Mihai Gagea
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View article: Engineered exosomes with KrasG12D specific siRNA in pancreatic cancer: a phase I study with immunological correlates
Engineered exosomes with KrasG12D specific siRNA in pancreatic cancer: a phase I study with immunological correlates Open
View article: KRAS<sup>G12D</sup>-Specific Targeting with Engineered Exosomes Reprograms the Immune Microenvironment to Enable Efficacy of Immune Checkpoint Therapy in PDAC Patients
KRAS<sup>G12D</sup>-Specific Targeting with Engineered Exosomes Reprograms the Immune Microenvironment to Enable Efficacy of Immune Checkpoint Therapy in PDAC Patients Open
Oncogenic KRAS drives initiation and maintenance of pancreatic ductal adenocarcinoma (PDAC). Here, we show that engineered exosomes with Kras G12D specific siRNA (iExoKras G12D ) reveal impressive biodistribution in pancreas with negligibl…
View article: Gut Microbiome and Hepatic Transcriptomic Determinants of HCC Development in Mice with Metabolic Dysfunction-Associated Steatohepatitis
Gut Microbiome and Hepatic Transcriptomic Determinants of HCC Development in Mice with Metabolic Dysfunction-Associated Steatohepatitis Open
We identified microbiome components contributing to liver carcinogenesis by inducing inflammation, and changes in hepatic gene expression and hepatic cells distribution that contribute to tumor growth. Such information can be highly valuab…
View article: Dysregulated KLF4 expression plays a pivotal role in the pathogenesis of pancreatic intraductal papillary mucinous neoplasms
Dysregulated KLF4 expression plays a pivotal role in the pathogenesis of pancreatic intraductal papillary mucinous neoplasms Open
View article: Age-specific induction of mutant p53 drives clonal hematopoiesis and acute myeloid leukemia in adult mice
Age-specific induction of mutant p53 drives clonal hematopoiesis and acute myeloid leukemia in adult mice Open
The investigation of the mechanisms behind p53 mutations in acute myeloid leukemia (AML) has been limited by the lack of suitable mouse models, which historically have resulted in lymphoma rather than leukemia. This study introduces two ne…
View article: Intratumoral Biosynthesis of Gold Nanoclusters by Pancreatic Cancer to Overcome Delivery Barriers to Radiosensitization
Intratumoral Biosynthesis of Gold Nanoclusters by Pancreatic Cancer to Overcome Delivery Barriers to Radiosensitization Open
Nanoparticle delivery to solid tumors is a prime challenge in nanomedicine. Here, we approach this challenge through the lens of biogeochemistry, the field that studies the flow of chemical elements within ecosystems as manipulated by livi…
View article: FIGURE 4 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
FIGURE 4 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
p53R245W GOF properties increase carcinoma incidence and mixed HCC-CCA cancers. A, Quantification of animals from LPfl/fl (N = 17), LP245/fl (N = 11) with hyperplasia (left), adenoma (middle), and…
View article: FIGURE 1 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
FIGURE 1 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
p53R245W induces fatty liver and compensatory proliferation in hepatocytes in vivo under metabolic challenges. A, Schematic of liver samples used. B, Expression of p53 target genes in the liver of animals fed regular c…
View article: FIGURE 4 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
FIGURE 4 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
p53R245W GOF properties increase carcinoma incidence and mixed HCC-CCA cancers. A, Quantification of animals from LPfl/fl (N = 17), LP245/fl (N = 11) with hyperplasia (left), adenoma (middle), and…
View article: Supplementary Table 1 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
Supplementary Table 1 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
A list of genotyping and RT-qPCR primers that were used in this study
View article: Data from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
Data from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
Obesity is a significant global health concern. Non-alcoholic fatty liver disease and non-alcoholic steatohepatitis (NASH) are common risk factors for hepatocellular carcinoma (HCC) and are closely associated with metabolic comorbidities, …
View article: Supplementary Table 3 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
Supplementary Table 3 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
Gene names, E-value, and motif diagrams from the MEME MAST analysis of 141 DEGs from Supplementary Table 2 examined for p53 response elements in 10KB upstream of the start site
View article: Supplementary Table 3 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
Supplementary Table 3 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
Gene names, E-value, and motif diagrams from the MEME MAST analysis of 141 DEGs from Supplementary Table 2 examined for p53 response elements in 10KB upstream of the start site
View article: Supplementary Table 1 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
Supplementary Table 1 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
A list of genotyping and RT-qPCR primers that were used in this study
View article: Supplementary Table 2 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
Supplementary Table 2 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
141 genes that had a descending slope >1 and determination correlation coefficient R2 value >0.6
View article: Supplementary Figure 2 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
Supplementary Figure 2 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
Tumor free survival curves of animals fed a regular or HFCD diet
View article: FIGURE 2 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
FIGURE 2 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
p53R245W suppresses transcriptional activity of WT p53 in the liver in vivo under metabolic challenges. A, Schematic of liver samples submitted for bulk RNA-seq (LP+/+, N = 3; LPfl/+, N = 2…
View article: Supplementary Figure 1 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
Supplementary Figure 1 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
Transcriptome analyses of the liver under metabolic challenges
View article: Supplementary Figure 1 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
Supplementary Figure 1 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
Transcriptome analyses of the liver under metabolic challenges
View article: Supplementary Figure 4 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
Supplementary Figure 4 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
Kaplan-Meier survival curves for animals with indicated genotypes
View article: Supplementary Figure 3 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
Supplementary Figure 3 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
The status of the WT p53 allele in 19 tumors with LP245/+ genotype
View article: FIGURE 5 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
FIGURE 5 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
p53R245 GOF properties triple metastatic incidence in liver tumors when compared with Trp53 loss. A–C, Kaplan–Meier survival curves for animals with genotypes LP245/fl (N = 35), LPfl/fl (
View article: FIGURE 5 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
FIGURE 5 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
p53R245 GOF properties triple metastatic incidence in liver tumors when compared with Trp53 loss. A–C, Kaplan–Meier survival curves for animals with genotypes LP245/fl (N = 35), LPfl/fl (
View article: FIGURE 1 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
FIGURE 1 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
p53R245W induces fatty liver and compensatory proliferation in hepatocytes in vivo under metabolic challenges. A, Schematic of liver samples used. B, Expression of p53 target genes in the liver of animals fed regular c…
View article: Supplementary Figure 4 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
Supplementary Figure 4 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
Kaplan-Meier survival curves for animals with indicated genotypes
View article: Supplementary Figure 3 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
Supplementary Figure 3 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
The status of the WT p53 allele in 19 tumors with LP245/+ genotype
View article: Supplementary Table 2 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
Supplementary Table 2 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
141 genes that had a descending slope >1 and determination correlation coefficient R2 value >0.6
View article: FIGURE 3 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
FIGURE 3 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
p53R245W displays GOF activities in the liver during tumorigenesis. A, Kaplan–Meier survival curves for animals with genotypes LP+/+ (N = 28), LPfl/+ (N = 28), and LP245/+ (N = 6…
View article: Supplementary Figure 2 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
Supplementary Figure 2 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
Tumor free survival curves of animals fed a regular or HFCD diet
View article: FIGURE 2 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis
FIGURE 2 from p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis Open
p53R245W suppresses transcriptional activity of WT p53 in the liver in vivo under metabolic challenges. A, Schematic of liver samples submitted for bulk RNA-seq (LP+/+, N = 3; LPfl/+, N = 2…