Cancer Biomarkers最新文献

BackgroundAs the role of physical activity in breast cancer management gains increasing recognition, understanding the effects of aerobic exercise on patients' quality of life and biological markers has emerged as a critical area of research to inform clinical practices and improve patient outcomes.ObjectiveThis study aims to investigate the impact of low-intensity resistance exercise training on serum tumor biomarkers and quality of life in women with breast cancer, providing evidence for its potential role as an adjunct therapy in improving clinical outcomes and patient well-being.MethodsThis study was carried out on 70 women between the ages of 18 and 65, who were included in the study while receiving chemotherapy treatment. The subject was divided into low-intensity resistance exercise (Group I) and control (Group II). Demographic characteristics, quality of life, and serum tumor biomarkers were evaluated. Participants in group I underwent a 12-week exercise programme of low-intensity resistance exercises three times a week (three metabolic equivalents, approximately 30 min/session).ResultsThe quality of life has been found to be significantly higher in the low-intensity resistance exercise group (p < 0.05). The serum tumor biomarker levels of CEA, CA15-3, and CA19-9 decreased across all participants. However, the reduction in serum tumor biomarker levels was found to be more pronounced in Group 1 (p < 0.05).ConclusionsLow-intensity resistance exercise has demonstrated a positive effect on the quality of life in women with breast cancer. Within the framework of oncological rehabilitation, aerobic exercise regimens may be preferred due to their role in promoting improvements in serum tumor biomarker levels and contributing to enhanced quality of life.

Objective: The aim of this study was to compare the competing risk model with the Cox model to evaluate prognostic markers in females with keratinized squamous cell carcinoma of the reproductive system and to develop predictive models. Methods: Patients with keratinizing squamous cell carcinoma of the female reproductive system were identified from the Surveillance, Epidemiology, and End Results (SEER) database. Using the cumulative incidence function (CIF) and Gray's test for univariate analysis, the competing risk and Cox models were used for multivariate analysis. A nomogram was developed based on the results of the competing risk model, and the C-index, net reclassification index (NRI), and integrated discrimination improvement (IDI) were used to evaluate the model's discrimination ability. The clinical validity of the model was assessed using calibration plots and decision curve analysis (DCA). Results: In this investigation, competing risk model analysis revealed that age, marital status, tumor size, AJCC stage, surgery, radiotherapy, chemotherapy, postoperative lymph node dissection, surgery and radiotherapy, and income were significant factors affecting the prognosis of patients with keratinizing squamous cell carcinoma of the female reproductive system. Based on these results, a nomogram for predicting the 3-year, 5-year, and 8-year survival rates was established. The nomogram demonstrated better clinical utility than the AJCC staging system. Conclusion: For the first time, the competing risk model was used in this study to assess the prognostic risk factors of keratinizing squamous cell carcinoma of the female reproductive system. The results may help clinicians make better clinical judgments. Additionally, we developed a nomogram to predict the likelihood of cancer-specific death (CSD) in patients at 3, 5, and 8 years. Physicians may use our nomogram to more accurately forecast the likelihood of CSD compared to the AJCC staging system.

Pancreatic cancer is a rare and refractory cancer, and the development of blood biomarkers for the enrichment of high-risk individuals who have risk factors for pancreatic cancer from the asymptomatic population is an unmet medical need. We identified abnormalities in the C-terminal truncation of the apolipoprotein A2 dimer (apoA2-isoforms: apoA2-i) in the blood of pancreatic cancer patients through proteomic analysis, and we have reported the potential for diagnosing resectable pancreatic cancer by detecting these abnormalities. We successfully developed enzyme-linked immunosorbent assay (ELISA) reagents for measuring apoA2-i for research use only, and then the basic data for diagnosing pancreatic cancer were accumulated by several studies using these reagents. In 2023, ELISA for measuring apoA2-i was regenerated by the regulation under the Japanese Quality Management System (QMS), it received marketing approval in Japan as an in vitro diagnostic (IVD) kit to aid in the diagnosis of pancreatic cancer, and it is now used in clinical practice. This review chronicles the journey from the initial discovery through omics research, to demonstrating clinical utility via multicenter studies in Japan and international collaborative research using the research reagent and validating the clinical performance of the IVD ELISA kit through a regulatory, science-guided, clinical trial in Japan, and finally to recent activities in the USA.

ARID1A mutations are a common occurrence in colorectal cancer (CRC) cells, but clinical therapeutic options targeting this anomaly remain unavailable. The loss of ARID1A functionality compromises DNA damage repair processes, potentially causing cancer cells to rely more heavily on PARP-dependent DNA repair pathways to preserve genomic integrity, thereby making them susceptible to PARP inhibitor (PARPi) therapy. To evaluate the suitability of PARPi treatment for CRC patients with ARID1A sufficiency (ARID1A+) and ARID1A deficiency (ARID1A-), our study enrolled 80 patients who had undergone surgical treatment for primary CRC. Surgical specimens underwent immunohistochemical examination to assess ARID1A protein expression. The study explored correlations between ARID1A expression loss and clinicopathological characteristics. Moreover, primary CRC cells were isolated through enzymatic digestion and validated using the colorectal carcinoma marker CK20. Subsequently, PARPi sensitivity was investigated in untreated ARID1A+ and ARID1A- CRC patients using an ATP-tumor chemosensitivity assay (ATP-TCA). Additionally, we confirmed the efficacy of PARPi in these primary CRC cells through clone formation and assessed its impact on cell cycle dynamics, apoptosis, and DNA damage repair signaling pathways using immunofluorescence and flow cytometry. The results demonstrated that the ARID1A- group displayed greater sensitivity to PARPi compared to the ARID1A+ group. PARPi treatment led to increased tumor cell death in the ARID1A- group. Mechanistically, ARID1A deficiency resulted in cell cycle abnormalities, particularly G2/M phase arrest, which was further exacerbated by PARPi treatment. Furthermore, PARPi treatment significantly increased the number of RAD51 foci in ARID1A- cell lines. In conclusion, our study highlights the potential of PARPi as an effective therapeutic option for ARID1A- CRC patients.

BackgroundCanopy FGF signalling regulator 3 (CNPY3) is involved in immune regulation, tumorigenesis and development, nevertheless, its role in glioma remains largely unexplored. Our study aimed to explore the regulatory role of CNPY3 as a prognostic biomarker in human glioma cell migration, invasion and immune infiltration.MethodsBioinformatics analysis of CNPY3 and clinical relevance of glioma in public databases was performed. COX regression analysis was performed to assess the relationship between CNPY3 and glioma prognosis. GO and Kyoto Encyclopedia of Genes and Genomes analyses were conducted to predict the signaling pathways of CNPY3 in gliomas. Tumor immune infiltration was explored using TIMER, CIBERSORT, and Pearson correlation analysis. GSVA analysis and single-cell sequencing data were employed for further validation. The effects of CNPY3 on the migration and invasion of glioma cells were investigated through cell scratch assay and transwell assay.ResultsCNPY3 was positively correlated with IDH mutation status, 1p/19q status, histopathologic grade, and MGMT promoter methylation status, but negatively with the overall survival of glioma patients (P < 0.05). CNPY3 was significantly associated with tumor immune response, inflammatory response, and lipopolysaccharide-mediated signaling pathway. CNPY3 influenced different types of immune cells which affected the immune microenvironment of glioma. CNPY3 promoted the increase of M2 macrophage and was negatively correlated with the positive regulation of macrophages apoptotic process. In vitro data suggested the promotion of CNPY3 in U87MG cells was associated with an increased capacity for cell migration and invasion (P < 0.05). Tumor drug sensitivity analysis showed more sensitivity towards temozolomide, irinotecan, and cisplatin among high CNPY3 expression patients (P < 0.05).ConclusionIncreased CNPY3 expression impacts the immune microenvironment of glioma and enhances the migration and invasion of glioma. CNPY3 is recommended as a prognostic biomarker for glioma patients.

Breast cancer, the most common cancer in women, is characterized by cell cycle dysregulation and chromosome segregation errors, leading to mitotic catastrophe and genomic instability. Understanding these molecular mechanisms is crucial for better diagnosis and treatment. We used databases like TIMER 2.0, UALCAN, and Oncomine to determine the differential expression of Budding uninhibited by benzimidazole 1 (BUB1) in normal and pan-cancer tissues. we also used the Kaplan-Meier Plotter database to analyze gene expression associations with survival outcomes, bc-GenExMiner v5.0 to analyze BUB1 gene expression and histological subtypes, and ctcRbase and miR-TV to identify microRNAs associated with BUB1 expression in breast cancer. Our data show that BUB1 expression is overexpressed in breast cancer tumors, metastatic tissues, and circulating tumor cells, leading to shorter overall survival, disease-free survival, and relapse-free survival compared to low-expression patients. BUB1 expression is strongly correlated with E2F1/E2F8 expression, suggesting a potential regulatory relationship between these genes. The study revealed a negative correlation between target miRNA miR-495-3p and BUB1 expression in breast cancer tumors, indicating a potential regulatory relationship between these genes. The BUB1 expression was also strongly correlated with the infiltration of CD4+ T helper 2 (Th2) subtypes in the tumors, suggesting a need for further research.

BackgroundCisplatin (DDP) resistance is a major challenge in the management of non-small cell lung cancer (NSCLC). Panax notoginseng has anticancer effects on a variety of solid tumors, but data on NSCLC and DDP resistance are lacking.ObjectiveTo investigate the effect of Panax notoginseng on DDP resistance in NSCLC in vitro and in vivo and explore the mechanisms involved.MethodsA 1 g/mL Panax notoginseng extract was prepared to treat the A549 and DDP-resistant A549/DDP cell lines. Cell proliferation was assessed using the CCK-8 assay, and apoptosis was measured via Annexin V-FITC/PI staining and flow cytometry. Glucose uptake, ATP production, and lactate levels were evaluated. Protein levels of p-AKT, GLUT1, HKII, and cleaved-caspase-3 were analyzed by Western blot. IGF1 was used to activate the Akt pathway. In vivo, A549/DDP cells were inoculated into nude mice to establish subcutaneous tumors, and tumor growth and apoptosis were assessed.ResultsPanax notoginseng inhibited A549/DDP cell proliferation, enhanced DDP-induced apoptosis, and reduced glucose uptake, ATP, and lactate levels (all p < 0.05). Combined treatment decreased p-AKT, GLUT1, and HKII expression while increasing cleaved-caspase-3(p < 0.05). IGF1 reversed these effects, indicating Akt pathway involvement (p < 0.05). In vivo, Panax notoginseng and DDP significantly suppressed tumor growth and increased apoptosis in tumors, confirming enhanced chemosensitivity (p < 0.05).ConclusionPanax notoginseng can improve the sensitivity of A549/DDP cells to DDP by inhibiting the effects of TRIM46 and Akt signaling pathways on glycolysis in vivo and in vitro.

BackgroundNeuroblastoma (NB) is one of the most common and aggressive pediatric solid tumors, characterized by a highly complex pathogenesis. Within the tumor microenvironment (TME), cancer-associated fibroblasts (CAFs) constitute a major cell population and play a pivotal role in facilitating communication among various stromal cells. However, the specific functions and contributions of CAFs in NB remain incompletely understood.ObjectiveTo investigate the impact of CAFs-related genes on the prognosis of NB, we developed a risk model to facilitate the diagnosis and prognostication of patients.MethodsIn this study, a CAFs gene prognostic model for NB was established using single-cell analysis and genomic sequencing data. The effectiveness of this prognostic model was subsequently evaluated through the development of a nomogram, immune infiltration analysis, drug prediction, and gene set enrichment analysis. Ultimately, the expression levels of the identified key genes were experimentally validated in NB tissues.ResultsA novel prognostic model for CAFs related to NB prognosis was established through single-cell analysis and transcriptome dataset analysis. The prognosis of the high-risk group was worse than that of the low-risk group. The validity of the model was confirmed by nomogram, drug sensitivity analysis, and immune infiltration methods. Finally, the high expression of the key gene STEAP2 in NB tissues was verified by experiments.ConclusionsThe study introduces a new predictive model that uses CAF markers to forecast the prognosis of NB. STEAP2 plays a key role in identifying high-risk neuroblastoma and may become a potential therapeutic target for NB.

BackgroundHypoxia and leptin receptors (also called obesity receptors, OB-R) are evident markers of tumor progression and have been demonstrated to be essential oncogenes in a variety of cancers. However, the specific role of OB-R in lung cancer, especially non-small cell lung cancer (NSCLC) and its correlation with HIF1α remains unclear. Present study aims to explore the potential functions and mechanisms of OB-R in NSCLC.MethodsThe RNA levels of HIF1α and OB-R in NSCLC cells were detected by quantitative real-time PCR (qRT-PCR) and western blotting. The HIF-1α, OB-R, and Ki67 levels in tumor tissues were detected by immunohistochemistry. CCK8 assays for proliferation, transwell assays for migration were performed to determine the role of HIF-1α and OB-R in vitro, while subcutaneous tumors in nude mice were used for in vivo functional studies. Mechanically, chromatin immunoprecipitation and luciferase reporter gene analyses were executed to determine the relationship between HIF-1α and OB-R.ResultsqRT-PCR and western blotting revealed that HIF-1α and OB-R was highly expressed in NSCLC cells. Moreover, hypoxia up-regulated OB-R expression in NSCLC cells via HIF-1α. Hence, down-regulating HIF-1α significantly reduced the mRNA level of OB-R. In addition, HIF-1α silencing reduced cell proliferation and migration in vitro. Xenograft mouse models indicated that decrease of HIF-1α led to tumor growth by decreasing OB-R in vivo. Mechanically, we unveiled that HIF-1α bound to the promoter region (-831 to -824) and positively regulated OB-R expression by activating its transcription. Additionally, by immunohistochemical staining, we observed that high levels of HIF-1α and OB-R were positively associated with tumor size and lymph node metastasis.ConclusionIn conclusion, our present results demonstrated that HIF-1α positively regulates the expression of OB-R, which acts as an oncogene in NSCLC. HIF-1α and OB-R are potential therapeutic targets in NSCLC.