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Autologous Hematopoietic Stem Cell Transplantation for Crohn’s Disease
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Robert M. Craig, Richard K. Burt
Over the past decade, there has been an increasing awareness that CD predisposes to malignant transformation, particularly in the colon, although not to the same extent as ulcerative colitis.47,48 In one group of patients with extensive Crohn’s colitis, the authors found an incidence of colonic carcinoma or dysplasia comparable to that found in CUC.45 Small intestinal cancer has also been reported in Crohn’s disease, usually in excluded segments of bowel. At this point it is not clear how prevalent Crohn’s colitis is complicated by cancer, and how this impacts on overall Crohn’s survival.
Cancer in IBD
Published in Peter Sagar, Andrew G. Hill, Charles H. Knowles, Stefan Post, Willem A. Bemelman, Patricia L. Roberts, Susan Galandiuk, John R.T. Monson, Michael R.B. Keighley, Norman S. Williams, Keighley & Williams’ Surgery of the Anus, Rectum and Colon, 2019
Several studies looked at risk factors for developing adenocarcinoma in the small intestine and concluded that strictures, chronic penetrating disease, young age at diagnosis and use of steroids and immunomodulators are amongst those.70 However, not all these factors demonstrated to be consistent throughout the studies, possibly due to the low incidence of small intestinal cancer.70 The ECCO consensus states that prolonged duration of stricturing disease may be associated with the development of small intestinal cancer in patients with Crohn’s disease. Due to the low absolute risk for small intestinal adenocarcinoma, there are no current screening guidelines.73 Indications for evaluation to detect a possible case of small bowel malignancy are prolonged duration of small bowel stricturing disease, symptomatic strictures after a prolonged period of remission and strictures that are refractory to medical therapy.70 Diagnostic modalities include CT, MRI, capsule endoscopy, double balloon enteroscopy or surgery.
Small Intestine Cancer
Published in Dongyou Liu, Tumors and Cancers, 2017
Andreas V. Hadjinicolaou, Christopher Hadjittofi
Neoplasms affecting the small intestine include primary benign tumors (adenoma, leiomyoma, fibroma, and lipoma), primary malignant tumors (adenocarcinoma, neuroendocrine tumor [NET], lymphoma, and sarcoma), and secondary tumors (lymphoma, melanoma, breast, lung, colon, and kidney tumors). Out of these, the most common histological types of primary small intestine cancer are adenocarcinoma (accounting for about 30% of small intestine malignancies), NET (or carcinoid tumor, 40%), lymphoma (20%), and sarcoma (10%).
A review of mammalian in vivo genotoxicity of hexavalent chromium: implications for oral carcinogenicity risk assessment
Published in Critical Reviews in Toxicology, 2021
Chad M. Thompson, Marilyn J. Aardema, Melissa M. Heintz, James T. MacGregor, Robert R. Young
In the AOP for small intestinal cancer arising from nongenotoxic mechanisms described in Bhat et al. (2020), two conditions were proposed for concluding that an intestinal carcinogen acts through a nongenotoxic MOA. The first condition is consistent evidence against genotoxicity in the intestine, ideally with corroborating dosimetry data in crypts and villi. The second condition is clear and consistent evidence for a plausible MOA containing key events that increase the chance of intestinal tumor formation such as, but not limited to, chronic regenerative hyperplasia. Evidence for the latter has been reviewed in several places (Thompson et al. 2013, 2017; Health Canada 2016; Moffat et al. 2018; Bhat et al. 2020), whereas this is the first such review of the in vivo oral genotoxicity of Cr(VI). Taken together, the MOA and genotoxicity data strongly support exploration and use of nonlinear risk assessment approaches for developing oral toxicity criteria for Cr(VI). Several organizations have already done so (Health Canada 2016; TCEQ 2016; FSCJ 2019; WHO 2019). Importantly, as new or improved genotoxicity assays and/or new guidance become available, information from future testing can be used to update and revise Cr(VI) risk assessments as warranted.