Abstract 2260: Defining molecular mechanisms linking Endophilin A2 to metastasis in human breast cancer models

2015 ◽  
Author(s):  
Tomas Baldassarre ◽  
Kathleen Watt ◽  
Peter Truesdell ◽  
Mark Schneider ◽  
Sandip Sengupta ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Molecular Mechanisms ◽  
Human Breast ◽  
Cancer Models

scholarly journals Structural and Molecular Mechanisms of Cytokine-Mediated Endocrine Resistance in Human Breast Cancer Cells

2017 ◽  
Vol 65 (6) ◽  
pp. 1122-1135.e5 ◽  
Author(s):  
Joshua D. Stender ◽  
Jerome C. Nwachukwu ◽  
Irida Kastrati ◽  
Yohan Kim ◽  
Tobias Strid ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Molecular Mechanisms ◽  
Endocrine Resistance ◽  
Human Breast Cancer Cells ◽  
Human Breast

Abstract 950: Src tyrosine kinase contributes to lapatinib resistance in human breast cancer models.

2013 ◽  
Author(s):  
Roberta Rosa ◽  
Lucia Nappi ◽  
Luigi Formisano ◽  
Claudia D'Amato ◽  
Valentina D'Amato ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tyrosine Kinase ◽  
Human Breast Cancer ◽  
Human Breast ◽  
Src Tyrosine Kinase ◽  
Cancer Models

5104 POSTER Vitamin D Analogs Enhance the Anastrozole Activity in Human Breast Cancer Models

2011 ◽  
Vol 47 ◽  
pp. S361
Author(s):  
B. Filip ◽  
P. Libako ◽  
A. Kutner ◽  
J. Wietrzyk
Keyword(s):  
Breast Cancer ◽  
Vitamin D ◽  
Human Breast Cancer ◽  
Human Breast ◽  
Vitamin D Analogs ◽  
Cancer Models

Positive interaction between lapatinib and capecitabine in human breast cancer models: study of molecular determinants

2011 ◽  
Vol 26 (4) ◽  
pp. 530-537 ◽  
Author(s):  
Mohamed Chefrour ◽  
Gérard Milano ◽  
Patricia Formento ◽  
Sarah Giacometti ◽  
Amine Denden ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Human Breast ◽  
Positive Interaction ◽  
Cancer Models ◽  
Molecular Determinants

scholarly journals Initiating oncogenic event determines gene-expression patterns of human breast cancer models

2002 ◽  
Vol 99 (10) ◽  
pp. 6967-6972 ◽  
Author(s):  
K. V. Desai ◽  
N. Xiao ◽  
W. Wang ◽  
L. Gangi ◽  
J. Greene ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Human Breast Cancer ◽  
Expression Patterns ◽  
Gene Expression Patterns ◽  
Human Breast ◽  
Cancer Models

scholarly journals A “NOTCH” Deeper into the Epithelial-To-Mesenchymal Transition (EMT) Program in Breast Cancer

Genes ◽  
2019 ◽  
Vol 10 (12) ◽  
pp. 961 ◽  
Author(s):  
Rohan Kar ◽  
Niraj Kumar Jha ◽  
Saurabh Kumar Jha ◽  
Ankur Sharma ◽  
Sunny Dholpuria ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Notch Signaling ◽  
Human Breast Cancer ◽  
Large Scale ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Epithelial Mesenchymal Transition ◽  
Human Breast ◽  
Breast Tumorigenesis ◽  
Mesenchymal Transition

Notch signaling is a primitive signaling pathway having various roles in the normal origin and development of each multicellular organisms. Therefore, any aberration in the pathway will inevitably lead to deadly outcomes such as cancer. It has now been more than two decades since Notch was acknowledged as an oncogene in mouse mammary tumor virus-infected mice. Since that discovery, activated Notch signaling and consequent up-regulation of tumor-promoting Notch target genes have been observed in human breast cancer. Moreover, consistent over-expression of Notch ligands and receptors has been shown to correlate with poor prognosis in human breast cancer. Notch regulates a number of key processes during breast carcinogenesis, of which, one key phenomenon is epithelial–mesenchymal transition (EMT). EMT is a key process for large-scale cell movement during morphogenesis at the time of embryonic development. Cancer cells aided by transcription factors usurp this developmental program to execute the multi-step process of tumorigenesis and metastasis. In this review, we recapitulate recent progress in breast cancer research that has provided new perceptions into the molecular mechanisms behind Notch-mediated EMT regulation during breast tumorigenesis.

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