Biomarkers of UC Tumorigenesis

病程超过8年的广泛溃疡性结肠炎(UC)患者患上 结直肠癌，每年约占结肠炎的1%。因此，有20年UC病史的患者将 有大约20%的肿瘤风险。目前的实践标准适用于所有患有 由来已久：UC将对结直肠癌进行终生结肠镜监测。有主要的 监测方面的问题包括：1)结肠表面积大；2)可能出现异型增生 在这个大范围内的任何地方，通常不会产生内窥镜下可见的损害；3)诊断 对于炎症性异型增生，肠病是一种主观的解释，需要有经验的 病理学家的最高精确度；近50万人患有UC，美国；癌症 对这些患者的监测是昂贵的、时间密集的、复发的(每1-2年)和终生的。《长河》 本研究的学期目标是更好地了解肿瘤的分子机制。 (UC)的进展，并利用这一知识改进对可治愈癌症及其 先驱物。 我们之前的研究已经明确，即使是非发育不良的粘膜在UC中也是遗传异常的 有黑色素瘤的患者。事实上，UC患者的整个结肠似乎表现出遗传不稳定性 患有癌症或不典型增生。我们相信，这些信息对于理解潜在的 肿瘤进展的原因和开发UC患者癌症监测的新方法。 这些新方法可能会改变这些患者及其提供者的临床护理面貌。 我们的目标仍然是更好地了解UC发病过程中的基因组变化，并利用这一点 现在寻找早期标志物，使我们能够将监测工作集中在这些患者身上 最有可能从中受益的是。这两个目标都将有助于为 未来的癌症预防策略。

Patients with extensive ulcerative colitis (UC) of more than 8 years duration have an increased risk of colorectal cancer which approximates 1% per year of colitis. Thus, a patient who has 20 years of UC will have a neoplastic risk that approximates 20%. The current standard of practice in all patients with longstanding :UC is to perform lifeHong colonoscopic surveillance for colorectal cancer. There are major problems regarding surveillance including: 1) the large surface area of the colon; 2):dysplasia may arise anywhere within this large area and frequently produces no endoscopically visible lesion; 3) the diagnosis of dysplasia in inflammatory, bowel disease is a subjective interpretation and requires an experienced pathologist forsptimum accuracy; Nearly half of a million people have UC iWIhe United States; cancer surveillance in these patients is costly, time intensive, recurrent (every 1-2 years), and life-long. The long term objectives of this research are to better understand the molecular mechanisms of neoplastic progression in (UC)and to use this knowledge for improved surveillance of curable cancer and its precursors. Our previous studies have made it clear that even the non-dysplastic mucosa is genetically abnormal in UC patients who have nebplasia. In fact, the entire colon appears to show genetic instability in UC patients with cancer or dysplasia. We believe that this information is central to understanding the underlying causes of neoplastic progression and for developing new methods for cancer surveillance of UC patients. Such new methods could change the face of clinical care for these patients and their providers. Our goals remain to better understand the genomic changes during earcinogenesis in UC, and to use this <nowledge to find early markers that will enable us to concentrate our surveillance efforts on those patients most likely to benefit from them. Both of these goals will help provide the underpinnings for development of cancer prevention strategies in the future.