Abstract 3728: Anti-Notch1 antibody (OMP-52M51) impedes tumor growth and cancer stem cell frequency (CSC) in a chemo-refractory breast cancer xenograft model with an activating Notch1 mutation and screening for activated Notch1 across multiple solid tumor types.

2013 ◽  
Author(s):  
Belinda Cancilla ◽  
Jennifer Cain ◽  
Min Wang ◽  
Lucia Beviglia ◽  
Jalpa Shah ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Tumor Growth ◽  
Solid Tumor ◽  
Xenograft Model ◽  
Cell Frequency ◽  
Breast Cancer Xenograft ◽  
Tumor Types

scholarly journals RUNX1 suppresses breast cancer stemness and tumor growth

2018 ◽  
Author(s):  
Deli Hong ◽  
Andrew J. Fritz ◽  
Kristiaan H. Finstad ◽  
Mark P. Fitzgerald ◽  
Adam L. Viens ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cell ◽  
Tumor Suppressor ◽  
Cancer Stem Cell ◽  
Tumor Growth ◽  
Epithelial Mesenchymal Transition ◽  
Ectopic Expression ◽  
Cell Activity ◽  
Mesenchymal Transition

SummaryRecent studies have revealed that mutations in the transcription factor Runx1 are prevalent in breast tumors. Yet, how loss of Runx1 contributes to breast cancer (BCa) remains unresolved. We demonstrate for the first time that Runx1 represses the breast cancer stem cell (BCSC) phenotype and consequently, functions as a tumor suppressor in breast cancer. Runx1 ectopic expression in MCF10AT1 and MCF10CA1a BCa cells reduces (60%) migration, invasion and in vivo tumor growth in mouse mammary fat pad (P<0.05). Runx1 is decreased in BCSCs, and overexpression of Runx1 suppresses tumorsphere formation and reduces the BCSC population. Furthermore, Runx1 inhibits Zeb1 expression, while Runx1 depletion activates Zeb1 and the epithelial-mesenchymal transition. Mechanistically Runx1 functions as a tumor suppressor in breast cancer through repression of cancer stem cell activity. This key regulation of BCSCs by Runx1 may be shared in other epithelial carcinomas, highlighting the importance of Runx1 in solid tumors.

scholarly journals ANTI-CSC COMBINATION THERAPY USING WNT SIGNALING-TARGETED DRUG

2018 ◽  
Vol 8 (5-s) ◽  
pp. 139-142 ◽  
Author(s):  
Muthu Dhandapani ◽  
Babu Balakrishnan ◽  
Ganesan Sivamani
Keyword(s):  
Breast Cancer ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Small Subset ◽  
Multiple Tumor ◽  
Promising Strategy ◽  
Keywords Cancer ◽  
Notch Pathways ◽  
Tumor Types

Dysfunctions of Wnt, Hedgehog and Notch pathways are evident in multiple tumor types and malignancies. A number of studies have suggested that dysregulation of Wnt/β-catenin signaling occurs in human breast cancer. Specifically, inhibition of Wnt/ β-catenin pathway is implicated in arresting of cancer stem cells (CSCs), a small subset of cancer cells capable of self-renewal and differentiation into heterogeneous tumor cells. Here, we investigated tumor initiating property of breast cancer stem cell in-vitro with XAV-939 an inhibitor of Wnt/β-catenin signaling pathway. Targeting Wnt/β-catenin signaling with this inhibitor represents a promising strategy to suppress metastasis. Keywords: Cancer Stem Cell, 3D Mammosphere, Wnt/β-catenin, metastasis, CD44+/CD24

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