Professor, Pathology, Anatomy and Cell Biology, Jefferson Medical College-Thos Jefferson Univ
Pathology
Dr. John L. Farber, MD
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John Farber is an expert in the field of Pathology. He over the years received 9 awards: "Burlington Resources Foundation Faculty Achievement Award for Excellence in Teaching and Research", "Associate Recipient, Book of the Year Award for Pathology, 1989 and Honorable Mention for Essential Pathology", "Christian R. and Mary P. Lindback Foundation (Honored for Excellence in Teaching)", "Nominated for Passano Award, Passsano Foundation", "Alpha Omega Alpha", "Upjohn Award", "Roche Award", "Phi Beta Kappa" and "Top MD". John Farber is also published. He has 101 publications published. The lastest publication: "Zinc replenishment reduces esophageal cell proliferation and N-nitrosomethylbenzylamine (NMBA)-induced esophageal tumor incidence in zinc-deficient rats.' He accepts Medicare payments and is listed with Medicare.gov.
Publications
- MicroRNA dysregulation and esophageal cancer development depend on the extent of zinc dietary deficiency.
- Repression of Esophageal Neoplasia and Inflammatory Signaling by Anti-miR-31 Delivery In Vivo.
- Humoral immunity in renal transplantation: epitopes, Cw and DP, and complement-activating capability - an update.
- Sensitization, pathologic, and imaging findings comparing symptomatic and quiescent failed renal allografts.
- CDK4/6 inhibition antagonizes the cytotoxic response to anthracycline therapy.
- Segmental Arterial Mediolysis: Report of 2 Cases and Review of the Literature.
- Zinc deficiency activates S100A8 inflammation in the absence of COX-2 and promotes murine oral-esophageal tumor progression.
- ERK-1 MAP kinase prevents TNF-induced apoptosis through bad phosphorylation and inhibition of Bax translocation in HeLa Cells.
- Foxp3-expressing T regulatory cells and mast cells in acute graft-versus-host disease of the skin.
- Zinc replenishment reverses overexpression of the proinflammatory mediator S100A8 and esophageal preneoplasia in the rat.
- Detailing the role of Bax translocation, cytochrome c release, and perinuclear clustering of the mitochondria in the killing of HeLa cells by TNF.
- Fatal aortic dissection in a patient with a family history of Marfan syndrome.
- Prevention of upper aerodigestive tract cancer in zinc-deficient rodents: inefficacy of genetic or pharmacological disruption of COX-2.
- Fez1/Lzts1 absence impairs Cdk1/Cdc25C interaction during mitosis and predisposes mice to cancer development.
- Re-evaluation of the distinction between type I and type II cells: the necessary role of the mitochondria in both the extrinsic and intrinsic signaling pathways upon F...
- The course of etoposide-induced apoptosis in Jurkat cells lacking p53 and Bax.
- Knockout mice reveal a tumor suppressor function for Testin.
- Dietary zinc modulation of COX-2 expression and lingual and esophageal carcinogenesis in rats.
- Crescentic glomerulonephritis and subepidermal blisters with autoantibodies to alpha5 and alpha6 chains of type IV collagen.
- p53 deficiency accelerates induction and progression of esophageal and forestomach tumors in zinc-deficient mice.
- Regulation of intracellular pH mediates Bax activation in HeLa cells treated with staurosporine or tumor necrosis factor-alpha.
- The course of etoposide-induced apoptosis from damage to DNA and p53 activation to mitochondrial release of cytochrome c.
- Cytochrome c release upon Fas receptor activation depends on translocation of full-length bid and the induction of the mitochondrial permeability transition.
- Zinc supplementation suppresses 4-nitroquinoline 1-oxide-induced rat oral carcinogenesis.
- Tacrolimus-induced thrombotic microangiopathy: natural history of a severe, acute vasculopathy.
- Characterization of rejection episodes in patients following positive crossmatch and ABO-incompatible live donor renal transplantation.
- Zinc deficiency potentiates induction and progression of lingual and esophageal tumors in p53-deficient mice.
- Arterial invasion predicts early mortality in stage I non-small cell lung cancer.
- Successful living donor renal transplantation despite ABO incompatibility and a positive crossmatch.
- Early deregulation of the the p16ink4a-cyclin D1/cyclin-dependent kinase 4-retinoblastoma pathway in cell proliferation-driven esophageal tumorigenesis in zinc-deficie...
- Induction of the mitochondrial permeability transition mediates the killing of HeLa cells by staurosporine.
- Esophageal cancer prevention in zinc-deficient rats: rapid induction of apoptosis by replenishing zinc.
- Cell proliferation and esophageal carcinogenesis in the zinc-deficient rat.
- The cytotoxicity of tumor necrosis factor depends on induction of the mitochondrial permeability transition.
- The overexpression of Bax produces cell death upon induction of the mitochondrial permeability transition.
- Zinc replenishment reduces esophageal cell proliferation and N-nitrosomethylbenzylamine (NMBA)-induced esophageal tumor incidence in zinc-deficient rats.
- Tumor necrosis factor induces phosphorylation and translocation of BAD through a phosphatidylinositide-3-OH kinase-dependent pathway.
- Functional consequences of the sustained or transient activation by Bax of the mitochondrial permeability transition pore.
- Cyclosporin and carnitine prevent the anoxic death of cultured hepatocytes by inhibiting the mitochondrial permeability transition.
- Protoporphyrin IX, an endogenous ligand of the peripheral benzodiazepine receptor, potentiates induction of the mitochondrial permeability transition and the killing o...
- Programmed cell death (apoptosis) of mouse fibroblasts is induced by the topoisomerase II inhibitor etoposide.
- Cytochrome c-dependent activation of caspase-3 by tumor necrosis factor requires induction of the mitochondrial permeability transition.
- The presence of B-cell nodules does not necessarily portend a less favorable outcome to therapy in patients with acute cellular rejection of a renal allograft.
- Mitochondrial damage as a mechanism of cell injury in the killing of cultured hepatocytes by tert-butyl hydroperoxide.
- Ca2+ depletion prevents anoxic death of hepatocytes by inhibiting mitochondrial permeability transition.
- Increases in cytosolic calcium ion concentration can be dissociated from the killing of cultured hepatocytes by tert-butyl hydroperoxide.
- Two mechanisms by which ATP depletion potentiates induction of the mitochondrial permeability transition.
- Analysis of cell type and radiographic presentation as predictors of the clinical course of patients with bronchioalveolar cell carcinoma.
- Peroxidation-dependent and peroxidation-independent mechanisms by which acetaminophen kills cultured rat hepatocytes.
- Evidence for the participation of activated oxygen species and the resulting peroxidation of lipids in the killing of cultured hepatocytes by aryl halides.
- The absence of extracellular calcium potentiates the killing of cultured hepatocytes by aluminum maltolate.
- Reversal of the ethionine-induced inhibition of rat liver ribonucleic acid polymerases in vivo by adenine.
- Cellular pool of transient ferric iron, chelatable by deferoxamine and distinct from ferritin, that is involved in oxidative cell injury.
- The killing of cultured hepatocytes by N-acetyl-p-benzoquinone imine (NAPQI) as a model of the cytotoxicity of acetaminophen.
- The inhibition of lipid peroxidation by disulfiram prevents the killing of cultured hepatocytes by allyl alcohol, tert-butyl hydroperoxide, hydrogen peroxide and dieth...
- ATP synthase activity is required for fructose to protect cultured hepatocytes from the toxicity of cyanide.
- Dexamethasone induces resistance to the lethal consequences of electron transport inhibition in cultured hepatocytes.
- Mechanisms of cell injury in the killing of cultured hepatocytes by bromobenzene.
- Protection by cyclosporin A of cultured hepatocytes from the toxic consequences of the loss of mitochondrial energization produced by 1-methyl-4-phenylpyridinium.
- Calcium ion-dependent signalling and mitochondrial dysfunction: mitochondrial calcium uptake during hormonal stimulation in intact liver cells and its implication for ...
- c-Kit-positive mast cells in portal tracts cannot be used to distinguish acute cellular rejection from recurrent hepatitis C infection in liver allografts.
- Dissociation of the accumulation of single-strand breaks in DNA from the killing of cultured hepatocytes by an oxidative stress.
- Roles for oxidative stress and poly(ADP-ribosyl)ation in the killing of cultured hepatocytes by methyl methanesulfonate.
- 1,3-(2-Chloroethyl)-1-nitrosourea potentiates the toxicity of acetaminophen both in the phenobarbital-induced rat and in hepatocytes cultured from such animals.
- Independent antioxidant action of vitamins E and C in cultured rat hepatocytes intoxicated with allyl alcohol.
- Sirolimus-induced pneumonitis complicated by pentamidine-induced phospholipidosis in a renal transplant recipient: a case report.
- Effects of ouabain on potassium transport and cell volume regulation in rat and rabbit liver.
- Metabolism of acetaminophen by cultured rat hepatocytes. Depletion of protein thiol groups without any loss of viability.
- Protein thiol depletion and the killing of cultured hepatocytes by hydrogen peroxide.
- N-hydroxy-2-acetylaminofluorene inhibition of rat live RNA polymerases.
- Bronchial atresia with relapsing pulmonary infection in a middle-aged man.
- Accelerated phospholipid degradation and associated membrane dysfunction in irreversible, ischemic liver cell injury.
- Intracellular calcium homeostasis in galactosamine-intoxicated rat liver cells. Active sequestration of calcium by microsomes and mitochondria.
- Oxygen-mediated cell injury in the killing of cultured hepatocytes by acetaminophen.
- Microtubule antagonists activate programmed cell death (apoptosis) in cultured rat hepatocytes.
- Intracellular acidosis protects cultured hepatocytes from the toxic consequences of a loss of mitochondrial energization.
- Increased sensitivity to oxidative injury in chinese hamster ovary cells stably transfected with rat liver S-adenosylmethionine synthetase cDNA.
- Mechanisms of cell injury by activated oxygen species.
- Growth inhibition and cell killing by N-methyl-N-nitrosourea: metabolic alterations that accompany poly(ADP-ribosyl)ation.
- Autophagic degradation of protein generates a pool of ferric iron required for the killing of cultured hepatocytes by an oxidative stress.
- Differing effects of the inhibition of poly(ADP-ribose) polymerase on the course of oxidative cell injury in hepatocytes and fibroblasts.
- Endocytosis of superoxide dismutase is required in order for the enzyme to protect hepatocytes from the cytotoxicity of hydrogen peroxide.
- Prevention of experimental allergic encephalomyelitis by targeting nitric oxide and peroxynitrite: implications for the treatment of multiple sclerosis.
- Human- and mouse-inducible nitric oxide synthase promoters require activation of phosphatidylcholine-specific phospholipase C and NF-kappa B.
- Oxidative cell injury in the killing of cultured hepatocytes by allyl alcohol.
- N-methyl-4-phenylpyridinium (MPP+) potentiates the killing of cultured hepatocytes by catecholamines.
- Relationship of the metabolism of vitamins C and E in cultured hepatocytes treated with tert-butyl hydroperoxide.
- Effects of cardiac-restricted overexpression of the A(2A) adenosine receptor on adriamycin-induced cardiotoxicity.
- Reversal of ischemic mitochondrial dysfunction.
- Calcium dependence of phalloidin-induced liver cell death.
- Ferric iron and superoxide ions are required for the killing of cultured hepatocytes by hydrogen peroxide. Evidence for the participation of hydroxyl radicals formed b...
- Early, reversible plasma membrane injury in galactosamine-induced liver cell death.
- Killing of cultured hepatocytes by the mixed-function oxidation of ethoxycoumarin.
- Potentiation in the intact rat of the hepatotoxicity of acetaminophen by 1,3-bis(2-chloroethyl)-1-nitrosourea.
- Effects of vitamin E on the killing of cultured hepatocytes by tert-butyl hydroperoxide.
- tert-butyl hydroperoxide kills cultured hepatocytes by peroxidizing membrane lipids.
- Toxic consequence of the abrupt depletion of glutathione in cultured rat hepatocytes.
- Ultrastruct pathology of phalloidin-intoxicated hepatocytes in the presence and absence of extracellular calcium.
- Effects of ouabain and chloride-free medium on isoosmotic volume control and ultrastructure of hepatocytes in primary culture.
- The antioxidant function of the physiological content of vitamin C.
Schools
University of California At San Francisco
Mass Gen Hospital
Doctors Specialties
- Anatomic Pathology
- Pathology
Accepted Insurances
Awards
- Burlington Resources Foundation Faculty Achievement Award for Excellence in Teaching and Research
- Associate Recipient, Book of the Year Award for Pathology, 1989 and Honorable Mention for Essential Pathology
- Christian R. and Mary P. Lindback Foundation (Honored for Excellence in Teaching)
- Nominated for Passano Award, Passsano Foundation
- Alpha Omega Alpha
- Upjohn Award
- Roche Award
- Phi Beta Kappa
- Top MD
Hospital
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Thomas Jefferson University Hospital
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Medicare Facts
| National Provider Identifier [NPI] | 1174531719 |
| Last Name Of The Provider | FARBER |
| First Name Of The Provider | JOHN |
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