Expression of CD44 variant exon epitopes in noninvasive breast carcinoma

1995 ◽  
Vol 121 (S1) ◽  
pp. A40-A40
Author(s):  
H. P. Sinn ◽  
P. Dallt ◽  
K. H. Heidert ◽  
M. Kaufmann
2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Primariadewi Rustamadji ◽  
Elvan Wiyarta ◽  
Kristina A. Bethania

Background. Invasive breast carcinoma of no special type (IBC-NST) is the most widespread invasive carcinoma subtype causing primarily regional metastases of the lymphatic node (LNM). The capacity of CD44 variant exon 6 (CD44v6) expression as an LNM predictor biomarker in IBC-NST was explored. Methods. We conducted a cross-sectional research with 48 paraffin blocks containing IBC-NST primary tumors that were divided into two groups by LNM. The assessment has been carried out in terms of age, tumor size, tumor grade, lymphovascular invasion (LVI), and CD44v6 expression. The expression of CD44v6 was analyzed on the grounds of immunohistochemical (IHC) staining, while other data were taken from archives. Statistical analysis is carried out by univariate, multivariate, and AUROC. Results. CD44v6 exhibits a dominant expression in IBC-NST tumor cells. Univariate analysis revealed a significant association between CD44v6 and LNM status ( p = 0.001 ). Multiple logistic regression results showed that CD44v6 expression and LVI were significantly associated with LNM with OR 10.7 (95% CI: 2.43 to 47.08) and 6.22 (95% CI: 1.4 to 27.88), respectively. CD44v6 expression was able to discriminate against LNM with AUROC 0.863 ± 0.053 (95% CI: 0.759 to 0.967) at the H-score cut-off 133.889 (75% sensitivity and 83.3% specificity). Conclusion. CD44v6 expression and LVI are potential predictors of LNM in IBC-NST. The H-score cut-off of the CD44v6 expression can also be used as a threshold for classification in further investigation.


1999 ◽  
Vol 154 (1) ◽  
pp. 291-300 ◽  
Author(s):  
Marco Paolo Martegani ◽  
Fabrizio Del Prete ◽  
Alessandra Gasbarri ◽  
Pier Giorgio Natali ◽  
Armando Bartolazzi

1998 ◽  
Vol 114 ◽  
pp. A1115
Author(s):  
B.M. Witting ◽  
U. Günthert ◽  
M. Zöller

1998 ◽  
Vol 255 (1) ◽  
pp. 74-80 ◽  
Author(s):  
Jonathan P. Sleeman ◽  
Ursula Rahmsdorf ◽  
Anja Steffen ◽  
Helmut Ponta ◽  
Peter Herrlich
Keyword(s):  

2000 ◽  
Vol 191 (12) ◽  
pp. 2053-2064 ◽  
Author(s):  
Bianca M. Wittig ◽  
Britt Johansson ◽  
Margot Zöller ◽  
Christoph Schwärzler ◽  
Ursula Günthert

Experimental colitis in mice is characterized by infiltration of activated T helper (Th) cells and macrophages into the lamina propria. Particularly, these cells expressed CD44 variant exon 7 (CD44v7)-containing isoforms. Upregulation of CD44v7 isoforms was induced by CD40 ligation, an inflammation-driving interaction between activated Th cells and macrophages. To define the role of CD44v7 in colitis, mice bearing a targeted deletion for exon v7 were generated. In trinitrobenzene sulfonic acid–induced colitis, wild-type mice developed severe signs of persistent inflammation. Mice lacking CD44v7 initially showed unspecific inflammation, then recovered completely. The pathogenic origin was shown to reside in bone marrow–derived CD44v7+ cells, because adoptive transfer experiments demonstrated an absolute requirement for CD44v7 on hematopoietic cells for maintenance of colitis. Interleukin (IL)-10–deficient mice, which develop a chronic Th1-driven enterocolitis, were crossbred with CD44v6/v7 null mice. In IL-10 × CD44v6/v7 double deficient mice, intestinal inflammation developed only weakly and at an older age. Analysis of cell death in the inflamed lesions revealed that mononuclear cells in the CD44v7 null infiltrates had higher rates of apoptosis than those from wild-type mice. Thus, the region encoded by CD44v7 appears to be essential for survival of effector lymphocytes, resulting in persistence of inflammation.


2014 ◽  
Vol 15 (16) ◽  
pp. 6761-6766 ◽  
Author(s):  
Shuang Zhao ◽  
Jin-Lan He ◽  
Zhi-Xin Qiu ◽  
Nian-Yong Chen ◽  
Zhuang Luo ◽  
...  

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