Annals of Coloproctology

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Case Report

Regression of Colonic Adenomas After Treatment With Sulindac in Familial Adenomatous Polyposis: A Case With a 2-Year Follow-up Without a Prophylactic Colectomy: Kyu Young Kim, Seong Woo Jeon, Jung Gil Park, Chung Hoon Yu, Se Young Jang, Jae Kwang Lee, Hee Young Hwang; Ann Coloproctol. 2014;30(4):201-204. Published online August 26, 2014; DOI: https://doi.org/10.3393/ac.2014.30.4.201

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Familial adenomatous polyposis (FAP) is an autosomal dominant disorder characterized by hundreds of colorectal adenomatous polyps that progress to colorectal cancer. Management of patients with FAP is with a total colectomy. Chemopreventive strategies have been studied in FAP patients in an effort to delay the development of adenomas in the upper and the lower gastrointestinal tract and to prevent recurrence of adenomas in the retained rectum of patients after prophylactic surgery. Sulindac, a nonsteroidal anti-inflammatory drug, causes regression of colorectal adenomas in the retained rectal segment of FAP patients. However, evidence regarding long-term use of this therapy and its effect on the intact colon has been insufficient. We report a case in which the long-term use of sulindac was effective in reducing the size and the number of colonic polyps in patients with FAP without a prophylactic colectomy and polypectomy; we also present a review of the literature.

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Emerging Strategies for Drug-Based Cancer Risk Reduction
Maria Daca-Álvarez, Angelo Brunori, Alessio Carbone, Chantelle Carbonell, Catherine M. Tangen, Joseph M. Unger, M. Scott Lucia, Martino Oliva, Andrea De Censi, Darren R. Brenner, Ian M. Thompson, Francesc Balaguer
American Society of Clinical Oncology Educational Book.2025;[Epub] CrossRef
Familial adenomatous polyposis: non-surgical management of large bowel disease: endoscopic and chemoprevention strategies
Maria Daca-Álvarez, Andrew Latchford, Maria Pellisé, Francesc Balaguer
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Sulindac sulfide suppresses oncogenic transformation through let-7b-mediated repression of K-Ras signaling
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Chemoprevention in hereditary digestive neoplasia: A comprehensive review
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Khalid Asadi, Lynnette R. Ferguson, Martin Philpott, Nishi Karunasinghe
Journal of Cancer Prevention.2017; 22(3): 135. CrossRef
Endogenous conversion of ω-6 to ω-3 polyunsaturated fatty acids infat-1 mice attenuated intestinal polyposis by either inhibiting COX-2/β-catenin signaling or activating 15-PGDH/IL-18
Young-Min Han, Jong-Min Park, Ji-Young Cha, Migyeong Jeong, Eun-Jin Go, Ki Baik Hahm
International Journal of Cancer.2016; 138(9): 2247. CrossRef
NOSH-sulindac (AVT-18A) is a novel nitric oxide- and hydrogen sulfide-releasing hybrid that is gastrointestinal safe and has potent anti-inflammatory, analgesic, antipyretic, anti-platelet, and anti-cancer properties
Khosrow Kashfi, Mitali Chattopadhyay, Ravinder Kodela
Redox Biology.2015; 6: 287. CrossRef
Sulindac

Reactions Weekly.2015; 1570(1): 198. CrossRef

Original Articles

A Combined Treatment of Tamoxifen, Goserelin, and Sulindac in 2 Cases of Recurrent Desmoid Tumor in the Abdomen.: Kim, Hee Cheol , Suh, Byung Sun , Lee, Dong Hee , Ahn, Byung Yool , Chung, Choon Sik , Kang, Gyeong hoon , Ha, Hyun Kwon , Kim, Jin Cheon; J Korean Soc Coloproctol. 1999;15(4):339-343.

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Abstract PDF: Desmoid tumor is a subtype of fibromatosis arising from deep fascial or soft tissue structure. It is characterized by locally aggressive behavior with a tendency to local recurrence, but is generally accepted the lack of ability for distant metastasis. Although excision is the best initial therapy, surgery is not always amenable in cases of lesions lying in difficult anatomical area. Two female patients with recurrent desmoid tumor in abdomen and pelvis after excision were treated with tamoxifen, goserelin, and sulindac. This therapy led to a progressive decrease of tumor size within 13 months in one patient. However, in the other patient, this combined therapy failed to reduce the size of the tumor. Despite the success of combined therapy with hormone and nonsteroidal anti-inflammatory drug is anecdotal, this treatment may improve the survival and reduce the recurrence in certain sub-group of desmoid tumor.

Effect of Lactacystin on the Sulindac-Induced Apoptosis Mechanisms in HT-29 Cells.: Kim, Jung Min , Park, Ki Jae , Kim, Sung Heun , Choi, Hong Jo; J Korean Soc Coloproctol. 2003;19(2):61-66.

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Abstract PDF: PURPOSE
One of possible mechanisms of the antineoplastic effect by nonsteroidal anti-inflammatory drugs (NSAIDs) is an induction of apoptosis. The NSAIDs-induced apoptosis appears to be caspase- and mitochondria-dependent. The ubiquitin-proteasome system, which is a fundamental non- lysosomal tool that cells use to process or degrade a variety of short-lived proteins, is known to be involved in apoptosis and to be located upstream of mitochondrial changes and caspase activation. The present study was conducted to explore the potential role of proteasome pathway in NSAIDs-induced apoptosis.
METHODS
We employed sulindac as a NSAID, and the lactacystin as a proteasome inhibitor to investigate the extent of the apoptosis in colon cancer cell line, HT-29 cells. The proteasome activity and the amount of apoptosis were quantified after cells were treated with 1 mM sulindac, 1micrometer lactacystin or both.
RESULTS
Sulindac treatment caused apoptosis of the HT-29 cells in a time-dependent manner with resultant changes in nuclear morphology. Western blots also showed caspase-3 activation and PARP cleavage after sulindac treatment. Not only single treatment with lactacystin decreased proteasome activity, but co-treatment with sulindac enhanced decrease in proteasome activity further (P<0.01). Treatment with lactacystin only did not induce apoptosis. However, lactacystin augmented the induction of sulindac-induced apoptosis (P<0.01). This synergistic effect was also proven by Western blot analyses, where co-treatment augmented the caspase-3 activation and PARP degradation.
CONCLUSIONS
The combination treatment of sulindac with a proteasome inhibitor lactacystin is suggested to be a very effective strategy for the induction of cancer cell apoptosis. Elucidation of the mechanism underlying the regression of colon cancers by combination of sulindac and lactacystin seems to be an immediate challenge in the near future.

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