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View article: Obesity drives depot-specific vascular remodeling in male white adipose tissue
Obesity drives depot-specific vascular remodeling in male white adipose tissue Open
Obesity-driven pathological expansion of white adipose tissue (WAT) is a key driver of endothelial dysfunction. However, early vascular alterations associated with over-nutrition also serve to exacerbate WAT dysfunction. Here, we conduct a…
Data from Endothelial RBPJ Is Essential for the Education of Tumor-Associated Macrophages Open
Epithelial ovarian cancer (EOC) is one of the most lethal gynecologic cancers worldwide. EOC cells educate tumor-associated macrophages (TAM) through CD44-mediated cholesterol depletion to generate an immunosuppressive tumor microenvironme…
Endothelial Notch1 signaling in white adipose tissue promotes cancer cachexia Open
Cachexia is a major cause of morbidity and mortality in individuals with cancer and is characterized by weight loss due to adipose and muscle tissue wasting. Hallmarks of white adipose tissue (WAT) remodeling, which often precedes weight l…
HAPLN1 potentiates peritoneal metastasis in pancreatic cancer Open
Pancreatic ductal adenocarcinoma (PDAC) frequently metastasizes into the peritoneum, which contributes to poor prognosis. Metastatic spreading is promoted by cancer cell plasticity, yet its regulation by the microenvironment is incompletel…
Data from Intraperitoneal Oil Application Causes Local Inflammation with Depletion of Resident Peritoneal Macrophages Open
Oil is frequently used as a solvent to inject lipophilic substances into the peritoneum of laboratory animals. Although mineral oil causes chronic peritoneal inflammation, little is known whether other oils are better suited. We show that …
Supplementary Figures 1-5 from Intraperitoneal Oil Application Causes Local Inflammation with Depletion of Resident Peritoneal Macrophages Open
S1. No changes in body weight of spleen histology. S2. Oil injection decreases the number of lymphocytes in peritoneal leverage. S3. Injection of saline does not generate inflammation in the peritoneum. S4. Macrophage foam cell formation u…
Data from Intraperitoneal Oil Application Causes Local Inflammation with Depletion of Resident Peritoneal Macrophages Open
Oil is frequently used as a solvent to inject lipophilic substances into the peritoneum of laboratory animals. Although mineral oil causes chronic peritoneal inflammation, little is known whether other oils are better suited. We show that …
Supplementary Figures 1-5 from Intraperitoneal Oil Application Causes Local Inflammation with Depletion of Resident Peritoneal Macrophages Open
S1. No changes in body weight of spleen histology. S2. Oil injection decreases the number of lymphocytes in peritoneal leverage. S3. Injection of saline does not generate inflammation in the peritoneum. S4. Macrophage foam cell formation u…
View article: Supplementary Fig. S1 from Genetic Evolution of T-cell Resistance in the Course of Melanoma Progression
Supplementary Fig. S1 from Genetic Evolution of T-cell Resistance in the Course of Melanoma Progression Open
Supplementary Fig. S1. Analysis of CD3 (T cells) and HMB-45 (melanoma cells) expression in serial sections from cryopreserved metastasis Ma-Mel-48b. Red staining indicates positive cells.
Supplementary Fig. S5 from Genetic Evolution of T-cell Resistance in the Course of Melanoma Progression Open
Supplementary Fig. S5. A, The different Ma-Mel-48 cell lines were treated with IFN-γ(500 U/ml) for 48 h, controls were left untreated. Cell lysates were analyzed by Western blot for the protein levels of JAK1, STAT1 and pSTAT1. GAPDH serve…
Supplementary Fig. S6 from Genetic Evolution of T-cell Resistance in the Course of Melanoma Progression Open
Supplementary Fig. S6. A, Analysis of HMB-45 (melanoma cells) and HLA class I antigen expression in serial sections from cryopreserved metastasis Ma-Mel-100b. Positive cells stain red. B, Localization of the 12 bp deletion in the B2M gene …
Supplementary material from Endothelial RBPJ Is Essential for the Education of Tumor-Associated Macrophages Open
It includes extended material and methods, and supplementary figures
Data from Genetic Evolution of T-cell Resistance in the Course of Melanoma Progression Open
Purpose: CD8+ T lymphocytes can kill autologous melanoma cells, but their activity is impaired when poorly immunogenic tumor phenotypes evolve in the course of disease progression. Here, we analyzed three consecutive melanoma lesions obtai…
Supplementary material from Endothelial RBPJ Is Essential for the Education of Tumor-Associated Macrophages Open
It includes extended material and methods, and supplementary figures
Supplementary Fig. S4 from Genetic Evolution of T-cell Resistance in the Course of Melanoma Progression Open
Supplementary Fig. S4. Real-time proliferation of Ma-Mel-48 cell lines was determined in an xCelligence device. 1,5 x 104 cells were seeded per well and proliferation was determined over time. Representative data from one of three independ…
Data from Genetic Evolution of T-cell Resistance in the Course of Melanoma Progression Open
Purpose: CD8+ T lymphocytes can kill autologous melanoma cells, but their activity is impaired when poorly immunogenic tumor phenotypes evolve in the course of disease progression. Here, we analyzed three consecutive melanoma lesions obtai…
Supplementary Fig. S1 from Genetic Evolution of T-cell Resistance in the Course of Melanoma Progression Open
Supplementary Fig. S1. Analysis of CD3 (T cells) and HMB-45 (melanoma cells) expression in serial sections from cryopreserved metastasis Ma-Mel-48b. Red staining indicates positive cells.
Supplementary Methods from Genetic Evolution of T-cell Resistance in the Course of Melanoma Progression Open
Supplementary Methods
Supplementary Fig. S2 from Genetic Evolution of T-cell Resistance in the Course of Melanoma Progression Open
Supplementary Fig. S2. The different Ma-Mel-48 cell lines were treated with IFN-γ (500 U/ml) for 48 h, controls were left untreated. Cells were stained with mAb L243 and mAb W6/32 for detection of HLA-DR and HLA class I antigen expression,…
Supplementary Fig. S4 from Genetic Evolution of T-cell Resistance in the Course of Melanoma Progression Open
Supplementary Fig. S4. Real-time proliferation of Ma-Mel-48 cell lines was determined in an xCelligence device. 1,5 x 104 cells were seeded per well and proliferation was determined over time. Representative data from one of three independ…
Supplementary Fig. S6 from Genetic Evolution of T-cell Resistance in the Course of Melanoma Progression Open
Supplementary Fig. S6. A, Analysis of HMB-45 (melanoma cells) and HLA class I antigen expression in serial sections from cryopreserved metastasis Ma-Mel-100b. Positive cells stain red. B, Localization of the 12 bp deletion in the B2M gene …
Supplementary Fig. S3 from Genetic Evolution of T-cell Resistance in the Course of Melanoma Progression Open
Supplementary Fig. S3. A, B, analysis of the T cell-stimulatory capacity of the different Ma-Mel-48 tumor cell lines. In autologous mixed lymphocyte-tumor cultures (MLTC) isolated CD8+ T cells were stimulated twice with Ma-Mel-48a (MLTC-48…
Supplementary Fig. S2 from Genetic Evolution of T-cell Resistance in the Course of Melanoma Progression Open
Supplementary Fig. S2. The different Ma-Mel-48 cell lines were treated with IFN-γ (500 U/ml) for 48 h, controls were left untreated. Cells were stained with mAb L243 and mAb W6/32 for detection of HLA-DR and HLA class I antigen expression,…
Supplementary Fig. S5 from Genetic Evolution of T-cell Resistance in the Course of Melanoma Progression Open
Supplementary Fig. S5. A, The different Ma-Mel-48 cell lines were treated with IFN-γ(500 U/ml) for 48 h, controls were left untreated. Cell lysates were analyzed by Western blot for the protein levels of JAK1, STAT1 and pSTAT1. GAPDH serve…
Supplementary Fig. S3 from Genetic Evolution of T-cell Resistance in the Course of Melanoma Progression Open
Supplementary Fig. S3. A, B, analysis of the T cell-stimulatory capacity of the different Ma-Mel-48 tumor cell lines. In autologous mixed lymphocyte-tumor cultures (MLTC) isolated CD8+ T cells were stimulated twice with Ma-Mel-48a (MLTC-48…
Data from Endothelial RBPJ Is Essential for the Education of Tumor-Associated Macrophages Open
Epithelial ovarian cancer (EOC) is one of the most lethal gynecologic cancers worldwide. EOC cells educate tumor-associated macrophages (TAM) through CD44-mediated cholesterol depletion to generate an immunosuppressive tumor microenvironme…
Supplementary Methods from Genetic Evolution of T-cell Resistance in the Course of Melanoma Progression Open
Supplementary Methods
Endothelial RBPJ Is Essential for the Education of Tumor-Associated Macrophages Open
Epithelial ovarian cancer (EOC) is one of the most lethal gynecologic cancers worldwide. EOC cells educate tumor-associated macrophages (TAM) through CD44-mediated cholesterol depletion to generate an immunosuppressive tumor microenvironme…
HAPLN1 is a driver for peritoneal carcinomatosis in pancreatic cancer Open
Pancreatic ductal adenocarcinoma (PDAC) frequently metastasizes into the peritoneum, which contributes to poor prognosis. Metastatic spreading is promoted by cancer cell plasticity, yet its regulation by the microenvironment is incompletel…
Ketone body oxidation increases cardiac endothelial cell proliferation Open
Blood vessel formation is dependent on metabolic adaption in endothelial cells. Glucose and fatty acids are essential substrates for ATP and biomass production; however, the metabolism of other substrates remains poorly understood. Ketone …