The origin of vimentin expression in invasive breast cancer:: epithelial-mesenchymal transition, myoepithelial histogenesis or histogenesis from progenitor cells with bilinear differentiation potential?

被引:170
作者
Korsching, E
Packeisen, J
Liedtke, C
Hungermann, D
Wülfing, P
van Diest, PJ
Brandt, B
Boecker, W
Buerger, H
机构
[1] Univ Munster, Inst Pathol, D-48149 Munster, Germany
[2] Klinikum Osnabruck, Inst Pathol, Osnabruck, Germany
[3] Univ Munster, Dept Obstet & Gynecol, Munster, Germany
[4] Univ Utrecht, Ctr Med, Dept Pathol, Utrecht, Netherlands
[5] Univ Munster, Inst Clin Chem & Lab Med, Munster, Germany
关键词
breast; vimentin; histogenesis; progenitor cells; cytokeratin;
D O I
10.1002/path.1797
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Vimentin expression is a rather rare finding in invasive breast cancer, and is associated with high tumour invasiveness and chemoresistance. It is currently explained by two different biological theories: direct histogenetic derivation from myoepithelial cells, and epithelial-mesenchymal transition (EMT) reflecting the end-stage of breast cancer dedifferentiation. In this study we aimed to obtain further insights into the biological hallmarks of these vimentin-expressing breast cancers. We applied inummohistochemistry for vimentin and 15 other differentiation markers to a series of 364 invasive breast cancer cases, using tissue microarray technology. 7.7% of all tumours expressed vimentin. Almost all of these cases (19/21) were Grade 3 invasive ductal carcinomas, and the majority (13/21) of these were associated with a ductal in situ component. Vimentin expression was also seen in the respective in situ components and correlated positively with the expression of SMA, CD10, CK 5, p53, Mib-1 and EGFR. A negative correlation was seen for the expression of CK 8/18 and the oestrogen receptor. Vimentin-expressing carcinomas revealed a significantly higher average absolute number of cytogenetic alterations per case, but a significantly lower frequency of chromosome 16q losses compared to vimentin-negative cases. Our present results demonstrate that, despite analogies between vimentin-positive breast cancers and myoepithelial cells in their expression of differentiation-related proteins, neither myoepithelial histogenesis nor EMT can exclusively explain the biology of these distinct tumours. This is mainly supported by the significantly higher incidence of vimentin-expressing breast cancers compared to any other myoepithelial breast tumours and the fact that vimentin is already observed in ductal in situ components. We therefore propose the alternative hypothesis that vimentin-expressing breast carcinomas may derive from breast progenitor cells with bilinear (glandular and myoepithelial) differentiation potential. Copyright (c) 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
引用
收藏
页码:451 / 457
页数:7
相关论文
共 58 条
[1]   Epidermal growth factor-induced epithelio-mesenchymal transition in human breast carcinoma cells [J].
Ackland, ML ;
Newgreen, DF ;
Fridman, M ;
Waltham, MC ;
Arvanitis, A ;
Minichiello, J ;
Price, JT ;
Thompson, EW .
LABORATORY INVESTIGATION, 2003, 83 (03) :435-448
[2]   Molecular classification of borderline ovarian tumors using hierarchical cluster analysis of protein expression profiles [J].
Alaiya, AA ;
Franzén, B ;
Hagman, A ;
Dysvik, B ;
Roblick, UJ ;
Becker, S ;
Moberger, B ;
Auer, G ;
Linder, S .
INTERNATIONAL JOURNAL OF CANCER, 2002, 98 (06) :895-899
[3]  
Alvi AJ, 2003, BREAST CANCER RES, V5, DOI [10.1186/bcr563, 10.1186/bcr547]
[4]  
Anbazhagan R, 1998, J PATHOL, V184, P197, DOI 10.1002/(SICI)1096-9896(199802)184:2&lt
[5]  
197::AID-PATH992&gt
[6]  
3.0.CO
[7]  
2-J
[8]   GROWTH AND DEVELOPMENT OF THE HUMAN INFANT BREAST [J].
ANBAZHAGAN, R ;
BARTEK, J ;
MONAGHAN, P ;
GUSTERSON, BA .
AMERICAN JOURNAL OF ANATOMY, 1991, 192 (04) :407-417
[9]  
[Anonymous], 1998, The Breast
[10]   Clinical presentation and long-term outcome of pure myoepithelial carcinoma of the breast [J].
Behranwala, KA ;
Nasiri, N ;
A'Hern, R ;
Gui, GPH .
EJSO, 2004, 30 (04) :357-361