PMID- 15831462
OWN - NLM
STAT- MEDLINE
DCOM- 20050614
LR  - 20181113
IS  - 0270-7306 (Print)
IS  - 1098-5549 (Electronic)
IS  - 0270-7306 (Linking)
VI  - 25
IP  - 9
DP  - 2005 May
TI  - Id2 mediates tumor initiation, proliferation, and angiogenesis in Rb mutant mice.
PG  - 3563-74
AB  - The inhibitor of differentiation Id2 is a target of the retinoblastoma (Rb) 
      protein during mouse embryogenesis. In Rb(+/-) mice, LOH at the wild-type Rb 
      allele initiates pituitary adenocarcinoma, a tumor derived from embryonic 
      melanotropes. Here we identify a critical role for Id2 in initiation, growth, and 
      angiogenesis of pituitary tumors from Rb(+/-) mice. We show that proliferation 
      and differentiation are intimately coupled in Rb(+/-) pituitary cells before 
      tumor initiation. In Id2-null pituitaries, premature activation of basic 
      helix-loop-helix-mediated transcription and expression of the cdk inhibitor 
      p27(Kip1) impairs the proliferation of melanotropes and tumor initiation. Without 
      Id2, Rb(+/-) mice have fewer early tumor lesions and a markedly decreased 
      proliferation rate of the tumor foci. Expression of Id2 by pituitary tumor cells 
      promotes growth and angiogenesis by functioning as a master regulator of vascular 
      endothelial growth factor (VEGF). In human neuroblastoma, the N-Myc-driven 
      expression of Id2 is sufficient and necessary for expression of VEGF. These 
      results establish that aberrant Id2 activity directs initiation and progression 
      of embryonal cancer.
FAU - Lasorella, Anna
AU  - Lasorella A
AD  - Institute for Cancer Genetics, Columbia University, 1150 St. Nicholas Avenue, New 
      York, NY 10032, USA.
FAU - Rothschild, Gerson
AU  - Rothschild G
FAU - Yokota, Yoshifumi
AU  - Yokota Y
FAU - Russell, Robert G
AU  - Russell RG
FAU - Iavarone, Antonio
AU  - Iavarone A
LA  - eng
GR  - R01 CA085628/CA/NCI NIH HHS/United States
GR  - R01 CA101644/CA/NCI NIH HHS/United States
GR  - R01 CA 101644/CA/NCI NIH HHS/United States
GR  - R01 CA 85628/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Mol Cell Biol
JT  - Molecular and cellular biology
JID - 8109087
RN  - 0 (CCNG1 protein, human)
RN  - 0 (Ccng1 protein, mouse)
RN  - 0 (Cdkn1b protein, mouse)
RN  - 0 (Cell Cycle Proteins)
RN  - 0 (Cyclin G)
RN  - 0 (Cyclin G1)
RN  - 0 (Cyclins)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Idb2 protein, mouse)
RN  - 0 (Inhibitor of Differentiation Protein 2)
RN  - 0 (Repressor Proteins)
RN  - 0 (Retinoblastoma Protein)
RN  - 0 (Transcription Factors)
RN  - 0 (Tumor Suppressor Proteins)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27)
SB  - IM
MH  - Animals
MH  - Cell Cycle/genetics/physiology
MH  - Cell Cycle Proteins/metabolism
MH  - Cell Differentiation/genetics/physiology
MH  - Cell Line, Tumor
MH  - Cell Proliferation
MH  - Cyclin G
MH  - Cyclin G1
MH  - Cyclin-Dependent Kinase Inhibitor p27
MH  - Cyclins/metabolism
MH  - DNA-Binding Proteins/genetics/*physiology
MH  - Inhibitor of Differentiation Protein 2
MH  - Mice
MH  - Mice, Mutant Strains
MH  - Mutation/genetics
MH  - Neovascularization, Pathologic/*genetics
MH  - Neuroblastoma/*genetics
MH  - Pituitary Gland/pathology
MH  - Pituitary Neoplasms/blood supply/*genetics
MH  - Repressor Proteins/genetics/*physiology
MH  - Retinoblastoma Protein/*genetics/physiology
MH  - Transcription Factors/genetics/*physiology
MH  - Tumor Suppressor Proteins/metabolism
MH  - Vascular Endothelial Growth Factor A/*metabolism
PMC - PMC1084294
EDAT- 2005/04/16 09:00
MHDA- 2005/06/15 09:00
PMCR- 2005/05/01
CRDT- 2005/04/16 09:00
PHST- 2005/04/16 09:00 [pubmed]
PHST- 2005/06/15 09:00 [medline]
PHST- 2005/04/16 09:00 [entrez]
PHST- 2005/05/01 00:00 [pmc-release]
AID - 25/9/3563 [pii]
AID - 1648-04 [pii]
AID - 10.1128/MCB.25.9.3563-3574.2005 [doi]
PST - ppublish
SO  - Mol Cell Biol. 2005 May;25(9):3563-74. doi: 10.1128/MCB.25.9.3563-3574.2005.