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Cancer stem cells in head and neck cancer.

Mitra D, Malkoski SP, Wang XJ - Cancers (Basel) (2011)

Bottom Line: Head and neck cancer (HNC) is the sixth most common malignancy world-wide, however the survival rate has not improved for the past 20 years.Here we review the progress of CSC studies in HNC, which suggest that HNC conforms to the CSC model.The identified CSC markers and their tumor initiation properties provide a framework for the development of novel therapeutic strategies for HNC.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, University of Colorado Denver, AMC 12800 E. 19th Ave., Aurora, CO 80045, USA. xj.wang@ucdenver.edu.

ABSTRACT
Head and neck cancer (HNC) is the sixth most common malignancy world-wide, however the survival rate has not improved for the past 20 years. In recent years, the cancer stem cell (CSC) hypothesis has gained ground in several malignancies and there is mounting evidence suggesting CSCs mediate tumor resistance to chemotherapy and radiation therapy. However, the CSC theory is also challenged at least in certain types of cancer. Here we review the progress of CSC studies in HNC, which suggest that HNC conforms to the CSC model. The identified CSC markers and their tumor initiation properties provide a framework for the development of novel therapeutic strategies for HNC.

No MeSH data available.


Related in: MedlinePlus

Cancer heterogeneity models. (A) Hierarchical model of Cancer Stem Cell (CSC). The CSC (in red) undergoes a division to give rise to a differentiated daughter cell (blue) and another CSC (red, self renewal depicted by red arrow). The CSC by virtue of its infinite proliferative potential will continue to divide as above (dotted arrow). The differentiated cell may undergo a few divisions before terminal differentiation or senescence or cell death as the case may be. The CSC may undergo clonal evolution and acquire even greater tumorigenicity and/or chemoresistance and/or radioresistance (brown). Alternatively, a differentiated cell may de-differentiate and acquire tumorigenicity (black arrow) and be converted to a CSC. (B) Clonal Evolution model. Normal cells (blue) acquire mutations stochastically (yellow), and over successive divisions and due to accrual of several mutations these cells become transformed (red) and/or acquire chemo-and/or radio-resistance and can divide indefinitely (dotted arrow).
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f1-cancers-03-00415: Cancer heterogeneity models. (A) Hierarchical model of Cancer Stem Cell (CSC). The CSC (in red) undergoes a division to give rise to a differentiated daughter cell (blue) and another CSC (red, self renewal depicted by red arrow). The CSC by virtue of its infinite proliferative potential will continue to divide as above (dotted arrow). The differentiated cell may undergo a few divisions before terminal differentiation or senescence or cell death as the case may be. The CSC may undergo clonal evolution and acquire even greater tumorigenicity and/or chemoresistance and/or radioresistance (brown). Alternatively, a differentiated cell may de-differentiate and acquire tumorigenicity (black arrow) and be converted to a CSC. (B) Clonal Evolution model. Normal cells (blue) acquire mutations stochastically (yellow), and over successive divisions and due to accrual of several mutations these cells become transformed (red) and/or acquire chemo-and/or radio-resistance and can divide indefinitely (dotted arrow).

Mentions: Head and neck cancer (HNC) is the sixth most common malignancy worldwide [1]. The head and neck is an anatomically complex region that gives rise to a wide variety of cancers varying in phenotype, histology, differentiation, tumorigenicity, and invasiveness [2]. Cancer heterogeneity has been explained by both clonal evolution and cancer stem cell models (Figure 1). In the clonal evolution model, all tumor cells are tumorigenic and heterogeneity arises from genetic or epigenetic changes occurring stochastically within individual clones [3]. The cancer stem cell (CSC) model proposes a hierarchical organization whereby tumor growth is dependent on CSCs that have the capacity for self renewal and to give rise to more differentiated tumor cells, analogous to the role of stem cells in normal tissue [3]. In this setting, small numbers of CSCs can produce a tumor recapitulating the heterogeneity of the original tumor when transplanted into immunocompromised mice [3]. In this model, differentiated daughter cells should not be tumorigenic and cannot recapitulate original tumor heterogeneity. It should be noted that the CSC model does not exclude the possibility that CSCs undergo clonal evolution, and thus these models are not mutually exclusive [3]. Furthermore, it is possible that different tumors follow either the clonal evolution or CSC hypothesis or some combination thereof.


Cancer stem cells in head and neck cancer.

Mitra D, Malkoski SP, Wang XJ - Cancers (Basel) (2011)

Cancer heterogeneity models. (A) Hierarchical model of Cancer Stem Cell (CSC). The CSC (in red) undergoes a division to give rise to a differentiated daughter cell (blue) and another CSC (red, self renewal depicted by red arrow). The CSC by virtue of its infinite proliferative potential will continue to divide as above (dotted arrow). The differentiated cell may undergo a few divisions before terminal differentiation or senescence or cell death as the case may be. The CSC may undergo clonal evolution and acquire even greater tumorigenicity and/or chemoresistance and/or radioresistance (brown). Alternatively, a differentiated cell may de-differentiate and acquire tumorigenicity (black arrow) and be converted to a CSC. (B) Clonal Evolution model. Normal cells (blue) acquire mutations stochastically (yellow), and over successive divisions and due to accrual of several mutations these cells become transformed (red) and/or acquire chemo-and/or radio-resistance and can divide indefinitely (dotted arrow).
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Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC3756369&req=5

f1-cancers-03-00415: Cancer heterogeneity models. (A) Hierarchical model of Cancer Stem Cell (CSC). The CSC (in red) undergoes a division to give rise to a differentiated daughter cell (blue) and another CSC (red, self renewal depicted by red arrow). The CSC by virtue of its infinite proliferative potential will continue to divide as above (dotted arrow). The differentiated cell may undergo a few divisions before terminal differentiation or senescence or cell death as the case may be. The CSC may undergo clonal evolution and acquire even greater tumorigenicity and/or chemoresistance and/or radioresistance (brown). Alternatively, a differentiated cell may de-differentiate and acquire tumorigenicity (black arrow) and be converted to a CSC. (B) Clonal Evolution model. Normal cells (blue) acquire mutations stochastically (yellow), and over successive divisions and due to accrual of several mutations these cells become transformed (red) and/or acquire chemo-and/or radio-resistance and can divide indefinitely (dotted arrow).
Mentions: Head and neck cancer (HNC) is the sixth most common malignancy worldwide [1]. The head and neck is an anatomically complex region that gives rise to a wide variety of cancers varying in phenotype, histology, differentiation, tumorigenicity, and invasiveness [2]. Cancer heterogeneity has been explained by both clonal evolution and cancer stem cell models (Figure 1). In the clonal evolution model, all tumor cells are tumorigenic and heterogeneity arises from genetic or epigenetic changes occurring stochastically within individual clones [3]. The cancer stem cell (CSC) model proposes a hierarchical organization whereby tumor growth is dependent on CSCs that have the capacity for self renewal and to give rise to more differentiated tumor cells, analogous to the role of stem cells in normal tissue [3]. In this setting, small numbers of CSCs can produce a tumor recapitulating the heterogeneity of the original tumor when transplanted into immunocompromised mice [3]. In this model, differentiated daughter cells should not be tumorigenic and cannot recapitulate original tumor heterogeneity. It should be noted that the CSC model does not exclude the possibility that CSCs undergo clonal evolution, and thus these models are not mutually exclusive [3]. Furthermore, it is possible that different tumors follow either the clonal evolution or CSC hypothesis or some combination thereof.

Bottom Line: Head and neck cancer (HNC) is the sixth most common malignancy world-wide, however the survival rate has not improved for the past 20 years.Here we review the progress of CSC studies in HNC, which suggest that HNC conforms to the CSC model.The identified CSC markers and their tumor initiation properties provide a framework for the development of novel therapeutic strategies for HNC.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, University of Colorado Denver, AMC 12800 E. 19th Ave., Aurora, CO 80045, USA. xj.wang@ucdenver.edu.

ABSTRACT
Head and neck cancer (HNC) is the sixth most common malignancy world-wide, however the survival rate has not improved for the past 20 years. In recent years, the cancer stem cell (CSC) hypothesis has gained ground in several malignancies and there is mounting evidence suggesting CSCs mediate tumor resistance to chemotherapy and radiation therapy. However, the CSC theory is also challenged at least in certain types of cancer. Here we review the progress of CSC studies in HNC, which suggest that HNC conforms to the CSC model. The identified CSC markers and their tumor initiation properties provide a framework for the development of novel therapeutic strategies for HNC.

No MeSH data available.


Related in: MedlinePlus