p53/MDM2 pathway aberrations in parathyroid tumors:: p21WAF-1 and MDM2 are frequently overexpressed in parathyroid adenomas

被引:5
作者
Arribas, B
Cristóbal, E
Alcázar, JA
Tardío, J
Martínez-Montero, JC
Polo, JR
Carrión, R
Gil, L
Azañedo, M
Rojas, JM
Menárguez, J
机构
[1] Univ Madrid, Hosp Gen Gregorio Maranon, Dept Pathol, Madrid 28007, Spain
[2] Univ Madrid, Hosp Gen Gregorio Maranon, Dept Surg, Madrid 28007, Spain
[3] Univ Madrid, Hosp Gen Gregorio Maranon, Dept Oncol, Madrid 28007, Spain
[4] Hosp El Escorial, Dept Pathol, Madrid, Spain
[5] Inst Oftalm, Dept Pathol, Madrid, Spain
[6] Ctr Nacl Biol Fundamental, Unidad Biol Celular, Inst Salud Carlos III, Madrid, Spain
关键词
parathyroid; adenoma; cell cycle; p21(WAF-1); p27(KIP1); MDM2; p53;
D O I
10.1385/EP:11:3:251
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Parathyroid adenomas (PTAs) are the main cause of primary hyperparathyroidism. Cell cycle regulation in normal parathyroid tissue (NPT) and PTA remains largely unknown. We have systematically explored several components involved in the p53/MDM2/p19(ARF) pathway in PTA and compared the results were with NPT. Forty-six PTA and 12 NPT were immunostained with anti-p21(WAF-1), MDM2, p53, and p27(KIP1) antibodies. The slides were processed by cytometry and the results were statistically analyzed using nonparametric methods (Mann-Whitney test), p21(WAF-1) and MDM2 expression were significantly higher in PTA compared with NPT (p < 0.05). The opposite results were found for p27(KIP1) (p < 0.05) Occasional p53 staining was found in some PTA, albeit no significant difference was found in comparison with NPT. In conclusion, MDM2 and p21(WAF-1) are the proteins more overexpressed in PTA. These findings are surprising taking into account the benign nature of PTA, making them suitable candidates for further molecular analysis.
引用
收藏
页码:251 / 257
页数:7
相关论文
共 41 条
[1]   PROLIFERATIVE ACTIVITY IN PARATHYROID TUMORS AS DETECTED BY KI-67 IMMUNOSTAINING [J].
ABBONA, GC ;
PAPOTTI, M ;
GASPARRI, G ;
BUSSOLATI, G .
HUMAN PATHOLOGY, 1995, 26 (02) :135-138
[2]   Comparative genomic hybridization analysis of human parathyroid tumors [J].
Agarwal, SK ;
Schröck, E ;
Kester, MB ;
Burns, AL ;
Heffess, CS ;
Ried, T ;
Marx, SJ .
CANCER GENETICS AND CYTOGENETICS, 1998, 106 (01) :30-36
[3]   MOLECULAR-CLONING AND CHROMOSOMAL MAPPING OF DNA REARRANGED WITH THE PARATHYROID-HORMONE GENE IN A PARATHYROID ADENOMA [J].
ARNOLD, A ;
KIM, HG ;
GAZ, RD ;
EDDY, RL ;
FUKUSHIMA, Y ;
BYERS, MG ;
SHOWS, TB ;
KRONENBERG, HM .
JOURNAL OF CLINICAL INVESTIGATION, 1989, 83 (06) :2034-2040
[4]   p14ARF links the tumour suppressors RB and p53 [J].
Bates, S ;
Phillips, AC ;
Clark, PA ;
Stott, F ;
Peters, G ;
Ludwig, RL ;
Vousden, KH .
NATURE, 1998, 395 (6698) :124-125
[5]   Centrosome hyperamplification in human cancer: chromosome instability induced by p53 mutation and/or Mdm2 overexpression [J].
Carroll, PE ;
Okuda, M ;
Horn, HF ;
Biddinger, P ;
Stambrook, PJ ;
Gleich, LL ;
Li, YQ ;
Tarapore, P ;
Fukasawa, K .
ONCOGENE, 1999, 18 (11) :1935-1944
[6]   FREQUENT LOSS OF CHROMOSOME ARM IP DNA IN PARATHYROID ADENOMAS [J].
CRYNS, VL ;
YI, SM ;
TAHARA, H ;
GAZ, RD ;
ARNOLD, A .
GENES CHROMOSOMES & CANCER, 1995, 13 (01) :9-17
[7]  
CRYNS VL, 1994, J CLIN ENDOCR METAB, V78, P1320, DOI 10.1210/jc.78.6.1320
[8]  
Doglioni C, 1996, J PATHOL, V179, P248, DOI 10.1002/(SICI)1096-9896(199607)179:3<248::AID-PATH571>3.0.CO
[9]  
2-6
[10]   Molecular genetics of primary and secondary hyperparathyroidism [J].
Dotzenrath, C ;
Goretzki, PE ;
Farnebo, F ;
Teh, BT ;
Weber, G ;
Roher, HD ;
Larsson, C .
EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES, 1996, 104 :105-107