Tumor-initiating activity and tumor morphology of HNSCC is modulated by interactions between clonal variants within the tumor

Cameron, Sarina R., Dahler, Alison L., Endo-Munoz, Liliana B., Jabbar, Ibtissam, Thomas, Gethin P., Leo, Paul J., Poth, Kim, Rickwood, Danny, Guminski, Alexander and Saunders, Nicholas A. (2010) Tumor-initiating activity and tumor morphology of HNSCC is modulated by interactions between clonal variants within the tumor. Laboratory Investigation, 90 11: 1594-1603. doi:10.1038/labinvest.2010.131


Author Cameron, Sarina R.
Dahler, Alison L.
Endo-Munoz, Liliana B.
Jabbar, Ibtissam
Thomas, Gethin P.
Leo, Paul J.
Poth, Kim
Rickwood, Danny
Guminski, Alexander
Saunders, Nicholas A.
Title Tumor-initiating activity and tumor morphology of HNSCC is modulated by interactions between clonal variants within the tumor
Journal name Laboratory Investigation   Check publisher's open access policy
ISSN 0023-6837
1530-0307
Publication date 2010-11
Sub-type Article (original research)
DOI 10.1038/labinvest.2010.131
Volume 90
Issue 11
Start page 1594
End page 1603
Total pages 10
Place of publication London, United Kingdom
Publisher Nature Publishing Group
Collection year 2011
Language eng
Abstract Tumor initiation (TI) in xenotransplantation models of head and neck squamous cell carcinoma (HNSCC) is an inefficient process. Poor TI could be due to (1) posttransplant cell loss, (2) a rare sub-population of cancer stem cells or (3) a requirement for specific cellular interactions, which rely on cell number. By tracking GFP-expressing HNSCC cells, we conclude that the posttransplant loss of cancer cells is minimal in the xenotransplant model. Furthermore, an examination of putative cancer stem cell markers (such as CD133, CD44, SP and label retention) in HNSCC cell lines revealed no correlation between marker expression and tumorigenicity. In addition, single-cell clones randomly isolated from HNSCC cell lines and then transplanted into mice were all capable of initiating tumors with efficiencies varying almost 34-fold. As the observed variation in the clones was both more and less tumorigenic than the parental cells, a combination of two clones, at suboptimal cell numbers for TI, was implanted into mice and was found to modulate the tumor-initiating activity, thus indicating that TI is dependent on a critical number of cells and, for the first time, that interactions between clonal variants within tumors can modulate the overall tumor-initiating activity. Put in context with previous literature on tumorigenic activity, we believe that interactions between clonal variants within a tumor as well as (1) stromal interactions, (2) angiogenic activity, (3) immunocompetence and (4) cancer stem cells may all contribute to tumorigenic potential and the propensity for tumor growth and recurrence.
Keyword Keratinocytes
Squamous cell carcinoma
Tumor initiation
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2011 Collection
UQ Diamantina Institute - Open Access Collection
UQ Diamantina Institute Publications
 
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Created: Sun, 21 Nov 2010, 00:02:18 EST