0-15. bcl-2 and p53 protein expression in ductal carcinoma in situ

The Breast ◽  
1997 ◽  
Vol 6 (4) ◽  
pp. 228-229
Author(s):  
C.M. Quinn ◽  
J.L. Ostrowski ◽  
L. Harkins ◽  
A.J. Rice ◽  
K. Horgan ◽  
...  
1997 ◽  
Vol 42 (3) ◽  
pp. 283-290 ◽  
Author(s):  
Prabha B. Rajan ◽  
David J. Scott ◽  
Robert H. Perry ◽  
Clive D.M. Griffith

2006 ◽  
Vol 124 (3) ◽  
pp. 121-124 ◽  
Author(s):  
Marcus Vinicius Martins de Menezes ◽  
Anna Letícia Oliveira Cestari ◽  
Orlando Almeida ◽  
Marcelo Alvarenga ◽  
Glauce Aparecida Pinto ◽  
...  

CONTEXT AND OBJECTIVE: Breast cancer is thought to derive from progressively aberrant, non-invasive breast lesions, but it is not known exactly how invasive breast cancer develops from these lesions. The aim of this study was to verify the changes in c-erbB-2 and p53 protein expression between non-neoplastic ducts, ductal carcinoma in situ and invasive ductal carcinoma found in the same breast. DESIGN AND SETTING: This was a cross-sectional study at Centro de Atenção Integral à Saúde da Mulher, Campinas, Brazil. METHODS: Fifty-six women with invasive ductal carcinoma and ductal carcinoma in situ in the same breast were included. The expression of c-erbB-2 and p53 proteins was assessed in non-neoplastic and neoplastic cells using immunohistochemical techniques. RESULTS: The c-erbB-2 protein was absent in non-neoplastic ducts but was present in 46% and 36% of in situ and invasive carcinoma components, respectively. Only 2% of non-neoplastic ducts, and 18% and 16% of ductal carcinoma in situ and invasive carcinoma components, respectively, were positive for p53 protein. No significant difference in c-erbB-2 and p53 protein expression was observed between in situ and invasive components. The nuclear grade agreement between in situ and invasive carcinoma was very good. CONCLUSIONS: The invasiveness of ductal carcinoma in situ seems to be independent of the Her-2/neu and TP53 genes. The general features of an occurrence of breast carcinoma are formulated at the outset of carcinogenesis, and the Her-2/neu and TP53 genes are involved.


1997 ◽  
Vol 33 (11) ◽  
pp. 1846-1850 ◽  
Author(s):  
L.G. Bobrow ◽  
R.R. Millis ◽  
L.C. Happerfield ◽  
W.J. Gullick

Biology ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 768
Author(s):  
Marie Colombe Agahozo ◽  
Marcel Smid ◽  
Ronald van Marion ◽  
Dora Hammerl ◽  
Thierry P. P. van den Bosch ◽  
...  

The identification of transcriptomic alterations of HER2+ ductal carcinoma in situ (DCIS) that are associated with the density of tumor-infiltrating lymphocytes (TILs) could contribute to optimizing choices regarding the potential benefit of immune therapy. We compared the gene expression profile of TIL-poor HER2+ DCIS to that of TIL-rich HER2+ DCIS. Tumor cells from 11 TIL-rich and 12 TIL-poor DCIS cases were micro-dissected for RNA isolation. The Ion AmpliSeq Transcriptome Human Gene Expression Kit was used for RNA sequencing. After normalization, a Mann–Whitney rank sum test was used to analyze differentially expressed genes between TIL-poor and TIL-rich HER2+ DCIS. Whole tissue sections were immunostained for validation of protein expression. We identified a 29-gene expression profile that differentiated TIL-rich from TIL-poor HER2+ DCIS. These genes included CCND3, DUSP10 and RAP1GAP, which were previously described in breast cancer and cancer immunity and were more highly expressed in TIL-rich DCIS. Using immunohistochemistry, we found lower protein expression in TIL-rich DCIS. This suggests regulation of protein expression at the posttranslational level. We identified a gene expression profile of HER2+ DCIS cells that was associated with the density of TILs. This classifier may guide towards more rationalized choices regarding immune-mediated therapy in HER2+ DCIS, such as targeted vaccine therapy.


2007 ◽  
Vol 451 (5) ◽  
pp. 877-881 ◽  
Author(s):  
Anja Dankof ◽  
Florian R. Fritzsche ◽  
Edgar Dahl ◽  
Stefan Pahl ◽  
Peter Wild ◽  
...  

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