Antonio Mazzocca
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View article: Dysfunctional mitochondrial bioenergetics sustains drug resistance in cancer cells
Dysfunctional mitochondrial bioenergetics sustains drug resistance in cancer cells Open
Cancer drug resistance (CDR) is increasingly becoming a concerning clinical problem. The mechanisms behind the onset of CDR are still not well defined. In this study, we demonstrated that a treatment mimicking long-term clinical protocols …
View article: The systemic evolutionary theory of the origin of cancer (SETOC): an update
The systemic evolutionary theory of the origin of cancer (SETOC): an update Open
The Systemic Evolutionary Theory of the Origin of Cancer (SETOC) is a recently proposed theory founded on two primary principles: the cooperative and endosymbiotic process of cell evolution as described by Lynn Margulis, and the integratio…
View article: Crithmum maritimum restores the lipid and metabolic profiles of liver cancer cells to a normal phenotype
Crithmum maritimum restores the lipid and metabolic profiles of liver cancer cells to a normal phenotype Open
Hepatocellular carcinoma (HCC) is becoming an alarming epidemiological clinical problem worldwide. Pharmacological approaches currently available do not provide adequate responses due to poor effectiveness, high toxicity, and serious side …
View article: Cellular Adaptation Takes Advantage of Atavistic Regression Programs during Carcinogenesis
Cellular Adaptation Takes Advantage of Atavistic Regression Programs during Carcinogenesis Open
Adaptation of cancer cells to extreme microenvironmental conditions (i.e., hypoxia, high acidity, and reduced nutrient availability) contributes to cancer resilience. Furthermore, neoplastic transformation can be envisioned as an extreme a…
View article: Supplementary Methods from DNA Damage Response Protein CHK2 Regulates Metabolism in Liver Cancer
Supplementary Methods from DNA Damage Response Protein CHK2 Regulates Metabolism in Liver Cancer Open
Description of supplementary methods
View article: Table S2 from DNA Damage Response Protein CHK2 Regulates Metabolism in Liver Cancer
Table S2 from DNA Damage Response Protein CHK2 Regulates Metabolism in Liver Cancer Open
Table S2. % 13C enrichment in cell culture media (CCM ) for 13C-glucose, 13C-alanine and 13C-lactate obtained by 1H NMR analysis.
View article: Supplementary Figure Legends from DNA Damage Response Protein CHK2 Regulates Metabolism in Liver Cancer
Supplementary Figure Legends from DNA Damage Response Protein CHK2 Regulates Metabolism in Liver Cancer Open
Description of supplementary figures
View article: Table S3 from DNA Damage Response Protein CHK2 Regulates Metabolism in Liver Cancer
Table S3 from DNA Damage Response Protein CHK2 Regulates Metabolism in Liver Cancer Open
Table S3. % 13C enrichment in cell lysates for13C-alanine (mitochondrial pyruvate labeling) and 13C-lactate (cytosol pyruvate labeling) obtained by 1H NMR analysis.
View article: Supplementary Methods from DNA Damage Response Protein CHK2 Regulates Metabolism in Liver Cancer
Supplementary Methods from DNA Damage Response Protein CHK2 Regulates Metabolism in Liver Cancer Open
Description of supplementary methods
View article: Table S2 from DNA Damage Response Protein CHK2 Regulates Metabolism in Liver Cancer
Table S2 from DNA Damage Response Protein CHK2 Regulates Metabolism in Liver Cancer Open
Table S2. % 13C enrichment in cell culture media (CCM ) for 13C-glucose, 13C-alanine and 13C-lactate obtained by 1H NMR analysis.
View article: Table S3 from DNA Damage Response Protein CHK2 Regulates Metabolism in Liver Cancer
Table S3 from DNA Damage Response Protein CHK2 Regulates Metabolism in Liver Cancer Open
Table S3. % 13C enrichment in cell lysates for13C-alanine (mitochondrial pyruvate labeling) and 13C-lactate (cytosol pyruvate labeling) obtained by 1H NMR analysis.
View article: Supplementary Figure Legends from DNA Damage Response Protein CHK2 Regulates Metabolism in Liver Cancer
Supplementary Figure Legends from DNA Damage Response Protein CHK2 Regulates Metabolism in Liver Cancer Open
Description of supplementary figures
View article: Table S1 from DNA Damage Response Protein CHK2 Regulates Metabolism in Liver Cancer
Table S1 from DNA Damage Response Protein CHK2 Regulates Metabolism in Liver Cancer Open
Table S1. Characteristics of the healthy subjects (HS) and patients with liver cirrhosis (LC) and hepatocellular carcinoma (HCC)
View article: Table S1 from DNA Damage Response Protein CHK2 Regulates Metabolism in Liver Cancer
Table S1 from DNA Damage Response Protein CHK2 Regulates Metabolism in Liver Cancer Open
Table S1. Characteristics of the healthy subjects (HS) and patients with liver cirrhosis (LC) and hepatocellular carcinoma (HCC)
View article: Supplementary Table S3 from Lysophosphatidic Acid Receptor LPAR6 Supports the Tumorigenicity of Hepatocellular Carcinoma
Supplementary Table S3 from Lysophosphatidic Acid Receptor LPAR6 Supports the Tumorigenicity of Hepatocellular Carcinoma Open
Grouped genes according to their functions (analysis for comparative cellular processes) using the publicly available software ToppCluster multiple gene analyzer.
View article: Supplementary Table S1 from Lysophosphatidic Acid Receptor LPAR6 Supports the Tumorigenicity of Hepatocellular Carcinoma
Supplementary Table S1 from Lysophosphatidic Acid Receptor LPAR6 Supports the Tumorigenicity of Hepatocellular Carcinoma Open
List of genes up-regulated in LPAR6 knocked down cells.
View article: Supplementary Methods from Lysophosphatidic Acid Receptor LPAR6 Supports the Tumorigenicity of Hepatocellular Carcinoma
Supplementary Methods from Lysophosphatidic Acid Receptor LPAR6 Supports the Tumorigenicity of Hepatocellular Carcinoma Open
Description of additional methods and procedures used in the study.
View article: Data from Lysophosphatidic Acid Receptor LPAR6 Supports the Tumorigenicity of Hepatocellular Carcinoma
Data from Lysophosphatidic Acid Receptor LPAR6 Supports the Tumorigenicity of Hepatocellular Carcinoma Open
The aberrant processes driving hepatocellular carcinoma (HCC) are not fully understood. Lysophosphatidic acid receptors (LPAR) are commonly overexpressed in HCC, but their contributions to malignant development are not well established. In…
View article: Supplementary Table S3 from Lysophosphatidic Acid Receptor LPAR6 Supports the Tumorigenicity of Hepatocellular Carcinoma
Supplementary Table S3 from Lysophosphatidic Acid Receptor LPAR6 Supports the Tumorigenicity of Hepatocellular Carcinoma Open
Grouped genes according to their functions (analysis for comparative cellular processes) using the publicly available software ToppCluster multiple gene analyzer.
View article: Supplementary Figures S1-S7 from Lysophosphatidic Acid Receptor LPAR6 Supports the Tumorigenicity of Hepatocellular Carcinoma
Supplementary Figures S1-S7 from Lysophosphatidic Acid Receptor LPAR6 Supports the Tumorigenicity of Hepatocellular Carcinoma Open
Expression of LPAR1-5 mRNA levels in peritumoral and HCC cell lines (S1); Cell cycle analysis of LPAR6-knocked-down cells versus controls (S2); Absence of apoptosis in stably LPAR6-knocked-down cells (S3); LPAR6 knockdown impairs HCC migra…
View article: Supplementary Methods from Lysophosphatidic Acid Receptor LPAR6 Supports the Tumorigenicity of Hepatocellular Carcinoma
Supplementary Methods from Lysophosphatidic Acid Receptor LPAR6 Supports the Tumorigenicity of Hepatocellular Carcinoma Open
Description of additional methods and procedures used in the study.
View article: Supplementary Table S2 from Lysophosphatidic Acid Receptor LPAR6 Supports the Tumorigenicity of Hepatocellular Carcinoma
Supplementary Table S2 from Lysophosphatidic Acid Receptor LPAR6 Supports the Tumorigenicity of Hepatocellular Carcinoma Open
List of genes down-regulated in LPAR6 knocked down cells.
View article: Supplementary Figure S2 from A Secreted Form of ADAM9 Promotes Carcinoma Invasion through Tumor-Stromal Interactions
Supplementary Figure S2 from A Secreted Form of ADAM9 Promotes Carcinoma Invasion through Tumor-Stromal Interactions Open
Supplementary Figure S2 from A Secreted Form of ADAM9 Promotes Carcinoma Invasion through Tumor-Stromal Interactions
View article: Supplementary Figure S1 from A Secreted Form of ADAM9 Promotes Carcinoma Invasion through Tumor-Stromal Interactions
Supplementary Figure S1 from A Secreted Form of ADAM9 Promotes Carcinoma Invasion through Tumor-Stromal Interactions Open
Supplementary Figure S1 from A Secreted Form of ADAM9 Promotes Carcinoma Invasion through Tumor-Stromal Interactions
View article: Supplementary Figures S1-S7 from Lysophosphatidic Acid Receptor LPAR6 Supports the Tumorigenicity of Hepatocellular Carcinoma
Supplementary Figures S1-S7 from Lysophosphatidic Acid Receptor LPAR6 Supports the Tumorigenicity of Hepatocellular Carcinoma Open
Expression of LPAR1-5 mRNA levels in peritumoral and HCC cell lines (S1); Cell cycle analysis of LPAR6-knocked-down cells versus controls (S2); Absence of apoptosis in stably LPAR6-knocked-down cells (S3); LPAR6 knockdown impairs HCC migra…
View article: Supplementary Table and Figure Legends from Lysophosphatidic Acid Receptor LPAR6 Supports the Tumorigenicity of Hepatocellular Carcinoma
Supplementary Table and Figure Legends from Lysophosphatidic Acid Receptor LPAR6 Supports the Tumorigenicity of Hepatocellular Carcinoma Open
Legends for Supplementary Tables S1-S3 and Supplementary Figures S1-S7.