scholarly journals Non-migratory tumorigenic intrinsic cancer stem cells ensure breast cancer metastasis by generation of CXCR4+ migrating cancer stem cells

Oncogene ◽  
2016 ◽  
Vol 35 (37) ◽  
pp. 4937-4948 ◽  
Author(s):  
S Mukherjee ◽  
A Manna ◽  
P Bhattacharjee ◽  
M Mazumdar ◽  
S Saha ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Metastasis ◽  
Breast Cancer Metastasis

scholarly journals The Role of Cancer Stem Cells in the Organ Tropism of Breast Cancer Metastasis: A Mechanistic Balance between the “Seed” and the “Soil”?

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Jenny E. Chu ◽  
Alison L. Allan
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Metastatic Disease ◽  
Cancer Metastasis ◽  
Metastatic Breast ◽  
Therapy Resistance ◽  
Breast Cancer Metastasis ◽  
Specific Pattern ◽  
Organ Tropism

Breast cancer is a prevalent disease worldwide, and the majority of deaths occur due to metastatic disease. Clinical studies have identified a specific pattern for the metastatic spread of breast cancer, termed organ tropism; where preferential secondary sites include lymph node, bone, brain, lung, and liver. A rare subpopulation of tumor cells, the cancer stem cells (CSCs), has been hypothesized to be responsible for metastatic disease and therapy resistance. Current treatments are highly ineffective against metastatic breast cancer, likely due to the innate therapy resistance of CSCs and the complex interactions that occur between cancer cells and their metastatic microenvironments. A better understanding of these interactions is essential for the development of novel therapeutic targets for metastatic disease. This paper summarizes the characteristics of breast CSCs and their potential metastatic microenvironments. Furthermore, it raises the question of the existence of a CSC niche and highlights areas for future investigation.

Abstract 4219: Biomarkers of cancer stem cells and invasion can predict breast cancer metastasis

2010 ◽  
Author(s):  
Robert Stobezki ◽  
Maja OKtay ◽  
Ester Adler ◽  
Frank Gertler ◽  
John S. Condeelis ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Metastasis ◽  
Breast Cancer Metastasis

scholarly journals Deep Tumor-Penetrated Nanocages Improve Accessibility to Cancer Stem Cells for Photothermal-Chemotherapy of Breast Cancer Metastasis

2018 ◽  
Vol 5 (12) ◽  
pp. 1801012 ◽  
Author(s):  
Tao Tan ◽  
Hong Wang ◽  
Haiqiang Cao ◽  
Lijuan Zeng ◽  
Yuqi Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Metastasis ◽  
Breast Cancer Metastasis

scholarly journals Dexamethasone promotes breast cancer stem cells in obese and not lean mice

2021 ◽  
Author(s):  
Stephanie L Annett ◽  
Orla Fox ◽  
Damir Vareslija ◽  
Tracy Robson
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Metastasis ◽  
Ex Vivo ◽  
Breast Cancer Metastasis ◽  
Obese Mice ◽  
Breast Cancer Patients ◽  
Mammosphere Formation ◽  
Cancer Specific Mortality

Obesity is highly prevalent in breast cancer patients and it is associated with increased recurrence and breast cancer specific mortality. Glucocorticoid (GC) use, in addition to obesity is associated with promoting breast cancer metastasis through activation of stemness-related pathways. Therefore, we utilised the synergetic allograft E0771 breast cancer model to investigate if treatment with GCs had differential effects on promoting cancer stem cells in lean and diet-induced obese mice. Indeed, both lean mice treated with dexamethasone and obese mice with no treatment had no effect on the ex vivo colony forming ability, mammosphere formation or ALDH bright subpopulation. However, treatment of obese mice with dexamethasone resulted in a significant increase in ex vivo colony formation, mammosphere formation, ALDH bright subpopulation and expression of pluripotency transcription factors. GC transcriptionally regulated genes were not altered in the dexamethasone treated groups compared to treatment controls. In summary, these results provide initial evidence that obesity presents a higher risk of GC induced cancer stemness via non-genomic GC signalling which is of potential translational significance.

Tumor Dormancy and Cancer Stem Cells: Implications for the Biology and Treatment of Breast Cancer Metastasis

2007 ◽  
Vol 26 (1) ◽  
pp. 87-98 ◽  
Author(s):  
Alison L. Allan ◽  
Sharon A. Vantyghem ◽  
Alan B. Tuck ◽  
Ann F. Chambers
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Metastasis ◽  
Breast Cancer Metastasis ◽  
Tumor Dormancy

scholarly journals Obesity-Altered Adipose Stem Cells Promote ER+ Breast Cancer Metastasis through Estrogen Independent Pathways

2019 ◽  
Vol 20 (6) ◽  
pp. 1419 ◽  
Author(s):  
Rachel A. Sabol ◽  
Adam Beighley ◽  
Paulina Giacomelli ◽  
Rachel M. Wise ◽  
Mark A. A. Harrison ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Estrogen Receptor ◽  
Tumor Growth ◽  
Estrogen Receptor Alpha ◽  
Cancer Metastasis ◽  
Breast Cancer Metastasis ◽  
Adipose Stem Cells ◽  
Estrogen Signaling ◽  
Promote Tumor Growth

Adipose stem cells (ASCs) play an essential role in tumor microenvironments. These cells are altered by obesity (obASCs) and previous studies have shown that obASCs secrete higher levels of leptin. Increased leptin, which upregulates estrogen receptor alpha (ERα) and aromatase, enhances estrogen bioavailability and signaling in estrogen receptor positive (ER+) breast cancer (BC) tumor growth and metastasis. In this study, we evaluate the effect of obASCs on ER+BC outside of the ERα signaling axis using breast cancer models with constitutively active ERα resulting from clinically relevant mutations (Y537S and D538G). We found that while obASCs promote tumor growth and proliferation, it occurs mostly through abrogated estrogen signaling when BC has constitutive ER activity. However, obASCs have a similar promotion of metastasis irrespective of ER status, demonstrating that obASC promotion of metastasis may not be completely estrogen dependent. We found that obASCs upregulate two genes in both ER wild type (WT) and ER mutant (MUT) BC: SERPINE1 and ABCB1. This study demonstrates that obASCs promote metastasis in ER WT and MUT xenografts and an ER MUT patient derived xenograft (PDX) model. However, obASCs promote tumor growth only in ER WT xenografts.

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