Breast cancer stem cells hard to kill?

Breast cancer stem cells may be hardest to kill by John Miner, The London Free Press, October 11, 2008. (Archived by WebCite^® at http://www.webcitation.org/5bgoyZhVX). The first two paragraphs:

A London researcher is investigating the possibility that the most dangerous breast cancer cells also are the hardest to kill with chemotherapy and radiation.

Alysha Croker, a trainee at the Lawson Health Research Institute, and graduate student at the University of Western Ontario, has already established cancer cells within a tumour can play different roles.

The article appears to be based on a press release: "Bright, Young Minds at Lawson Fight Breast Cancer" [PDF] from the Lawson Health Research Institute (London, Ontario, Canada) dated September 10, 2008. The first paragraph:

The future of breast cancer treatment may involve targeting cancerous stem-like cells (cancer stem cells). These cancer stem cells have recently been identified as the cells that initiate and maintain tumor growth. The same cells seem to play a key role in breast cancer metastasis. What is more, these cells may be resistant to both radiation and chemotherapy. Alysha Croker, a trainee at Lawson Health Research Institute (Lawson) and a graduate student at the Schulich School of Medicine & Dentistry at The University of Western Ontario (Western), has been awarded a fellowship from the Canadian Breast Cancer Foundation (CBCF) to investigate the behaviour and response of cancer stem cells to commonly used chemotherapy agents and to radiation.

The Canadian Breast Cancer Foundation (CBCF) "allocates funds to high-quality research and community grants" across Canada.

Alysha Croker has worked under the guidance of Alison L Allan, an Oncology Scientist at the London Regional Cancer Program. For a recent review based on their work, see: Cancer stem cells: implications for the progression and treatment of metastatic disease by Alysha K Croker and Alison L Allan, J Cell Mol Med 2008(Apr); 12(2): 374-90. On October 19, 2008, both the HTML and PDF versions of the full-text were freely accessible. The PubMed Abstract:

Metastasis is the major cause of death for cancer patients with solid tumours, due mainly to the ineffectiveness of current therapies once metastases begin to form. Further insight into the biology of metastasis is therefore essential in order to gain a greater understanding of this process and ultimately to develop better cancer therapies. Metastasis is an inefficient process, such that very few cells that leave a tumour successfully form macrometastases in distant sites. This suggests that only a small subset of cells can successfully navigate the metastatic cascade and eventually re-initiate tumour growth to form life-threatening metastases. Recently, there has been growing support for the cancer stem cell (CSC) hypothesis which stipulates that primary tumours are initiated and maintained by a small subpopulation of cancer cells that possess "stem-like" characteristics. Classical properties of normal stem cells are strikingly reminiscent of the observed experimental and clinical behaviour of metastatic cancer cells, including an unlimited capacity for self renewal; the requirement for a specific 'niche' or microenvironment to grow; use of the stromal cell-derived factor 1 (SDF-1)/chemokine receptor 4 (CXCR4) axis for migration; enhanced resistance to apoptosis and an increased capacity for drug resistance. Therefore, in addition to playing a role in primary tumour formation, we believe that CSCs are also key players in the metastatic process. We will review the current evidence supporting this idea and discuss the potential implications of the CSC hypothesis with regards to experimental investigation and treatment of metastatic disease.

The Journal of Cellular and Molecular Medicine is published by Wiley-Blackwell, which offers a hybrid Open Access option called OnlineOpen. For 2008, the OnlineOpen fee is US$3000. See also the Journal of Cellular and Molecular Medicine Open Access Exclusive Licence Form [PDF].

Delayed OA, after an embargo period, is also available free of charge. According to the Journal of Cellular and Molecular Medicine Exclusive Licence Form [PDF], "12 months after publication you may post an electronic version of the Article on your own personal website, on your employer’s website/repository and on free public servers in your subject area" but "you are not permitted to post the Blackwell Publishing PDF version of the Article online". Some Wiley-Blackwell journals make their backfiles openly accessible after an embargo period (usually, a year or more), but the Journal of Cellular and Molecular Medicine isn't included in the current list of such journals. (See the section entitled "Wiley-Blackwell Open Access Backfiles" in the page entitled "Wiley-Blackwell and Open Access").

Added October 20, 2008:

See also another recent article: High aldehyde dehydrogenase and expression of cancer stem cell markers selects for breast cancer cells with enhanced malignant and metastatic ability by Alysha K Croker and 6 co-authors, including Alison L Allan, J Cell Mol Med 2008(Aug 4). [Epub ahead of print]. [PubMed Abstract]. A PDF version of the full text of this article is currently freely accessible.