments had more integral vascular structures compared with the control. Immunofluorescence staining showed that tumors received multiple USMC treatments had higher overlap coefficient of CD31 and intercellular cell adhesion molecule-1, indicating the normalization of tumor vasculature. In conclusion, USMC with appropriate parameters has stability and reproducibility in improving tumor perfusion. And multiple USMC treatments could potentially promote tumor vascular normalization, which is beneficial for tumor therapy.

Epigenetic modifications act as crucial controllers of gene expression in nasopharyngeal carcinoma (NPC), with DNA hypermethylation of tumour suppressor genes and alterations in histone modification patterns playing a major role in oncogenesis. EBV-encoded proteins directly modulate host epigenetic machinery, promoting stable silencing of critical genes. Environmental exposures, such as nitrosamines and tobacco smoke, further influence epigenetic risk. Non-coding RNAs, especially miRNAs and lncRNAs, modulate epigenetic regulators and contribute to tumour behaviour. Several epigenetic markers show strong potential as non-invasive diagnostic and prognostic tools. Epigenetic drugs, such as HDAC and DNMT inhibitors, therapeutically show promise in reactivating silenced genes and sensitising tumours to conventional treatments. Epigenomic alterations offer profound insights into NPC pathogenesis and present valuable opportunities for early detection, risk assessment and targeted therapy. With the advances in epigenomic profiling technologies and increasing clinical validation, epigenetic biomarkers and therapeutics may become integral to precision oncology approaches in NPC. Continued interdisciplinary research is essential to fully harness these insights and translate them into improved outcomes for patients. This review presents an in-depth summary of the current understanding regarding epigenomic alterations in NPC, with a focus on their biological significance, diagnostic utility, and therapeutic potential in NPC initiation, progression and treatment.