Contribution of an aged microenvironment to aging-associated myeloproliferative disease. - Wikidata - awgldk - TriplyDB

Contribution of an aged microenvironment to aging-associated myeloproliferative disease.

Contribution of an aged microenvironment to aging-associated myeloproliferative disease.

http://www.wikidata.org/entity/Q34171027

about

Aging of hematopoietic stem cells: DNA damage and mutations?Toward an evolutionary model of cancer: Considering the mechanisms that govern the fate of somatic mutations Aging-associated inflammation promotes selection for adaptive oncogenic events in B cell progenitors Regulation of tumor growth and metastasis: the role of tumor microenvironment.Cdc42 and aging of hematopoietic stem cells.The crossroads between cancer stem cells and aging.Mesenchymal stromal cells derived from acute myeloid leukemia bone marrow exhibit aberrant cytogenetics and cytokine elaboration.The stem cell niche: tissue physiology at a single cell level Reactive Oxygen Species Limit the Ability of Bone Marrow Stromal Cells to Support Hematopoietic Reconstitution in Aging Mice.Tissue resident stem cells: till death do us part.Aging promotes neoplastic disease through effects on the tissue microenvironment.An evolutionary perspective on chronic myelomonocytic leukemia.Aging of the hematopoietic stem cells niche.Aging, Clonality, and Rejuvenation of Hematopoietic Stem Cells.Immune senescence: significance of the stromal microenvironment.The aging hematopoietic stem cell niche: Phenotypic and functional changes and mechanisms that contribute to hematopoietic aging.The evolution of lifespan and age-dependent cancer risk Angelica sinensis Polysaccharides Ameliorate Stress-Induced Premature Senescence of Hematopoietic Cell via Protecting Bone Marrow Stromal Cells from Oxidative Injuries Caused by 5-Fluorouracil.Heterodimerization of AML1/ETO with CBFβ is required for leukemogenesis but not for myeloproliferation.Endothelial transplantation rejuvenates aged hematopoietic stem cell function.

P2860

Q26741217-2CC8F1B6-AC67-4346-A735-156FD9B1DD89 Q28384546-57D9E231-EA26-4B5E-9D20-6722B739C537 Q28395194-D0553DAE-0A95-43C2-AE16-CD7041B92DB1 Q33734780-A1D268E1-CA83-439C-A329-450E3B03B428 Q33753610-26330BBE-19CB-4273-B92C-E1E9FAB3FA90 Q35566484-330482DE-E9D9-42A9-8B83-E73BD511625D Q35669055-72797B3B-C6FE-4E0F-8244-A57BC0D2F58D Q36190672-F5E73093-7A64-4D6D-BF6D-D572E398647F Q37054482-7A3D9F00-2D20-463B-8B5C-D72F61079141 Q37429379-021B0D3B-06B7-403A-AA11-80F241A397E1 Q37610201-EB7A4FE7-898A-4D46-9878-9ADEDAD92276 Q38096235-C691E148-D394-447F-B219-5DF578ECC5B7 Q38237265-6DCC4B52-1C15-4290-9ACC-875BF4DBADBA Q38887008-40440E63-B849-4FB1-9D5F-DF0E16E3CD73 Q38928710-5A41451E-0198-42AF-AEA2-1F7216E182BA Q39089125-65D454F8-2A4B-4458-8A0C-0CDBFA52A70E Q39260251-85FBD2E5-BDFF-43EA-A4FF-426514B9BA5E Q46260486-023BAC6E-BFB3-4B0D-BC2A-9B0138366364 Q47127883-1AF6C0E5-7F2F-4AAC-B6A9-ED24918E0EFC Q47441774-5D4EB4CA-6F0E-4564-9078-D8D9F118F0B8

P2860

Contribution of an aged microenvironment to aging-associated myeloproliferative disease.

http://www.wikidata.org/entity/Q34171027

description

2012 nî lūn-bûn

@nan

2012 թուականի Փետրուարին հրատարակուած գիտական յօդուած

@hyw

2012 թվականի փետրվարին հրատարակված գիտական հոդված

@hy

2012年の論文

@ja

2012年論文

@yue

2012年論文

@zh-hant

2012年論文

@zh-hk

2012年論文

@zh-mo

2012年論文

@zh-tw

2012年论文

@wuu

name

Contribution of an aged microenvironment to aging-associated myeloproliferative disease.

@ast

Contribution of an aged microenvironment to aging-associated myeloproliferative disease.

@en

Contribution of an aged microenvironment to aging-associated myeloproliferative disease.

@nl

type

label

Contribution of an aged microenvironment to aging-associated myeloproliferative disease.

@ast

Contribution of an aged microenvironment to aging-associated myeloproliferative disease.

@en

Contribution of an aged microenvironment to aging-associated myeloproliferative disease.

@nl

prefLabel

Contribution of an aged microenvironment to aging-associated myeloproliferative disease.

@ast

Contribution of an aged microenvironment to aging-associated myeloproliferative disease.

@en

Contribution of an aged microenvironment to aging-associated myeloproliferative disease.

@nl

P1433

Q34171027-37EAE6CD-5036-4803-8704-D0B20ADBB34C

P1476

Q34171027-28CD0695-AE73-4A5F-8E88-0B2F71715D43

P2093

Q34171027-19AE540A-B0FF-4441-A3B5-963DA1687042

Q34171027-1F3EF58D-AACB-4CC5-B6D9-1EEFA7385B78

Q34171027-5B93F3D8-9735-412C-9499-466D8270C1C5

Q34171027-5DB968CD-8283-45DC-A99A-C20A36599EA7

P2860

Q34171027-00B14716-F702-425E-842C-5ACCF93485AE

Q34171027-07A0F39F-7E63-4D22-A715-D3492B74388E

Q34171027-0F87101E-8C31-481E-9061-2A73CA3420B0

Q34171027-0FEAB173-F734-4BFE-B958-3E3277640C47

Q34171027-1055DEAF-9409-43AE-BE47-1A53B25FABCF

Q34171027-10B5F8F9-8CD3-4A45-ADA9-BFA93778934C

Q34171027-17809C5E-6366-4ECB-AE20-31808BD34C82

Q34171027-1F2870DF-9599-4F32-8350-9CC0E31FE77D

Q34171027-23E61808-425F-4E99-9C55-9834BE74B00D

Q34171027-252D3C63-87C0-4E73-BDE0-252196446A57

P304

Q34171027-D916D818-30B6-4DCB-8D1A-BAA265DCC65F

P31

Q34171027-2F223543-6F0A-4D7D-A7D1-EF83256F5E92

P356

Q34171027-E7B11D3A-5EA8-4145-BD7E-EE496AB1CA10

P407

Q34171027-C299AA6A-A099-47A8-AACD-F3D4603FC071

P433

Q34171027-936EEFFA-9CF2-4D73-BFD9-F9DF8F8A7A76

P478

Q34171027-64A68522-3891-491D-A6DF-33011623E595

P50

Q34171027-6395B5CE-1216-4BDE-95B3-F59FCA073519

P577

Q34171027-D8F3A12D-D24B-46BE-8EFE-3D681792CAB9

P5875

Q34171027-5943F251-AA65-44D6-A75C-C7C98CE6D2B8

P698

Q34171027-031368CC-84BE-4DA0-8DE1-65695D4CEEB3

P932

Q34171027-4F40D3C5-F79B-44D8-A5E8-B1562ED44515

P356

JOURNAL.PONE.0031523

P1433

P1476

Contribution of an aged microenvironment to aging-associated myeloproliferative disease.

@en

P2093

Anja Niebel

http://www.w3.org/2001/XMLSchema#string

Corinna Wandhoff

http://www.w3.org/2001/XMLSchema#string

Hartmut Geiger

http://www.w3.org/2001/XMLSchema#string

Karin Dörr

http://www.w3.org/2001/XMLSchema#string

P2860

Deficiencies in DNA damage repair limit the function of haematopoietic stem cells with age

Distinct hematopoietic stem cell subtypes are differentially regulated by TGF-beta1.

Functionally distinct hematopoietic stem cells modulate hematopoietic lineage potential during aging by a mechanism of clonal expansion

Cell intrinsic alterations underlie hematopoietic stem cell aging.

The AML1-ETO fusion gene and the FLT3 length mutation collaborate in inducing acute leukemia in mice.

Hematopoietic stem cell quiescence promotes error-prone DNA repair and mutagenesis

Declining lymphoid progenitor fitness promotes aging-associated leukemogenesis.

C-KIT mutation cooperates with full-length AML1-ETO to induce acute myeloid leukemia in mice

Prognostic factors of acute myelocytic leukemia: an analysis of 132 patients in a single institution

Contribution of bone microenvironment to leukemogenesis and leukemia progression.

P304

e31523

http://www.w3.org/2001/XMLSchema#string

P31

scholarly article

P356

10.1371/JOURNAL.PONE.0031523

http://www.w3.org/2001/XMLSchema#string

P407

P433

2

http://www.w3.org/2001/XMLSchema#string

P478

7

http://www.w3.org/2001/XMLSchema#string

P50

P577

2012-02-21T00:00:00Z

http://www.w3.org/2001/XMLSchema#dateTime

P5875

221859943

http://www.w3.org/2001/XMLSchema#string

P698

22363661

http://www.w3.org/2001/XMLSchema#string

P932

3283638

http://www.w3.org/2001/XMLSchema#string