Circulating growth factors data associated with insulin secretagogue use in women with incident breast cancer.
Ontology highlight
ABSTRACT:
SUBMITTER: Wintrob ZA
PROVIDER: S-EPMC5338905 | biostudies-literature | 2017 Apr
REPOSITORIES: biostudies-literature
Publications
Circulating growth factors data associated with insulin secretagogue use in women with incident breast cancer.
Wintrob Zachary A P ZA Hammel Jeffrey P JP Nimako George K GK Gaile Dan P DP Forrest Alan A Ceacareanu Alice C AC
Data in brief 20170222
Oral drugs stimulating insulin production may impact growth factor levels. The data presented shows the relationship between pre-existing insulin secretagogues use, growth factor profiles at the time of breast cancer diagnosis and subsequent cancer outcomes in women diagnosed with breast cancer and type 2 diabetes mellitus. A Pearson correlation analysis evaluating the relationship between growth factors stratified by diabetes pharmacotherapy and controls is also provided. ...[more]
Similar Datasets
Project description:Oral drugs stimulating endogenous insulin production (insulin secretagogues) may have detrimental effects on breast cancer outcomes. The data presented shows the relationship between pre-existing insulin secretagogues use, adipokine profiles at the time of breast cancer (BC) diagnosis and subsequent cancer outcomes in women diagnosed with BC and type 2 diabetes mellitus (T2DM). The Pearson correlation analysis evaluating the relationship between adipokines stratified by T2DM pharmacotherapy and controls is also provided. This information is the extension of the data presented and discussed in "Insulin use, adipokine profiles and breast cancer prognosis" (Wintrob et al., in press) [1].
| S-EPMC5155039 | biostudies-literature
Project description:Monocytes' infiltration into the tumor tissue and their activation to tumor-associated macrophages is an essential step in tumor development, also playing a critical role in an eventual metastasis. Stimulation of endogenous insulin production by oral insulin secretagogue treatment has the potential to interfere with the production and release of C-C chemokines, a group of potent inflammatory cytokines acting as monocyte chemo-attractants and influencing their behavior in the tumor microenvironment. Studied plasma samples were collected under a previously reported study design involving a population of women diagnosed with breast cancer presenting with or without type 2 diabetes mellitus at the time of breast cancer diagnosis (Wintrob et al., 2017, 2016) [1,2]. The data presented here shows the relationship between pre-existing use of insulin secretagogue, the inflammatory C-C chemokine profiles at the time of breast cancer diagnosis, and subsequent cancer outcomes. A Pearson correlation analysis stratified by secretagogue use and controls was implemented to evaluate the relationship between the investigated biomarkers and respectively each of these biomarkers and the other relevant reported cytokine datasets derived from the same patient population (Wintrob et al., 2017, 2016) [1,2].
| S-EPMC5331147 | biostudies-literature
Project description:GM-CSF and G-CSF are widely used for their benefit in reducing chemotherapy-associated neutropenia. However, whether GM- or G-CSF administration could have tumorigenic or pro-metastatic effects or whether insulin resistance could negatively impact such effects is not known. Their ability to stimulate monocyte production at the same time with the highly sought after neutrophils' production, enables an enhanced potential for activation of tumor-associated macrophages. At the same time, IL-7 remains the main driver of B and T cell differentiation and maturation, a process linked to the development of insulin resistance and response to diabetes pharmacotherapy. Insulin secretagogues have the potential to interfere with the hematopoiesis process, respectively with the formation of lineages that may lead to a tumorigenic or pro-metastatic phenotype, but this relationship has not been yet investigated. The data presented here shows the relationship between pre-existing use of insulin secretagogues in women diagnosed with breast cancer and type 2 diabetes mellitus, the GM-CSF, G-CSF and IL-7 cytokine profiles at the time of breast cancer diagnosis, and subsequent cancer outcomes. A Pearson correlation analysis evaluating the relationship between investigated cytokines stratified by secretagogue use and controls, and interferon is also provided.
| S-EPMC5328709 | biostudies-literature
Project description:Background: Studies on the association between circulating insulin-like growth factor 1 (IGF1) and prognosis of breast cancer are limited. Whether this association is modified by insulin levels and clinical characteristics is unclear. Methods: Serum concentrations of IGF1 as well as IGF binding protein 3 (IGFBP3), IGF1/IGFBP3 ratio, insulin, and C-peptide were prospectively examined in 2,682 invasive breast cancer patients who received surgery in Ruijin Hospital, Shanghai, between 2012 and 2017. Cox proportional hazards models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause mortality, breast cancer-specific mortality, and breast cancer recurrence associated with different levels of IGF1 and other biomarkers with multivariable adjustment. Results: Compared with patients with low IGF1, patients with high IGF1 had a significantly lower risk of all-cause mortality (HR, 0.53; 95% CI, 0.29-0.96) and a borderline lower risk of breast cancer-specific mortality (HR, 0.53; 95% CI, 0.27-1.02). The inverse association between IGF1 and all-cause mortality was consistent across stratification subgroups but was more pronounced among patients with high insulin (HR, 0.40; 95% CI, 0.18-0.89), were premenopausal (HR, 0.34; 95% CI, 0.12-0.97), with a tumor size >2 cm (HR, 0.35; 95% CI, 0.17-0.73), with positive lymph node (HR, 0.49; 95% CI, 0.25-0.98), and with a high Ki-67 level (HR, 0.49; 95% CI, 0.26-0.95) (all P for interaction >0.05). No significant associations were found for IGFBP3, IGF1/IGFBP3 ratio, insulin, and C-peptide levels with all-cause mortality, breast cancer-specific mortality, and breast cancer recurrence. Conclusion: Circulating IGF1 was inversely and independently associated with all-cause mortality in invasive breast cancer patients, and this association was consistent across clinical risk factors.
| S-EPMC7466632 | biostudies-literature
Project description:The purpose of this study was to evaluate whether antihypertensive medication use, including long-term use, is associated with increased breast cancer incidence in women. We studied 210,641 U.S. registered nurses participating in the Nurses' Health Study (NHS) and Nurses' Health Study II (NHS II). Information on antihypertensive medication use was collected on biennial questionnaires in both cohorts, and breast cancer cases were ascertained during this period. Multivariable-adjusted Cox proportional hazard models were used to estimate relative risks of invasive breast cancer over follow-up (1988-2012 in NHS, 1989-2011 in NHS II) across categories of overall antihypertensive medication use and use of specific classes (diuretics, beta blockers, calcium channel blockers, and angiotensin-converting enzyme inhibitors). During follow-up, 10,012 cases of invasive breast cancer developed (6718 cases in NHS and 3294 in the NHS II). Overall, current use of any antihypertensive medication was not associated with breast cancer risk compared with past/never use in NHS (multivariable-adjusted relative risk = 1.00, 95 % CI = 0.95-1.06) or NHS II (multivariable-adjusted relative risk = 0.94, 95 % CI = 0.86-1.03). Furthermore, no specific class of antihypertensive medication was consistently associated with breast cancer risk. Results were similar when we considered hypertensive women only, and when we evaluated consistency and duration of medication use over time. Overall, antihypertensive medication use was largely unrelated to the risk of invasive breast cancer among women in the NHS cohorts.
| S-EPMC4381798 | biostudies-literature
Project description:Growth factor profiles could be influenced by the utilization of exogenous insulin. The data presented shows the relationship between pre-existing use of injectable insulin in women diagnosed with breast cancer and type 2 diabetes mellitus, the growth factor profiles at the time of breast cancer diagnosis, and subsequent cancer outcomes. A Pearson correlation analysis evaluating the relationship between growth factors stratified by of insulin use and controls is also provided.
| S-EPMC5315441 | biostudies-literature
Project description:ObjectiveTo examine whether genetically predicted variation in circulating insulin-like growth factor 1 (IGF1) or its binding protein, IGFBP3, are associated with risk of Alzheimer disease (AD), using a mendelian randomization study design.MethodsWe first examined disease risk by genotypes of 9 insulin-like growth factor (IGF)-related single nucleotide polymorphisms (SNPs) using published summary genome-wide association statistics from the International Genomics of Alzheimer's Project (IGAP; n = 17,008 cases; 37,154 controls). We then assessed whether any SNP-disease results replicated in an independent sample derived from the Swedish Twin Registry (n = 984 cases; 10,304 controls).ResultsMeta-analyses of SNP-AD results did not suggest that variation in IGF1, IGFBP3, or the molar ratio of these affect AD risk. Only one SNP appeared to affect AD risk in IGAP data. This variant is located in the gene FOXO3, implicated in human longevity. In a meta-analysis of both IGAP and secondary data, the odds ratio of AD per FOXO3 risk allele was 1.04 (95% confidence interval 1.01-1.08; p = 0.008).ConclusionsThese findings suggest that circulating IGF1 and IGFBP3 are not important determinants of AD risk. FOXO3 function may influence AD development via pathways that are independent of IGF signaling (i.e., pleiotropic actions).
| S-EPMC5798653 | biostudies-literature
Project description:BackgroundDyslipidaemias are common in patients with diabetes mellitus. A high prevalence of type 2 diabetes in hyperlipidaemic patients also exists. The aim of this study was to find a treatment that lowers both blood glucose and lipid levels simultaneously.MethodsThe hypolipidaemic effect of (R)-(-)-carvone was investigated in a tyloxapol-induced hyperlipidaemia mice model. Furthermore, its effect on insulin secretion and proliferation of 1.1E7 human pancreatic β-cells was studied. In addition, using molecular docking, the binding affinity of (R)-(-)-carvone against 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase was estimated.Results(R)-(-)-carvone (100 mg/kg) decreased plasma triglyceride, total cholesterol, low-density lipoprotein cholesterol (LDL-C) levels and atherogenic index by 90.6%, 49.3%, 56.6% and 70.3%, respectively, but it had no effect on high-density lipoprotein cholesterol (HDL-C). Furthermore, it increased hepatic triglyceride level and catalase activity by 79.6% and 59.6%, respectively. In-vitro, 500 μM (R)-(-)-carvone increased insulin secretion by 454.4% and proliferation of 1.1E7 cells with no cytotoxic effects up to a concentration of 100 μM. Molecular docking simulation demonstrated a good binding affinity with -5.03 Kcal/mol of (R)-(-)-carvone to HMG-CoA reductase.ConclusionThe hypolipidaemic effect of (R)-(-)-carvone is comparable to that of fenofibrate. (R)-(-)-carvone has the advantage over fenofibrate of not producing hypoglycaemia in animals. Furthermore, (R)-(-)-carvone increased proliferation and insulin secretion of human pancreatic β-cells.
| S-EPMC7785269 | biostudies-literature
Project description:Reproductive factors are well-established risk factors for breast cancer. The prevailing hypothesis suggested that stem cell changes may be the key underlying mechanisms, but epidemiological evidence has been notably scarce. Herein we examined the relationship between reproductive risk factors and the expression of well-established stem cell markers CD44, CD24, and ALDH1A1 in benign breast biopsy non-cancerous samples. Our study included 735 participants from the Nurses' Health Study II who were diagnosed with biopsy-confirmed incident benign breast disease (BBD). Reproductive history and other BBD/breast cancer risk factors were measured from self-reported biennial questionnaires. Immunohistochemistry was performed on breast tissue microarrays from normal terminal ductal-lobular units (TDLU) cores. Marker expression in epithelium and stroma was quantified using semi-automated image analysis. The generalized linear regression was used to examine the associations of reproductive factors with the positive expression of CD44, CD24, and ALDH1A1, adjusted for known breast cancer risk factors. Age at first birth ≥30 years old (vs. <25 years) was associated with lower ALDH1A1 expression in the epithelium (β for ≥30 vs. <25 years = -0.30, 95% CI -0.57; -0.03, p-trend = 0.03). Parity, breastfeeding, age at menarche, and the time interval between menarche and age at first birth were not associated with the expression of any of the three markers in epithelium or stroma. These findings suggest age at first birth may influence the ALDH1A1 expression in breast tissue. Our study added to the very limited evidence regarding the potential impact of reproductive factors on breast stem cell markers.
| S-EPMC11626268 | biostudies-literature
Project description:BackgroundMammographic density (MD) is a strong breast cancer risk factor that reflects fibroglandular and adipose tissue composition, but its biologic underpinnings are poorly understood. Insulin-like growth factor binding proteins (IGFBPs) are markers that may be associated with MD given their hypothesized role in breast carcinogenesis. IGFBPs sequester IGF-I, limiting its bioavailability. Prior studies have found positive associations between circulating IGF-I and the IGF-I:IGFBP-3 ratio and breast cancer risk. We evaluated the associations of IGF-I, IGFBP-3, and six other IGFBPs with MD.MethodsSerum IGF measures were quantified in 296 women, ages 40-65, undergoing diagnostic image-guided breast biopsy. Volumetric density measures (MD-V) were assessed in pre-biopsy digital mammograms using single X-ray absorptiometry. Area density measures (MD-A) were estimated by computer-assisted thresholding software. Age, body mass index (BMI), and BMI2-adjusted linear regression models were used to examine associations of serum IGF measures with MD. Effect modification by BMI was also assessed.ResultsIGF-I and IGFBP-3 were not strongly associated with MD after BMI adjustment. In multivariable analyses among premenopausal women, IGFBP-2 was positively associated with both percent MD-V (β = 1.49, p value = 0.02) and MD-A (β = 1.55, p value = 0.05). Among postmenopausal women, positive relationships between IGFBP-2 and percent MD-V (β = 2.04, p = 0.003) were observed; the positive associations between IGFBP-2 and percent MD-V were stronger among lean women (BMI < 25 kg/m2) (β = 5.32, p = 0.0002; p interaction = 0.0003).ConclusionsIn this comprehensive study of IGFBPs and MD, we observed a novel positive association between IGFBP-2 and MD, particularly among women with lower BMI. In concert with in vitro studies suggesting a dual role of IGFBP-2 on breast tissue, promoting cell proliferation as well as inhibiting tumorigenesis, our findings suggest that further studies assessing the role of IGFBP-2 in breast tissue composition, in addition to IGF-1 and IGFBP-3, are warranted.
| S-EPMC6651938 | biostudies-literature