Jaime Abrego
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View article: Data from A Cancer Cell–Intrinsic GOT2–PPARδ Axis Suppresses Antitumor Immunity
Data from A Cancer Cell–Intrinsic GOT2–PPARδ Axis Suppresses Antitumor Immunity Open
Despite significant recent advances in precision medicine, pancreatic ductal adenocarcinoma (PDAC) remains near uniformly lethal. Although immune-modulatory therapies hold promise to meaningfully improve outcomes for patients with PDAC, th…
View article: Data from A Cancer Cell–Intrinsic GOT2–PPARδ Axis Suppresses Antitumor Immunity
Data from A Cancer Cell–Intrinsic GOT2–PPARδ Axis Suppresses Antitumor Immunity Open
Despite significant recent advances in precision medicine, pancreatic ductal adenocarcinoma (PDAC) remains near uniformly lethal. Although immune-modulatory therapies hold promise to meaningfully improve outcomes for patients with PDAC, th…
View article: Supplementary Figure from A Cancer Cell–Intrinsic GOT2–PPARδ Axis Suppresses Antitumor Immunity
Supplementary Figure from A Cancer Cell–Intrinsic GOT2–PPARδ Axis Suppresses Antitumor Immunity Open
Supplementary Figure from A Cancer Cell–Intrinsic GOT2–PPARδ Axis Suppresses Antitumor Immunity
View article: Supplementary Figure from A Cancer Cell–Intrinsic GOT2–PPARδ Axis Suppresses Antitumor Immunity
Supplementary Figure from A Cancer Cell–Intrinsic GOT2–PPARδ Axis Suppresses Antitumor Immunity Open
Supplementary Figure from A Cancer Cell–Intrinsic GOT2–PPARδ Axis Suppresses Antitumor Immunity
View article: Figures S1 and S2 from MUC1-Mediated Metabolic Alterations Regulate Response to Radiotherapy in Pancreatic Cancer
Figures S1 and S2 from MUC1-Mediated Metabolic Alterations Regulate Response to Radiotherapy in Pancreatic Cancer Open
Figure S1. BrPA inhibits MUC1-mediated nucleotide metabolism. Figure S2. Immunohistochemical staining for MUC1 in tumor sections.
View article: Data from <i>De Novo</i> Lipid Synthesis Facilitates Gemcitabine Resistance through Endoplasmic Reticulum Stress in Pancreatic Cancer
Data from <i>De Novo</i> Lipid Synthesis Facilitates Gemcitabine Resistance through Endoplasmic Reticulum Stress in Pancreatic Cancer Open
Pancreatic adenocarcinoma is moderately responsive to gemcitabine-based chemotherapy, the most widely used single-agent therapy for pancreatic cancer. Although the prognosis in pancreatic cancer remains grim in part due to poor response to…
View article: Figures S1 and S2 from MUC1-Mediated Metabolic Alterations Regulate Response to Radiotherapy in Pancreatic Cancer
Figures S1 and S2 from MUC1-Mediated Metabolic Alterations Regulate Response to Radiotherapy in Pancreatic Cancer Open
Figure S1. BrPA inhibits MUC1-mediated nucleotide metabolism. Figure S2. Immunohistochemical staining for MUC1 in tumor sections.
View article: Supplementary Figures S1-S8; Supplementary Tables S1-S8; Supplementary methods from <i>De Novo</i> Lipid Synthesis Facilitates Gemcitabine Resistance through Endoplasmic Reticulum Stress in Pancreatic Cancer
Supplementary Figures S1-S8; Supplementary Tables S1-S8; Supplementary methods from <i>De Novo</i> Lipid Synthesis Facilitates Gemcitabine Resistance through Endoplasmic Reticulum Stress in Pancreatic Cancer Open
Figure S1: FASN inhibition with orlistat shows synergistic activity with gemcitabine in AsPC-1 cells; Figure S2: Effect of orlistat on the lipid content of pancreatic cancer cells; Figure S3: Platensimycin shows synergistic activity with g…
View article: Data from MUC1-Mediated Metabolic Alterations Regulate Response to Radiotherapy in Pancreatic Cancer
Data from MUC1-Mediated Metabolic Alterations Regulate Response to Radiotherapy in Pancreatic Cancer Open
Purpose: MUC1, an oncogene overexpressed in multiple solid tumors, including pancreatic cancer, reduces overall survival and imparts resistance to radiation and chemotherapies. We previously identified that MUC1 facilitates g…
View article: Data from <i>De Novo</i> Lipid Synthesis Facilitates Gemcitabine Resistance through Endoplasmic Reticulum Stress in Pancreatic Cancer
Data from <i>De Novo</i> Lipid Synthesis Facilitates Gemcitabine Resistance through Endoplasmic Reticulum Stress in Pancreatic Cancer Open
Pancreatic adenocarcinoma is moderately responsive to gemcitabine-based chemotherapy, the most widely used single-agent therapy for pancreatic cancer. Although the prognosis in pancreatic cancer remains grim in part due to poor response to…
View article: Supplementary Figures S1-S8; Supplementary Tables S1-S8; Supplementary methods from <i>De Novo</i> Lipid Synthesis Facilitates Gemcitabine Resistance through Endoplasmic Reticulum Stress in Pancreatic Cancer
Supplementary Figures S1-S8; Supplementary Tables S1-S8; Supplementary methods from <i>De Novo</i> Lipid Synthesis Facilitates Gemcitabine Resistance through Endoplasmic Reticulum Stress in Pancreatic Cancer Open
Figure S1: FASN inhibition with orlistat shows synergistic activity with gemcitabine in AsPC-1 cells; Figure S2: Effect of orlistat on the lipid content of pancreatic cancer cells; Figure S3: Platensimycin shows synergistic activity with g…
View article: Data from MUC1-Mediated Metabolic Alterations Regulate Response to Radiotherapy in Pancreatic Cancer
Data from MUC1-Mediated Metabolic Alterations Regulate Response to Radiotherapy in Pancreatic Cancer Open
Purpose: MUC1, an oncogene overexpressed in multiple solid tumors, including pancreatic cancer, reduces overall survival and imparts resistance to radiation and chemotherapies. We previously identified that MUC1 facilitates g…
View article: A Cancer Cell–Intrinsic GOT2–PPARδ Axis Suppresses Antitumor Immunity
A Cancer Cell–Intrinsic GOT2–PPARδ Axis Suppresses Antitumor Immunity Open
Despite significant recent advances in precision medicine, pancreatic ductal adenocarcinoma (PDAC) remains near uniformly lethal. Although immune-modulatory therapies hold promise to meaningfully improve outcomes for patients with PDAC, th…
View article: A cancer cell-intrinsic GOT2-PPARδ axis suppresses antitumor immunity
A cancer cell-intrinsic GOT2-PPARδ axis suppresses antitumor immunity Open
Despite significant recent advances in precision medicine 1,2 , pancreatic ductal adenocarcinoma (PDAC) remains near-uniformly lethal. While the most frequent genomic alterations in PDAC are not presently druggable 3 and conventional thera…
View article: JNK signaling contributes to skeletal muscle wasting and protein turnover in pancreatic cancer cachexia
JNK signaling contributes to skeletal muscle wasting and protein turnover in pancreatic cancer cachexia Open
View article: SIRT1–NOX4 signaling axis regulates cancer cachexia
SIRT1–NOX4 signaling axis regulates cancer cachexia Open
Approximately one third of cancer patients die due to complexities related to cachexia. However, the mechanisms of cachexia and the potential therapeutic interventions remain poorly studied. We observed a significant positive correlation b…
View article: Metabolic Alterations in Pancreatic Cancer Progression
Metabolic Alterations in Pancreatic Cancer Progression Open
Pancreatic cancer is the third leading cause of cancer-related deaths in the USA. Pancreatic tumors are characterized by enhanced glycolytic metabolism promoted by a hypoxic tumor microenvironment and a resultant acidic milieu. The metabol…
View article: Fibroblasts as Modulators of Local and Systemic Cancer Metabolism
Fibroblasts as Modulators of Local and Systemic Cancer Metabolism Open
Fibroblast activation is an accompanying feature of solid tumor progression, resembling a conserved host response to tissue damage. Cancer-associated fibroblasts (CAFs) comprise a heterogeneous and plastic population with increasingly appr…
View article: MUC1 and HIF-1alpha Signaling Crosstalk Induces Anabolic Glucose Metabolism to Impart Gemcitabine Resistance to Pancreatic Cancer
MUC1 and HIF-1alpha Signaling Crosstalk Induces Anabolic Glucose Metabolism to Impart Gemcitabine Resistance to Pancreatic Cancer Open
View article: <i>De Novo</i> Lipid Synthesis Facilitates Gemcitabine Resistance through Endoplasmic Reticulum Stress in Pancreatic Cancer
<i>De Novo</i> Lipid Synthesis Facilitates Gemcitabine Resistance through Endoplasmic Reticulum Stress in Pancreatic Cancer Open
Pancreatic adenocarcinoma is moderately responsive to gemcitabine-based chemotherapy, the most widely used single-agent therapy for pancreatic cancer. Although the prognosis in pancreatic cancer remains grim in part due to poor response to…
View article: Glucose Limitation Alters Glutamine Metabolism in MUC1-Overexpressing Pancreatic Cancer Cells
Glucose Limitation Alters Glutamine Metabolism in MUC1-Overexpressing Pancreatic Cancer Cells Open
Pancreatic cancer cells overexpressing Mucin 1 (MUC1) rely on aerobic glycolysis and, correspondingly, are dependent on glucose for survival. Our NMR metabolomics comparative analysis of control (S2-013.Neo) and MUC1-overexpressing (S2-013…
View article: MUC1-Mediated Metabolic Alterations Regulate Response to Radiotherapy in Pancreatic Cancer
MUC1-Mediated Metabolic Alterations Regulate Response to Radiotherapy in Pancreatic Cancer Open
Purpose: MUC1, an oncogene overexpressed in multiple solid tumors, including pancreatic cancer, reduces overall survival and imparts resistance to radiation and chemotherapies. We previously identified that MUC1 facilitates growth-promotin…
View article: MUC1 and HIF-1alpha Signaling Crosstalk Induces Anabolic Glucose Metabolism to Impart Gemcitabine Resistance to Pancreatic Cancer
MUC1 and HIF-1alpha Signaling Crosstalk Induces Anabolic Glucose Metabolism to Impart Gemcitabine Resistance to Pancreatic Cancer Open
View article: GOT1-mediated anaplerotic glutamine metabolism regulates chronic acidosis stress in pancreatic cancer cells
GOT1-mediated anaplerotic glutamine metabolism regulates chronic acidosis stress in pancreatic cancer cells Open
View article: Metabolic Reprogramming of Pancreatic Ductal Adenocarcinoma Cells in Response to Chronic Low pH Stress
Metabolic Reprogramming of Pancreatic Ductal Adenocarcinoma Cells in Response to Chronic Low pH Stress Open
Pancreatic ductal adenocarcinoma (PDAC) is among the most lethal of all cancers with a 5-year survival rate of only 8.2%. This is because PDAC is diagnosed in its advanced stages and is characterized by radio and chemotherapy resistance. A…
View article: MUC16-mediated activation of mTOR and c-MYC reprograms pancreatic cancer metabolism
MUC16-mediated activation of mTOR and c-MYC reprograms pancreatic cancer metabolism Open
MUC16, a transmembrane mucin, facilitates pancreatic adenocarcinoma progression and metastasis. In the current studies, we observed that MUC16 knockdown pancreatic cancer cells exhibit reduced glucose uptake and lactate secretion along wit…