Patel Kepal N, Singh Bhuvanesh
Department of Surgery, Stony Brook University Hospital, Stony Brook, New York, USA.
Cancer Control. 2006 Apr;13(2):111-8. doi: 10.1177/107327480601300205.
Recent molecular studies have described a number of abnormalities associated with the progression and dedifferentiation of thyroid carcinoma. These distinct molecular events are often associated with specific stages of tumor development. A better understanding of the mechanisms involved in thyroid cancer pathogenesis may help to translate these discoveries toward improvements in patient care.
We reviewed the literature on the molecular pathogenesis of thyroid cancer and compared clinical, histopathologic, and genetic features important in defining the disease process.
The progression of thyroid cancer from well-differentiated to poorly differentiated and undifferentiated carcinoma represents a biological continuum. Specific genetic events serve as early initiating and late triggering events. Poorly differentiated thyroid carcinomas occupy an intermediate position in this progression model.
With sophisticated genetic tools generating a wealth of information, we have gained better insight into the mechanisms driving thyroid tumor progression. Recognition of these features is crucial to the management of patients with thyroid cancer. Novel treatments are being designed based on our enhanced understanding of this disease process.
近期的分子研究描述了许多与甲状腺癌进展和去分化相关的异常情况。这些独特的分子事件通常与肿瘤发展的特定阶段相关。更好地理解甲状腺癌发病机制中涉及的机制可能有助于将这些发现转化为改善患者护理的措施。
我们回顾了关于甲状腺癌分子发病机制的文献，并比较了在定义疾病过程中重要的临床、组织病理学和遗传学特征。
甲状腺癌从高分化癌发展为低分化癌和未分化癌代表了一个生物学连续过程。特定的基因事件作为早期启动和晚期触发事件。低分化甲状腺癌在这个进展模型中占据中间位置。
借助先进的基因工具产生了大量信息，我们对驱动甲状腺肿瘤进展的机制有了更好的了解。认识到这些特征对于甲状腺癌患者的管理至关重要。基于我们对这一疾病过程的深入理解，正在设计新的治疗方法。
