PMID- 11414476
OWN - NLM
STAT- MEDLINE
DCOM- 20011204
LR  - 20210904
IS  - 1015-6305 (Print)
IS  - 1750-3639 (Electronic)
IS  - 1015-6305 (Linking)
VI  - 11
IP  - 3
DP  - 2001 Jul
TI  - Tumor suppressor loss in pituitary tumors.
PG  - 342-55
AB  - The current model of human neoplasia invokes a number of potential genomic 
      alterations that impact cellular phenotype and proliferative rates. In the 
      majority of human tumor models, the transformation from normal cells to 
      neoplastic lesion is a multistep process. This review offers a specific overview 
      of the involvement of tumor suppressor genes (TSGs) in the pathogenesis of human 
      pituitary adenomas. TSG genetic lesions, such as BRCA1 in breast cancer and p53 
      in Li-Fraumeni Syndrome, have been identified in both sporadic and heritable 
      human endocrine tumors. Familial neoplastic syndromes like multiple endocrine 
      neoplasia type 1 (MEN1) that include pituitary tumor formation as part of a broad 
      clinical spectrum of disease represent a unique opportunity to investigate the 
      general mechanisms of tumorigenesis, and well as genes responsible for sporadic 
      endocrine tumors. Similarly, homologous recombination knockout mice with 
      selectively ablated candidate TSGs have also shed light on the molecular 
      mechanisms of pituitary cell proliferation and tumor suppression. However, 
      despite insights into pituitary tumorigenesis generated by heritable neoplasia 
      syndromes and mouse knockout of critical TSGs that display a pituitary tumor 
      phenotype, the molecular pathogenesis of human pituitary adenomas remains largely 
      an enigma. Thus, the role of TSGs, if any, in sporadic pituitary adenoma 
      formation has yet to be determined, despite our greater understanding of the 
      molecular mechanisms underlying pituitary cell function and phenotype.
FAU - Alexander, J M
AU  - Alexander JM
AD  - Harvard Medical School, Boston, MA, USA. jalexand@caregroup.harvard.edu
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Switzerland
TA  - Brain Pathol
JT  - Brain pathology (Zurich, Switzerland)
JID - 9216781
RN  - 0 (Cdkn1b protein, mouse)
RN  - 0 (Cell Cycle Proteins)
RN  - 0 (Tumor Suppressor Proteins)
RN  - 12629-01-5 (Human Growth Hormone)
RN  - 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27)
RN  - EC 2.7.11.22 (Cyclin-Dependent Kinases)
SB  - IM
MH  - Adenoma/*genetics/pathology
MH  - Animals
MH  - Cell Cycle Proteins/genetics
MH  - Cell Division/genetics
MH  - Chromosome Aberrations
MH  - Chromosome Disorders
MH  - Cyclin-Dependent Kinase Inhibitor p27
MH  - Cyclin-Dependent Kinases/antagonists & inhibitors
MH  - Female
MH  - Gene Deletion
MH  - Genes, Retinoblastoma
MH  - *Genes, Tumor Suppressor
MH  - Human Growth Hormone/metabolism
MH  - Humans
MH  - Loss of Heterozygosity
MH  - Male
MH  - Mice
MH  - Mice, Knockout
MH  - Minisatellite Repeats
MH  - Multiple Endocrine Neoplasia Type 1/genetics
MH  - Neoplastic Syndromes, Hereditary/genetics
MH  - Pituitary Neoplasms/*genetics/pathology
MH  - Syndrome
MH  - Tumor Suppressor Proteins/genetics
MH  - von Hippel-Lindau Disease/genetics
PMC - PMC8098364
EDAT- 2001/06/21 10:00
MHDA- 2002/01/05 10:01
PMCR- 2006/04/05
CRDT- 2001/06/21 10:00
PHST- 2001/06/21 10:00 [pubmed]
PHST- 2002/01/05 10:01 [medline]
PHST- 2001/06/21 10:00 [entrez]
PHST- 2006/04/05 00:00 [pmc-release]
AID - BPA342 [pii]
AID - 10.1111/j.1750-3639.2001.tb00404.x [doi]
PST - ppublish
SO  - Brain Pathol. 2001 Jul;11(3):342-55. doi: 10.1111/j.1750-3639.2001.tb00404.x.