Ulcerative colitis is characterized by chronic inflammation originating in the rectum and involving the proximal colon to varying degrees, with varying lengths of involvement. Between 15% and 30% of patients with UC require surgical treatment. Indications for surgery include acute colitis, malignancy, etc. Complete removal of all possible diseased tissues can theoretically cure UC. Doctors and patients often worry that long-term chronic inflammation of UC will cause cancer, so will UC cause cancer or not? 1.Will UC become cancerous or not? Not all UC patients will become cancerous. Then what are the high-risk factors for cancer? It was found that the severity of colonic inflammation, total colitis (involving the proximal splenic flexure) and long duration of disease (>8 years, total colitis) are high-risk factors. In addition, UC is diagnosed at a young age, which is often strongly associated with an increased risk of colorectal cancer. Some other high-risk factors include family history of IBD, and combined primary sclerosing cholangitis (PSC). A meta-analysis showed that the cumulative risk of colorectal cancer in UC patients was 2.1% at 10 years, 8.5% at 20 years, and 17.8% at 30 years. However, population-based series have reported lower annual incidence rates of 0.06% to 0.2%. Nevertheless, chronic ulcerative colitis is generally considered to be associated with an increased risk of malignancy. Therefore, surveillance by colonoscopy is recommended for these patients, even in the absence of data on survival benefit. Patients who undergo regular endoscopic surveillance are usually able to detect cancer at an early stage and have a relatively good overall prognosis. 2. How to monitor for cancer? Since there is a risk of cancer in UC, how should it be prevented? Currently, 5-ASA, or mesalazine, is considered to have a role in reducing the risk of cancer. However, more important is the review by endoscopist and the fire eye of pathologist. For patients with extensive colitis (lesions involving the proximal splenic flexure), it is recommended that they begin endoscopy 8 years after onset and maintain regular colonoscopic surveillance every 1 to 2 years. The timing of monitoring will depend on whether atypical hyperplasia is detected in the biopsy specimen. In patients with left-sided lesions (lesions located distal to the splenic flexure), surveillance may begin 15 years after onset or earlier. Patients with two consecutive negative colonoscopies can be monitored at intervals of 1 to 3 years, depending on the condition. In addition, patients with primary sclerosing cholangitis (PSC) have a higher risk of malignancy, with a cumulative risk of cancer or atypical hyperplasia approaching 50% over 25 years of presentation. Therefore, it is recommended that such patients adhere to annual endoscopic surveillance. 3. What should be done for biopsy? Endoscopic surveillance should include two random biopsies from each of the four quadrants of the entire colorectal segment at 10 cm intervals, as well as targeted biopsies of suspicious lesions. The recommended endoscopic surveillance includes two biopsies from each of the four quadrants of the colon (including right hemicolectomy, transverse colon, left hemicolectomy, and sigmoid colon), for a total of 32 random biopsies in four sample cups. A minimum of 32 random biopsies had a sensitivity of 80% to 90% for detecting atypical hyperplasia. Targeted biopsies are also required for polypoid lesions, masses, strictures, or obvious irregularities in the mucosa around inflammation. In addition, the presence of adjacent apparently “normal” tissue should also be submitted as a normal control. Polypectomy is performed for polyps with suspected atypical hyperplasia, and the adjacent mucosa should also be biopsied to rule out atypical hyperplasia. The magnification staining targeted biopsy technique allows better detection of smaller, flattened, atypical hyperplastic lesions. This technique applies a stain or dye (such as indigo carmine or methylene blue) throughout the colorectum to improve detection of microscopic mucosal changes. The technique can also be combined with advanced image processing capabilities including narrow-band imaging and laser confocal microendoscopy to further increase the detection rate of atypical hyperplastic areas. A small number of prospective studies have demonstrated that this approach offers significant advantages over conventional light source endoscopy for the detection of intraepithelial cancers.