Chemoprevention in familial adenomatous polyposis

Kim, Brian; Giardiello, Francis M.

doi:10.1016/j.bpg.2011.08.002

Cited by 88 publications

(65 citation statements)

References 91 publications

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“…At present, no optimal adjuvant chemotherapy exists for clinical use; therefore, developing rationally designed, novel adjuvant therapeutic tools for the treatment of colon cancer is a constant requirement (2). Previously, the use of natural substances, including curcumin, eicosapentaenoic acid, apple polyphenols, capsaicin and thymoquinone (TQ), for cancer chemoprevention has been investigated (3)(4)(5). TQ is the primary active ingredient of volatile Nigella sativa (black cumin) seed oil, which is used as a spice in countries with a low incidence of colorectal cancer, including Egypt, Pakistan and India (6).…”

Section: Introductionmentioning

confidence: 99%

Thymoquinone chemosensitizes colon cancer cells through inhibition of NF-κB

2016

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Abstract. In the present study, the effects and molecular mechanisms of thymoquinone (TQ) on colon cancer cells were investigated. Cell viability was determined using a Cell Counting Kit-8 assay, and the results revealed that treatment with TQ significantly decreased cell viability in COLO205 and HCT116 cells in a dose-dependent manner. TQ treatment additionally sensitized COLO205 and HCT116 cells to cisplatin therapy in a concentration-dependent manner. To investigate the molecular mechanisms of TQ action, western blot analysis was used to determine the levels of phosphorylated p65 and nuclear factor-κB (NF-κB)-regulated gene products vascular endothelial growth factor (VEGF), c-Myc and B-cell lymphoma 2 (Bcl-2). The results indicated that TQ treatment significantly decreased the level of phosphorylated p65 in the nucleus, which indicated the inhibition of NF-κB activation by TQ treatment. Treatment with TQ also decreased the expression levels of VEGF, c-Myc and Bcl-2. In addition, the inhibition of NF-κB activation with a specific inhibitor, pyrrolidine dithiocarbamate, potentiated the induction of cell death and caused a chemosensitization effect of TQ in colon cancer cells. Overall, the results of the present study suggested that TQ induced cell death and chemosensitized colon cancer cells by inhibiting NF-κB signaling.

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Section: Introductionmentioning

confidence: 99%

Thymoquinone chemosensitizes colon cancer cells through inhibition of NF-κB

2016

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“…Colectomy should be considered when the patient presents with more than 20 adenomas, with the diameter of the adenoma exceeding 1cm or advanced histology findings (Jasperson et al, 2010). Chemoprevention with medications such as nonsteroidal anti-inflammatory drugs (NSAID) and selective cyclooxygenase-2 (COX-2) inhibitors delay the development of adenomas and prevent recurrence of adenomas in the retained rectum after prophylactic surgery (Kim and Giardiello, 2011). Long term adverse effects of these medications limit their use as medication chemoprophylaxis.…”

Section: Discussionmentioning

confidence: 99%

Colon Cancer Prevention by Detection of APC Gene Mutation in a Family with Attenuated Familial Adenomatous Polyposis

Poovorawan

Suksawatamnuay²,

Sahakitrungruang³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Background: Genetic mutation is a significant factor in colon CA pathogenesis. Familial adenomatous polyposis (FAP) is an autosomal dominant hereditary disease characterized by multiple colorectal adenomatous polyps affecting a number of cases in the family. This report focuses on a family with attenuated familial adenomatous polyposis (AFAP) with exon 4 mutation, c.481C>T p.Q161X of the APC gene. Methods: We analyzed 20 members of a family with AFAP. Clinical and endoscopic data were collected for phenotype determination. Genetic analysis was also performed by direct sequencing of the APC gene. Result: Five patients with a phenotype of AFAP were found. Endoscopic polyposis was demonstrated among the second generation with genotype mutation of the disease (age > 50 years) consistent with delayed phenotypic adenomatous polyposis in AFAP. APC gene mutation was identified in exon 4 of the APC gene, with mutation points of c.481C>T p.Q161X. Laparoscopic subtotal colectomy was performed to prevent carcinogenesis. Conclusion: A family with attenuated familial adenomatous polyposis of APC related to exon 4 mutation, c.481C>T p.Q161X, was reported and the phenotypic finding was confirmed by endoscopic examination. Genetic mutation analysis might be advantageous in AFAP for long term colon cancer prevention and management due to subtle or asymptomatic phenotype presentation in early adulthood.

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“…Prostaglandins have been postulated in having a role in altering cell adhesion, inhibiting apoptosis and promoting angiogenesis [ 109 , 110 ], all important components that are implicated in transforming tumors from benign to malignant lesions. Subsequent studies have suggested that NSAIDS exert most of their antineoplastic effects via the inhibition of the COX-2 enzyme and inhibition of other biochemical pathways independent of COX suppression [ 111 ].…”

Section: Chemopreventionmentioning

confidence: 99%