Long-term safety of Infliximab for the treatment of inflammatory bowel disease: does blocking TNF  reduce colitis-associated colorectal carcinogenesis?

Biancone, Livia; Petruzziello, C.; Calabrese, Emma; Zorzi, Francesca; Naccarato, Patrizia; Onali, S.; Pallone, Francesco

doi:10.1136/gut.2008.176461

Cited by 18 publications

(5 citation statements)

References 7 publications

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“…30 Targeting TNF-a has therefore been suggested for treating colitisassociated colon cancers, as in ulcerative colitis (UC). 30 Whether targeting TNF may reduce the cancer risk associated with chronic inflammation in IBD needs further investigation, 31 as other antiinflammatory drugs (i.e., mesalazine) have already been shown to exert this effect. 32 The present findings therefore support that infliximab use does not increase the cancer risk in the long term.…”

Section: Discussionmentioning

confidence: 99%

Cancer in Crohnʼs Disease patients treated with infliximab: A long-term multicenter matched pair study

Biancone

Petruzziello

Orlando

et al. 2011

Inflammatory Bowel Diseases

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Section: Discussionmentioning

confidence: 99%

Cancer in Crohnʼs Disease patients treated with infliximab: A long-term multicenter matched pair study

Biancone

Petruzziello

Orlando

et al. 2011

Inflammatory Bowel Diseases

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“…Patients who have been exposed to anti-TNF antibodies were determined to be at increased risk of developing cancers, in a study that included patients who developed colon cancer (Bongartz et al, 2006). However, no safety concerns regarding the incidence of IBD-associated colon carcinoma were identified in a recent study of patients who were administered infliximab (Biancone et al, 2009). …”

Section: Cytokinesmentioning

confidence: 99%

Inflammatory bowel disease and intestinal cancer: a paradigm of the Yin–Yang interplay between inflammation and cancer

Danese¹,

2010

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Colon cancer represents a paradigm for the connection between inflammation and cancer in terms of epidemiology and mechanistic studies in preclinical models. Key components of cancer promoting inflammation include master transcription factors (for example, nuclear factor jB, STAT3), proinflammatory cytokines (for example, tumor necrosis factor, interleukin-6 (IL-6)), cyclooxygenase-2 and selected chemokines (for example, CCL2). Of no less importance are mediators that keep inflammation in check, including IL-10, transforming growth factorb, toll-like receptor and the IL-1 receptor inhibitor TIR8/ SIGIRR, and the chemokine decoy and scavenger receptor D6. Dissection of molecular pathways involved in colitis-associated cancer may offer opportunities for innovative therapeutic strategies.

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“…However, while it efficiently blocks the tumor formation in AOM-induced CAC model, the efficacy of Etanercept in IBD is quite limited as compared to monoclonal antibodies directed against TNF α (e.g., Infliximab) [ 138 ]. In contrast, anti-TNF antibodies show unclear efficacy (anti- or procarcinogenic effects) in colorectal cancer development [ 139 , 140 ].…”

Section: Involvement Of Soluble Mediators In Cacmentioning

confidence: 99%

Animal Models of Colitis‐Associated Carcinogenesis

Kanneganti

Mino‐Kenudson

Mizoguchi

2011

BioMed Research International

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Inflammatory bowel disease (IBD) is a group of chronic inflammatory disorders that affect individuals throughout life. Although the etiology and pathogenesis of IBD are largely unknown, studies with animal models of colitis indicate that dysregulation of host/microbial interactions are requisite for the development of IBD. Patients with long-standing IBD have an increased risk for developing colitis-associated cancer (CAC), especially 10 years after the initial diagnosis of colitis, although the absolute number of CAC cases is relatively small. The cancer risk seems to be not directly related to disease activity, but is related to disease duration/extent, complication of primary sclerosing cholangitis, and family history of colon cancer. In particular, high levels and continuous production of inflammatory mediators, including cytokines and chemokines, by colonic epithelial cells (CECs) and immune cells in lamina propria may be strongly associated with the pathogenesis of CAC. In this article, we have summarized animal models of CAC and have reviewed the cellular and molecular mechanisms underlining the development of carcinogenic changes in CECs secondary to the chronic inflammatory conditions in the intestine. It may provide us some clues in developing a new class of therapeutic agents for the treatment of IBD and CAC in the near future.

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Long-term safety of Infliximab for the treatment of inflammatory bowel disease: does blocking TNF reduce colitis-associated colorectal carcinogenesis?

Cited by 18 publications

References 7 publications

Cancer in Crohnʼs Disease patients treated with infliximab: A long-term multicenter matched pair study

Cancer in Crohnʼs Disease patients treated with infliximab: A long-term multicenter matched pair study

Inflammatory bowel disease and intestinal cancer: a paradigm of the Yin–Yang interplay between inflammation and cancer

Animal Models of Colitis‐Associated Carcinogenesis

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