University of Texas Southwestern Medical Center, Dallas, TX 75093-8576, USA.
Proc Natl Acad Sci U S A. 2011 Jul 26;108(30):12396-400. doi: 10.1073/pnas.1106613108. Epub 2011 Jul 11.
Clinical cancer dormancy is defined as an unusually long time between removal of the primary tumor and subsequent relapse in a patient who has been clinically disease-free. The condition is frequently observed in certain carcinomas (e.g., breast cancer), B-cell lymphoma, and melanoma, with relapse occurring 5-25 y later. Clinical data suggest that a majority of breast cancer survivors have cancer cells for decades but can remain clinically cancer-free for their lifetime. Thus, there is a major effort to characterize the molecular mechanisms responsible for inducing tumor cell dormancy using experimental models or studying the early phases of cancer growth in humans. Many molecules and signaling pathways have been characterized and have led to concepts that dominate the field, such as the possible role of innate and adaptive immunity in immune surveillance and initiation and maintenance of dormancy. However, recent clinical data do not support many of these concepts. Several areas need further study to determine their relevance to clinical cancer dormancy. We suggest hypotheses that may contribute to elucidation of the mechanisms underlying the dormant state.
临床癌症休眠是指在患者临床无病的情况下，从切除原发肿瘤到随后复发之间的异常长时间。这种情况在某些癌（如乳腺癌）、B 细胞淋巴瘤和黑色素瘤中经常观察到，复发发生在 5-25 年后。临床数据表明，大多数乳腺癌幸存者的癌细胞存在数十年，但可以终生保持临床无癌症状态。因此，人们正在努力使用实验模型来描述诱导肿瘤细胞休眠的分子机制，或研究人类癌症生长的早期阶段。许多分子和信号通路已经被描述，并形成了主导该领域的概念，例如先天和适应性免疫在免疫监视以及休眠的启动和维持中的可能作用。然而，最近的临床数据并不支持这些概念中的许多概念。还需要进一步研究几个领域，以确定它们与临床癌症休眠的相关性。我们提出了一些假设，这些假设可能有助于阐明休眠状态的潜在机制。
