Researchers from Stanford University earlier this month reported in Nature that they had found a marker, CD271, that identified a somewhat unique population of cells that could produce melanoma in highly immunocompromised mice; anywhere from 2.5 percent to 41 percent of cells in their human tumor samples expressed the marker. In additional experiments using similar mice on which human skin was engrafted, only tumor cells with the marker could produce tumors and metastases in the mice. (In his lab, Dr. Morrison noted, the same marker did not differentiate tumor-forming from nontumor-forming cells.)The publication about CD271 is: Human melanoma-initiating cells express neural crest nerve growth factor receptor CD271 by Alexander D Boiko and 11 colleagues, Nature 2010(Jul 1); 466(7302): 133-7. [PubMed citation].
Comments: The sentence: "In his lab, Dr. Morrison noted, the same marker did not differentiate tumor-forming from nontumor-forming cells" is noteworthy. Why the difference in results for CD271?
The publication by Boiko and co-authors was cited in a previous post to this blog, "Melanoma-initiating cells identified", dated July 1, 2010.
See also an earlier post to this blog, "Tumorigenic cells not rare in human melanoma", dated December 3, 2008.
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See also the Twitter Trackbacks for NCI Cancer Bulletin for July 27, 2010.
ReplyDeleteSee also: The Melanoma Stem Cell Controversy Continues by Hensin Tsao, Journal Watch Dermatology, July 30, 2010.
ReplyDeleteLast sentence of Comments section: "Lastly, the clinical implications are a bit disturbing. If the stem cell population is unaffected by antimelanoma immunity, current immunotherapeutic approaches that rely on TYR, MART1 or MAGE as antigens may not be properly targeting the mother lode."
A relevant article: Melanoma stem cells - are there devils in the detail? by Mark Shackleton, Pigment Cell Melanoma Res 2010(Aug 5). [Epub ahead of print][PubMed citation]. Excerpt from the "Accepted Article" version: "Since both studies evaluated tumors that were at similar stages of disease progression and that were obtained directly from patients, these data suggest that Boiko et al. used a tumorigenesis assay that was several orders of magnitude less sensitive than the assay used by Quintana et al."
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