Professor, Pediatrics, University of Pittsburgh School of Medicine
Hematology
Dr. Edward V. Prochownik, MD
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Edward Prochownik works in the field of Hematology. He went to University of Chicago Pritzker School of Medicine. University of Chicago Pritzker School of Medicine is ranked 10/19 in Research/PrimaryCare. He over the years received 1 awards: "Elected Member". Edward Prochownik is a published physician as well. He has 101 publications published. The latest was: Differential apoptotic behaviors of c-myc, N-myc, and L-myc oncoproteins.
Publications
- Complex I assembly function and fatty acid oxidation enzyme activity of ACAD9 both contribute to Disease severity in ACAD9 deficiency.
- c-Myc Programs Fatty Acid Metabolism and Dictates Acetyl-CoA Abundance and Fate.
- Discovery of Methyl 4'-Methyl-5-(7-nitrobenzo[c][1,2,5]oxadiazol-4-yl)-[1,1'-biphenyl]-3-carboxylate, an Improved Small-Molecule Inhibitor of c-Myc-Max Dimerization.
- Small-molecule inhibitors of the Myc oncoprotein.
- Pharmacophore identification of c-Myc inhibitor 10074-G5.
- Breast Cancer Stem Cell-Like Cells Are More Sensitive to Ionizing Radiation than Non-Stem Cells: Role of ATM.
- Phenotypic Screening Reveals ¬Topoisomerase I as a Breast Cancer Stem Cell Therapeutic Target.
- Pten mediates Myc oncogene dependence in a conditional zebrafish model of T cell Acute lymphoblastic leukemia.
- In vitro cytotoxicity and in vivo efficacy, pharmacokinetics, and metabolism of 10074-G5, a novel small-molecule inhibitor of c-Myc/Max dimerization.
- Endothelial-like Cells derived directly from human tumor xenografts.
- c-Myc is required for the CHREBP-dependent activation of glucose-responsive genes.
- Permanently blocked stem Cells derived from breast cancer Cell lines.
- Therapeutic Targeting of Myc.
- Widespread genomic instability mediated by a pathway involving glycoprotein Ib alpha and Aurora B kinase.
- The c-Myc target glycoprotein1balpha links cytokinesis failure to oncogenic signal transduction pathways in cultured human Cells.
- Point mutations in c-Myc uncouple neoplastic transformation from multiple other phenotypes in rat fibroblasts.
- Multiple independent binding sites for small-molecule inhibitors on the oncoprotein c-Myc.
- Discovery of novel Myc-Max heterodimer disruptors with a three-dimensional pharmacophore model.
- Regulation of reactive oxygen species homeostasis by peroxiredoxins and c-Myc.
- Modularity of the oncoprotein-like properties of platelet glycoprotein Ibalpha.
- Improved low molecular weight Myc-Max inhibitors.
- Dual role for SUMO E2 conjugase Ubc9 in modulating the transforming and growth-promoting properties of the HMGA1b architectural transcription factor.
- The ever expanding role for c-Myc in promoting genomic instability.
- c-Myc-mediated genomic instability proceeds via a megakaryocytic endomitosis pathway involving Gp1balpha.
- The negative c-Myc target onzin affects proliferation and apoptosis via its obligate interaction with phospholipid scramblase 1.
- A functional hierarchy for c-Myc target genes? Lessons from MT-MC1.
- Deregulation of common genes by c-Myc and its direct target, MT-MC1.
- C-Myc-independent restoration of multiple phenotypes by two C-Myc target genes with overlapping functions.
- Cyclin B1 is a critical target of RhoB in the Cell suicide program triggered by farnesyl transferase inhibition.
- The CCL6 chemokine is differentially regulated by c-Myc and L-Myc, and promotes tumorigenesis and metastasis.
- Pag, a putative tumor suppressor, interacts with the Myc Box II domain of c-Myc and selectively alters its biological function and target gene expression.
- Myc target in myeloid Cells-1, a novel c-Myc target, recapitulates multiple c-Myc phenotypes.
- Rapid in vitro derivation of endothelium directly from human cancer Cells.
- Endothelial Progenitors Exist within the Kidney and Lung Mesenchyme.
- Myc-induced T cell Leukemia in transgenic zebrafish.
- c-Myc depletion inhibits proliferation of human tumor Cells at various stages of the Cell cycle.
- C-MYC overexpression is required for continuous suppression of oncogene-induced senescence in melanoma Cells.
- Transformation, genomic instability and senescence mediated by platelet/megakaryocyte glycoprotein Ibalpha.
- Increased Cell-substrate adhesion accompanies conditional reversion to the normal phenotype in ras-oncogene-transformed NIH-3T3 Cells.
- Assignment of the human MAD and MXI1 genes to chromosomes 2p12-p13 and 10q24-q25.
- Mutation of the MXI1 gene in prostate cancer.
- Isolation of a cDNA clone for human antithrombin III.
- Molecular heterogeneity of inherited antithrombin III deficiency.
- In vivo transcription of a human antithrombin III "minigene".
- Molecular genetic survey of 16 kindreds with hereditary antithrombin III deficiency.
- Two regions downstream of AATAAA in the human antithrombin III gene are important for cleavage-polyadenylation.
- Deregulated expression of c-myc by murine erythroleukaemia Cells prevents differentiation.
- Changes in protein kinase C activity are associated with the differentiation of Friend erythroLeukemia cells.
- Antithrombin-III-Hamilton: a gene with a point mutation (guanine to adenine) in codon 382 causing impaired serine protease reactivity.
- Relationship between an enhancer element in the human antithrombin III gene and an immunoglobulin light-chain gene enhancer.
- Intron structure of the human antithrombin III gene differs from that of other members of the serine protease inhibitor superfamily.
- Constitutive expression of a c-myb cDNA blocks Friend murine erythroLeukemia cell differentiation.
- Expression and analysis of COOH-terminal deletions of the human thrombospondin molecule.
- c-myb but not c-myc suppresses the hemin-induced nonterminal expression of hemoglobin by murine erythroLeukemia cells.
- Molecular genetics of inherited antithrombin III deficiencies.
- Protooncogenes and Cell differentiation.
- The antimitogenic action of tumor necrosis factor is associated with increased AP-1/c-jun proto-oncogene transcription.
- c-myc antisense transcripts accelerate differentiation and inhibit G1 progression in murine erythroLeukemia cells.
- Tumor necrosis factor-alpha induction of novel gene products in human endothelial Cells including a macrophage-specific chemotaxin.
- Regulation of megakaryocyte phenotype in human erythroLeukemia cells.
- Embryonal rhabdomyosarcoma of the ampulla of Vater with long-term survival following pancreaticoduodenectomy.
- The leucine zipper of c-Myc is required for full inhibition of erythroLeukemia differentiation.
- Amplified expression of three jun family members inhibits erythroLeukemia differentiation.
- Depletion of c-myc with specific antisense sequences reverses the transformed phenotype in ras oncogene-transformed NIH 3T3 Cells.
- Antisense-mediated reduction in thrombospondin reverses the malignant phenotype of a human squamous carcinoma.
- Modulation of cis-platinum resistance in Friend erythroLeukemia cells by c-myc.
- Regulation of the junB gene by v-src.
- Inhibition of c-jun causes reversible proliferative arrest and withdrawal from the Cell cycle.
- A point mutation in the MyoD basic domain imparts c-Myc-like properties.
- The interferon refractory state. II. Biological characterization of a refractoriness-inducing protein.
- Type C virus induced by iododeoxyuridine in the human embryonic Cell strain HEL-12.
- Kinetics of type C virion release from a human diploid fibroblast strain.
- Cell generation and type C virus expression in the human embryonic Cell strain HEL-12.
- Inhibition of reverse transcriptases of primate type C viruses by 7S immunoglobulin from patients with leukaemia.
- Induction of type C virions from normal rat kidney Cells by 2-deoxy-D-glucose.
- Isolation of type C virions from a normal human fibroblast strain.
- Biological and physical modifications of a murine oncornavirus by 2-deoxy-D-glucose.
- Functional and physical communication between oncoproteins and tumor suppressors.
- Nucleic acid sequences of primate type C viruses in normal and neoplastic human tissues.
- Inverse regulation of cyclin B1 by c-Myc and p53 and induction of tetraploidy by cyclin B1 overexpression.
- Dynamic in vivo interactions among Myc network members.
- Mmip-2/Rnf-17 enhances c-Myc function and regulates some target genes in common with glucocorticoid hormones.
- Genetic dissection of c-myc apoptotic pathways.
- Promotion of growth and apoptosis in c-myc nullizygous fibroblasts by other members of the myc oncoprotein family.
- Mmip-2, a novel RING finger protein that interacts with mad members of the Myc oncoprotein network.
- MYC oncogenes and human neoplastic Disease.
- Establishment of an apoptosis-resistant and growth-controllable Cell line by transfecting with inducible antisense c-Jun gene.
- C-myc overexpression and p53 loss cooperate to promote genomic instability.
- Differential apoptotic behaviors of c-myc, N-myc, and L-myc oncoproteins.
- Distinct apoptotic responses imparted by c-myc and max.
- Commonly occurring loss and mutation of the MXI1 gene in prostate cancer.
- Lack of transcriptional repression by max homodimers.
- Mmip1: a novel leucine zipper protein that reverses the suppressive effects of Mad family members on c-myc.
- Differential interactions of Id proteins with basic-helix-loop-helix transcription factors.
- Novel regulation of the helix-loop-helix protein Id1 by S5a, a subunit of the 26 S proteasome.
- A rapid method for the preparation of yeast lysates that facilitates the immunodetection of proteins generated by the yeast two-hybrid system.
- Distinct roles for MAX protein isoforms in proliferation and apoptosis.
- Proximal promoter region of the junB gene mediates attenuation of serum inducibility in Src-transformed Cells.
- Differential patterns of DNA binding by myc and max proteins.
- Attenuation of serum inducibility of immediate early genes by oncoproteins in tyrosine kinase signaling pathways.
Schools
U Of Chgo Div Of Bio Sci Pritzker Sch Of Med
Children39s Hospital Boston
Conditions Treated
- Acute Leukemia
- Sickle Cell Disease
Doctors Specialties
- Hematology
Accepted Insurances
Awards
- Elected Member
Education
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Boston Children's Hospital -
University of Chicago Pritzker School of Medicine
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