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Article: Genomic technologies for detecting structural variations in hematologic malignancies.

Jang, Mi-Ae

2024 Volume 59, Issue 1, Page(s) 1

Abstract: ... Several molecular diagnostic approaches play a central role in evaluating hematological malignancies. Traditional cytogenetic ... components of the current diagnostic workup that guide clinical care for most hematologic ... the clinical relevance of structural variations in hematologic malignancies and introduce genomic technologies ...

Abstract	Genomic structural variations in myeloid, lymphoid, and plasma cell neoplasms can provide key diagnostic, prognostic, and therapeutic information while elucidating the underlying disease biology. Several molecular diagnostic approaches play a central role in evaluating hematological malignancies. Traditional cytogenetic diagnostic assays, such as chromosome banding and fluorescence in situ hybridization, are essential components of the current diagnostic workup that guide clinical care for most hematologic malignancies. However, each assay has inherent limitations, including limited resolution for detecting small structural variations and low coverage, and can only detect alterations in the target regions. Recently, the rapid expansion and increasing availability of novel and comprehensive genomic technologies have led to their use in clinical laboratories for clinical management and translational research. This review aims to describe the clinical relevance of structural variations in hematologic malignancies and introduce genomic technologies that may facilitate personalized tumor characterization and treatment.
Language	English
Publishing date	2024-02-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2711910-5
ISSN	2288-0011 ; 2287-979X
ISSN (online)	2288-0011
ISSN	2287-979X
DOI	10.1007/s44313-024-00001-1
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Article: Viral parkinsonism.

Jang, Haeman / Boltz, David A / Webster, Robert G / Smeyne, Richard Jay

Biochimica et biophysica acta

2008 Volume 1792, Issue 7, Page(s) 714–721

Abstract: Parkinson's disease is a debilitating neurological disorder that affects 1-2% of the adult population over 55 years of age. For the vast majority of cases, the etiology of this disorder is unknown, although it is generally accepted that there is a ... ...

Abstract	Parkinson's disease is a debilitating neurological disorder that affects 1-2% of the adult population over 55 years of age. For the vast majority of cases, the etiology of this disorder is unknown, although it is generally accepted that there is a genetic susceptibility to any number of environmental agents. One such agent may be viruses. It has been shown that numerous viruses can enter the nervous system, i.e. they are neurotropic, and induce a number of encephalopathies. One of the secondary consequences of these encephalopathies can be parkinsonism, that is both transient as well as permanent. One of the most highlighted and controversial cases of viral parkinsonism is that which followed the 1918 influenza outbreak and the subsequent induction of von Economo's encephalopathy. In this review, we discuss the neurological sequelae of infection by influenza virus as well as that of other viruses known to induce parkinsonism including Coxsackie, Japanese encephalitis B, St. Louis, West Nile and HIV viruses.
MeSH term(s)	Animals ; Encephalitis Virus, Japanese/isolation & purification ; Encephalitis Virus, St. Louis/isolation & purification ; Enterovirus/isolation & purification ; HIV/isolation & purification ; Humans ; Influenza, Human/complications ; Orthomyxoviridae/isolation & purification ; Parkinson Disease, Postencephalitic/etiology ; Parkinson Disease, Postencephalitic/virology ; West Nile virus/isolation & purification
Language	English
Publishing date	2008-08-12
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2008.08.001
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Article ; Online: Parkinsonism and neurological manifestations of influenza throughout the 20th and 21st centuries.

Henry, Julia / Smeyne, Richard J / Jang, Haeman / Miller, Bayard / Okun, Michael S

Parkinsonism & related disorders

2010 Volume 16, Issue 9, Page(s) 566–571

Abstract: Purpose: Given the recent paper by Jang et al. on "A Highly Pathogenic H5N1 Influenza Virus ...

Abstract	Purpose: Given the recent paper by Jang et al. on "A Highly Pathogenic H5N1 Influenza Virus" which reported a novel animal model of parkinsonism, we aimed to perform a complete historical review of the 20th and 21st century literature on parkinsonism and neurological manifestations of influenza. Scope: There were at least twelve major flu pandemics reported in the literature in the 20th and 21st century. Neurological manifestations most prevalent during the pandemics included delirium, encephalitis, ocular abnormalities, amyotrophy, myelopathy, radiculopathy, ataxia and seizures. Very little parkinsonism was reported with the exception of the 1917 cases originally described by von Economo. Conclusions: To date there have been surprisingly few cases of neurological issues inclusive of parkinsonism associated with influenza pandemics. Given the recent animal model of H5N1 influenza associated parkinsonism, the medical establishment should be prepared to evaluate for the re-emergence of parkinsonism during future outbreaks.
MeSH term(s)	Animals ; Birds ; Databases, Factual/statistics & numerical data ; History, 16th Century ; History, 19th Century ; History, 20th Century ; History, 21st Century ; Humans ; Influenza in Birds ; Influenza, Human/complications ; Influenza, Human/epidemiology ; Influenza, Human/history ; Nervous System Diseases/epidemiology ; Nervous System Diseases/etiology ; Nervous System Diseases/history ; Pandemics ; Parkinsonian Disorders/epidemiology ; Parkinsonian Disorders/etiology ; Parkinsonian Disorders/history
Language	English
Publishing date	2010-07-21
Publishing country	England
Document type	Historical Article ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1311489-x
ISSN	1873-5126 ; 1353-8020
ISSN (online)	1873-5126
ISSN	1353-8020
DOI	10.1016/j.parkreldis.2010.06.012
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Article ; Online: Inflammatory effects of highly pathogenic H5N1 influenza virus infection in the CNS of mice.

Jang, Haeman / Boltz, David / McClaren, Jennifer / Pani, Amar K / Smeyne, Michelle / Korff, Ane / Webster, Robert / Smeyne, Richard Jay

The Journal of neuroscience : the official journal of the Society for Neuroscience

2012 Volume 32, Issue 5, Page(s) 1545–1559

Abstract: The A/VN/1203/04 strain of the H5N1 influenza virus is capable of infecting the CNS of mice and inducing a number of neurodegenerative pathologies. Here, we examined the effects of H5N1 on several pathological aspects affected in parkinsonism, including ... ...

Abstract	The A/VN/1203/04 strain of the H5N1 influenza virus is capable of infecting the CNS of mice and inducing a number of neurodegenerative pathologies. Here, we examined the effects of H5N1 on several pathological aspects affected in parkinsonism, including loss of the phenotype of dopaminergic neurons located in the substantia nigra pars compacta (SNpc), expression of monoamines and indolamines in brain, alterations in SNpc microglia number and morphology, and expression of cytokines, chemokines, and growth factors. We find that H5N1 induces a transient loss of the dopaminergic phenotype in SNpc and now report that this loss recovers by 90 d after infection. A similar pattern of loss and recovery was seen in monoamine levels of the basal ganglia. The inflammatory response in lung and different regions of the brain known to be targets of the H5N1 virus (brainstem, substantia nigra, striatum, and cortex) were examined at 3, 10, 21, 60, and 90 d after infection. In each of these brain regions, we found a significant increase in the number of activated microglia that lasted at least 90 d. We also quantified expression of IL-1α, IL-1β, IL-2, IL-6, IL-9, IL-10, IL-12(p70), IL-13, TNF-α, IFN-γ, granulocyte-macrophage colony-stimulating factor, granulocyte colony-stimulating factor, macrophage colony-stimulating factor, eotaxin, interferon-inducible protein 10, cytokine-induced neutrophil chemoattractant, monocyte chemotactic protein-1, macrophage inflammatory protein (MIP) 1α, MIP-1β, and VEGF, and found that the pattern and levels of expression are dependent on both brain region and time after infection. We conclude that H5N1 infection in mice induces a long-lasting inflammatory response in brain and may play a contributing factor in the development of pathologies in neurodegenerative disorders.
MeSH term(s)	Animals ; Brain/metabolism ; Brain/pathology ; Brain/virology ; Central Nervous System Viral Diseases/metabolism ; Central Nervous System Viral Diseases/pathology ; Central Nervous System Viral Diseases/virology ; Chick Embryo ; Female ; Humans ; Inflammation/pathology ; Inflammation/virology ; Inflammation Mediators/adverse effects ; Inflammation Mediators/metabolism ; Influenza A Virus, H5N1 Subtype/pathogenicity ; Influenza, Human/metabolism ; Influenza, Human/pathology ; Influenza, Human/virology ; Mice ; Mice, Inbred C57BL
Chemical Substances	Inflammation Mediators
Language	English
Publishing date	2012-02-02
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.5123-11.2012
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Article: Why should we monitor for hematologic adverse drug reactions to oxcarbazepine?

Jang, Gwang Cheon

Korean journal of pediatrics

2019 Volume 62, Issue 8, Page(s) 299–300

Language	English
Publishing date	2019-06-24
Publishing country	Korea (South)
Document type	Editorial
ZDB-ID	2594966-4
ISSN	2092-7258 ; 1738-1061
ISSN (online)	2092-7258
ISSN	1738-1061
DOI	10.3345/kjp.2019.00472
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Article: Highly pathogenic H5N1 influenza virus can enter the central nervous system and induce neuroinflammation and neurodegeneration

Jang, Haeman / Boltz, David / Sturm-Ramirez, Katharine / Shepherd, Kennie R / Jiao, Yun / Webster, Robert / Smeyne, Richard J

Proceedings of the National Academy of Sciences of the United States of America. 2009 Aug. 18, v. 106, no. 33

2009

Abstract: One of the greatest influenza pandemic threats at this time is posed by the highly pathogenic H5N1 avian influenza viruses. To date, 61% of the 433 known human cases of H5N1 infection have proved fatal. Animals infected by H5N1 viruses have demonstrated ... ...

Abstract	One of the greatest influenza pandemic threats at this time is posed by the highly pathogenic H5N1 avian influenza viruses. To date, 61% of the 433 known human cases of H5N1 infection have proved fatal. Animals infected by H5N1 viruses have demonstrated acute neurological signs ranging from mild encephalitis to motor disturbances to coma. However, no studies have examined the longer-term neurologic consequences of H5N1 infection among surviving hosts. Using the C57BL/6J mouse, a mouse strain that can be infected by the A/Vietnam/1203/04 H5N1 virus without adaptation, we show that this virus travels from the peripheral nervous system into the CNS to higher levels of the neuroaxis. In regions infected by H5N1 virus, we observe activation of microglia and alpha-synuclein phosphorylation and aggregation that persists long after resolution of the infection. We also observe a significant loss of dopaminergic neurons in the substantia nigra pars compacta 60 days after infection. Our results suggest that a pandemic H5N1 pathogen, or other neurotropic influenza virus, could initiate CNS disorders of protein aggregation including Parkinson's and Alzheimer's diseases.
Keywords	Alzheimer disease ; Influenza A virus ; central nervous system ; coma ; encephalitis ; hosts ; humans ; influenza ; mice ; neurodegenerative diseases ; neuroglia ; neurons ; pandemic ; pathogens ; peripheral nervous system ; phosphorylation ; viruses
Language	English
Dates of publication	2009-0818
Size	p. 14063-14068.
Publishing place	National Academy of Sciences
Document type	Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.0900096106
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Article: Impacts of Temperature on the Growth, Feed Utilization, Stress, and Hemato-Immune Responses of Cherry Salmon (

Lee, Jang-Won / Balasubramanian, Balamuralikrishnan

Animals : an open access journal from MDPI

2023 Volume 13, Issue 24

Abstract: Cherry salmon ( ...

Abstract	Cherry salmon (
Language	English
Publishing date	2023-12-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606558-7
ISSN	2076-2615
ISSN	2076-2615
DOI	10.3390/ani13243870
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Article ; Online: Highly pathogenic H5N1 influenza virus can enter the central nervous system and induce neuroinflammation and neurodegeneration.

Jang, Haeman / Boltz, David / Sturm-Ramirez, Katharine / Shepherd, Kennie R / Jiao, Yun / Webster, Robert / Smeyne, Richard J

Proceedings of the National Academy of Sciences of the United States of America

2009 Volume 106, Issue 33, Page(s) 14063–14068

Abstract	One of the greatest influenza pandemic threats at this time is posed by the highly pathogenic H5N1 avian influenza viruses. To date, 61% of the 433 known human cases of H5N1 infection have proved fatal. Animals infected by H5N1 viruses have demonstrated acute neurological signs ranging from mild encephalitis to motor disturbances to coma. However, no studies have examined the longer-term neurologic consequences of H5N1 infection among surviving hosts. Using the C57BL/6J mouse, a mouse strain that can be infected by the A/Vietnam/1203/04 H5N1 virus without adaptation, we show that this virus travels from the peripheral nervous system into the CNS to higher levels of the neuroaxis. In regions infected by H5N1 virus, we observe activation of microglia and alpha-synuclein phosphorylation and aggregation that persists long after resolution of the infection. We also observe a significant loss of dopaminergic neurons in the substantia nigra pars compacta 60 days after infection. Our results suggest that a pandemic H5N1 pathogen, or other neurotropic influenza virus, could initiate CNS disorders of protein aggregation including Parkinson's and Alzheimer's diseases.
MeSH term(s)	Animals ; Central Nervous System/immunology ; Central Nervous System/virology ; Ganglia, Spinal/metabolism ; Immunohistochemistry/methods ; Inflammation/metabolism ; Influenza A Virus, H5N1 Subtype/metabolism ; Influenza A Virus, H5N1 Subtype/pathogenicity ; Influenza A Virus, H5N1 Subtype/physiology ; Mice ; Mice, Inbred C57BL ; Neurodegenerative Diseases/metabolism ; Neurons/metabolism ; Orthomyxoviridae Infections/immunology ; Orthomyxoviridae Infections/virology ; Phenotype ; Phosphorylation ; Virus Diseases/metabolism ; alpha-Synuclein/metabolism
Chemical Substances	alpha-Synuclein
Language	English
Publishing date	2009-08-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.0900096106
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Article: Autoantibodies that recognize functional domains of hnRNPA1 implicate molecular mimicry in the pathogenesis of neurological disease.

Lee, Sang Min / Dunnavant, Floyd D / Jang, Haeman / Zunt, Joseph / Levin, Michael C

Neuroscience letters

2006 Volume 401, Issue 1-2, Page(s) 188–193

Abstract: As a model for molecular mimicry in neurological disease, we study people infected with human T-lymphotropic virus type 1 (HTLV-1) who develop HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP), an immune-mediated disease of the central ... ...

Abstract	As a model for molecular mimicry in neurological disease, we study people infected with human T-lymphotropic virus type 1 (HTLV-1) who develop HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP), an immune-mediated disease of the central nervous system (CNS). In HAM/TSP, data suggests molecular mimicry is the result of cross-reactive antibodies between HTLV-1-tax and heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1), a protein over-expressed in human CNS neurons. The hnRNP A1 epitope recognized by autoantibodies was unknown. In this study, we hypothesized that antibodies purified from HAM/TSP patients would react with functionally significant domains of hnRNP A1. Western blotting of functionally significant deletion mutants and overlapping fusion proteins using HAM/TSP IgG revealed two core epitopes within the C-terminal region of hnRNP A1. The first (aminoacids 191-SSQRGRSGSGNF-202), overlapped the RGG domain and the second (aminoacids 293-GQYFAKPRNQGG-304), with the M9 shuttling sequence, two functionally important regions of hnRNP A1. Monoclonal antibodies to HTLV-1-tax also reacted with the epitopes. These data fulfill an important criterion of molecular mimicry, namely that mimicking epitopes are not random, but include biologically significant regions of target proteins. This suggests an important role for the cross-reactive immune response between HTLV-1 and hnRNP A1 in the pathogenesis of immune-mediated neurological diseases via molecular mimicry.
MeSH term(s)	Autoantibodies/immunology ; Cross Reactions/genetics ; Cross Reactions/immunology ; Epitopes/genetics ; Epitopes/immunology ; HTLV-I Infections/genetics ; HTLV-I Infections/immunology ; HTLV-I Infections/physiopathology ; Heterogeneous Nuclear Ribonucleoprotein A1 ; Heterogeneous-Nuclear Ribonucleoprotein Group A-B/chemistry ; Heterogeneous-Nuclear Ribonucleoprotein Group A-B/genetics ; Heterogeneous-Nuclear Ribonucleoprotein Group A-B/immunology ; Humans ; Immunoglobulin G/immunology ; Molecular Mimicry/genetics ; Molecular Mimicry/immunology ; Mutation/genetics ; Mutation/immunology ; Neurons/immunology ; Neurons/metabolism ; Neurons/pathology ; Paraparesis, Tropical Spastic/genetics ; Paraparesis, Tropical Spastic/immunology ; Paraparesis, Tropical Spastic/physiopathology ; Protein Structure, Tertiary/genetics ; Recombinant Fusion Proteins/genetics ; Recombinant Fusion Proteins/immunology ; Spinal Cord/immunology ; Spinal Cord/metabolism ; Spinal Cord/pathology
Chemical Substances	Autoantibodies ; Epitopes ; Heterogeneous Nuclear Ribonucleoprotein A1 ; Heterogeneous-Nuclear Ribonucleoprotein Group A-B ; Immunoglobulin G ; Recombinant Fusion Proteins ; hnRNPA1 protein, human
Language	English
Publishing date	2006-04-05
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	194929-9
ISSN	1872-7972 ; 0304-3940
ISSN (online)	1872-7972
ISSN	0304-3940
DOI	10.1016/j.neulet.2006.03.016
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Article: Mysterious Arm Swelling in a Patient With Non-Hodgkin Lymphoma Complicated by Superior Vena Cava Syndrome.

Jang, Jessica S / Jang, Jeffrey S

Journal of the advanced practitioner in oncology

2022 Volume 13, Issue 1, Page(s) 87–92

Abstract: Hematologic malignancies often create difficult venous complications. Specifically, with lymphoma ...

Abstract	Hematologic malignancies often create difficult venous complications. Specifically, with lymphoma, the risk of venous thromboembolism (VTE) is high, often requiring highly specialized accuracy in balancing this coagulopathy. This case study demonstrates a situation where the advanced practitioner participated in the differential diagnosis of VTEs, management, and workup of subsequent central venous complications in a patient with non-Hodgkin lymphoma and superior vena cava syndrome.
Language	English
Publishing date	2022-02-01
Publishing country	United States
Document type	Journal Article
ISSN	2150-0878
ISSN	2150-0878
DOI	10.6004/jadpro.2022.13.1.8
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