7 results match your criteria: "The Beckman Research Institute at the City of Hope National Medical Center[Affiliation]"

Cytokine induction of VCAM-1 but not IL13Rα2 on glioma cells: a tale of two antibodies.

PLoS One

December 2014

Departments of Hematology and Hematopoietic Cell Transplantation, Cancer Immunotherapy & Tumor Immunology, Beckman Research Institute at the City of Hope National Medical Center, Duarte, California, United States of America.

The interleukin-13 receptor alpha2 (IL13Rα2) is a cell surface receptor that is over-expressed by a subset of high-grade gliomas, but not expressed at significant levels by normal brain tissue. For both malignant and non-malignant cells, IL13Rα2 surface expression is reported to be induced by various cytokines such as IL-4 or IL-13 and tumor necrosis factor (TNF). Our group has developed a therapeutic platform to target IL13Rα2-positive brain tumors by engineering human cytotoxic T lymphocytes (CTLs) to express the IL13-zetakine chimeric antigen receptor.

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The active, potent, and selective Farnesoid X Receptor (FXR) agonist 6α-ethylchenodeoxycholic acid (6ECDCA) has been synthesized in improved yield compared to the published methodologies. The synthesis employed selective oxidation of one of the two hydroxyls of the readily-available starting material chenodeoxycholic acid (CDCA) as a key step. After protection of the remaining hydroxyl, LDA/HMPA/EtI/PPTS provided an efficient deprotonation/ethylation/deprotection sequence.

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BRCA1 and BRCA2 are the most well-known breast cancer susceptibility genes. Additional genes involved in DNA repair have been identified as predisposing to breast cancer. One such gene, RAD51C, is essential for homologous recombination repair.

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Identification of an endogenous ligand bound to a native orphan nuclear receptor.

PLoS One

August 2009

Department of Gene Regulation and Drug Discovery, Gonda Diabetes Research Center, The Beckman Research Institute at the City of Hope National Medical Center, Duarte, California, United States of America.

Orphan nuclear receptors have been instrumental in identifying novel signaling pathways and therapeutic targets. However, identification of ligands for these receptors has often been based on random compound screens or other biased approaches. As a result, it remains unclear in many cases if the reported ligands are the true endogenous ligands,--i.

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Immune cells in the tumour microenvironment not only fail to mount an effective anti-tumour immune response, but also interact intimately with the transformed cells to promote oncogenesis actively. Signal transducer and activator of transcription 3 (STAT3), which is a point of convergence for numerous oncogenic signalling pathways, is constitutively activated both in tumour cells and in immune cells in the tumour microenvironment. Constitutively activated STAT3 inhibits the expression of mediators necessary for immune activation against tumour cells.

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Detection of designer steroids.

Nucl Recept Signal

May 2006

Gene Regulation and Drug Discovery Department, The Beckman Research Institute at The City of Hope National Medical Center, Gonda Diabetes Research Center, Duarte, CA 91010, USA.

Illicit use of performance-enhancing steroids has proliferated among a wide range of professional and amateur athletes. This problem has attracted broad public attention and has led the United States Congress to draft legislation that proposes frequent testing of athletes. However, current testing protocols are inadequate as athletes can evade detection by using novel steroids that are unknown to authorities.

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Are those phospholipids in your pocket?

Cell Metab

March 2005

Gene Regulation and Drug Discovery, The Beckman Research Institute at The City of Hope National Medical Center, Gonda Diabetes Research Center, 1500 East Duarte Road, Duarte, California 91010, USA.

The identification of phospholipids ligands for the nuclear receptors SF-1 and LRH-1 raise exciting new questions in the areas of signaling and metabolism. Do these receptors provide cells with a mechanism to alter genomic activities in response to phospholipid flux? The tools now exist to address these questions, and more.

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