Benign Neoplasms of the Colon and Rectum
Philip H. Gordon, Santhat Nivatvongs, Lee E. Smith, Scott Thorn Barrows, Carla Gunn, Gregory Blew, David Ehlert, Craig Kiefer, Kim Martens in Neoplasms of the Colon, Rectum, and Anus, 2007
The concept that carcinomas of the colon and rectum derived from benign adenoma was observed by C. Dukes of St. Mark’s Hospital, London, in 1926. Numerous studies, based on tumor registry reports, hospital records, pathology reports, surgical specimens, and colonoscopy show a coexistence of adenomas and adenocarcinomas of the colon and rectum ranging from 13% to 62%. Colonoscopy has revolutionized the management of large bowel polyps. Most polyps throughout the entire colon and rectum can be excised through the colonoscope with minimal morbidity. Polyps of the colon and rectum that are too numerous for colonoscopy and polypectomies should have an abdominal colectomy with ileorectal anastomosis or proctocolectomy with ileal pouch-anal anastomosis or an ileostomy. M. Miettinen et al studied all the mesenchymal neoplasms involving the rectum and anus coded as leiomyoma, leiomyosarcoma, smooth muscle neoplasm, schwannomas, neurofibromas, nerve sheath, stromal neoplasm.
Large Bowel Carcinoma: Screening, Surveillance, and Follow-Up
Philip H. Gordon, Santhat Nivatvongs, Lee E. Smith, Scott Thorn Barrows, Carla Gunn, Gregory Blew, David Ehlert, Craig Kiefer, Kim Martens in Neoplasms of the Colon, Rectum, and Anus, 2007
Survival for colon and rectal carcinoma is closely related to the clinical and pathologic stage of the disease at diagnosis. Colorectal carcinoma fulfills all the criteria for justified screening. Screening identifies individuals who are more likely to have colorectal carcinoma or adenomatous polyps from among those without signs or symptoms of disease. The goal of screening for colorectal carcinoma is to reduce mortality from the disease. Screening people at average risk for colorectal carcinoma is different from screening people at high risk. Clinicians should determine an individual patient’s risk status well before the earliest potential initiation of screening. Case-controlled studies have reported that sigmoidoscopy was associated with reduced mortality for colorectal carcinoma. A randomized controlled trial of sigmoidoscopy with follow-up colonoscopy for all patients with polyps compared with no screening demonstrated a significant reduction in colorectal carcinoma incidence in the screened patients.
Laparoscopic Colon and Rectal Surgery
Philip H. Gordon, Santhat Nivatvongs, Lee E. Smith, Scott Thorn Barrows, Carla Gunn, Gregory Blew, David Ehlert, Craig Kiefer, Kim Martens in Neoplasms of the Colon, Rectum, and Anus, 2007
Colectomy is termed an advanced laparoscopic technique because the colon is a large, mobile organ, spanning each abdominal quadrant, a specimen must be removed intact, and an anastomosis is often required; therefore, the visualization and dissection of the colon must move from abdominal quadrant to quadrant. Advocates of laparoscopic colectomy believe that the shorter hospital stay and better quality of life clearly qualify as advantages, but equipment is clearly more expensive, and an exact evaluation is often difficult because of the sometimes-perverted calculations that may involve actual cost or charges to patients. Hand-assisted laparoscopic surgery is a technique that involves the intra-abdominal placement of a hand or a forearm through a minilaparotomy incision while pneumoperitoneum is maintained. The identification of small neoplasms or areas presenting lesions associated with previous endoscopic polypectomy is one of the major problems in laparoscopic colon resection.
Th22 cells control colon tumorigenesis through STAT3 and Polycomb Repression complex 2 signaling
Published in OncoImmunology, 2016
Danfeng Sun, Yanwei Lin, Jie Hong, Haoyan Chen, Nisha Nagarsheth, Dongjun Peng, Shuang Wei, Emina Huang, Jingyuan Fang, Ilona Kryczek, Weiping Zou
ABSTRACT Th22 cells traffic to and retain in the colon cancer microenvironment, and target core stem cell genes and promote colon cancer stemness via STAT3 and H3K79me2 signaling pathway and contribute to colon carcinogenesis. However, whether Th22 cells affect colon cancer cell proliferation and apoptosis remains unknown. We studied the interaction between Th22 cells and colon cancer cells in the colon cancer microenvironment. Colon cancer proliferation was examined by flow cytometry analysis and H3 thymidine incorporation. Cell cycle related genes were quantified by real-time PCR and Western blotting. We transfected colon cancer cells with lentiviral vector encoding specific gene shRNAs and used chromatin immunoprecipitation (ChIP) assay to determine the genetic signaling involved in interleukin (IL)-22-mediated colon cancer cell proliferation. We showed that Th22 cells released IL-22 and stimulated colon cancer proliferation. Mechanistically, IL-22 activated STAT3, and subsequently STAT3 bound to the promoter areas of the Polycomb Repression complex 2 (PRC2) components SUZ12 and EED, and stimulated the expression of PRC2. Consequently, the activated PRC2 catalyzed the promoters of the cell cycle check-point genes p16 and p21, and inhibited their expression through H3K27me3-mediated histone methylation, and ultimately caused colon cancer cell proliferation. Bioinformatics analysis revealed that the levels of IL-22 expression positively correlated with the levels of genes controlling cancer proliferation and cell cycling in colon cancer. In addition to controlling colon cancer stemness, Th22 cells support colon carcinogenesis via affecting colon cancer cell proliferation through a distinct histone modification.
S-methyltransferases in human intestine: differential distribution of the microsomal thiol methyltransferase and cytosolic thiopurine methyltransferase along the human bowel
Published in Xenobiotica, 1993
G. M. Pacifici, P. Romiti, S. Santerini, L. Giuliani
1. The activities of the microsomal thiol methyltransferase and the cytosolic thiopurine methyltransferase were measured with 2-mercaptoethanol and 6-mercaptopurine as substrates in human ileum, ascending colon, transverse colon, descending colon and liver. 2. Thiol methyltransferase activity (pmol/min per mg) (mean±SD) was 495±280 (ileum), 786±454 (ascending colon), 1791±233 (transverse colon), 964±484 (descending colon) and 4800±1194 (liver). 3. Thiopurine methyltransferase (pmol/min per mg) (mean±SD) was 53.5±15.4 (ileum), 34.6±11.4 (ascending colon), 64.3±12.1 (transverse colon), 57.0±10.1 (descending colon) and 106±20.4 (liver). 4. Transferases in intestinal mucosa followed non-Michaelis-Menten kinetics, and two phases representing high and low affinity forms, for the acceptor methyl substrates were observed. 5. Comparison of intestinal with hepatic activities showed that thiopurine methyltransferase is better expressed than thiol methyltransferase in the human intestine, at least with the substrates studied.
Microenvironment influence on human colon adenocarcinoma phenotypes and matrix metalloproteinase-2, p53 and β-catenin tumor expressions from identical monoclonal cell tumor in the orthotopic model in athymic nude rats
Published in Scandinavian Journal of Gastroenterology, 2014
Denise Gonçalves Priolli, Ana Margarida Abrantes, Silvia Neves, Ana Cristina Gonçalves, Camila Oliveira Lopes, Natalia Peres Martinez, Izilda Aparecida Cardinalli, Ana Bela Sarmento Ribeiro, Maria Filomena Botelho
The present study aims to identify differences between left and right colon adenocarcinoma arising from identical clonal cell and to find out if microenvironment has any influence on matrix metalloproteinase-2 (MMP2), p53 and β-catenin tumor expressions. Material and methods. Rats (RNU) were submitted to cecostomy to obtain the orthotopic model of right colon tumor (n = 10), while for the left colon model (n = 10), a colon diversion and distal mucous fistula in the descending colon was used. Cultivated human colon adenocarcinoma cells (WiDr) were inoculated in stomas submucosa. Histopathological analysis, real-time reverse transcription-PCR for β-catenin, p53 and MMP2, as well as immunohistochemical analysis for p53 and β-catenin expression were conducted. Central tendency, variance analysis and the Livak delta-delta–CT method were used for statistical analysis, adopting a 5% significance level. Results. All tumors from the left colon exhibited infiltrative ulceration, while in the right colon tumor growth was predominantly exophytic (67%). In the left colon, tumor growth was undifferentiated (100%), while it was moderately differentiated in the right colon (83%). In right colon tumors, MMP2, p53, and β-catenin gene expressions were higher than compared to left colon (p = 4.59354E-05, p = 0.0035179, p = 0.00093798, respectively, for MMP2, p53 and β-catenin). β-catenin and p53 results obtained by real-time polymerase chain reaction were confirmed by immunohistochemistry assay (p = 0.01 and p = 0.001, respectively, for β-catenin and p53). Conclusion. Left and right human colon adenocarcinomas developed in animal models have distinct phenotypes even when they have the same clonal origin. Microenvironment has influenced p53, β-catenin, and MMP2 expression in animal models of colon cancer.