4 results on '"Catalani, S."'
Search Results
2. Occupational exposure to formaldehyde and risk of non hodgkin lymphoma: a meta-analysis.
- Author
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Catalani S, Donato F, Madeo E, Apostoli P, De Palma G, Pira E, Mundt KA, and Boffetta P
- Subjects
- Humans, Lymphoma, Non-Hodgkin chemically induced, Occupational Diseases chemically induced, Occupational Exposure adverse effects, Risk Assessment methods, Risk Factors, Disinfectants poisoning, Formaldehyde poisoning, Lymphoma, Non-Hodgkin epidemiology, Occupational Diseases epidemiology, Occupational Exposure statistics & numerical data
- Abstract
Background: Formaldehyde, a widely used chemical, is considered a human carcinogen. We report the results of a meta-analyses of studies on the relationship between occupational exposure to formaldehyde and risk of non-Hodgkin lymphoma (NHL)., Methods: We performed a systematic review and meta-analysis according to international guidelines and we identified 12 reports of occupational populations exposed to formaldehyde. We evaluated inter-study heterogeneity and we applied a random effects model. We conducted a cumulative meta-analysis and a meta-analysis according to estimated average exposure of each study population., Results: The meta-analysis resulted in a summary relative risk (RR) for NHL of 0.93 (95% confidence interval 0.83-1.04). The cumulative meta-analysis suggests that higher RRs were detected in studies published before 1986, while studies available after 1986 did not show an association. No differences were found between different levels of occupational exposure. Conclusions Notwithstanding some limitations, the results of this meta-analysis do not support the hypothesis of an association between occupational exposure to formaldehyde and risk of NHL.
- Published
- 2019
- Full Text
- View/download PDF
3. CELLFOOD™ induces apoptosis in human mesothelioma and colorectal cancer cells by modulating p53, c-myc and pAkt signaling pathways.
- Author
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Nuvoli B, Santoro R, Catalani S, Battistelli S, Benedetti S, Canestrari F, and Galati R
- Subjects
- Cell Line, Tumor, Cell Survival drug effects, Colorectal Neoplasms, Cyclin-Dependent Kinase Inhibitor p21 metabolism, Cyclin-Dependent Kinase Inhibitor p27 metabolism, Humans, Mesothelioma, Signal Transduction drug effects, Amino Acids pharmacology, Apoptosis drug effects, Enzymes pharmacology, Minerals pharmacology, Proto-Oncogene Proteins c-akt metabolism, Proto-Oncogene Proteins c-myc metabolism, Sulfates pharmacology, Tumor Suppressor Protein p53 metabolism
- Abstract
Background: CELLFOOD™ (CF) is a nutraceutical non-addictive, non-invasive, and completely non-toxic unique proprietary colloidal-ionic formula. Little is known about its effect on cancer cells in solid tumors. The aim of this study was to evaluate the effect that CF has on different cancer cell lines and the mechanism by which the nutraceutical works., Methods: The effect of CF on HFF (normal fibroblasts), Met5A (mesothelium), MSTO-211H, NCI-2452, Ist-Mes1, MPP89, Ist-Mes2 (mesothelioma), M14 (melanoma), H1650, H1975 (lung cancer), SKRB3 (breast cancer), and HCT-116 (colorectal cancer) cell growth was tested by cell proliferation and clonogenic assay. Among all of them, MSTO-211 and HCT-116 were analyzed for cell cycle by flow cytometry and western blot., Results: All human cancer lines were suppressed on cell growth upon 1:200 CF treatment for 24 and 48 hours. Death was not observed in HFF and Met5A cell lines. Cell cycle analysis showed an increased sub-G1 with reduction of G1 in MSTO-211 and a cell cycle arrest of in G1 in HCT116. Activation of caspase-3 and cleavage of PARP confirmed an apoptotic death for both cell lines. Increased expression levels of p53, p21, and p27, downregulation of c-myc and Bcl-2, and inhibition of Akt activation were also found in CF-treated MSTO-211 and HCT-116 cells., Conclusions: These findings ascertained an interaction between p53, c-myc, p21, p27, Bcl-2, PI3K/Akt pathway, and CF-induced apoptosis in MSTO-211H and HCT-116 cells, suggesting that CF acts as an important regulator of cell growth in human cancer cell lines. CF could be a useful nutraceutical intervention for prevention in colon cancer and mesothelioma.
- Published
- 2014
- Full Text
- View/download PDF
4. Metabolism modifications and apoptosis induction after Cellfood™ administration to leukemia cell lines.
- Author
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Catalani S, Carbonaro V, Palma F, Arshakyan M, Galati R, Nuvoli B, Battistelli S, Canestrari F, and Benedetti S
- Subjects
- Amino Acids pharmacology, Apoptosis drug effects, Cell Growth Processes physiology, Cell Hypoxia physiology, Cell Line, Tumor, Enzymes pharmacology, Humans, Hypoxia-Inducible Factor 1, alpha Subunit metabolism, Jurkat Cells, K562 Cells, Leukemia pathology, Minerals pharmacology, Rhodophyta chemistry, Sulfates pharmacology, U937 Cells, Dietary Supplements, Leukemia drug therapy, Leukemia metabolism, Plant Extracts pharmacology
- Abstract
Background: Cellfood™ (CF) is a nutritional supplement containing deuterium sulphate, minerals, amino acids, and enzymes, with well documented antioxidant properties. Its organic and inorganic components are extracted from the red algae Lithothamnion calcareum, whose mineral extract has shown growth-inhibitory effect both on in vitro and in vivo models. The purpose of this study was to evaluate the antiproliferative effects of CF on leukemic cells. In fact, according to its capacity to modulate O2 availability and to improve mitochondrial respiratory metabolism, we wondered if CF could affect cancer cell metabolism making cells susceptible to apoptosis., Methods: Three leukemic cell lines, Jurkat, U937, and K562, were treated with CF 5 μl/ml up to 72 hours. Cell viability, apoptosis (i.e. caspase-3 activity and DNA fragmentation), hypoxia inducible factor 1 alpha (HIF-1α) concentration, glucose transporter 1 (GLUT-1) expression, lactate dehydrogenase (LDH) activity and lactate release in the culture medium were detected and compared with untreated cells., Results: CF significantly inhibited leukemic cell viability by promoting cell apoptosis, as revealed by caspase-3 activation and DNA laddering. In particular, CF treated cells showed lower HIF-1α levels and lower GLUT-1 expression as compared to untreated cells. At the same time, CF was able to reduce LDH activity and, consequently, the amount of lactate released in the extracellular environment., Conclusions: We supplied evidence for an antiproliferative effect of CF on leukemia cell lines by inducing cell death through an apoptotic mechanism and by altering cancer cell metabolism through HIF-1α and GLUT-1 regulation. Thanks to its antioxidative and proapoptotic properties, CF might be a good candidate for cancer prevention.
- Published
- 2013
- Full Text
- View/download PDF
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