Aldehyde dehydrogenase 1 is a putative marker for cancer stem cells in head and neck squamous cancer

Chen, Yu‐Chih; Chen, Yi Wei; Hsu, Han Shui; Tseng, Ling Ming; Huang, Pin I.; Lü, Kai; Chen, Dow Tien; Tai, Lung Kuo; Yung, Ming Chi; Chang, Shih Ching; Ku, Hung Hai; Chiou, Shih Hwa; Lo, Wen-Liang

doi:10.1016/j.bbrc.2009.05.048

Cited by 433 publications

(416 citation statements)

References 23 publications

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“…The resulting tumors, derived from the CD44 high injections, demonstrated renewal of CD44 high cells, indicating self-renewal, and regeneration of a heterogeneous tumor, thus meeting the definition of a CSC. Similar experiments using the enzymatic marker ALDH were also able to demonstrate that cells with ALDH+ expression had greater rates of tumorigenesis in mouse flank and neck injections (Chen et al, 2009).…”

Section: Tumorigenesismentioning

confidence: 55%

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Cancer Stem Cells in Head and Neck Squamous Cell Carcinoma: A Review

Satpute

Hazarey²,

Ahmed³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Research indicates that a small population of cancer cells is highly tumorigenic, endowed with the capacity for self-renewal, and has the ability to differentiate into cells that constitute the bulk of tumors. These cells are considered the ''drivers'' of the tumorigenic process in some tumor types, and have been named cancer stem cells (CSC). Epithelial-mesenchymal transition (EMT) appears to be involved in the process leading to the acquisition of stemness by epithelial tumor cells. Through this process, cells acquire an invasive phenotype that may contribute to tumor recurrence and metastasis. CSC have been identified in human head and neck squamous cell carcinomas (HNSCC) using markers such as CD133 and CD44 expression, and aldehyde dehydrogenase (ALDH) activity. Head and neck cancer stem cells reside primarily in perivascular niches in the invasive fronts where endothelial-cell initiated events contribute to their survival and function. Clinically, CSC enrichment has been shown to be enhanced in recurrent disease, treatment failure and metastasis. CSC represent a novel target of study given their slow growth and innate mechanisms conferring treatment resistance. Further understanding of their unique phenotype may reveal potential molecular targets to improve therapeutic and survival outcomes in patients with HNSCC. Here, we discuss the state-of-the-knowledge on the pathobiology of cancer stem cells, with a focus on the impact of these cells on head and neck tumor progression, metastasis and recurrence due to treatment failure.

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Section: Tumorigenesismentioning

confidence: 55%

“…In these tumors, ALDH+ cells were characterized as highly tumorigenic cells that can self-renew, which are hallmarks of cancer stem cells. In HNSCC, ALDH enriches for cancer stem cells and is involved in epithelial-to-mesenchymal transition (EMT) (Chen et al, 2009). …”

Section: Methods Of Identification Of Cancer Stem Cellsmentioning

confidence: 99%

Cancer Stem Cells in Head and Neck Squamous Cell Carcinoma: A Review

Satpute

Hazarey²,

Ahmed³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…36 -42 Moreover, several studies have described a clinical influence of ALDH1A1-expressing tumor cells in cancers of breast, colon, prostate, and head and neck, as well as in leukemia. 36,39,40,43,44 These findings raise the intriguing question of how ALDH1A1, in charge of activating the prodifferentiation factor RA, is associated with worsened clinical outcome and an undifferentiated phenotype in both healthy and neoplastic tissues. Taking into account possible mechanisms of alternative RA signaling, it could be of great interest to investigate whether stem and progenitor cells are capable of steering self-generated intracellular RA levels.…”

Section: Discussionmentioning

confidence: 99%

Aberrant Expression of Retinoic Acid Signaling Molecules Influences Patient Survival in Astrocytic Gliomas

Campos

Centner

Bermejo

et al. 2011

The American Journal of Pathology

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Undifferentiated cell populations may influence tumor growth in malignant glioma. We investigated potential disruptions in the retinoic acid (RA) differentiation pathway that could lead to a loss of differentiation capacity, influencing patient prognosis. Expression of key molecules belonging to the RA differentiation pathway was analyzed in 283 astrocytic gliomas and was correlated with tumor proliferation, tumor differentiation, and patient survival. In addition, in situ concentrations of retinoids were measured in tumors, and RA signaling events were studied in vitro. Unlike other tumors, in gliomas expression of most RA signaling molecules increased with malignancy and was associated with augmented intratumoral retinoid levels in high-grade gliomas. Aberrantly expressed RA signaling molecules included i) the retinol-binding protein CRBP1, which facilitates cellular retinoid uptake; ii) ALDH1A1, capable of activating RA precursors; iii) the RA-degrading enzyme CYP26B1; and iv) the RA-binding protein FABP5, which can inhibit RA-induced differentiation. In contrast, expression of the RA-binding protein CRABP2, which fosters differentiation, was decreased in high-grade tumors. Moreover, expression of CRBP1 correlated with tumor proliferation, and FABP5 expression correlated with an undifferentiated tumor phenotype. CRBP1 and ALDH1A1 were independent prognostic markers for adverse patient survival. Our data indicate a complex and clinically relevant deregulation of RA signaling, which seems to be a central event in glioma pathogenesis.

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“…Immediately following this discovery, CD133+ cells were identified as tumor stem cells in glioblastoma brain tumors [27] and thereafter in colon cancer [28]. In the past few years, high ALDH1 activity levels have been used to identify CSCs in a variety of tumors including liver, head and neck, colorectal, breast, multiple myeloma, acute myeloid leukemia, and brain cancers [29][30][31][32][33][34][35]. Moreover, a link between poor prognosis and increased ALDH1 activity was found in breast tumors [33].…”

Section: Cancer Stem Cells-past and Currentmentioning

confidence: 99%

Targeted therapy aimed at cancer stem cells: Wilms’ tumor as an example

2013

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Wilms' tumor (WT), a common renal pediatric solid tumor, serves as a model for a malignancy formed by renal precursor cells that have failed to differentiate properly. Here we review recent evidence showing that the tumors' heterogeneous cell population contains a small fraction of cancer stem cells (CSC) identified by two markers: Neural Cell Adhesion Molecule 1 (NCAM1) expression and Aldehyde dehydrogenase 1 (ALDH1) enzymatic activity. In vivo studies show these CSCs to both self-renew and differentiate to give rise to all tumor components. Similar to other malignancies, the identification of a specific CSC fraction has allowed the examination of a novel targeted therapy, aimed at eradicating the CSC population. The loss of CSCs abolishes the tumor's ability to sustain and propagate, hence, causing tumor degradation with minimal damage to normal tissue.

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Aldehyde dehydrogenase 1 is a putative marker for cancer stem cells in head and neck squamous cancer

Cited by 433 publications

References 23 publications

Cancer Stem Cells in Head and Neck Squamous Cell Carcinoma: A Review

Cancer Stem Cells in Head and Neck Squamous Cell Carcinoma: A Review

Aberrant Expression of Retinoic Acid Signaling Molecules Influences Patient Survival in Astrocytic Gliomas

Targeted therapy aimed at cancer stem cells: Wilms’ tumor as an example

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