Breast cancer is one of the most common malignancies in females. It is an etiologically complex disease driven by a multitude of cellular pathways. The proliferation and spread of breast cancer is intimately linked to cellular glucose metabolism, given that glucose is an essential cellular metabolic substrate and that insulin signalling has mitogenic effects. Growing interest has focused on anti-diabetic agents in the management of breast cancer. Epidemiologic studies show that metformin reduces cancer incidence and mortality among type 2 diabetic patients.
The authors showed that metformin has a protective Free picture seductive sister on BC risk among postmenopausal females with diabetes. With Sandhya Pruthi, M. Evidence that metformin exerts its anti-diabetic effects through inhibition of complex 1 of the mitochondrial respiratory chain. Results obtained were limited by the observational nature of the reports and different comparison groups that were not age- race- or stage-matched. Results showed that metformin may reduce cancer incidence and mortality in diabetics, but the reduction is modest and does not affect all populations equally The limitations of the study included heterogeneity of study design and treatment comparators. Finally, we examined associations with an insulin genetic score comprising 18 insulin-associated variants see details below Diabetes breast enhancement drugs an instrument to proxy long-term exposure to circulating insulin levels. Hyperglycemia Diabetes breast enhancement drugs a risk factor for cancer progression. Activation of AMPK has been shown to inhibit the mammalian target of rapamycin mTOR and therefore inhibit pathological cell proliferation in different cancer cell lines [ 56 — 59 ] Figure 1 1.
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Metrics details. Long-term insulin exposure has been implicated in breast cancer etiology, but epidemiological evidence remains inconclusive. The aims of this study were to investigate the association of insulin therapy with mammographic density MD as an intermediate phenotype for breast cancer and to assess associations with long-term elevated circulating insulin levels using a genetic score comprising 18 insulin-associated variants.
We assessed associations with treatment duration and insulin glargine use, and we further examined MD differences using non-insulin-treated T2D patients as an active comparator. MD was measured using a fully automated volumetric method, and analyses were adjusted for multiple potential confounders.
Associations with the insulin genetic score were assessed in study participants without diabetes. Compared with age-matched women without diabetes, insulin-treated T1D patients had greater percent dense 8. Similar associations were observed for insulin-treated T2D, and estimates were not materially different in analyses comparing insulin-treated T2D patients with T2D patients receiving noninsulin glucose-lowering medication.
No consistent evidence of differential associations by insulin treatment duration or type was found for percent dense and absolute nondense volumes. The consistency in direction of association for insulin treatment and the insulin genetic score with the absolute dense volume suggest a causal influence of long-term increased insulin exposure on mammographic dense breast tissue.
The role of insulin in breast cancer etiology has received growing attention in recent years [ 1 ]. Basic research suggests that long-term exposure to elevated exogenous and endogenous insulins promotes breast tumor growth, either directly by signaling mitogenic effects through the insulin receptor isoform A and the insulin-like growth factor 1 IGF-1 receptor [ 2 , 3 ] or indirectly by altering the levels of circulating estrogens [ 4 ].
The potential carcinogenic effect of insulin has been demonstrated in vitro in terms of increased proliferation in human breast epithelial cells and breast cancer cell lines [ 2 , 3 ]. Whether these in vitro observations are relevant to humans and concerns surrounding risks of long-term exogenous insulin use and elevated circulating insulin levels are justified remains uncertain [ 5 , 6 , 7 , 8 ].
Thus far, observational studies [ 6 , 9 ] and randomized clinical trials [ 10 , 11 , 12 ] have found no compelling evidence of an increased breast cancer incidence in insulin-treated diabetes patients, although recently some studies have suggested a possible elevated risk with long-term insulin glargine use [ 5 , 13 , 14 ], which might be related to the more constant pharmacokinetic profile and enhanced IGF-1 receptor affinity of this insulin analog [ 15 , 16 ].
However, because of methodological limitations including short-term follow-up and confounding by indication, definitive conclusions cannot be drawn.
Many agents affecting carcinogenesis have long latencies and require a minimum length of exposure. Most studies addressing recency or duration effects had limited control for confounding factors or were insufficiently powered to assess associations with long-term insulin therapy [ 6 ].
While randomized clinical trials are limited in size and follow-up to study cancer-specific outcomes, confounding by indication is a concern in observational studies, and the use of different comparators is necessary to disentangle treatment effects from their underlying indications. Studies investigating associations of circulating insulin levels with breast cancer risk have also yielded conflicting results, with either positive [ 17 , 18 , 19 ] or null associations [ 20 ].
Most of these findings, however, were based on small numbers of breast cancer patients and a single insulin measurement, which is not an ideal proxy for long-term insulin exposure 18]. Mammographic density MD refers to the amount of radiologically dense fibroglandular tissue in the breast, and high MD levels are a strong and independent predictor of breast cancer risk [ 21 , 22 ].
Both traits also have several reproductive and lifestyle determinants in common, and MD is viewed as an intermediate phenotype in breast cancer etiology [ 23 ]. Because many insulin-treated diabetes patients are below the age at which breast cancer is usually diagnosed, and given the long latency of breast cancer, MD serves as an attractive intermediate endpoint for identifying potential carcinogenic effects. In the present study, we aimed to investigate the association of long-term insulin exposure with MD in a mammography screening cohort using different methodological approaches.
First, we assessed associations of insulin therapy with MD by comparing insulin-treated type 1 T1D and type 2 T2D diabetes patients with age-matched individuals without diabetes, overall and stratified by duration of insulin treatment and insulin glargine use.
Second, as an alternative means of overcoming confounding, we explored associations with an insulin genetic score in nondiabetic women. This score comprising 18 insulin-associated variants represents genetic predisposition to elevated circulating insulin levels over the life course. Because genotypes sort randomly at conception, genetic association analyses are less likely affected by confounding and hence can provide additional evidence of the likelihood of a causal effect of long-term increased insulin exposure [ 24 ].
This study was nested within the KARolinska MAmmography Project for Risk Prediction of Breast Cancer Karma , a prospective cohort of 70, women attending mammography screening or clinical mammography at one of four mammography units in Sweden between January and March [ 25 ]. Information on diabetes diagnoses and insulin prescriptions was retrieved through linkage with the Swedish Patient Register [ 26 ] and Prescribed Drug Register [ 27 ].
The Patient Register has nationwide coverage and includes inpatient hospitalizations since and outpatient physician visits since The Prescribed Drug Register covers all drugs sold and dispensed by prescription since July 1, Diabetes diagnoses were retrieved from the Karma questionnaire and Patient Register.
Using these prescription and diagnostic criteria, insulin-treated diabetes patients were identified, including T1D and T2D patients of whom 97 T1D [ For each patient, we randomly sampled up to five individuals without a diabetes diagnosis from the study base, matched on birth year. In total, 21 T2D patients could not be matched to a maximum of 5 individuals, leaving age-matched individuals without diabetes for analyses i.
Because insulin is the mainstay of therapy for T1D, we were unable to do a similar analysis for this group of patients. Finally, we examined associations with an insulin genetic score comprising 18 insulin-associated variants see details below as an instrument to proxy long-term exposure to circulating insulin levels. Associations with the insulin genetic score were assessed in a subcohort of participants with available genotyping data. All women in the subcohort had no history of cancer or diabetes at the time of study entry when blood samples were obtained.
The Karma study was approved by the ethical review committee at Karolinska Institutet, and all participants provided written informed consent. Volpara volumetric MD measures show good agreement with breast magnetic resonance imaging data [ 31 ] and have been validated as being predictive of breast cancer risk [ 30 , 32 ].
The Volpara algorithm estimates the thickness of dense tissue at each pixel using the X-ray attenuation of an entirely fatty region as an internal reference. The absolute dense volume cm 3 is computed by integrating the dense thickness at each pixel over the whole mammogram, and the total breast volume cm 3 is derived by multiplying the breast area by the recorded breast thickness, with an appropriate correction for the breast edge.
The average measurement of the left and right breasts of the mediolateral oblique view was taken for all analyses. Associations with the insulin genetic score were assessed in the Karma subcohort with genotyping data. Differences in MD by insulin therapy were analyzed using generalized linear models, including a basic model with adjustment for age and BMI and a multivariable model with inclusion of other potential confounders education level, age at menarche, parity and age at first birth, oral contraceptives, menopausal status, hormone replacement therapy, alcohol intake, smoking status, statins, low-dose aspirin, Charlson comorbidity index, history of benign breast disease, and family history of breast cancer.
Analyses were additionally adjusted for metformin comedication to account for potential antiproliferative effects of this diabetes drug [ 6 ]. Differences in MD were assessed overall and by insulin glargine use and treatment duration.
In T2D patients, treatment duration was defined from the first dispensed insulin prescription encountered in the Prescribed Drug Register. Because age at T1D onset is well below the age at which women undergo mammography screening, and with prescription data being available only from July onward, insulin treatment duration in T1D patients was calculated from the age at T1D diagnosis to study entry.
To address possible residual confounding by underlying disease, we also examined MD differences comparing insulin-treated with non-insulin-treated T2D patients. This active comparator analysis was adjusted for the same covariates as listed above and additionally for diabetes duration to account for differences in disease onset between the two patient groups. Associations with the insulin genetic score were assessed using linear regression, with beta values representing percentage differences in MD per 1-SD increment in the score.
Because there was no evidence of heterogeneity by genotyping array iCOGS vs. OncoArray , a one-sample approach was undertaken. Genetic score analyses were adjusted for age, BMI, menopausal status, genotyping array, and six principal components to account for population stratification.
To investigate the independence of genetic effects of other potential confounders, we also examined associations of the score with covariates entered in the insulin treatment analysis.
Missing values on covariates were imputed using multivariate multiple imputation with chained equations, and ten imputed datasets were generated [ 39 ]. As expected, insulin-treated T1D and T2D patients also presented with more comorbid conditions and were more often on statin and low-dose aspirin medications.
Univariate associations with other participant characteristics were comparable for the two patient groups, except for BMI and age at menarche. Study participants of the subcohort for genetic analysis had characteristics similar to those of the age-matched individuals without T2D, except for a larger proportion being premenopausal.
Compared with T2D patients receiving other glucose-lowering medication, insulin-treated T2D patients were younger, had a lower BMI, and were more likely to have comorbid conditions and a history of benign breast disease.
They also had a longer disease duration 8. Compared with age-matched women without diabetes, T1D patients had a greater percent dense These associations were not materially different after multivariable adjustment percent dense volume [ Compared with women without diabetes, the largest difference in absolute dense volume was found for current use of insulin glargine, whereas for percent dense and absolute nondense volumes, no notable difference in magnitude of association was observed by insulin type.
Overall, similar associations were found for insulin-treated T2D. Compared with age-matched individuals without diabetes, insulin-treated T2D patients had greater percent dense 7. Results of analyses by insulin treatment duration are summarized in Fig. Compared with age-matched individuals without diabetes, a gradual increase in absolute dense volume was found with duration of insulin treatment in T1D patients.
In T2D patients, a similar increase in absolute dense volume was observed with treatment duration. Associations of duration of insulin therapy with volumetric mammographic density in type 1 diabetes T1D and type 2 diabetes T2D patients. Model 1 open circles : adjusted for age and body mass index. Model 2 closed circles : adjusted for age, body mass index, education level, age at menarche, parity, age at first birth, menopausal status, oral contraceptives use, hormone replacement therapy, alcohol intake, physical activity, smoking status, statins, low-dose aspirin, Charlson comorbidity index, benign breast disease, family history of breast cancer, and metformin therapy.
Associations of the insulin genetic score with MD are shown in Fig. Genetically predicted insulin levels were positively associated with both percent dense and absolute dense volume Fig. Association of the insulin genetic score with volumetric mammographic density. Association of single-nucleotide polymorphism insulin genetic score with volumetric mammographic density in nondiabetic women, overall and stratified by genotyping array. Associations with volumetric mammographic density were analyzed in a linear regression model, adjusted for age, body mass index, menopausal status, and six principal components.
Analyses in the total study population were additionally adjusted for genotyping array. All volumetric mammographic density measures were log-transformed prior to analyses, with beta values representing percentage differences in volumetric mammographic density per 1-SD increase in insulin genetic score.
Associations with the absolute dense volume were driven mainly by long-term insulin use and the long-acting insulin analog glargine, whereas no associations with treatment duration or insulin type were found for the absolute nondense volume. We further observed positive associations of genetically predicted insulin levels with percent dense and absolute dense volumes, but not with absolute nondense volume. The consistency in direction of association for insulin treatment and the insulin genetic score with the absolute dense volume strengthen the evidence of a potential causal effect of long-term increased insulin exposure on mammographic dense breast tissue.
Observational studies and randomized clinical trials are limited in their ability to investigate associations of long-term insulin exposure with relatively rare outcomes such as breast cancer. As a continuous intermediate trait, MD represents an attractive endpoint for identifying potential carcinogenic effects [ 40 ]. Because MD was routinely collected in all study participants regardless of screening outcome, this outcome is also not susceptible to ascertainment bias. To date, only one study assessed associations between exogenous insulin use and MD.
Though previous observational data on breast cancer risk have been somewhat conflicting, recent findings [ 14 ] of a positive association between long-term insulin glargine use and breast cancer risk cohere with the results for the absolute dense volume reported herein. Altogether, these findings suggest that the carcinogenic potential of exogenous insulins might be greatest for insulin glargine, possibly because of its unique characteristics in terms of receptor affinity and pharmacokinetic profile with prolonged duration of action.
Because our study is observational in nature, we aimed to integrate evidence from different methodological approaches to assess the likelihood of a potential causal effect of long-term insulin exposure.
To address confounding by indication, we assessed associations with insulin-treated T1D and T2D separately. Because T1D and T2D differ in pathophysiology and underlying risk factors with T1D being an autoimmune disease, whereas insulin resistance, driven mainly by obesity, is the hallmark of T2D , consistent results for insulin-treated T1D and T2D are suggestive of an insulin therapy effect independent of underlying disease etiology.
This analysis approach using nondiabetics as a comparator, however, does not rule out confounding by the indication itself T1D or T2D. Hence, to address possible residual confounding, we also assessed MD differences by duration of insulin treatment and insulin glargine use in case-only analyses, and we performed additional analyses using non-insulin-treated diabetes patients as an active comparator.
Although none of these observational assessments may be completely free of bias, sources and directions of bias in each of these are likely to be different. Therefore, consistency of direction of association across the different approaches can be interpreted as evidence for a potential causal association.
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