The role of head and neck squamous cell carcinoma cancer stem cells in tumorigenesis, metastasis, and treatment failure.

The role of head and neck squamous cell carcinoma cancer stem cells in tumorigenesis, metastasis, and treatment failure.
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头部和颈部鳞状细胞癌癌干细胞在肿瘤发生,转移和治疗衰竭中的作用。

DOI:
10.3389/fendo.2012.00090
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发表时间:
2012
影响因子:
5.2
通讯作者:
Prince ME
Prince ME
中科院分区:
医学2区
文献类型:
--
作者:
Chinn SB;Darr OA;Peters RD;Prince ME

文献摘要

被引文献

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头颈鳞状细胞癌(HNSCC)是全球第六大常见癌症。尽管诊断和治疗方法取得了进步,但 HNSCC 的生存率在过去 30 年中保持不变,治疗失败和转移是预后不良的最有力指标。癌症干细胞 (CSC) 已在多种其他实体瘤中被发现,包括乳腺癌、前列腺癌和胰腺癌。最近,基于细胞标记物 CD44 的过度表达和乙醛脱氢酶活性的增加,在 HNSCC 中鉴定出了肿瘤细胞亚群。这些细胞因其干细胞样特性而被指定为 CSC:自我更新、肿瘤发生以及再现异质性肿瘤的能力。最近研究 HNSCC CSC 在肿瘤发生中的作用表明,CSC 具有更强的肿瘤生长能力、增强的运动性和侵袭性特征;体内实验证实,与非 CSC 相比,CSC 具有更大的转移潜力。临床上,CSC 富集已被证明在复发性疾病、治疗失败和转移时会增强。鉴于 CSC 生长缓慢且具有治疗耐药性的先天机制,它们代表了一个新的研究目标。进一步了解其独特的表型可能会揭示潜在的分子靶点,以改善 HNSCC 患者的治疗和生存结果。
Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide. Despite advances in diagnostic and therapeutic methods, survival of HNSCC remains unchanged over the last 30 years with treatment failure and metastases being the strongest indicators of poor outcome. Cancer stem cells (CSC) have been identified in multiple other solid tumors, including breast, prostate, and pancreatic carcinoma. Recently, a subpopulation of tumor cells has been identified in HNSCC based on the overexpression of the cellular marker CD44 and increased activity of aldehyde dehydrogenase. These cells have been designated CSC based on their stem cell-like properties: self-renewal, tumorigenesis, and the ability to recapitulate a heterogeneous tumor. Recent work looking at the role of HNSCC CSC in tumorigenesis has shown that CSC have a greater capacity for tumor growth, increased motility, and invasive characteristics; in vivo experiments confirm greater metastatic potential in CSC compared to non-CSC. 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.