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  1. Book: Myeloproliferative disorders

    Green, Anthony R.

    (Baillière's clinical haematology ; 11,4)

    1998  

    Author's details A. R. Green ..., guest ed
    Series title Baillière's clinical haematology ; 11,4
    Collection
    Keywords Myeloproliferatives Syndrom
    Subject MPS ; Chronische myeloproliferative Krankheit ; Myeloproliferative Erkrankung ; Myeloproliferative Neoplasie
    Language English
    Size X S., S. 695 - 904
    Publisher Baillière Tindall
    Publishing place London u.a.
    Publishing country Great Britain
    Document type Book
    HBZ-ID HT011085288
    ISBN 0-7020-2462-7 ; 978-0-7020-2462-7
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Se 1029 -11,4- verfügbar in Königswinter Königswinter

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  2. Article ; Online: Mutant CALR functions: gains and losses.

    Prins, Daniel / Green, Anthony R

    Blood

    2020  Volume 136, Issue 1, Page(s) 6–7

    MeSH term(s) Animals ; Calreticulin/genetics ; Calreticulin/metabolism ; Haploinsufficiency ; Mice ; Myeloproliferative Disorders ; Neoplasms ; Stem Cells/metabolism
    Chemical Substances Calreticulin
    Language English
    Publishing date 2020-07-02
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2020005805
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  3. Article ; Online: Order Matters: The Order of Somatic Mutations Influences Cancer Evolution.

    Kent, David G / Green, Anthony R

    Cold Spring Harbor perspectives in medicine

    2017  Volume 7, Issue 4

    Abstract: Cancers evolve as a consequence of multiple somatic lesions, with competition between subclones and sequential subclonal evolution. Some driver mutations arise either early or late in the evolution of different individual tumors, suggesting that the ... ...

    Abstract Cancers evolve as a consequence of multiple somatic lesions, with competition between subclones and sequential subclonal evolution. Some driver mutations arise either early or late in the evolution of different individual tumors, suggesting that the final malignant properties of a subclone reflect the sum of mutations acquired rather than the order in which they arose. However, very little is known about the cellular consequences of altering the order in which mutations are acquired. Recent studies of human myeloproliferative neoplasms show that the order in which individual mutations are acquired has a dramatic impact on the cell biological and molecular properties of tumor-initiating cells. Differences in clinical presentation, complications, and response to targeted therapy were all observed and implicate mutation order as an important player in cancer biology. These observations represent the first demonstration that the order of mutation acquisition influences stem and progenitor cell behavior and clonal evolution in any cancer. Thus far, the impact of different mutation orders has only been studied in hematological malignancies, and analogous studies of solid cancers are now required.
    MeSH term(s) Animals ; Clonal Evolution/genetics ; Disease Models, Animal ; Humans ; Mice ; Mutation ; Neoplasms/genetics
    Language English
    Publishing date 2017-04-03
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2157-1422
    ISSN (online) 2157-1422
    DOI 10.1101/cshperspect.a027060
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Myeloproliferative neoplasms: from origins to outcomes.

    Nangalia, Jyoti / Green, Anthony R

    Hematology. American Society of Hematology. Education Program

    2017  Volume 2017, Issue 1, Page(s) 470–479

    Abstract: Substantial progress has been made in our understanding of the pathogenetic basis of myeloproliferative neoplasms. The discovery of mutations ... ...

    Abstract Substantial progress has been made in our understanding of the pathogenetic basis of myeloproliferative neoplasms. The discovery of mutations in
    MeSH term(s) Animals ; DNA Mutational Analysis ; Hematologic Neoplasms/drug therapy ; Hematologic Neoplasms/enzymology ; Hematologic Neoplasms/genetics ; Humans ; Janus Kinase 2/antagonists & inhibitors ; Janus Kinase 2/genetics ; Janus Kinase 2/metabolism ; Mutation ; Myelopoiesis/drug effects ; Myelopoiesis/genetics ; Myeloproliferative Disorders/drug therapy ; Myeloproliferative Disorders/enzymology ; Myeloproliferative Disorders/genetics ; Protein Kinase Inhibitors/therapeutic use
    Chemical Substances Protein Kinase Inhibitors ; JAK2 protein, human (EC 2.7.10.2) ; Janus Kinase 2 (EC 2.7.10.2)
    Language English
    Publishing date 2017-12-13
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2084287-9
    ISSN 1520-4383 ; 1520-4391
    ISSN (online) 1520-4383
    ISSN 1520-4391
    DOI 10.1182/asheducation-2017.1.470
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Myeloproliferative neoplasms: from origins to outcomes.

    Nangalia, Jyoti / Green, Anthony R

    Blood

    2017  Volume 130, Issue 23, Page(s) 2475–2483

    Abstract: Substantial progress has been made in our understanding of the pathogenetic basis of myeloproliferative neoplasms. The discovery of mutations ... ...

    Abstract Substantial progress has been made in our understanding of the pathogenetic basis of myeloproliferative neoplasms. The discovery of mutations in
    MeSH term(s) Animals ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Clonal Evolution ; Disease Progression ; Epistasis, Genetic ; Genetic Association Studies ; Genetic Predisposition to Disease ; Humans ; Janus Kinases/metabolism ; Mutation ; Myeloproliferative Disorders/diagnosis ; Myeloproliferative Disorders/etiology ; Myeloproliferative Disorders/metabolism ; Phenotype ; STAT Transcription Factors/metabolism ; Signal Transduction
    Chemical Substances STAT Transcription Factors ; Janus Kinases (EC 2.7.10.2)
    Language English
    Publishing date 2017-09-27
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2017-06-782037
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  6. Article ; Online: Clonal approaches to understanding the impact of mutations on hematologic disease development.

    Nangalia, Jyoti / Mitchell, Emily / Green, Anthony R

    Blood

    2019  Volume 133, Issue 13, Page(s) 1436–1445

    Abstract: Interrogation of hematopoietic tissue at the clonal level has a rich history spanning over 50 years, and has provided critical insights into both normal and malignant hematopoiesis. Characterization of chromosomes identified some of the first genetic ... ...

    Abstract Interrogation of hematopoietic tissue at the clonal level has a rich history spanning over 50 years, and has provided critical insights into both normal and malignant hematopoiesis. Characterization of chromosomes identified some of the first genetic links to cancer with the discovery of chromosomal translocations in association with many hematological neoplasms. The unique accessibility of hematopoietic tissue and the ability to clonally expand hematopoietic progenitors in vitro has provided fundamental insights into the cellular hierarchy of normal hematopoiesis, as well as the functional impact of driver mutations in disease. Transplantation assays in murine models have enabled cellular assessment of the functional consequences of somatic mutations in vivo. Most recently, next-generation sequencing-based assays have shown great promise in allowing multi-"omic" characterization of single cells. Here, we review how clonal approaches have advanced our understanding of disease development, focusing on the acquisition of somatic mutations, clonal selection, driver mutation cooperation, and tumor evolution.
    MeSH term(s) Animals ; Carcinogenesis/genetics ; Carcinogenesis/pathology ; Hematologic Diseases/genetics ; Hematologic Diseases/pathology ; Hematologic Neoplasms/genetics ; Hematologic Neoplasms/pathology ; Hematopoiesis ; Hematopoietic Stem Cells/metabolism ; Hematopoietic Stem Cells/pathology ; High-Throughput Nucleotide Sequencing ; Humans ; Mutation
    Language English
    Publishing date 2019-02-06
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2018-11-835405
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Microsimulation of SARS-CoV-2 Transmission in Society

    Green, Anthony R / Keep, Daniel / Piper, Ian

    medRxiv

    Abstract: The outbreak of the pandemic disease, COVID-19, has shown that the approaches by different countries has resulted in a range of infection rates through their societies. This has arisen from the varying personal behaviour and tactical use of lockdown ... ...

    Abstract The outbreak of the pandemic disease, COVID-19, has shown that the approaches by different countries has resulted in a range of infection rates through their societies. This has arisen from the varying personal behaviour and tactical use of lockdown strategies within each country. We report the use of microsimulation of a simulated community in Australia, using a discrete infection model within a community of residences, places of work and recreation to demonstrate the applicability of this method to both the current pandemic and to infection more generally. Simulations without any societal intervention on infection spread provided base simulations that could be compared with social and societal controls in the future and which were compared with the initial doubling times of country outbreaks across the world. Different population sizes were represented in some simulations and in other simulations the effects of either social distancing or the use of facial masks as personal behaviours was investigated within the community. Good agreement is found between the initial doubling times for several countries and the simulations that suggests that modelling infection as a collection of individual infections provides an alternative to current epidemiological models. The variation of the basic reproductive number, R0, with time and population size, suggests that one of the fundamentals assumptions in SIR type models is wrong, but varies according to the properties of the population being modelled. Investigation of the infection spread shows that the number of super-spreaders varies with the size of the population and occurs through contacts in clubs, supermarkets, schools and theatres where the source of infection is an employee and where there are high numbers of contacts. The simulations of individual control show that the benefits of social distancing or wearing masks is only fully realised where there is considerable compliance within society to these measures.
    Keywords covid19
    Language English
    Publishing date 2021-05-18
    Publisher Cold Spring Harbor Laboratory Press
    Document type Article ; Online
    DOI 10.1101/2021.05.16.21257298
    Database COVID19

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  8. Article ; Online: Inherited polygenic effects on common hematological traits influence clonal selection on JAK2

    Guo, Jing / Walter, Klaudia / Quiros, Pedro M / Gu, Muxin / Baxter, E Joanna / Danesh, John / Di Angelantonio, Emanuele / Roberts, David / Guglielmelli, Paola / Harrison, Claire N / Godfrey, Anna L / Green, Anthony R / Vassiliou, George S / Vuckovic, Dragana / Nangalia, Jyoti / Soranzo, Nicole

    Nature genetics

    2024  Volume 56, Issue 2, Page(s) 273–280

    Abstract: Myeloproliferative neoplasms (MPNs) are chronic cancers characterized by overproduction of mature blood cells. Their causative somatic mutations, for example, ... ...

    Abstract Myeloproliferative neoplasms (MPNs) are chronic cancers characterized by overproduction of mature blood cells. Their causative somatic mutations, for example, JAK2
    MeSH term(s) Humans ; Mutation ; Myeloproliferative Disorders/genetics ; Myeloproliferative Disorders/diagnosis ; Phenotype ; Neoplasms ; Janus Kinase 2/genetics ; Genetic Risk Score
    Chemical Substances Janus Kinase 2 (EC 2.7.10.2) ; JAK2 protein, human (EC 2.7.10.2)
    Language English
    Publishing date 2024-01-17
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1108734-1
    ISSN 1546-1718 ; 1061-4036
    ISSN (online) 1546-1718
    ISSN 1061-4036
    DOI 10.1038/s41588-023-01638-x
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  9. Article ; Online: Mutant Calreticulin in the Myeloproliferative Neoplasms.

    Prins, Daniel / González Arias, Carlos / Klampfl, Thorsten / Grinfeld, Jacob / Green, Anthony R

    HemaSphere

    2020  Volume 4, Issue 1, Page(s) e333

    Abstract: Mutations in the gene for calreticulin ( ...

    Abstract Mutations in the gene for calreticulin (
    Language English
    Publishing date 2020-01-15
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2572-9241
    ISSN (online) 2572-9241
    DOI 10.1097/HS9.0000000000000333
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Pathogenesis of Myeloproliferative Disorders.

    Nangalia, Jyoti / Grinfeld, Jacob / Green, Anthony R

    Annual review of pathology

    2016  Volume 11, Page(s) 101–126

    Abstract: Myeloproliferative neoplasms (MPNs) are a set of chronic hematopoietic neoplasms with overlapping clinical and molecular features. Recent years have witnessed considerable advances in our understanding of their pathogenetic basis. Due to their protracted ...

    Abstract Myeloproliferative neoplasms (MPNs) are a set of chronic hematopoietic neoplasms with overlapping clinical and molecular features. Recent years have witnessed considerable advances in our understanding of their pathogenetic basis. Due to their protracted clinical course, the evolution to advanced hematological malignancies, and the accessibility of neoplastic tissue, the study of MPNs has provided a window into the earliest stages of tumorigenesis. With the discovery of mutations in CALR, the majority of MPN patients now bear an identifiable marker of clonal disease; however, the mechanism by which mutated CALR perturbs megakaryopoiesis is currently unresolved. We are beginning to understand better the role of JAK2(V617F) homozygosity, the function of comutations in epigenetic regulators and spliceosome components, and how these mutations cooperate with JAK2(V617F) to modulate MPN phenotype.
    MeSH term(s) Animals ; Cell Transformation, Neoplastic/pathology ; Humans ; Myeloproliferative Disorders/physiopathology
    Language English
    Publishing date 2016-05-17
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2227429-7
    ISSN 1553-4014 ; 1553-4006
    ISSN (online) 1553-4014
    ISSN 1553-4006
    DOI 10.1146/annurev-pathol-012615-044454
    Database MEDical Literature Analysis and Retrieval System OnLINE

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