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The Duodenum and Small Bowel
Published in E. George Elias, CRC Handbook of Surgical Oncology, 2020
While adenomatous polyps can be removed either endoscopically or via an enterotomy, other benign tumors are managed by segmental resection whether these are located in the ileum, jejunum, or third or first part of duodenum. In addition, benign periampullary duodenal lesions can be managed by duodenotomy with excision of the lesion. On the other hand, large sessile villous adenoma of the small bowel is treated by segmental resection with the resection of the related mesentery of the small bowel, but such lesions may require a proximal pancreaticoduodenectomy (Whipple’s procedure) if they located in the periampullary area as the nature of malignancy cannot be determined. Bruner’s adenomas are usually treated by local resection; however, large ones can also be by-passed without submitting the patient to a Whipple’s procedure for a benign disease that has no malignant potential. Patients with Peutz-Jegher’s syndrome may require several exploratory laparotomies to remove the symptomatic part of the polyps or small segment of the bowel to avoid complications related to those false polyps. In addition, the remaining benign tumors can be resected locally by a simple excision or segmental resection without radical resection.
The gastrointestinal system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Sharon J. White, Francis A. Carey
Adenomatous polyps are important in their own right as causes of bleeding and anaemia due to traumatic surface ulceration by the passing faecal stream. Nevertheless, it is the association between these lesions and the development of invasive malignancy (adenocarcinoma) that is of greatest clinical concern.
Comparative Pathology — Human Large Intestinal Cancer And Animal Models
Published in Herman Autrup, Gary M. Williams, Experimental Colon Carcinogenesis, 2019
Also called villous adenoma, villous polyps are less common than the adenomatous polyps and have distinctly different morphological as well as biological features. These are most often sessile lesions with broad base. Unlike the adenomatous polyps, the entire polyp is neoplastic. The polyp appears as if it has been plastered on to the mucosa. The surface of the polyp is characterized by finger-shaped structures reminiscent of the villi in the small intestine and, hence, the name villous polyps. Generally the morphological features of malignancy are more predominant throughout the entire polyp than that seen in adenomatous polyps. Villous polyps are also generally larger than the adenomatous polyps and the potential to progress to carcinomas is likewise much higher than any other polyps described earlier.5
Circulating microRNA-944 and its target gene EPHA7 as a potential biomarker for colorectal cancer
Published in Archives of Physiology and Biochemistry, 2022
Olfat G. Shaker, Ghada Ayeldeen, Amr M. Abdelhamid
In our study, according to pathology results and positive colonoscopy to settle the diagnosis, we recruited 150 CRC patients and 50 patients with adenomatous polyps (AP). Full case history was collected for all the subjects in addition to the clinical investigation and the routine laboratory investigations including complete blood count, carcinoembryonic antigen assay (CEA), erythrocyte sedimentation rate (ESR), stool analysis and faecal occult blood test in addition to assessment of liver biomarkers. Moreover, full colonoscopy, using abdominal ultrasound for imaging and computed tomography to CRC stages as reported by the American Joint Committee on Cancer (2010) (Edge and Compton 2010). Exclusion criteria for the subjects: 1. Patients previously received chemotherapy and/or radiotherapy for CRC, 2. Patients diagnosed with inflammatory bowel disease (IBD). 3. Patients with cancer at another site during the time of selection or with recurrent tumours history.
Colorectal cancer management: strategies in drug delivery
Published in Expert Opinion on Drug Delivery, 2022
Prabha Singh, Pramita Waghambare, Tabassum Asif Khan, Abdelwahab Omri
CRC begins with projection of a tissue called ‘polyp’ that can be cancerous or noncancerous [5]. In general, there are two main types of polyps—adenomatous polyp (adenomas) and hyperplastic polyps. Adenomatous polyps are precancerous and can change into cancer, whereas hyperplastic polyps are the most common type of polyp and are generally not precancerous [6]. In stage 0 of CRC, the tumor growth starts from the inner lining of mucosa and patients are diagnosed easily. In stage I, CRC has spread to the upper layer, i.e. sub mucosa and surgery is the best option. In stage II, CRC spreads to the third layer, i.e. muscular layer and sometimes to lymph node and beyond colon. Resection surgery is the best option to treat this stage. In stage III, CRC spreads to the serosa and lymph nodes and surgery is used to eradicate the section of the colon together with nearby lymph nodes, followed by adjuvant chemotherapy. In stage IV (advanced stage), the cancer spreads to other vital organs like liver and lungs [7]. Figure 3 depicts the different stages of CRC.
Gut Bacteroides species in health and disease
Published in Gut Microbes, 2021
Around 5% of colorectal cancers occur in individuals who have an inherited mutation.133 Familial adenomatous polyposis is a hereditary condition caused by germline mutations in the adenomatous polyposis coli tumor suppressor gene.134 In this genetic background, numerous adenomatous polyps form in the epithelium of the colon, and malignant transformation may lead to colorectal cancer. Dejea et al. examined surgically resected tissue of patients with familial adenomatous polyposis and found that Bfr and E. coli (positive for the polyketide synthase (pks) island responsible for the synthesis of genotoxic colibactin) dominated the observed biofilms.135 Further experiments in mice showed that mono-colonization with either species resulted in few to no tumors. However, tumorigenesis was observed in the mice colonized with both species. In vitro trials using mucin monolayers indicated that degradation of mucin by Bfr enhanced colonization by E. coli. Thus, a shift in the niche of this species could facilitate the delivery of genotoxic colibactin to colonic epithelial cells, increasing the risk of mutations in genes such as that of adenomatous polyposis. This revealed another association of Bacteroides spp. with another gut resident, this time as a partner in crime for the initiation of colon tumorigenesis.