Nuclear β-catenin expression distinguishes deep fibromatosis from other benign and malignant fibroblastic and myofibroblastic lesions

被引:207
作者
Bhattacharya, B
Dilworth, HP
Iacobuzio-Donahue, C
Ricci, F
Weber, K
Furlong, MA
Fisher, C
Montgomery, E
机构
[1] Johns Hopkins Med Inst, Dept Pathol, Baltimore, MD 21231 USA
[2] Georgetown Univ, Washington, DC USA
[3] Royal Marsden Hosp, London SW3 6JJ, England
关键词
beta-catenin; fibromatosis; low-grade fibromyxoid sarcoma; myofibrosarcoma; myofibroma; myofibromatosis; scar; nodular fasciitis; leiomyosarcoma;
D O I
10.1097/01.pas.0000157938.95785.da
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Deep fibromatoses (desmoid tumors) are clonal myofibroblastic proliferations that are prone to aggressive local recurrences but that do not metastasize. They must be distinguished from a host of fibroblastic and myofibroblastic lesions as well as from smooth muscle neoplasms. Virtually all deep fibromatoses have somatic beta-catenin or adenomatous polyposis coli (APC) gene mutations leading to intranuclear accumulation of beta-catenin. Since low-grade sarcomas in general lack P-catenin and since reactive proliferations would not be expected to have it, we predicted that nuclear beta-catenin expression would be detected in deep fibromatoses but absent in other entities in the differential diagnosis. We evaluated the role of beta-catenin to help differentiate distinguish deep fibromatoses from congeners. Formalin-fixed, paraffin-embedded sections from 21 lesions from 20 patients with deep fibromatoses were stained with monoclonal beta-catenin antibody (Transduction Laboratories) and compared with low-grade fibromyxoid sarcoma (n = 12), leiomyosarcoma (n = 10), various other fibrosarcoma variants (n = 13, including 3 myofibrosarcomas, 3 sclerosing epithelioid fibrosarcomas, 5 low-grade fibrosarcomas, I classic fibrosarcoma arising in dermatofibrosarcoma protuberans, I inflammatory myxohyaline tumor/myxoinflammatory fibroblastic sarcoma), myofibroma/myofibromatosis (n = 12), nodular fasciitis (n = 11), and scars (n = 9). Nuclear and cytoplasmic staining was assessed. All 21 examples of deep fibromatosis displayed nuclear beta-catenin (focal nuclear staining in one case to 90% staining). All other lesions tested (n = 67) lacked nuclear labeling for beta-catenin, showing only cytoplasmic accumulation. beta-Catenin immunohistochemistry separates deep fibromatosis from entities in the differential diagnosis, a finding that can be exploited for diagnosis. Most fibromatoses have diffuse nuclear staining although occasional examples only focally label.
引用
收藏
页码:653 / 659
页数:7
相关论文
共 46 条
[1]   Fibromatosis of the breast and mutations involving the APC/β-catenin pathway [J].
Abraham, SC ;
Reynolds, C ;
Lee, JH ;
Montgomery, EA ;
Baisden, BL ;
Krasinskas, AM ;
Wu, TT .
HUMAN PATHOLOGY, 2002, 33 (01) :39-46
[2]   Distinctive molecular genetic alterations in sporadic and familial adenomatous polyposis-associated pancreatoblastomas -: Frequent alterations in the APC/β-catenin pathway and chromosome 11p [J].
Abraham, SC ;
Wu, TT ;
Klimstra, DS ;
Finn, LS ;
Lee, JH ;
Yeo, CJ ;
Cameron, JL ;
Hruban, RH .
AMERICAN JOURNAL OF PATHOLOGY, 2001, 159 (05) :1619-1627
[3]   Frequent β-catenin mutations in juvenile nasopharyngeal angiofibromas [J].
Abraham, SC ;
Montgomery, EA ;
Giardiello, FM ;
Wu, TT .
AMERICAN JOURNAL OF PATHOLOGY, 2001, 158 (03) :1073-1078
[4]   Sporadic fundic gland polyps -: Common gastric polyps arising through activating mutations in the β-catenin gene [J].
Abraham, SC ;
Nobukawa, B ;
Giardiello, FM ;
Hamilton, SR ;
Wu, TT .
AMERICAN JOURNAL OF PATHOLOGY, 2001, 158 (03) :1005-1010
[5]  
Alman BA, 1997, AM J PATHOL, V151, P329
[6]  
Anna CH, 2000, CANCER RES, V60, P2864
[7]   Sclerosing epithelioid fibrosarcoma - A study of 16 cases and confirmation of a clinicopathologically distinct tumor [J].
Antonescu, CR ;
Rosenblum, MK ;
Pereira, P ;
Nascimento, AG ;
Woodruff, JM .
AMERICAN JOURNAL OF SURGICAL PATHOLOGY, 2001, 25 (06) :699-709
[8]   FAMILIAL ADENOMATOUS POLYPOSIS - DESMOID TUMORS AND LACK OF OPHTHALMIC LESIONS (CHRPE) ASSOCIATED WITH APC MUTATIONS BEYOND CODON-1444 [J].
CASPARI, R ;
OLSCHWANG, S ;
FRIEDL, W ;
MANDL, M ;
BOISSON, C ;
BOKER, T ;
AUGUSTIN, A ;
KADMON, M ;
MOSLEIN, G ;
THOMAS, G ;
PROPPING, P .
HUMAN MOLECULAR GENETICS, 1995, 4 (03) :337-340
[9]  
CHUNG EB, 1981, CANCER, V48, P1807, DOI 10.1002/1097-0142(19811015)48:8<1807::AID-CNCR2820480818>3.0.CO
[10]  
2-G