Cancer among patients with type 2 diabetes mellitus: A population-based cohort study in northeastern Italy

Gini, Andrea; Bidoli, Ettore; Zanier, Loris; Clagnan, Elena; Zanette, Giorgio; Gobbato, Michele; Paoli, Paolo De; Serraino, Diego

doi:10.1016/j.canep.2016.01.011

Cited by 27 publications

(45 citation statements)

References 35 publications

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“…Regarding small intestine cancer, we found that adults with midlife diabetes had higher risk of small intestine cancer. Our results are in line with those reported by some studies showing that people with diabetes have 1.5‐ to 2.2‐fold higher risk of small intestine cancer . However, another study showed no association between diabetes and small intestine cancer in women .…”

Section: Discussionsupporting

confidence: 93%

“…8,9 However, results have been inconsistent regarding the forms of cancer for which diabetes may be a risk factor. 10,11 In some studies, diabetes has been associated with increased risk of liver, 12 breast, 13 oropharyngeal, 14 endometrial, 15 bladder 16 and kidney 17,18 cancers and a decreased risk of prostate cancer. [19][20][21] However, other studies did not find such associations.…”

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confidence: 99%

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Diabetes in midlife and risk of cancer in late life: A nationwide Swedish twin study

Bao

Pedersen

Yang

et al. 2018

Intl Journal of Cancer

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The association between diabetes and cancer risk remains controversial. Hence, we examined whether midlife diabetes is related to the risk of cancer in late-life, and whether genetic and early-life environmental factors play a role in this association. This study included 25,154 twin individuals born in 1958 or earlier from the Swedish Twin Registry. Information on cancer diagnosis in late life (aged ≥ 65) during 1998-2014, was derived from the National Patient and Cancer Registries. Diabetes was ascertained based on self- or informant-reported history, patient registry and antidiabetic medication use. Midlife diabetes was defined when diabetes was diagnosed before 65 years. Data were analyzed following two strategies: (i) unmatched case-control analysis for all participants using generalized estimating equation (GEE) models, and (ii) co-twin control analysis for cancer-discordant twin pairs using conditional logistic regression. Overall, 1,766 (7.0%) had midlife diabetes and 5,293 (21.0%) had cancer in late-life. In multiadjusted GEE models, the odds ratios (95% CIs) of diabetes were 10.55 (2.95-37.67) for pharynx cancer, 5.78 (1.72-19.40) for small intestine cancer, 2.37 (1.14-4.91) for liver cancer and 0.48 (0.35-0.67) for prostate cancer. In people with diabetes, diabetes duration was dose-dependently associated with cancer risk. In conditional logistic regression analysis of 176 prostate cancer-discordant twin pairs, the association between midlife diabetes and prostate cancer in later life became stronger. Midlife diabetes increases the risk of pharynx, small intestine and liver cancers, but reduces prostate cancer risk in late life. Genetic and early-life environmental factors may partially contribute to the diabetes-prostate cancer association.

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Section: Discussionsupporting

confidence: 93%

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confidence: 99%

Diabetes in midlife and risk of cancer in late life: A nationwide Swedish twin study

Bao

Pedersen

Yang

et al. 2018

Intl Journal of Cancer

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“…Because cancer risk among patients with T2D may vary by specific cancer site, we systematically investigated 23 common cancers. This study showed a significantly increased risk of overall cancer among patients with T2D, which is consistent with most previous studies . Increased risks were noted for 11 cancers in males, with SIRs ranging from 1.16 to 1.86, and 13 cancers in females, with SIRs ranging from 1.30 to 2.33.…”

Section: Discussionsupporting

confidence: 91%

Cancer risk among patients with type 2 diabetes: A real‐world study in Shanghai, China

Jing

Yao

et al. 2019

Journal of Diabetes

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Background The aim of this study was to investigate the risk of 23 common types of cancer among patients with type 2 diabetes (T2D) compared with the general Chinese population. Methods Based on the Shanghai Hospital Link database, 410 191 patients with T2D (age 20‐99 years) were identified from July 2013 to December 2016, and were followed‐up for cancer incidence until December 2017. Results In all, 8485 cases of newly diagnosed cancer were identified. The standardized incidence ratios (SIRs) of total cancer were 1.34 and 1.62 among males and females, respectively. Among males with T2D, the risk of cancer of the prostate (highest SIR of 1.86), blood (leukemia, lymphoma), skin, thyroid, kidney, liver, pancreas, lung, colorectum, and stomach was increased significantly. There was a significant decrease in the risk of esophageal cancer. In females with T2D, there were significantly greater risks of cancer of the nasopharynx (highest SIR of 2.33), liver, esophagus, thyroid, lung, pancreas, blood (lymphoma, leukemia), uterus, colorectum, breast, cervix, and stomach. In contrast, there was significantly decrease risk of gallbladder cancer in females with T2D. Conclusions This study shows significantly increased risks of overall and some site‐specific cancers among patients with T2D. We suggest that establishing strategies for regular cancer‐specific screening and prevention care among patients with T2D are necessary.

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“…In another study, it was found that pioglitazone use might increase the risk of cancers [Lewis et al, ]. Nevertheless, a population based study found an overall relationship between cancer and type II diabetes, with type II diabetic patients displaying a 28% higher cancer risk, especially for liver and pancreas [Gini et al, ]. These studies also found that diabetic patients with breast cancer had a lower 5‐year survival rate compared to patients without diabetes [Gini et al, ].…”

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confidence: 99%

“…Nevertheless, a population based study found an overall relationship between cancer and type II diabetes, with type II diabetic patients displaying a 28% higher cancer risk, especially for liver and pancreas [Gini et al, ]. These studies also found that diabetic patients with breast cancer had a lower 5‐year survival rate compared to patients without diabetes [Gini et al, ]. Additionally, a pilot study of women with breast cancer undergoing short term rosiglitazone treatment did not demonstrate significant effects on breast tumor growth [Yee et al, ].…”

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confidence: 99%

PPARγ Modulation of Cytokine‐Stimulated MUC16 (CA125) Expression in Breast and Ovarian Cancer‐Derived Cells

Morgado

Carson

2016

J of Cellular Biochemistry

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CA125 is serum tumor marker consisting of an epitope carried by a portion of the extremely large (>3 MDa), heavily glycosylated cell surface transmembrane mucin, MUC16. In malignancies, membrane bound mucins lose their polarized distribution, become aberrantly over-expressed and protect tumor cells from the actions of chemotherapeutic agents as well as the immune system. Previously, we described stimulation of MUC16 expression by the proinflammatory cytokines, tumor necrosis factor α (TNFα) and interferon γ (IFNγ), in breast and ovarian cancer cells and tissues. Herein, we show that PPARγ modulates cytokine-stimulated MUC16 in a complex manner: at low concentrations (<10 µM) rosiglitazone further potentiates cytokine-driven MUC16 expression while at high concentrations (>20 µM) rosiglitazone antagonizes cytokine stimulation. Rosiglitazone actions were fully reversible by the PPARγ antagonist, GW9662. Furthermore, siRNA-mediated PPARγ knockdown also prevented a large portion of high dose rosiglitazone suppression of MUC16 expression indicating that rosiglitazone inhibition is largely PPARγ-dependent. Cytokines greatly (>75%) suppressed PPARγ expression. Conversely, PPARγ activation by rosiglitazone at either low or high concentrations greatly (>75%) suppressed NFκB/p65 expression. NFκB/p65 expression was largely preserved in the presence of cytokines at low, but not high, rosiglitazone concentrations accounting for the different concentration dependent effects on MUC16 expression. Collectively, these studies demonstrate that PPARγ is an important modulator of MUC16 expression. The ability to deliver high doses of PPARγ agonists to MUC16-expressing tumors offers an avenue to reduce expression of this protective glycoprotein and increase tumor sensitivity to killing by chemotherapeutic drugs and the immune system. J. Cell. Biochem. 118: 163-171, 2017. © 2016 Wiley Periodicals, Inc.

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Cancer among patients with type 2 diabetes mellitus: A population-based cohort study in northeastern Italy

Cited by 27 publications

References 35 publications

Diabetes in midlife and risk of cancer in late life: A nationwide Swedish twin study

Diabetes in midlife and risk of cancer in late life: A nationwide Swedish twin study

Cancer risk among patients with type 2 diabetes: A real‐world study in Shanghai, China

PPARγ Modulation of Cytokine‐Stimulated MUC16 (CA125) Expression in Breast and Ovarian Cancer‐Derived Cells

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