ArticleCancer science2010
Insulin-independent promotion of chemically induced hepatocellular tumor development in genetically diabetic mice.
Article in Cancer science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- The crosstalk within the breast tumor microenvironment in type II diabetes: Implications for cancer disparities.Frontiers in endocrinology · 2022Review
- Legacy effect of high glucose on promoting survival of HCT116 colorectal cancer cells by reducing endoplasmic reticulum stress response.American journal of cancer research · 2021Article
- Hyperinsulinaemia in cancer.Nature reviews. Cancer · 2020Review
- Evolution of Diabetes Care in Hong Kong: From the Hong Kong Diabetes Register to JADE-PEARL Program to RAMP and PEP Program.Endocrinology and metabolism (Seoul, Korea) · 2018Review
- Dietary sugar intake increases liver tumor incidence in female mice.Scientific reports · 2016Article
- NOTCH2 signaling confers immature morphology and aggressiveness in human hepatocellular carcinoma cells.Oncology reports · 2015Article
- Drug-subphenotype interactions for cancer in type 2 diabetes mellitus.Nature reviews. Endocrinology · 2015Review
- Diabetes and cancer: Associations, mechanisms, and implications for medical practice.World journal of diabetes · 2014Review
- Additive effects of blood glucose lowering drugs, statins and renin-angiotensin system blockers on all-site cancer risk in patients with type 2 diabetes.BMC medicine · 2014Article
- Diabetes and risk of cancer.ISRN oncology · 2013Article
- Cancer incidence and mortality in patients with type 2 diabetes treated with human insulin: a cohort study in Shanghai.PloS one · 2013Article
- Diabetes, insulin and cancer risk.World journal of diabetes · 2012Article
- Metformin prevents liver tumorigenesis by inhibiting pathways driving hepatic lipogenesis.Cancer prevention research (Philadelphia, Pa.) · 2012Article
- Fascin-1 expression correlates with repression of E-cadherin expression in hepatocellular carcinoma cells and augments their invasiveness in combination with matrix metalloproteinases.Cancer science · 2011Article
- Meta-analysis of trial data may support a causal role of hyperglycaemia in cancer.Diabetologia · 2011Article
- Enhanced tumorigenesis of forestomach tumors induced by N-Methyl-N'-nitro-N-nitrosoguanidine in rats with hypoinsulinemic diabetes.Cancer science · 2010Article
- Inflammation and oncogenesis: a vicious connection.Current opinion in genetics & development · 2010Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes mellitus has been proposed as an epidemiological risk factor for human liver cancer development. One reasonable possibility is that this is attributable to hyperinsulinemia compensatory for obesity-related insulin resistance. However, diabetes mellitus is a complex disease with multiple abnormal conditions essentially caused by hyperglycemia. Therefore, it is not evident whether hyperinsulinemia is prerequisite for the elevated cancer risk. To gain a clue to answer this question, we characterized chemically induced hepatocarcinogenesis in diabetic model mice genetically deficient for insulin. Akita inbred mice originating from the C57BL/6 strain carry a heterozygous germline mutation of the insulin II gene and suffer from inherited insulin deficiency and diabetes in an autosomal dominant manner. They were mated with normal C3H/HeJ mice with high sensitivity to liver carcinogenesis and the resultant F(1) littermates, which were either normal or insulin deficient, were exposed to diethylnitrosamine and induced hepatocellular tumors were evaluated for number, size, proliferative activity, and apoptosis. Unexpectedly, both mean and total volumes of hepatocellular tumors in the insulin-deficient animals were more than twofold larger than those in the normal controls, with no significant difference in tumor number. The tumors in insulin-deficient mice showed a significantly lower frequency of apoptosis but no alteration in cell proliferation. In conclusion, our results indicate that insulin-independent liver tumor promotion occurred in diabetic mice. Clearly, insulin-independent mechanisms for the human case also deserve consideration.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.