P53 EXPRESSION AND DNA-PLOIDY OF CARTILAGE LESIONS

被引:59
作者
COUGHLAN, B
FELIZ, A
ISHIDA, T
CZERNIAK, B
DORFMAN, HD
机构
[1] MONTEFIORE MED CTR,DEPT ORTHOPED SURG,DIV ORTHOPED PATHOL,ORTHOPED PATHOL SECT,BRONX,NY 10467
[2] ALBERT EINSTEIN COLL MED,BRONX,NY 10467
[3] UNIV TEXAS,MD ANDERSON CANC CTR,DEPT PATHOL,HOUSTON,TX 77030
关键词
P53; EXPRESSION; DNA PLOIDY; CARTILAGE LESIONS;
D O I
10.1016/0046-8177(95)90166-3
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
The aim of this study was to investigate the expression of a tumor suppressor gene (p53) in cartilage lesions of bone and its relationship to their histological grade and DNA ploidy. An immunohistochemical assay for p53 and Feulgen-stained DNA preparations was subjected to computerized image analysis. Enchondromas, vial chondromatosis, and low grade (grade I and II) chondrosarcomas were diploid. High grade (grade III) chondrosarcomas and high grade sarcomatous components of dedifferentiated chondrosarcomas were aneuploid. Well differentiated cartilaginous components of dedifferentiated chondrosarcomas were diploid. Microscopic examination showed weak focal positivity for p53 in one of 10 enchondromas one of six examples of synovial chondromatosis, and three of four low grade (grade I and II) chondrosarcomas. All three high grade (grade III) chondrosarcomas were strongly positive for p53. The high grade sarcomatous component of all four dedifferentiated chondrosarcomas was strongly positive for p53, whereas only focal weak positivity was noted in the well differentiated cartilaginous areas. These results were confirmed by quantitative computer-assisted image analysis, which showed that high grade aneuploid cartilage tumors demonstrated strikingly higher levels of p53 than did diploid low grade malignant tumors or benign cartilage lesions. Copyright (C) 1995 by W.B. Saunders Company
引用
收藏
页码:620 / 624
页数:5
相关论文
共 35 条
[1]  
ANDREASSEN A, 1993, CANCER RES, V53, P468
[2]   SUPPRESSION OF HUMAN COLORECTAL-CARCINOMA CELL-GROWTH BY WILD-TYPE-P53 [J].
BAKER, SJ ;
MARKOWITZ, S ;
FEARON, ER ;
WILLSON, JKV ;
VOGELSTEIN, B .
SCIENCE, 1990, 249 (4971) :912-915
[3]  
BARTEK J, 1991, ONCOGENE, V6, P1699
[4]   ASYMMETRIC DISTRIBUTION OF ONCOGENE PRODUCTS AT MITOSIS [J].
CZERNIAK, B ;
HERZ, F ;
WERSTO, RP ;
KOSS, LG .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (11) :4860-4863
[5]   QUANTITATION OF ONCOGENE PRODUCTS BY COMPUTER-ASSISTED IMAGE-ANALYSIS AND FLOW-CYTOMETRY [J].
CZERNIAK, B ;
HERZ, F ;
WERSTO, RP ;
ALSTER, P ;
PUSZKIN, E ;
SCHWARZ, E ;
KOSS, LG .
JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY, 1990, 38 (04) :463-466
[6]   P53 FUNCTIONS AS A CELL-CYCLE CONTROL PROTEIN IN OSTEOSARCOMAS [J].
DILLER, L ;
KASSEL, J ;
NELSON, CE ;
GRYKA, MA ;
LITWAK, G ;
GEBHARDT, M ;
BRESSAC, B ;
OZTURK, M ;
BAKER, SJ ;
VOGELSTEIN, B ;
FRIEND, SH .
MOLECULAR AND CELLULAR BIOLOGY, 1990, 10 (11) :5772-5781
[7]   WAF1, A POTENTIAL MEDIATOR OF P53 TUMOR SUPPRESSION [J].
ELDEIRY, WS ;
TOKINO, T ;
VELCULESCU, VE ;
LEVY, DB ;
PARSONS, R ;
TRENT, JM ;
LIN, D ;
MERCER, WE ;
KINZLER, KW ;
VOGELSTEIN, B .
CELL, 1993, 75 (04) :817-825
[8]   PRESENCE OF A POTENT TRANSCRIPTION ACTIVATING SEQUENCE IN THE P53 PROTEIN [J].
FIELDS, S ;
JANG, SK .
SCIENCE, 1990, 249 (4972) :1046-1049
[9]   ACTIVATING MUTATIONS FOR TRANSFORMATION BY P53 PRODUCE A GENE-PRODUCT THAT FORMS AN HSC70-P53 COMPLEX WITH AN ALTERED HALF-LIFE [J].
FINLAY, CA ;
HINDS, PW ;
TAN, TH ;
ELIYAHU, D ;
OREN, M ;
LEVINE, AJ .
MOLECULAR AND CELLULAR BIOLOGY, 1988, 8 (02) :531-539
[10]   THE P53 PROTO-ONCOGENE CAN ACT AS A SUPPRESSOR OF TRANSFORMATION [J].
FINLAY, CA ;
HINDS, PW ;
LEVINE, AJ .
CELL, 1989, 57 (07) :1083-1093