UCSD School of Medicine, La Jolla, USA.
Department of Surgery, Stanford University School of Medicine, CJ Huang Bldg, Palo Alto, CA, 94306, USA.
Dig Dis Sci. 2023 Sep;68(9):3504-3513. doi: 10.1007/s10620-023-08006-z. Epub 2023 Jul 5.
In this installment of the "Paradigm Shifts in Perspective" series, the authors, all scientists who have been involved in colorectal cancer (CRC) research for most or all of their careers, have watched the field develop from early pathological descriptions of tumor formation to the current understanding of tumor pathogenesis that informs personalized therapies. We outline how our understanding of the pathogenetic basis of CRC began with seemingly isolated discoveries-initially with the mutations in RAS and the APC gene, the latter of which was initially found in the context of intestinal polyposis, to the more complex process of multistep carcinogenesis, to the chase for tumor suppressor genes, which led to the unexpected discovery of microsatellite instability (MSI). These discoveries enabled the authors to better understand how the DNA mismatch repair (MMR) system not only recognizes DNA damage but also responds to damage by DNA repair or by triggering apoptosis in the injured cell. This work served, in part, to link the earlier findings on the pathogenesis of CRC to the development of immune checkpoint inhibitors, which has been transformative-and curative-for certain types of CRCs and other cancers as well. These discoveries also highlight the circuitous routes that scientific progress takes, which can include thoughtful hypothesis testing and at other times recognizing the importance of seemingly serendipitous observations that substantially change the flow and direction of the discovery process. What has happened over the past 37 years was not predictable when this journey began, but it does speak to the power of careful scientific experimentation, following the facts, perseverance in the face of opposition, and the willingness to think outside of established paradigms.
在本系列的“视角转变”这一集中,作者都是从事结直肠癌 (CRC) 研究的科学家,他们的职业生涯大多或全部都投入到了该领域。他们目睹了该领域从肿瘤形成的早期病理描述发展到当前的肿瘤发病机制理解,而后者为个性化治疗提供了信息。我们概述了我们对 CRC 发病基础的理解是如何从看似孤立的发现开始的——最初是 RAS 和 APC 基因的突变,后者最初是在肠息肉的背景下发现的,到更复杂的多步骤致癌过程,再到寻找肿瘤抑制基因,这导致了意想不到的微卫星不稳定性 (MSI) 的发现。这些发现使作者能够更好地理解 DNA 错配修复 (MMR) 系统不仅如何识别 DNA 损伤,还如何通过 DNA 修复或触发受损细胞中的细胞凋亡来响应损伤。这项工作部分将 CRC 发病机制的早期发现与免疫检查点抑制剂的开发联系起来,这对某些类型的 CRC 和其他癌症的治疗产生了变革性的影响。这些发现还突出了科学进步所采取的迂回路线,其中包括深思熟虑的假设检验,以及在其他时候认识到看似偶然的观察的重要性,这些观察大大改变了发现过程的流程和方向。在这段旅程开始时,过去 37 年来发生的事情是不可预测的,但它确实说明了仔细的科学实验、遵循事实、面对反对时的坚持以及愿意跳出既定范式思考的力量。