King Fahd Professor of Medicine, Oncology, Molecular Biology and Genetics, Professor of Medicine and Oncology, Johns Hopkins University School of Medicine; Chief, Division of Molecular Medicine, Department of Medicine; Director, Center for Epigenetics; Gi
Medical Genetics
Dr. Andrew G. Feinberg, MD
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Doctor Andrew G. Feinberg, MD works in the field of Medical Genetics. He graduated from Johns Hopkins University School of Medicine. Johns Hopkins University School of Medicine is a one of the best medicals schools. Johns Hopkins University School of Medicine has a rank of 3 in research and a 29 in primary care He has 3 awards "Elected Member", "Investigator Alumnus" and "Whos Who in Medicine and Healthcare". Andrew Feinberg has written publications. He has 100 publications published with PubMed. The lastest paper is: 'Genomic imprinting, DNA methylation, and cancer.'
Publications
- Mouse-human experimental epigenetic analysis unmasks dietary targets and genetic liability for diabetic phenotypes.
- A comparison of non-integrating reprogramming methods.
- Mutant WT1 is associated with DNA hypermethylation of PRC2 targets in AML and responds to EZH2 inhibition.
- A Selective Phenelzine Analogue Inhibitor of Histone Demethylase LSD1.
- GeMes, Clusters of DNA Methylation under Genetic Control, Can Inform Genetic and Epigenetic Analysis of Disease.
- Epigenetic stochasticity, nuclear structure and cancer: the implications for medicine.
- Minfi: a flexible and comprehensive Bioconductor package for the analysis of Infinium DNA methylation microarrays.
- Common DNA methylation alterations in multiple brain regions in autism.
- Cancer as a dysregulated epigenome allowing cellular growth advantage at the expense of the host.
- A third-generation method reveals cell lineage ancestry.
- Epigenome-wide association data implicate DNA methylation as an intermediary of genetic risk in rheumatoid arthritis.
- Higher order chromatin organization in cancer.
- Reversible switching between epigenetic states in honeybee behavioral subcastes.
- Regulated noise in the epigenetic landscape of development and disease.
- Erratum: Donor cell type can influence the epigenome and differentiation potential of human induced pluripotent stem cells.
- Stem cell differentiation as a renewal-reward process: predictions and validation in the colonic crypt.
- Adaptation of the CHARM DNA methylation platform for the rat genome reveals novel brain region-specific differences.
- A nucleolar protein, H19 opposite tumor suppressor (HOTS), is a tumor growth inhibitor encoded by a human imprinted H19 antisense transcript.
- Genome-scale epigenetic reprogramming during epithelial-to-mesenchymal transition.
- Increased methylation variation in epigenetic domains across cancer types.
- Significance analysis and statistical dissection of variably methylated regions.
- Donor cell type can influence the epigenome and differentiation potential of human induced pluripotent stem cells.
- Epigenomics reveals a functional genome anatomy and a new approach to common disease.
- Personalized epigenomic signatures that are stable over time and covary with body mass index.
- Addition of H19 'loss of methylation testing' for Beckwith-Wiedemann syndrome (BWS) increases the diagnostic yield.
- Comprehensive high-throughput arrays for relative methylation (CHARM).
- Evolution in health and medicine Sackler colloquium: Stochastic epigenetic variation as a driving force of development, evolutionary adaptation, and disease.
- Differential methylation of tissue- and cancer-specific CpG island shores distinguishes human induced pluripotent stem cells, embryonic stem cells and fibroblasts.
- A species-generalized probabilistic model-based definition of CpG islands.
- Temporal stability and age-related prevalence of loss of imprinting of the insulin-like growth factor-2 gene.
- Large histone H3 lysine 9 dimethylated chromatin blocks distinguish differentiated from embryonic stem cells.
- The human colon cancer methylome shows similar hypo- and hypermethylation at conserved tissue-specific CpG island shores.
- A new link between epigenetic progenitor lesions in cancer and the dynamics of signal transduction.
- Overlapping euchromatin/heterochromatin- associated marks are enriched in imprinted gene regions and predict allele-specific modification.
- BAT3 and SET1A form a complex with CTCFL/BORIS to modulate H3K4 histone dimethylation and gene expression.
- CTCFL/BORIS is a methylation-independent DNA-binding protein that preferentially binds to the paternal H19 differentially methylated region.
- Intra-individual change over time in DNA methylation with familial clustering.
- SNP-specific array-based allele-specific expression analysis.
- DNA methyltransferase 1 and 3B activate BAG-1 expression via recruitment of CTCFL/BORIS and modulation of promoter histone methylation.
- Epigenetics at the epicenter of modern medicine.
- Enhanced sensitivity to IGF-II signaling links loss of imprinting of IGF2 to increased cell proliferation and tumor risk.
- DNA methylation signatures within the human brain.
- Epigenetic specificity of loss of imprinting of the IGF2 gene in Wilms tumors.
- The commonality of plasticity underlying multipotent tumor cells and embryonic stem cells.
- Genetics and epigenetics--nature's pen-and-pencil set.
- An X chromosome gene, WTX, is commonly inactivated in Wilms tumor.
- Detailed DNA methylation profiles of the E-cadherin promoter in the NCI-60 cancer cells.
- An epigenetic approach to cancer etiology.
- Loss of imprinting of IGF2: a common epigenetic modifier of intestinal tumor risk.
- Children with idiopathic hemihypertrophy and beckwith-wiedemann syndrome have different constitutional epigenotypes associated with wilms tumor.
- Cancer epigenetics is no Mickey Mouse.
- Inheritance pattern of Beckwith-Wiedemann syndrome is heterogeneous in 291 families with an affected proband.
- Association of chromosome arm 16q loss with loss of imprinting of insulin-like growth factor-II in Wilms tumor.
- Factors associated with preterm delivery in mothers of children with Beckwith-Wiedemann syndrome: a case cohort study from the BWS registry.
- Loss of imprinting of Igf2 alters intestinal maturation and tumorigenesis in mice.
- Association between Beckwith-Wiedemann syndrome and assisted reproductive technology: a case series of 19 patients.
- The epigenetics of cancer etiology.
- Microdeletion of LIT1 in familial Beckwith-Wiedemann syndrome.
- Distinct effects on gene expression of chemical and genetic manipulation of the cancer epigenome revealed by a multimodality approach.
- Poly(ADP-ribosyl)ation regulates CTCF-dependent chromatin insulation.
- Loss of imprinting of insulin growth factor II gene: a potential heritable biomarker for colon neoplasia predisposition.
- Epigenetics and assisted reproductive technology: a call for investigation.
- Lack of parental origin specificity of altered alleles at 11p15 in testicular germ cell tumors.
- Loss of IGF2 imprinting: a potential marker of colorectal cancer risk.
- Wilms' tumor as a model for cancer biology.
- Association of in vitro fertilization with Beckwith-Wiedemann syndrome and epigenetic alterations of LIT1 and H19.
- Epigenetic variability and the evolution of human cancer.
- Epigenetic mechanisms in human disease.
- Loss of imprinting in colorectal cancer linked to hypomethylation of H19 and IGF2.
- SIRT3, a human SIR2 homologue, is an NAD-dependent deacetylase localized to mitochondria.
- DNA methylation and genomic imprinting: insights from cancer into epigenetic mechanisms.
- Monoallelic expression and methylation of imprinted genes in human and mouse embryonic germ cell lineages.
- BORIS, a novel male germ-line-specific protein associated with epigenetic reprogramming events, shares the same 11-zinc-finger domain with CTCF, the insulator protein ...
- A genome-wide screen for normally methylated human CpG islands that can identify novel imprinted genes.
- Epigenetic alterations of H19 and LIT1 distinguish patients with Beckwith-Wiedemann syndrome with cancer and birth defects.
- Tumor-associated zinc finger mutations in the CTCF transcription factor selectively alter tts DNA-binding specificity.
- Accurate genome-scale percentage DNA methylation estimates from microarray data.
- Comprehensive methylome map of lineage commitment from haematopoietic progenitors.
- Redefining CpG islands using hidden Markov models.
- Genome-scale approaches to the epigenetics of common human disease.
- An integrated epigenetic and genetic approach to common human disease.
- Epigenetic silencing of tumour suppressor gene p15 by its antisense RNA.
- Phenotypic plasticity and the epigenetics of human disease.
- Gene-based SNP mapping of a psychotic Bipolar affective disorder linkage region on 22q12.3: association with HMG2L1 and TOM1.
- The epigenetic progenitor origin of human cancer.
- The emerging science of epigenomics.
- The history of cancer epigenetics.
- DNMT1 and DNMT3b cooperate to silence genes in human cancer cells.
- Targeted regulation of imprinted genes by synthetic zinc-finger transcription factors.
- Microallelotyping defines the sequence and tempo of allelic losses at tumour suppressor gene loci during colorectal cancer progression.
- Loss of imprinting in human cancer.
- Loss of imprinting in hepatoblastoma.
- Epigenetic effects in eukaryotic gene expression.
- A developmental context for multiple genetic alterations in Wilms'' tumor.
- Parental imprinting of human chromosome region 11p15.3-pter involved in the Beckwith-Wiedemann syndrome and various human neoplasia.
- Loss of imprinting of IGF2 is linked to reduced expression and abnormal methylation of H19 in Wilms' tumour.
- Transcribed dinucleotide repeat polymorphism in the IGF2 gene.
- Simple purification of human chromosomes to homogeneity using muntjac hybrid cells.
- Genomic imprinting, DNA methylation, and cancer.
Schools
University of Medicine And Dentistry of New Jersey Newark
Johns Hopkins
Conditions Treated
- Bipolar Disorder
- Major Depressive Disorder
Doctors Specialties
- Geriatric Psychiatry
- Medical Genetics
Accepted Insurances
Awards
- Elected Member
- Investigator Alumnus
- Whos Who in Medicine and Healthcare
Education
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Johns Hopkins University -
Johns Hopkins University School of Medicine
Hospital
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Johns Hopkins Hospital
Drug Facts
| NPI NUMBER | 1316959802 | |
| NPPES Provider LastName | FEINBERG | |
| NPPES Provider FirstName | ANDREW | |
| NPPES Provider ZIPCode | 303082247 | |
| NPPES Provider State | GA | |
| Specialty Description | Ophthalmology | |
| Total Claim Count | 1631.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
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Medicare Facts
| National Provider Identifier [NPI] | 1316959802 |
| Last Name Of The Provider | FEINBERG |
| First Name Of The Provider | ANDREW |
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