Discover. Oncology最新文献

Background: Tripartite motif-containing 44 (TRIM44) involves in various tumor development. This study investigated role of TRIM44 in multiple myeloma (MM).

Materials and methods: TRIM44 levels in bone marrow tissues and MM cell lines was detected by quantitative reverse transcription PCR (RT-qPCR). Cell viability, migration, and invasion of MM cells were evaluated under the interference of TRIM44 expression. The role of TRIM44 on regulating tumor growth in vivo was also investigated in subcutaneous tumor xenograft models. The protein interact between TRIM44 and Zinc Finger E-Box Binding Homeobox 1 (ZEB1) was also studied according IP followed by western blotting assay.

Results: TRIM44 was all highly expressed in collected bone marrow tissues and MM cell lines. Cell viability, migration, and invasion of MM cells with low expression of TRIM44 was significantly inhibited. Over-expression of TRIM44 can down-regulate the ZEB1 ubiquitination to enhance the protein stability.

Conclusions: TRIM44 exerts as an oncogenic factor to induce the oncogenesis of MM by stabilizing ZEB1.

Women with breast cancer are predisposed to muscle mass loss, to compromised muscle quality, and to decreased strength, and these abnormalities may serve as important predictors of adverse outcomes, including mortality. The aim of this study was to evaluate the possible associations between muscle mass markers, assessed by computed tomography with the phase angle (PhA) obtained by Bioelectrical impedance analysis (BIA), and health outcomes in women with breast cancer.

Methods: retrospective study with 54 women newly diagnosed with breast cancer, aged ≥ 18 years and < 65 years; histologically confirmed diagnosis of early breast cancer (stage I-III range), and in the first chemotherapy-cycled treatment. Measurements performed: anthropometric assessments, BIA, third lumbar vertebra by computed tomography (CT) and physical function (handgrip strength, gait speed test 4 m, fatigue assessment), and blood biochemical analysis.

Results: Lower skeletal muscle index were correlated with reduced PhA values (R² = 0.222, p = 0.0047), suggesting a worse prognosis. Logistic regression analysis showed that individuals with low muscle mass had a significantly lower likelihood of survival compared to those with normal muscle mass regardless of age and cancer stage.

Conclusion: low muscle mass negatively affected patient survival and was associated with lower PhA values. Phase angle emerges as a promising marker of overall health and could be a valuable clinical tool in assessing prognosis.

Skin cutaneous melanoma (SKCM) is one of the most lethal cancers translating into 75% of skin cancer-related deaths. Despite the advances in SKCM management and treatment strategies, the overall survival of patients remains unsatisfactory due to the metastatic properties of SKCM as well as the absence of effective prognostic biomarkers. Recent studies have shown that overload copper renders accumulation of mitochondrial proteins and fuels a form of cell death at odds with known death mechanisms and is hinged on mitochondrial respiration, the so-called cuproptosis. However, the exact role of cuproptosis in SKCM development and progression is unknown, and painting a clear picture of its functions in SKCM is fraught with challenges. A more systematic investigation is justified. In this study, we were posed to dissect the clout and latent regulatory mechanisms of cuproptosis-related genes (CRGs) in reining in SKCM progression. Also, we identified three CRGs that stood out were used to construct a prognostic model, which could be employed to predict the prognosis of patients with SKCM. Finally, through pan-cancer analysis, we found that the four cuproptosis key genes play a role in multiple tumors, suggesting that cuproptosis may impact tumor progression at the pan-cancer level. Taken together, these findings may not only contribute to the development of treatment strategies but also provide clues for treatment decision-making.

Gliomas, a heterogeneous group of tumors affecting the brain and spinal cord, present a significant clinical challenge. Ephrin B1 (EFNB1) has been implicated in various malignancies. However, its role in gliomas remained poorly understood. Hence, this study aimed to elucidate the connection between EFNB1 and the progression of glioma. A retrospective RNA-seq analysis was conducted by utilizing the data from glioma patients in the TCGA and CGGA databases. Kaplan-Meier survival analysis and multivariate regression models were employed to evaluate the prognostic significance of EFNB1. RT-PCR was used to quantify EFNB1 expression in glioma tissues and cell lines. Meanwhile, in vitro assays were carried out to assess its functional roles in glioma cells. Our findings demonstrated that EFNB1 expression was significantly elevated in gliomas and other cancers. Moreover, high EFNB1 expression was closely correlated with advanced clinical stages and poor prognosis. Notably, multivariate analysis identified EFNB1 as an independent prognostic factor for overall survival. KEGG pathway analysis suggested that EFNB1 was involved in critical biological processes, including the cell cycle, protein processing in the endoplasmic reticulum, Epstein-Barr virus infection, and Salmonella infection. Furthermore, EFNB1 expression was associated with immune cell infiltration, particularly Th2 cells, macrophages, and plasmacytoid dendritic cells. In glioma cells, EFNB1 expression was markedly increased. Consequently, functional experiments demonstrated that EFNB1 knockdown inhibited glioma cell proliferation, invasion, and migration. These results highlighted EFNB1 as a novel independent prognostic biomarker and suggest its potential role in shaping the immunological microenvironment of gliomas.

Osteosarcoma, a malignant bone tumor, faces significant treatment challenges. Enhancer of zeste homolog 2 (EZH2) shows aberrant expression in various tumors including osteosarcoma, which is identified as a potential therapeutic target. The anti-cancer efficacy of EZH2 inhibitor GSK126 has attracted attention, yet its impact on osteosarcoma cells was not fully understood. The study investigated the effects of GSK126 on osteosarcoma cells, particularly in apoptosis, autophagy, and cell motility. Our findings revealed that GSK126 induced apoptosis and autophagy, evidenced by increased markers like cleaved caspase-3 and LC3-II, and decreased cellular migration, through downregulation of the Fuse Binding Protein 1 (FBP1)/C-Myc axis. These findings suggest GSK126 as a promising therapeutic against osteosarcoma, offering a dual action of promoting cell death and hindering migration.

Background: Several studies have used demographic characteristics to examine differences in survival time for patients with malignant meningioma (MM). Latent class analysis (LCA), with its ability to identify mutually patterns of patients in a heterogeneous population. The aim of our study was to analyze the heterogeneity of sociodemographic characteristics in meningioma.

Methods: The data of patients diagnosed with malignant meningioma (n = 1,562, age > 18 years old) were extracted from the Surveillance, Epidemiology, and End Result database. Data on sociodemographic characteristics such as age, sex, race, NHIA, marital status, household income, rural or urban residential area, and overall survival time were included. LCA was used to identify heterogeneous patterns of MM. each group was explored using Bayesian network analysis.

Results: In total, 1562 patients with MM were processed by the LCA model; the 4-class latent class models were the best fit. LCA identified four survival groups: highest, intermediate-high, low-to-moderate, and lowest survival groups. Patients with the longest survival times-93.59 months-were 40-59 years old, female, Black, non-Hispanic, married, and had a family income of $60,000-$74,999 and lived in densely populated areas. Bayesian networks revealed correlations between patients with MM and sociodemographic characteristics in different latent class groups.

Conclusion: We identified and verified differences in clinical and sociodemographic characteristics between survival groups. A comprehensive understanding of the "people-oriented" subgroup characteristics will greatly benefit the diagnosis and treatment of MM.

The potential oncogenic role of Baculoviral inhibitor of apoptosis (IAP) Repeat-Containing (BIRC) genes in prostate cancer (PCa) has yet to be fully investigated. Two genes associated with disease recurrence, BIRC5 and BIRC7, were identified through survival analysis, and prostate cancer patients were categorized into two subtypes, C1 and C2, based on these genes. We performed survival analyses to assess the relationship between subtypes and the prognosis of PCa. Single-cell dataset analysis was used to identify specific cell types with enriched expression of BIRC family genes. Our findings show that BIRC5 and BIRC7 exhibit higher expression in PCa tissues compared to non-cancerous tissues. High expression of BIRC5 and BIRC7 independently correlates with an adverse prognosis in PCa. The analysis of mechanisms reveals that the differentially expressed genes impact signaling pathways associated with cancer and immunity. BIRC5/BIRC7 correlate with several immune cells infiltrating levels including T cells and macrophages. Furthermore, our research indicates that elevated expression of BIRC5 is associated with immune infiltration in PCa. These findings highlight the potential of BIRC5/BIRC7 or C1 subtype as prognostic biomarkers, offering new insights into possible targets for the development of therapeutic biomarkers and immunotherapeutic for PCa.

A growing body of research indicates that a wide range of cancer types may correlate with human microbiome components. On the other hand, little is known about the potential contribution of the oral microbiota to oral cancer. However, some oral microbiome components can stimulate different tumorigenic processes associated with the development of cancer. In this line, two prevalent oral infections, Porphyromonas gingivalis, and Fusobacterium nucleatum can increase tumor growth. The microbiome can impact the course of the illness through direct interactions with the human body and major modifications to the toxicity and responsiveness to different kinds of cancer therapy. Recent research has demonstrated a relationship between specific phylogenetic groupings and the results of immunotherapy treatment for particular tumor types. Conversely, there has been a recent upsurge in interest in the possibility of using microbes to treat cancer. At the moment, some species, such as Salmonella typhimurium and Clostridium spp., are being explored as possible cancer treatment vectors. Thus, understanding these microbial interactions highlights the importance of maintaining a healthy oral microbiome in preventing oral cancers. From this perspective, this review will discuss the role of the microbiome on oral cancers and their possible application in oral cancer treatment/improvement.

Background: Colorectal cancer (CRC) is known for its high heterogeneity, with liver metastases significantly impairing survival outcomes. Understanding the tumor microenvironment (TME) and genomic alterations in metastatic sites is crucial for developing personalized therapies that overcome drug resistance and improve prognosis.

Methods: We profiled 54 CRC liver metastases, comparing them with 198 other metastatic lesions and normal liver tissues. By analyzing immune cell infiltration, stromal interactions, and key genomic alterations, we constructed an 11-gene prognostic model to predict survival and immunotherapy outcomes.

Results: CRC liver metastases with high-risk profiles demonstrated enriched follicular helper T cells, activated dendritic cells, and M2 macrophages in the TME. Frequent mutations in APC, TP53, KRAS, and PIK3CA were identified, alongside altered EGFR signaling. The 11-gene model effectively stratified patients by prognosis and predicted immunotherapy responses, emphasizing the therapeutic potential of targeting resistance mechanisms.

Conclusions: This study reveals how genomic and TME-driven factors contribute to drug resistance in CRC liver metastases. Integrating these insights with clinical data could advance precision therapies, addressing the evolving challenge of tumor drug resistance in CRC.