Experimental and Therapeutic Medicine

Our medical research library holds 8 studies published in Experimental and Therapeutic Medicine (2010–2025). Each entry links to the study's record on PubMed and, where there is one, to the publisher's page and a free full text. 8 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it.

About the journal

• Publisher: Spandidos Pub.]
• Published: 2010 to the present, Greece
• Language: English
• ISSN: 1792-0981 (print), 1792-1015 (electronic)
• Its record in the NLM Catalog

2020s

• Analysis of a pan-cancer panel reveals the amino acid metabolism-related gene MTHFD1 as a potential prognostic and immunotherapeutic biomarker. S. Gong, J. Yang, C. Pan, et al. 2025;30(1):142. PubMed · Publisher · Free full text

  Abstract

  Methylenetetrahydrofolate dehydrogenase 1 (MTHFD1) serves a role in amino acid metabolism and may influence tumor progression. However, to the best of our knowledge, a comprehensive analysis of MTHFD1 in various types of cancer has not been previously performed. Therefore, the present study aimed to investigate the expression profile and prognostic implication of MTHFD1 across various types of cancer, whilst assessing its potential as a novel biomarker and therapeutic target. The expression of MTHFD1 in tissues from various types of cancer was analyzed using online tools based on data from the Cancer Cell Line Encyclopedia and Clinical Proteomic Tumor Analysis Consortium, as well as in-house differential expression analysis using data from The Cancer Genome Atlas (TCGA). The association between MTHFD1 and prognosis was investigated using Kaplan-Meier survival analysis and Cox proportional hazards regression analysis based on TCGA datasets. Furthermore, the association between MTHFD1 and the tumor microenvironment (TME) was investigated using the 'estimation of stromal and immune cells in malignant tumor tissues using expression data' and 'cell-type identification by estimating relative subsets of RNA transcripts' algorithms. The correlation between MTHFD1 expression and tumor mutational burden (TMB), microsatellite instability (MSI) or 48 immune checkpoint blockade-related gene expression levels was investigated using Pearson correlation analyses. The predictive potential of MTHFD1 for immunotherapy efficacy was evaluated using the tumor immune dysfunction and exclusion (TIDE) algorithm with the IMvigor210 dataset. Subsequently, the effects of MTHFD1 on the proliferation and invasion of A549 and 786-O cell lines were assessed using colony formation and Transwell assays. Analysis across 33 tumor types revealed that MTHFD1 expression was significantly upregulated in 12 cancers (e.g., bladder urothelial carcinoma) and downregulated in 6 cancers (e.g., breast invasive carcinoma). Moreover, high MTHFD1 expression was associated with a poorer prognosis in kidney chromophobe and lung adenocarcinoma, but with better prognosis in kidney renal clear cell carcinoma. Additionally, the activity of MTHFD1, evaluated using the single-sample Gene Set Enrichment Analysis algorithm, was significantly upregulated in 21 cancer types, including bladder urothelial carcinoma and breast invasive carcinoma, compared with corresponding normal tissues. MTHFD1expression levels were negatively correlated with immune cell infiltration in 16 tumor types [e.g., adrenocortical carcinoma (ACC)] and positively correlated only in uveal melanoma (UVM). Additionally, MTHFD1 expression levels showed significant correlations with TMB in 17 tumors (e.g., ACC), were negatively correlated with TIDE scores in most tumors except mesothelioma, liver hepatocellular carcinoma, diffuse large B-cell lymphoma and cholangiocarcinoma, and were associated with MSI in 9 tumor types (e.g., UVM). Multivariant Cox regression analysis revealed that MTHFD1 expression was an independent risk factor for prognosis in lung adenocarcinoma, whilst it was an independent protective factor in clear cell renal cell carcinoma, highlighting its distinct prognostic roles in these two tumor types. In vitro experiments found that knocking down or overexpressing MTHFD1 in A549 and 786-O cells, respectively, reduced the corresponding malignant phenotypes. Overall, to the best of our knowledge, results of the present study provided the first comprehensive analysis of MTHFD1 as a potential cancer biomarker and highlighted its role in immune suppression within the TME. These findings suggested that targeting MTHFD1 may be a novel therapeutic strategy, which may enhance the efficacy of immunotherapy and improve the outcomes of patients with various types of cancer.

  Copyright: © 2025 Gong et al.

• Morphine poisoning in a patient with malignant peritoneal mesothelioma: A case report. C. Zhao, J. Bai, S. Jia, et al. 2023;25(5):197. Case report PubMed · Publisher · Free full text

  Abstract

  Pain is one of the most common symptoms of malignant peritoneal mesothelioma. Therefore, analgesia serves an indispensable role in the treatment of this condition. Morphine is a representative opioid, which is widely used in clinical practice; however, excessive or unreasonable application can cause poisoning. Few cases of morphine poisoning have been reported, and cases of morphine poisoning in patients with malignant peritoneal mesothelioma are even more rare. Here, we present a case of morphine poisoning in a patient with malignant peritoneal mesothelioma. The patient had a high abdominal tumor load, hepatorenal insufficiency, and was treated with a combination of morphine and the sedative benzodiazepine, eventually leading to morphine poisoning. Therefore, for cancer pain, omni-directional and whole-process management should be emphasized. In patients with hepatorenal insufficiency, those treated with morphine combined with benzodiazepines, or those with a high abdominal tumor load, attention should be paid to drug absorption, excretion and interaction, and the drug dose during administration should be reduced to avoid drug poisoning. If poisoning symptoms occur, timely measures should be taken to reduce poison absorption and increase poison excretion, and antagonists should be used to reverse the poisoning and reduce the damage caused.

  Copyright: © Zhao et al.

2010s

• Mesothelin-targeted second generation CAR-T cells inhibit growth of mesothelin-expressing tumors in vivo. L. Ye, Y. Lou, L. Lu, et al. 2019;17(1):739-747. PubMed · Publisher · Free full text

  Abstract

  Non-small cell lung cancer (NSCLC) and mesothelioma are renowned for being diagnosed at a late stage and poor prognosis. Although surgery, chemotherapy, and radiotherapy have yielded successful outcomes, the improvement on the survival rate of NSCLC and mesothelioma have been less marked. Recently, adoptive immunotherapy, particularly chimeric antigen receptor T (CAR-T) cell therapy demonstrated promise for improving the survival of acute lymphoblastic leukemia with minimum toxicity. However, its application in solid tumors still warrants in-depth investigations and multiple consistent trial results, particularly in eliminating 'off-tumor' toxicity. To explore CAR-T therapy in NSCLC and mesothelioma, second-generation CAR-T cells were constructed targeting mesothelin (MSLN), which is abundant in NSCLC and mesothelioma but is under expressed in normal tissues. The second-generation design incorporated co-stimulatory CD28 and 4-1BB signaling domains to enhance the proliferation. Following the successful analysis of CAR-T cells by flow cytometry, cytotoxicity experiments were performed using the LDH kit to verify the killing effect of CAR-T cells on target cells. Otherwise, the in vivo killing tumor activity of MSLN CAR-T cells was verified by constructing a mouse model using tumor-derived cells from patients to inoculate the mice. When the effector-to-target ratio is >0.5:1, CAR-T MSLN cells exhibited significantly higher ability to kill tumor cells than T cells. In in vivo experiments, mice whose tail vein was injected with CAR-T MSLN cells demonstrated significantly slower tumor growth. Without continuous administration, both groups became gradually synchronized in growth of tumor size, which suggests that the persistence of CAR-T cells is an important issue in preclinical studies.

• Pravastatin reduces radiation-induced damage in normal tissues. H. Doi, S. Matsumoto, S. Odawara, et al. 2017;13(5):1765-1772. PubMed · Publisher · Free full text

  Abstract

  Pravastatin is an inhibitor of 3-hydroxy-3-methyl- glutaryl-coenzyme A reductase that has been reported to have therapeutic applications in a range of inflammatory conditions. The aim of the present study was to assess the radioprotective effects of pravastatin in an experimental animal model. Mice were divided into two groups: The control group received ionizing radiation with no prior medication, while the pravastatin group received pravastatin prior to ionizing radiation. Pravastatin was administered orally at 30 mg/kg body weight in drinking water at 24 and 4 h before irradiation. Intestinal crypt epithelial cell survival and the incidence of apoptosis in the intestine and lung were measured post-irradiation. The effect of pravastatin on intestinal DNA damage was determined by immunohistochemistry. Finally, the effect of pravastatin on tumor response to radiotherapy was examined in a mouse mesothelioma xenograft model. Pravastatin increased the number of viable intestinal crypts and this effect was statistically significant in the ileum (P<0.0001). The pravastatin group showed significantly lower apoptotic indices in all examined parts of the intestine (P<0.0001) and tended to show reduced apoptosis in the lung. Pravastatin reduced the intestinal expression of ataxia-telangiectasia mutated and gamma-H2AX after irradiation. No apparent pravastatin-related differences were observed in the response of xenograft tumors to irradiation. In conclusion, pravastatin had radioprotective effects on the intestine and lung and reduced radiation-induced DNA double-strand breaks. Pravastatin may increase the therapeutic index of radiotherapy.

• Fluoro-edenite and carbon nanotubes: The health impact of 'asbestos-like' fibres. E. Miozzi, V. Rapisarda, A. Marconi, et al. 2016;11(1):21-27. PubMed · Publisher · Free full text

  Abstract

  Several decades have passed since Wagner et al demonstrated a causal link between asbestos fibre inhalation and the development of pleural mesothelioma in 1960. It was later suggested that pleural plaques are a benign consequence of exposure to these fibres. Most recently, a significant association between exposure to asbestos and cancer diagnosed at various sites, such as the peritoneum, stomach, pharynx, colon and ovaries has been demonstrated. The great concerns about public health that arose from the scientific evidence presented above have led to the banning of asbestos in several countries. Over the years, the suspicion that particles with a high aspect ratio may have asbestos-like pathogenicity has been supported by increasing evidence. Natural occurring minerals, as well as man-made fibres, have proven capable of inducing either chronic inflammation of serous membranes, or, in some cases, the development of peritoneal and pleural mesothelioma. The pathogenic role of both fluoro-edenite and carbon nanotubes, two 'asbestos-like' fibres is summarized and discussed in this review. The data presented herein support the notion that occupational exposure to these two types of fibre contributes to the development of different types of cancer.

• Computed tomography-guided cutting needle pleural biopsy: Accuracy and complications. Y.Y. Cao, N. Fan, F. Xing, et al. 2015;9(1):262-266. PubMed · Publisher · Free full text

  Abstract

  In cases of pleural lesion, tissue samples can be obtained through thoracoscopy or closed needle biopsy for histopathological analysis. Cutting needle biopsy is a relatively recent addition to these techniques. The aim of this study was to evaluate the diagnostic accuracy and safety of computed tomography-guided cutting needle pleural biopsy (CT-CNPB), as well as the associated complications, in patients with pleural lesion. This study was a retrospective analysis of 92 percutaneous CT-CNPBs on 90 patients between March 2008 and May 2013. For group comparisons, χ2 tests were used to detect the risk factors for diagnostic accuracy (false-negative rate). Of the 92 CT-CNPBs, malignant lesions were diagnosed in 55 cases (mesothelioma in 12, metastatic pleural disease in 36, synoviosarcoma in one, indeterminate-origin disease in one and false-negative lesion in five) and benign pleural disease was diagnosed in 37 cases (inflammation in 15, tuberculosis in 10, granuloma in three, solitary fibrous tumor in two, hematoma in one, fungus in one and indeterminate-origin disease in five). The sensitivity of diagnostic malignant lesion was 90.9%, and the specificity and positive and negative predictive values were 100, 100 and 88.1%, respectively. The overall diagnostic accuracy was 94.6%. A specific diagnosis was achieved in 89.1% of malignant lesions and 86.4% of benign lesions. Univariate analysis of the risk factors affecting accuracy (false-negative rate) did not reveal any significant differences (all P>0.05). The complication rates were 6.5% for pneumothorax, 8.7% for hemorrhage and 1.1% for hemothorax. In conclusion, CT-CNPB is a safe and accurate diagnostic technique that can be recommended as the primary method of diagnosis in patients with pleural thickening or lesions observed by CT scan.

• Clinical utility of 18-fluorodeoxyglucose positron emission tomography/computed tomography in malignant pleural mesothelioma. T. Terada, C. Tabata, R. Tabata, et al. 2012;4(2):197-200. PubMed · Publisher · Free full text

  Abstract

  Malignant pleural mesothelioma (MPM) is an aggressive malignant tumor of mesothelial origin associated with asbestos exposure. MPM has a limited response to conventional chemotherapy and radiotherapy, thus early diagnosis of MPM is extremely critical. CT scans have limited accuracy in the differentiation between benign and malignant pleural disease. Several studies have reported that 18-fluorodeoxyglucose (FDG) positron emission tomography (PET) plays an important role in the assessment of thoracic malignancy such as lung cancer. Here, we investigated the clinical utility of PET in patients with MPM. The maximum SUV (SUVmax) of 18F-FDG was measured in 47 MPM patients and 29 non-MPM patients including those with pleural thickening. We demonstrated that patients with MPM had significantly higher SUVmax levels than a population with non-malignant pleural disease. The Kaplan-Meier method revealed significant differences in overall survival between groups with SUVmax levels lower and higher than the assumed cut-off. Our data suggest that SUVmax levels are useful as an aid for diagnosis and prognosis of MPM.

• Soluble mesothelin-related protein in pleural effusion from patients with malignant pleural mesothelioma. N. Fujimoto, K. Gemba, M. Asano, et al. 2010;1(2):313-317. PubMed · Publisher · Free full text

  Abstract

  Malignant pleural mesothelioma (MPM) is a highly aggressive neoplasm primarily arising from surface serosal cells of the pleura and is strongly associated with asbestos exposure. Patients with MPM often develop pleural fluid as initial presentation. However, cytological diagnosis using pleural fluid is usually difficult and has limited utility. A useful molecular marker for differential diagnosis particularly with lung cancer (LC) is urgently needed. The aim of the present study was to investigate the diagnostic value of soluble mesothelin-related protein (SMRP) in pleural fluid. Pleural fluids were collected from 23 patients with MPM, 38 with LC, 26 with benign asbestos pleurisy (BAP), 5 with tuberculosis pleurisy (TP) and 4 with chronic heart failure (CHF), and the SMRP concentration was determined. All data were analyzed by using non-parametric two-sided statistical tests. The median concentration of SMRP in MPM, LC, BAP, TP and CHF were 11.5 (range 0.90-82.80), 5.20 (0.05-36.40), 6.65 (1.45-11.25), 3.20 (1.65-6.50) and 2.03 (1.35-2.80) nmol/l, respectively. The SMRP concentration was significantly higher in MPM than in the other diseases (P=0.001). The area under the ROC curve (AUC) values of the MPM diagnosis was 0.75 for the differential diagnosis from the other groups. Based on the cut-off value of 8 nmol/l, the sensitivity and specificity for diagnosis of MPM were 70.0 and 68.4%, respectively. These results indicate that the SMRP concentration in pleural fluid is a useful marker for the diagnosis of MPM.

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