CSCs responsible for metastasis identified

Cancer stem cells responsible for metastasis identified: HK study, Xinhua News Agency, June 4, 2010. Excerpt:

Hong Kong researchers have identified a subset of cancer stem cells responsible for metastasis in human colorectal cancer which can help better predict the prognosis and design a more suitable treatment for patients, according to a study made public by the University of Hong Kong on Friday.

The researchers from the university's medicine school discovered that cancer stem cells with a surface marker CD26, which marks a subset of cancer stem cells with metastatic capacity, are present in all terminal colon cancer cells and all metastatic cancer cells.

This news item is about the publication: A Subpopulation of CD26+ Cancer Stem Cells with Metastatic Capacity in Human Colorectal Cancer by Roberta Pang and 13 co-authors, including Wai Lun Law, Ronnie T Poon and Benjamin CY Wong [photos of authors], Cell Stem Cell 2010(Jun 4); 6(6): 603-15. [Summary][Twitter entry][Commentary][FriendFeed entry][Science Pond entry].

Progression of primary tumours and metastases

Parallel progression of tumour and metastases by Serge Koscielny and Maurice Tubiana, Nat Rev Cancer 2010(Feb); 10(2): 156 [PubMed citation]. Commentary on an opinion article: Parallel progression of primary tumours and metastases by Christoph Klein, Nat Rev Cancer 2009(Apr); 9(4): 302-12 [PubMed citation]. An excerpt from the full text of the commentary:

[Data are presented that] are consistent with the linear progression model when it is assumed that there are two types of cells in tumours: those that can initiate metastases (metastasis-forming cells (MFCs)), which probably derive from tumour stem cells[ref 7] and those that probably cannot initiate metastasis because their proliferative ability is limited[refs 7,8,9].

Response to the commentary: Tumour cell dissemination and growth of metastasis by Christoph A Klein, Nat Rev Cancer 2010(Feb); 10(2): 156. Excerpt from the full text of the response:

Finally, the authors declare that the parallel progression model is incompatible with the cancer stem cell hypothesis. As defined above, parallel progression does not address this issue.

The 'linear progression model' described by Christoph Klein "places major evolutionary events in the primary tumour and late dissemination of fully malignant cells that subsequently grow to manifest metastases". In the 'parallel progression model', there is "early dissemination of tumour cells from the primary tumour and ectopic selective adaptation (which is associated with the emergence of genomes fully able to form metastases)" (see Christoph Klein's response).