Objective: Lung cancer is a leading cause of cancer-related mortality, primarily due to its high metastatic potential, particularly to the brain and bones. Brain metastases significantly challenge clinical management, impacting treatment efficacy and patient survival, while bone metastases cause severe complications such as pathological fractures and hypercalcemia. Understanding the clinico-pathological factors influencing these metastases is essential for improving patient outcomes. Materials and Methods: This study examined a cohort of 158 patients with primary lung cancer treated at the Cheikh Zaid International University Hospital in Rabat, Morocco. Clinical data, including demographic information, smoking status, and histological and molecular characteristics, were collected. The incidences of bone and brain metastases were analyzed. Statistical analysis was performed using Excel and Jamovi software, with qualitative variables expressed as frequencies and quantitative variables as central tendencies. Associations between variables were evaluated using Chi-square and Fisher's exact tests, with a significance threshold set at p < 0.05. Results: Bone metastases were identified in 31 patients (19.6%) via bone scintigraphy, while brain metastases were confirmed in 29 patients (18.4%) through cerebral MRI. No significant differences were observed between males and females or among different age groups. However, smoking was significantly associated with bone metastases (p = 0.034), with smokers exhibiting a higher incidence. A significant association was found between brain metastases and the adenocarcinoma histological subtype (p = 0.001), indicating that specific tumor characteristics influence metastatic patterns. No significant correlation was observed between molecular status and the occurrence of metastases. Conclusions: This study underscores the importance of clinico-pathological factors in lung cancer metastasis. Smoking is significantly correlated with bone metastases, while adenocarcinoma is closely linked with brain metastases. These findings highlight the need for personalized management strategies and improved data documentation to enhance clinical care.
Objective: This study aimed to evaluate the anticancer activity of cryptotanshinone (CPT) in estrogen and progesterone receptor-positive (ER+/PR+) MCF-7 breast cancer cells and to determine whether delivery via the filamentous M13 bacteriophage enhances CPT's functional effect, with a focus on FOXM1 gene expression. Materials and Methods: MCF-7 cells were treated with CPT across a concentration range to establish dose-response behavior and calculate IC50 values at 24 and 48 h using an MTT viability assay. For phage-mediated delivery, cells were exposed to M13 alone, free CPT, CPT co-administered with M13 without loading, and preformed M13-CPT complexes, followed by MTT-based viability assessment. FOXM1 messenger ribonucleic acid (mRNA) levels were quantified at 24 and 48 h by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and normalized to a housekeeping gene using Delta Ct-based analysis. Results: CPT decreased cell viability in a dose- and time-dependent manner, yielding IC50 values of 19.82 & micro;M at 24 h and 16.14 & micro;M at 48 h. CPT also suppressed FOXM1 expression, with a stronger inhibitory effect at 48 h rather than at 24 h. M13 alone did not produce a meaningful change in viability. Compared with free CPT and the non-loaded CPT+M13 mixture, M13-CPT induced a markedly greater reduction in cell viability. In addition, Annexin V-fluorescein isothiocyanate/propidium iodide (V-FITC/PI) analysis showed that CPT increased apoptosis, with a stronger effect in the M13-CPT group than free CPT. Conclusions: CPT reduces MCF-7 cell viability and downregulates FOXM1 expression, and delivery through M13 bacteriophage further enhances in vitro cytotoxic efficacy without requiring additional targeting ligands.
The osteosarcoma tumor microenvironment has both cellular and non-cellular components. Among the cellular components, both immune and non-immune cells can be derived. The immune cells include infiltrating T lymphocytes, B cells, and dendritic cells, while the non-immune cells include macrophages and cancer-associated fibroblasts. The extracellular matrix, blood vessels, and all cytokines and chemokines are included in the non-cellular portion. Hypoxia-inducible factor-1 alpha (HIF-1 alpha) is up-regulated during the early stages of tumor formation due to an induced hypoxic drive. Tumor suppression, progression, or relapse may result from the interplay of various elements in the tumor microenvironment. Tumor suppression occurs when immune cells cooperate to eliminate cancer cells, whereas tumor formation occurs when an immunosuppressive microenvironment is created. Tumor growth or recurrence might result from some components of the tumor microenvironment releasing chemicals that hinder other immune cells from defending the tumor. T regulatory cells release the inhibitory cytokines interleukin (IL)-10 and IL-35, produce bioactive transforming growth factor beta (TGF-(3), and induce death in effector T cells. Macrophages and dendritic cells produce HIF-1 alpha, which directly reduces tumor cells' vulnerability to doxorubicin (DOX)-induced apoptosis. Doxorubicin, narasin, ifosfamide, cisplatin, methotrexate, gemcitabine, etoposide, carboplatin, and cyclophosphamide have all been used to treat osteosarcoma. Modest doses of doxorubicin are recommended because of the cardiotoxic effects alone, but these leave some cancer cells alive. This review explicitly describes how the changes in the tumor microenvironment contribute specifically to doxorubicin resistance and how doxorubicin-resistant cells affect the components in the tumor microenvironment.
Objective: Chemotherapy-induced peripheral neuropathy (CIPN) is a common and debilitating side effect of chemotherapeutic agents used in the treatment of cancer patients. Peripheral Neuropathy (PN) may arise due to the disease itself or as a consequence of treatment with chemotherapeutic agents, such as proteasome inhibitors, platinum-based compounds, and vinca alkaloids, which are widely known as CIPN. However, the underlying mechanisms of CIPN remain poorly understood. The objective of this study was to investigate the presence of CIPN in a rat model and identify potential biomarkers associated with the induction of neuronal damage and consequent neuropathy. Materials and Methods: CIPN was induced in experimental rats by administering Bortezomib (BTZ), Cisplatin (CIS), and Vincristine (VIN). The onset and progression of CIPN in these rats were assessed by the Hot and Cold plate experiments. The ELISA method was used to measure the levels of neuronal damage-related biomarkers NSE, S100B, and inflammatory biomarkers IL-6, TNF alpha, and IL-10 using plasma and sciatic nerve, collected from the experimental rats. Results: Our findings revealed significant alterations in body weight, as well as abnormal responses in the hot plate and cold plate tests, which are indicative of CIPN. Our results showed a significant increase in NSE, S100B, IL-6, and TNF alpha levels in the plasma of rats that showed symptoms of CIPN. However, the IL-10 levels were elevated in the sciatic nerve and plasma of the CIPN rats. Conclusion: These findings suggest that NSE, S100B, IL-6, TNF alpha, and IL-10 could serve as biomarkers for detecting CIPN induced by chemotherapeutic agents. Further research is necessary to fully understand the roles of these biomarkers in the development and progression of CIPN.
cell lung cancer (NSCLC) remains the most frequently diagnosed malignancy and the leading cause of cancer-related death worldwide. Although targeted therapies for actionable alterations and immune checkpoint inhibitors (ICIs) have improved outcomes, clinical benefit is highly heterogeneous, with frequent primary non-response and early acquired resistance. This unmet need has intensified the search for robust prognostic factors and predictive biomarkers. The human microbiota has emerged as a relevant candidate within this landscape, given its central role in immune modulation, systemic inflammation, epithelial barrier integrity, and the production of bioactive metabolites. Increasing evidence supports a gut-lung axis in NSCLC, with dysregulated intestinal and airway microbial profiles associated with aggressive phenotypes, metastatic patterns, and survival endpoints. Mechanistically, dysbiosis may influence tumor progression and therapy response through microbe-associated molecular pattern signaling and metabolite-driven effects on antigen presentation, interferon pathways, and regulatory T-cell balance, ultimately reshaping the tumor microenvironment. In immunotherapy, baseline gut microbiome features and iatrogenic perturbations have been linked to reduced ICI efficacy, while microbiota-restoring strategies such as fecal microbiota transplantation can rescue anti-PD-1 activity in translational models. Importantly, emerging data extend the relevance of the microbiome to oncogene-addicted NSCLC: baseline fecal signatures have been associated with the efficacy and gastrointestinal toxicity of Epidermal Growth Factor Receptor-tyrosine kinase inhibitors (EGFR-TKIs), and experimental microbiota perturbation can suppress EGFR-TKIs' antitumor effects, whereas microbiota-supporting interventions may enhance response. Despite promising signals, inter-study variability and confounding exposures limit comparability. This narrative short review is based on a non-systematic search of PubMed/MEDLINE, Embase, and Scopus focused on NSCLC microbiome/gut-lung axis and outcomes with ICIs and EGFR-TKIs. Prospective, well-controlled multi-omics studies integrating microbiome, metabolome, immune profiling, and rigorous clinical annotation are needed to validate actionable signatures and define microbiota-informed strategies to optimize NSCLC treatment.
