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Margaryan NV, Seftor EA, Seftor REB, et al. Targeting the Stem Cell Properties of Adult Breast Cancer Cells: Using Combinatorial Strategies to Overcome Drug Resistance. Curr Mol Biol Rep. 2017;3(3):159-164doi: 10.1007/s40610-017-0067-5.
Margaryan, N. V., Seftor, E. A., Seftor, R. E. B., & Hendrix, M. J. C. (2017). Targeting the Stem Cell Properties of Adult Breast Cancer Cells: Using Combinatorial Strategies to Overcome Drug Resistance. Current molecular biology reports, 3(3), 159-164. https://doi.org/10.1007/s40610-017-0067-5
Margaryan, Naira V, et al. "Targeting the Stem Cell Properties of Adult Breast Cancer Cells: Using Combinatorial Strategies to Overcome Drug Resistance." Current molecular biology reports vol. 3,3 (2017): 159-164. doi: https://doi.org/10.1007/s40610-017-0067-5
Margaryan NV, Seftor EA, Seftor REB, Hendrix MJC. Targeting the Stem Cell Properties of Adult Breast Cancer Cells: Using Combinatorial Strategies to Overcome Drug Resistance. Curr Mol Biol Rep. 2017 Sep;3(3):159-164. doi: 10.1007/s40610-017-0067-5. Epub 2017 Jul 10. PMID: 29152453; PMCID: PMC5687579.
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Curr Mol Biol Rep. 2017 Sep;3(3):159-164. doi: 10.1007/s40610-017-0067-5. Epub 2017 Jul 10.

Targeting the Stem Cell Properties of Adult Breast Cancer Cells: Using Combinatorial Strategies to Overcome Drug Resistance.

Current molecular biology reports

Naira V Margaryan, Elisabeth A Seftor, Richard E B Seftor, Mary J C Hendrix

Affiliations

  1. Department of Biochemistry, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, WV 26506 USA.
  2. Cancer Institute, West Virginia University, Morgantown, WV 26506 USA.
  3. Department of Biology, Shepherd University, Shepherdstown, WV 25443 USA.
  4. Department of Internal Medicine, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, WV 26506 USA.

PMID: 29152453 PMCID: PMC5687579 DOI: 10.1007/s40610-017-0067-5

Abstract

PURPOSE OF REVIEW: Cancer is a major public health problem worldwide. In aggressive cancers, which are heterogeneous in nature, there exists a paucity of targetable molecules that can be used to predict outcome and response to therapy in patients, especially those in the high risk category with a propensity to relapse following chemotherapy. This review addresses the challenges pertinent to treating aggressive cancer cells with inherent stem cell properties, with a special focus on triple-negative breast cancer (TNBC).

RECENT FINDINGS: Plasticity underlies the cancer stem cell (CSC) phenotype in aggressive cancers like TNBC. Progenitors and CSCs implement similar signaling pathways to sustain growth, and the convergence of embryonic and tumorigenic signaling pathways has led to the discovery of novel oncofetal targets, rigorously regulated during normal development, but aberrantly reactivated in aggressive forms of cancer.

SUMMARY: Translational studies have shown that Nodal, an embryonic morphogen, is reactivated in aggressive cancers, but not in normal tissues, and underlies tumor growth, invasion, metastasis and drug resistance. Front-line therapies do not inhibit Nodal, but when a combinatorial approach is used with an agent such as doxorubicin followed by anti-Nodal antibody therapy, significant decreases in cell growth and viability occur. These findings are of special interest in the development of new therapeutic interventions that target the stem cell properties of cancer cells to overcome drug resistance and metastasis.

Keywords: Breast cancer; Cancer stem cells; Combinatorial therapy; Doxorubicin; Nodal; Predictive biomarker

References

  1. Med Oncol. 2013;30(3):653 - PubMed
  2. Expert Opin Ther Targets. 2007 Apr;11(4):497-505 - PubMed
  3. Breast Cancer Res. 2004;6(6):R605-15 - PubMed
  4. Nature. 2000 Aug 3;406(6795):536-40 - PubMed
  5. Cancer Res. 2005 Dec 15;65(24):11520-8 - PubMed
  6. Mol Cancer Ther. 2015 Mar;14 (3):779-787 - PubMed
  7. Cell Stem Cell. 2011 Nov 4;9(5):433-46 - PubMed
  8. Expert Rev Dermatol. 2009;4(1):67-78 - PubMed
  9. Br J Cancer. 2008 Jan 15;98(1):137-42 - PubMed
  10. Cancer Biol Ther. 2010 Nov 15;10(10):955-60 - PubMed
  11. J Cell Biochem. 2007 Jul 1;101(4):908-17 - PubMed
  12. Breast Cancer Res Treat. 1999 May;55(2):127-36 - PubMed
  13. Oncology (Williston Park). 2008 Oct;22(11):1233-9; discussion 1239-40, 1243 - PubMed
  14. Int J Biochem Cell Biol. 2013 Apr;45(4):885-98 - PubMed
  15. Prostate. 2011 Aug 1;71(11):1198-209 - PubMed
  16. Semin Cancer Biol. 2014 Dec;29:1-2 - PubMed
  17. Nature. 2000 Aug 17;406(6797):747-52 - PubMed
  18. Nature. 1994 Feb 17;367(6464):645-8 - PubMed
  19. Cancer Res. 2009 Sep 15;69(18):7131-4 - PubMed
  20. Onco Targets Ther. 2015 Jan 16;8:177-93 - PubMed
  21. Nat Rev Mol Cell Biol. 2009 Feb;10(2):91-103 - PubMed
  22. Epigenomics. 2009 Dec;1(2):387-98 - PubMed
  23. Nature. 2000 Jan 27;403(6768):385-9 - PubMed
  24. Nature. 2015 Apr 16;520(7547):358-62 - PubMed
  25. Clin Cancer Res. 2010 Jan 1;16(1):45-55 - PubMed
  26. Breast Cancer Res. 2012 May 11;14(3):R75 - PubMed
  27. J Clin Oncol. 2008 Jul 1;26(19):3153-8 - PubMed
  28. J Natl Cancer Inst. 2004 Oct 6;96(19):1473-7 - PubMed
  29. Nat Med. 2006 Aug;12(8):925-32 - PubMed
  30. Lab Invest. 2017 Feb;97(2):176-186 - PubMed
  31. Mol Cancer Res. 2015 Apr;13(4):670-80 - PubMed
  32. Semin Cancer Biol. 2014 Dec;29:40-50 - PubMed
  33. Cell Cycle. 2016 May 2;15(9):1295-302 - PubMed
  34. Clin Cancer Res. 2009 Mar 15;15(6):1845-7 - PubMed
  35. Oncotarget. 2015 Oct 27;6(33):34071-86 - PubMed
  36. Breast Cancer Res. 2000;2(6):417-22 - PubMed
  37. Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):3983-8 - PubMed
  38. Nat Rev Cancer. 2003 Jun;3(6):411-21 - PubMed
  39. Proc Natl Acad Sci U S A. 2008 Mar 18;105(11):4329-34 - PubMed
  40. Cancer Res. 2009 Feb 15;69(4):1302-13 - PubMed

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