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 Table of Contents 
Year : 2018  |  Volume : 9  |  Issue : 2  |  Page : 85-91  

Association of dyslipidemia, increased insulin resistance, and serum CA 15-3 with increased risk of breast cancer in urban areas of North and Central India

1 Department of Biochemistry, Saraswathi Institute of Medical Sciences, Hapur, Uttar Pradesh, India
2 Department of Biochemistry, Mahaveer Institute of Medical Sciences and Research, Madhya Pradesh, Bhopal, India
3 Department of Anatomy, GSL Medical College, Rajahmundry, Andhra Pradesh, India
4 Department of Biochemistry, Mahatma Gandhi Memorial Medical College, Indore, Madhya Pradesh, India
5 Department of Pharmacology, GSL Medical College, Rajahmundry, Andhra Pradesh, India

Date of Web Publication13-Jun-2018

Correspondence Address:
Dr. Sanjay Kumar
Department of Pharmacology, GSL Medical College and GSL General Hospital, Rajahmundry - 533 296, Andhra Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jmh.JMH_77_17

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Objective: This study aims to determine the association of dyslipidemia and increased insulin resistance (IR) with increased breast cancer (BC) risk. Materials and Methods: The study group comprised 110 premenopausal and 143 postmenopausal, untreated female BC patients in the age range of 29–72 years. Control group consisted of 117 premenopausal and 141 postmenopausal healthy females in the age range of 23–75. Approximately 8-ml blood samples were drawn to measure various biochemical parameters. Serum glucose, total cholesterol, triglyceride (TG), and high-density lipoprotein-cholesterol were measured. Very low-density lipoprotein-cholesterol (VLDL-C) and LDL-C were calculated using Friedewald's formula. Serum insulin and serum CA 15-3 were estimated by immune enzymatic assay. IR was assessed using homeostasis model assessment IR index (HOMA-IR). Results: Clinical variables in the case and control groups were compared using the unpaired Student's t-test. The crude and adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by binary logistic regression analysis. Pearson's correlation analysis was used to determine the association between CA 15-3 and variables of interest. Total cholesterol, TG, LDL, VLDL, serum glucose, serum insulin, HOMA-IR, and serum CA 15-3 were significantly higher (P < 0.001) in BC patients compared to those in controls. Significant adjusted ORs with 95% CI were found to be fasting glucose, total cholesterol, and TGs. We also found a significant positive correlation between total cholesterol, TG, LDL, serum glucose, serum insulin, HOMA-IR, and serum CA 15-3.
Conclusion: This study confirms the association between dyslipidemia, IR, and increased BC risk.

Keywords: Breast cancer, cholesterol, homeostasis model assessment-insulin resistance, risk factors

How to cite this article:
Kachhawa P, Kachhawa K, Agrawal D, Sinha V, Sarkar PD, Kumar S. Association of dyslipidemia, increased insulin resistance, and serum CA 15-3 with increased risk of breast cancer in urban areas of North and Central India. J Mid-life Health 2018;9:85-91

How to cite this URL:
Kachhawa P, Kachhawa K, Agrawal D, Sinha V, Sarkar PD, Kumar S. Association of dyslipidemia, increased insulin resistance, and serum CA 15-3 with increased risk of breast cancer in urban areas of North and Central India. J Mid-life Health [serial online] 2018 [cited 2022 Oct 6];9:85-91. Available from:

   Introduction Top

Breast cancer (BC) is the most common cancer affecting female individuals in the world with an estimated 1.67 million new cancer patients diagnosed in 2012. In India, the incidence of BC is significantly lower than in western countries. With an annual incidence of approximately 144,000 BC has now become the most common cancer affecting female individuals in urban India.[1] The incidence of BC in India varies from 5/100,000 women per year in rural areas to 30/100,000 women per year in urban areas.[2] The incidence of BC increases with age in India, as is the case in the rest of the world. Genetic predisposition is the main risk factor in 5%–10% cases of BCs. Risk factors identified for the remaining 90% spontaneous BCs are reproductive, lifestyle, or environmental factors, primarily through their influence on the hormonal milieu. The precise etiology of BC is unknown. However, the female sex hormone, estrogen, is reported to be carcinogenic, promoting cell proliferation in breast tissues and reproductive organs. In addition, environmental factors such as exposure to radiation and chemicals may trigger the onset of BC.[3] Important lifestyle factors believed to contribute toward the development of BC include obesity after menopause, decreased physical activity, high-fat diet, use of contraceptives, and lack or short duration of breastfeeding.[4]

In the past few years, extensive efforts have been dedicated to understanding the relationship between dyslipidemia, insulin resistance (IR), type 2 diabetes mellitus and metabolic syndrome, and BC risk.[5],[6],[7],[8],[9] Several reports showed that the levels of circulating lipids and lipoproteins are high in pre- and postmenopausal BC patients.[5],[6],[7],[10],[11] It has been postulated that changes in the concentration of serum lipids in the BC patients could result in an increased production of tumor necrosis factor-alpha and inhibition of adipose lipoprotein lipase activity by insulin.[12] These changes impair the catabolism of very low-density lipoprotein-cholesterol (VLDL-C), leading to an increase in high-density lipoprotein-cholesterol (HDL-C). Epidemiology studies reveal that HDL-C and BC are influenced by variables such as dietary fat intake, alcohol consumption, body weight, country of residence, pregnancy, endogenous hormones, smoking, exercise, and socioeconomic status.[13] HDL-C level has been shown to be higher in participants with mammography dysphasia and family history of BC.[14],[15] However, it has also been reported that HDL-C level was either elevated or depressed in women with BC.[9] Thus, HDL-C level alone, at present, cannot be taken into consideration as a causative factor. It was found that patients with more advanced Breast Cancer have significantly lower concentration of HDL-C than do patients with less advanced disease.[12],[16] Plasma total cholesterol and LDL-C were found to be significantly elevated whereas HDL-C was significantly decreased in BC patients. These studies suggest that higher level of total cholesterol may play an important role in carcinogenesis.[9],[17],[18] The role of lipoprotein levels in the development and advancement of BC has been reported in many in vitro studies.[19],[20],[21] The role of different lipids in cancer has been studied extensively in developed countries, but it is still a matter of controversy.[11],[20],[21] Levels of exposure to carcinogens and prevalence of established risk factors may be different in developing and developed nations.

This study aims to compare the serum lipid levels in female BC patients with those in normal healthy controls and to discover the effect of dyslipidemia and increased IR on BC risk.

   Materials and Methods Top


The case group comprised 110 premenopausal and 143 postmenopausal female BC patients. A case was defined as an untreated female patient with histopathologically confirmed BC. The age group of the cases ranged from 29 to 72 years. Control group consisted of 117 premenopausal and 141 postmenopausal healthy women in the age range of 23–75. These were apparently healthy volunteers, who were not taking oral contraceptives or any form of hormonal medication. Women were classified as postmenopausal if they had no menstrual cycles during the preceding 3 years or if they had undergone a hysterectomy without complete oophorectomy before menopause and were 47 years of age or older.

Exclusion criteria

Patients were excluded if they were suffering from diabetes mellitus or dyslipidemia and those taking statins or any drugs that interfere with blood glucose, serum lipid profile, and serum insulin.

Blood sample collection and preparation

Approximately 8-ml blood sample was withdrawn from the antecubital vein after overnight fasting. The blood sample was collected in plain vacutainers. Serum was separated from the clotted blood by centrifugation for 15 min at 3000 rpm at room temperature. All serum samples were stored at −80°C until use.

Biochemical assays

Serum total cholesterol (normal value: 150–200 mg/dl), HDL-C (normal value: 35–70 mg/dl), and triglycerides (TGs) (normal value: 60–170 mg/dl) were measured using commercially available kits for autoanalyzer. VLDL-C (normal value: 12–34 mg/dl) and LDL-C (normal value: 50–100 mg/dl) were calculated by Friedewald's formula. Serum glucose level (normal value: 70–140 mg/dl) was estimated by glucose oxidase and peroxidase method. All biochemical investigations were performed using a fully automated analyzer, Turbo cam 100 (CPC Diagnostics Pvt. Ltd., Alwarpet, Chennai, Tamil Nadu, India). Serum insulin (normal value: <10 μlU/ml) was measured using enzyme-linked immunosorbent assay (ELISA), a solid-phase two-site enzyme immunoassay (Calbiotech, Inc., Insulin ELISA kit, Catalog No. IS130D, 96 Tests). Serum CA 15-3 (normal value: <35 U/ml) was measured using the CA 15-3 ELISA kit (Calbiotech, Inc., Catalog No. CA153T). All assays were performed according to the respective manufacturer's instructions. Homeostasis model assessment-IR index (HOMA-IR) to indicate IR was calculated as: “fasting glucose (mg/dl) × fasting insulin (μlU/ml)/405.” The cutoff point was 2.5 or greater. Body mass index (BMI) was calculated as “weight in kilograms/height in meters squared (kg/m 2).” Blood pressure (systolic and diastolic) was measured in the sitting position after a 10-min resting period.

Statistical analysis

Statistical analysis was performed using SPSS version 21 (SPSS Inc., 233, South Wacker Drive, 11th Floor, Chicago, IL, 60606-6412, USA). Metabolic parameters such as BMI, systolic blood pressure (SBP), diastolic blood pressure (DBP), lipid profile, serum glucose, serum insulin, HOMA-IR, and serum CA 15-3 were compared between cases and controls, using an unpaired Student's t-test. Crude odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated using crosstab analysis. In univariate analysis, the significance level was <10%. The binary logistic regression analysis was done using the presence of BC as dependent variable and parameters of interest (age, menopausal status, BMI, total cholesterol, TGs, HDL, fasting glucose, serum insulin, and HOMA-IR) as independent variables. Pearson's correlation analysis was used to determine the association between serum CA 15-3 and variables of interest. P < 0.05 was considered statistically significant.

Ethics statement

The study was approved by the Ethical Committee of the Institute. Informed consent was obtained from each patient.

   Results Top

[Table 1] highlights the clinical characteristics of BC cases and healthy controls. Data revealed that BC cases had significantly higher (P< 0.001) SBP, DBP, fasting glucose, total cholesterol, triglyceride, LDL-C, VLDL-C, serum insulin, HOMA-IR, and serum CA 15-3 than did the controls. There was no significant difference in age, BMI, and HDL-C between the cases and controls.
Table 1: Clinical characteristics of breast cancer cases and healthy controls

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[Table 2] shows the comparison of biochemical parameters between premenopausal and postmenopausal BC cases and healthy controls. The data indicated that SBP, DBP, total cholesterol, LDL-C, TGs, VLDL-C, serum glucose, HOMA-IR, and CA 15-3 were significantly different (P< 0.001) between premenopausal and postmenopausal cases and controls. Serum insulin was significantly high (P< 0.05) only in postmenopausal cases compared to that in postmenopausal controls. The differences in BMI and HDL-C between premenopausal and postmenopausal cases and controls were not significant. Similarly, there was no significant difference in serum insulin levels between premenopausal cases and controls.
Table 2: Comparison of biochemical variables between premenopausal and postmenopausal breast cancer cases and healthy controls

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[Table 3] shows crude and adjusted ORs and 95% CIs for BC in relation to age, menopausal status, BMI, total cholesterol, HDL-C, TGs, fasting glucose, insulin, and HOMA-IR. Crude ORs with 95% CI (P< 0.001) were significant for fasting glucose (3.83 [2.64–5.55]), total cholesterol (8.23 [5.26–12.8]), TGs (11.13 [7.37–16.8]), and HOMA-IR (2.14 [1.49–3.07]). On the other hand, HDL-C had a mitigating effect on the risk of developing BC (OR [95% CI]: 0.86 [0.59–0.99]), P < 0.001. In univariate analysis, the significant variables were taken for binary logistic regression. Significant adjusted OR with 95% CI and P < 0.001 were found to be fasting glucose (4.87 [2.73–8.70]), total cholesterol (6.76 [3.98–11.5]), and TGs (10.49 [6.50–16.9]).
Table 3: Crude and adjusted odds ratios and 95% confidence interval for breast cancer with respect to menopausal status, age, body mass index, total cholesterol, high-density lipoprotein-cholesterol, triglycerides, fasting glucose, insulin, homeostasis model assessment index-insulin resistance, calculated using binary logistic regression

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[Table 4] shows Pearson's correlation analysis between CA 15-3 and variables of interest. [Figure 1], [Figure 2], [Figure 3], [Figure 4] also depict the correlation [Figure 1], [Figure 2], [Figure 3], [Figure 4] between CA 15-3 and other variables. The results showed that serum CA 15-3 was significantly positively associated with fasting glucose (r = 0.35, P > 0.001) shown in [Figure 4], serum insulin (r = 0.29, P > 0.05), HOMA-IR (r = 0.36, P > 0.001) shown in [Figure 3], total cholesterol (r = 0.48, P > 0.001) shown in [Figure 1], TGs (r = 0.34, P > 0.001), LDL-C (r = 0.49, P > 0.001), and VLDL-C (r = 0.34, P > 0.001) and significant negative association with HDL-C (r = −0.26, P< 0.05) shown in [Figure 2]. No significant correlation was found with age, BMI, SBP, and DBP.
Table 4: Pearson's correlation coefficient (r) between serum CA 15-3 and various metabolic variables of breast cancer patients

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Figure 1: Positive Pearson's correlation between serum CA 15-3 and total cholesterol

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Figure 2: Negative Pearson's correlation between serum CA 15-3 and high-density lipoprotein-cholesterol

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Figure 3: Positive Pearson's correlation between serum CA 15-3 and homeostasis model assessment-insulin resistance

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Figure 4: Positive Pearson's correlation between serum CA 15-3 and fasting sugar

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   Discussion Top

BC results in the death of millions of women worldwide every year. This study confirms the occurrence of dyslipidemia and IR in women with BC. In this study, we have found higher levels of total cholesterol, TGs, LDL-C, VLDL-C, fasting glucose, fasting serum insulin, and HOMA-IR in BC cases compared to those in healthy controls.

Ray et al. suggested that an increased serum total cholesterol level may play a significant role in carcinogenesis.[22] Some of the studies also find similar results.[23],[24],[25] A few other studies reported that plasma total cholesterol level was significantly lower in patients with BC.[26],[27] Agurs-Collins et al. and Hoyer and Engholm did not find any significant difference in the serum total cholesterol levels between BC patients and controls.[28],[29]

In our study, TG levels were significantly higher in both pre- and postmenopausal BC patients than in controls. These results are consistent with those of other studies.[10],[23],[28],[30] Bani et al. showed that there was a significant increase in the TG levels in postmenopausal cancer patients.[11] Goodwin et al. reported elevated serum TG levels in premenopausal BC patients.[31] The high concentration of TGs may lead to a decreased level of sex hormone-binding globulin, resulting in higher levels of free estradiol, which may increase BC risk.[32]

In this study, we did not observe any significant difference in the HDL-C levels in pre- and postmenopausal BC patients and controls. Ray et al. and Kachhawa et al. reported that plasma HDL-C levels were significantly lower in BC patients.[22],[23] At least two prospective studies reported the association between low HDL-C levels and increased risk of BC.[29],[33] Since endogenous sex steroids are closely associated with the development of BC, it has been hypothesized that cholesterol is an important risk factor for the development of BC.[34] It has also been reported that low HDL-C is a marker of relative androgen excess.[35] Aromatization of the excess androgen in the body promotes BC development.

The LDL-C level was significantly higher in pre- and postmenopausal BC patients than in controls in this study, consistent with results reported in other studies.[22],[23] The elevated serum LDL-C, which is more susceptible to oxidation, may result in high lipid peroxidation in BC patients. This may cause the accumulation of reactive oxygen species and free radicals (oxidative stress), which may, in turn, lead to cellular and molecular damage, ultimately resulting in malignant transformation.

High blood glucose was associated with increased BC risk in five of seven cohort studies,[36],[37],[38],[39],[40],[41],[42] but the association was significant only in three.[36],[37],[38] Some other studies have reported higher fasting blood glucose, serum insulin, and HOMA-IR in BC patients.[36],[41],[43],[44] The results of the present study are consistent with these findings. Muti et al. and Stattin et al. have reported that elevated blood glucose levels were associated with a significantly higher risk of BC in premenopausal women, compared to the lower risk in postmenopausal women.[36],[38] A study conducted with 77,228 women participants, during a screening program in Austria, found that elevated blood glucose was associated with BC risk. The risk was the highest among those older than 65 years of age.[42]

Only one of the four cohort studies that have examined fasting insulin levels in relation to BC risk reported a significant positive association.[40],[45],[46],[47] HOMA-IR, based on a measurement of fasting insulin and glucose, by the euglycemic clamp method, has been shown to reflect IR more accurately than fasting insulin alone.[48] Thus, the positive association of HOMA-IR with BC risk adds to the evidence for a possible role of IR in the etiology of BC. The results of the repeated measures analysis supported the findings of the analyses using baseline values for glucose, insulin, and HOMA-IR.

   Conclusion Top

Our study suggests that dyslipidemia and disturbed glucose metabolism are correlated with BC and supports the hypothesis that total cholesterol, LDL-C, and TGs and serum glucose are important risk factors in the development of BC. It also reinforces the importance of controlling these factors, thereby reducing the incidence and mortality associated with BC. Our study has particularly highlighted the significant differences in metabolic indices and lipid profile between BC patients and controls. Among the biochemical parameters, serum glucose, total cholesterol, TG, LDL-C, VLDL-C, serum insulin, HOMA-IR, and serum CA 15-3 are significantly elevated in patients with BC compared to those in controls, suggesting a significant positive correlation between serum CA 15-3 and total cholesterol, TGs, LDL-C, serum insulin, and HOMA-IR in BC patients. There was no significant difference between the serum HDL-C levels in BC patients and controls. There was a negative correlation between serum HDL-C and CA 15-3. HOMA-IR is an indicator of IR, which is an important risk factor in the development of BC. Our study confirms that total cholesterol, TG, serum glucose, and HOMA-IR are important risk factors for BC.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

   References Top

Agency for Cancer Research (Homepage on the Internet) Cancer Fact Sheets. Available from:  Back to cited text no. 1
Nandakumar A, Ramnath T. Consolidated Report of Hospital Based Registries 2004-2006. Bangalore, India: National Cancer registry programme, Indian Council for Medical Research; 2009. p. 54.  Back to cited text no. 2
Paley PJ. Screening for the major malignancies affecting women: Current guidelines. Am J Obstet Gynecol 2001;184:1021-30.  Back to cited text no. 3
Yoo KY, Kang D, Park SK, Kim SU, Kim SU, Shin A, et al. Epidemiology of breast cancer in korea: Occurrence, high-risk groups, and prevention. J Korean Med Sci 2002;17:1-6.  Back to cited text no. 4
Abdelsalam KE, Hassan IK, Sadig IA. The role of developing BC in alteration of serum lipid profile. J Res Med Sci 2012;17:562-5.  Back to cited text no. 5
Laisupasin P, Thompat W, Sukarayodhin S, Sornprom A, Sudjaroen Y. Comparison of serum lipid profiles between normal controls and breast cancer patients. J Lab Physicians 2013;5:38-41.  Back to cited text no. 6
[PUBMED]  [Full text]  
Peela JR, Jarari AM, El Alsoaeiti SO, El Busaifi S, El Awamy H, Shakila S. The relationship between serum lipids and BC in libya. Biochem Anal Biochem 2012;1:117.  Back to cited text no. 7
Owiredu WK, Donkor S, Addai BW, Amidu N. Serum lipid profile of BC patients. Pak J Biol Sci 2009;12:332-8.  Back to cited text no. 8
Hasija K, Bagga HK. Alterations of serum cholesterol and serum lipoprotein in BC of women. Indian J Clin Biochem 2005;20:61-6.  Back to cited text no. 9
Naval KY, Bibek P, Thanpari C, Bidhan CK. Assessment of biochemical profiles in premenopausal and postmenopausal women with BC. Asian Pac J Cancer Prev 2012;13:3385-8.  Back to cited text no. 10
Bani IA, Williams CM, Boulter PS, Dickerson JW. Plasma lipids and prolactin in patients with breast cancer. Br J Cancer 1986;54:439-46.  Back to cited text no. 11
Knapp ML, Al Sheibani S, Riches PG. Alterations of serum lipids in BC: Effects of disease activity, treatment, and hormonal factors. Clin Chem 1991;37:2093-101.  Back to cited text no. 12
Boyd NF, McGuire V. Evidence of association between plasma high-density lipoprotein cholesterol and risk factors for breast cancer. J Natl Cancer Inst 1990;82:460-8.  Back to cited text no. 13
Saftlas AF, Szklo M. Mammographic parenchymal patterns and breast cancer risk. Epidemiol Rev 1987;9:146-74.  Back to cited text no. 14
Rössner S, Wallgren A. Serum lipoproteins and proteins after breast cancer surgery and effects of tamoxifen. Atherosclerosis 1984;52:339-46.  Back to cited text no. 15
Pushpalatha M, Smitha KS, Gilsa ES, Nimi B. Lipid profile in female BC: A study from Kerala, South India. Intl J Adv Res 2015;3:472-5.  Back to cited text no. 16
Antalis CJ, Uchida A, Buhman KK, Siddiqui RA. Migration of MDA-MB-231 BC cells depends on the availability of exogenous lipids and cholesterol esterification. Clin Exp Metastasis 2011;28:733-41.  Back to cited text no. 17
Danilo C, Gutierrez-Pajares JL, Mainieri MA, Mercier I, Lisanti MP, Frank PG, et al. Scavenger receptor class B type I regulates cellular cholesterol metabolism and cell signaling associated with breast cancer development. Breast Cancer Res 2013;15:R87.  Back to cited text no. 18
Alikhani N, Ferguson RD, Novosyadlyy R, Gallagher EJ, Scheinman EJ, Yakar S, et al. Mammary tumor growth and pulmonary metastasis are enhanced in a hyperlipidemic mouse model. Oncogene 2013;32:961-7.  Back to cited text no. 19
Vatten LJ, Foss OP. Total serum cholesterol and triglycerides and risk of breast cancer: A prospective study of 24,329 Norwegian women. Cancer Res 1990;50:2341-6.  Back to cited text no. 20
Alexopoulos CG, Blatsios B, Avgerinos A. Serum lipids and lipoprotein disorders in cancer patients. Cancer 1987;60:3065-70.  Back to cited text no. 21
Ray G, Husain SA. Role of lipids, lipoproteins and vitamins in women with breast cancer. Clin Biochem 2001;34:71-6.  Back to cited text no. 22
Kachhawa P, Kachhawa K, Singh S, Sarkar PD, Agrawal D, Kumar S, et al. Relationship of dyslipidemia, insulin resistance, and prostatespecific antigen with prostate cancer. Oncobiol Targets 2016;3:7.  Back to cited text no. 23
  [Full text]  
Chow LW, Cheng CW, Wong JL, Toi M. Serum lipid profiles in patients receiving endocrine treatment for breast cancer – The results from the celecoxib anti-aromatase neoadjuvant (CAAN) trial. Biomed Pharmacother 2005;59 Suppl 2:S302-5.  Back to cited text no. 24
Qi XY, Zhang AY, Wu GL, Pang WZ. The association between BC and diet and other factors. Asia Pac J Public Health 1994;7:98-104.  Back to cited text no. 25
Shah FD, Shukla SN, Shah PM, Patel HR, Patel PS. Significance of alterations in plasma lipid profile levels in BC. Integr Cancer Ther 2008;7:33-41.  Back to cited text no. 26
Kokoglu E, Karaarslan I, Karaarslan HM, Balogu H. Alterations of serum lipids and lipoproteins in BC. Cancer Lett 1994;82:175-8.  Back to cited text no. 27
Agurs-Collins T, Kim KS, Dunston GM, Adams-Campbell LL. Plasma lipid alterations in African-American women with BC. J Cancer Res Clin Oncol 1998;124:186-90.  Back to cited text no. 28
Hoyer AP, Engholm G. Serum lipids and BC risk: A cohort study of 5,207 Danish women. Cancer Causes Control 1992;3:403-8.  Back to cited text no. 29
Abu-Bedair FA, El-Gamal BA, Ibrahim NA, El-Aaser AA. Serum lipids and tissue DNA content in Egyptian female BC patients. Jpn J Clin Oncol 2003;33:278-82.  Back to cited text no. 30
Goodwin PJ, Boyd NF, Hanna W, Hartwick W, Murray D, Qizilbash A, et al. Elevated levels of plasma triglycerides are associated with histologically defined premenopausal breast cancer risk. Nutr Cancer 1997;27:284-92.  Back to cited text no. 31
Takatani O, Okumoto T, Kosano H. Genesis of breast cancer in Japanese: A possible relationship between sex hormone binding globulin (SHBG) and serum lipid components. Breast Cancer Res Treat 1991;18 Suppl 1:S27-9.  Back to cited text no. 32
Furberg AS, Veierød MB, Wilsgaard T, Bernstein L, Thune I. Serum high-density lipoprotein cholesterol, metabolic profile, and breast cancer risk. J Natl Cancer Inst 2004;96:1152-60.  Back to cited text no. 33
Key T, Appleby P, Barnes I, Reeves G, Endogenous Hormones and Breast Cancer Collaborative Group. Endogenous sex hormones and breast cancer in postmenopausal women: Reanalysis of nine prospective studies. J Natl Cancer Inst 2002;94:606-16.  Back to cited text no. 34
Gillmer MD. Mechanism of action/effects of androgens on lipid metabolism. Int J Fertil 1992;37 Suppl 2:83-92.  Back to cited text no. 35
Stattin P, Björ O, Ferrari P, Lukanova A, Lenner P, Lindahl B, et al. Prospective study of hyperglycemia and cancer risk. Diabetes Care 2007;30:561-7.  Back to cited text no. 36
Haseen SD, Khanam A, Sultan N, Idrees F, Akhtar N, Imtiaz F, et al. Elevated fasting blood glucose is associated with increased risk of breast cancer: Outcome of case-control study conducted in Karachi, Pakistan. Asian Pac J Cancer Prev 2015;16:675-8.  Back to cited text no. 37
Muti P, Quattrin T, Grant BJ, Krogh V, Micheli A, Schünemann HJ, et al. Fasting glucose is a risk factor for breast cancer: A prospective study. Cancer Epidemiol Biomarkers Prev 2002;11:1361-8.  Back to cited text no. 38
Manjer J, Kaaks R, Riboli E, Berglund G. Risk of BC in relation to anthropometry, blood pressure, blood lipids and glucose metabolism: A prospective study within the Malmo preventive project. Eur J Cancer Prev 2001;10:33-42.  Back to cited text no. 39
Mink PJ, Shahar E, Rosamond WD, Alberg AJ, Folsom AR. Serum insulin and glucose levels and BC incidence: The atherosclerosis risk in communities study. Am J Epidemiol 2002;156:349-52.  Back to cited text no. 40
Kabat GC, Kim M, Caan BJ, Chlebowski RT, Gunter MJ, Ho GY, et al. Repeated measures of serum glucose and insulin in relation to postmenopausal breast cancer. Int J Cancer 2009;125:2704-10.  Back to cited text no. 41
Rapp K, Schroeder J, Klenk J, Ulmer H, Concin H, Diem G, et al. Fasting blood glucose and cancer risk in a cohort of more than 140,000 adults in Austria. Diabetologia 2006;49:945-52.  Back to cited text no. 42
Sieri S, Muti P, Claudia A, Berrino F, Pala V, Grioni S, et al. Prospective study on the role of glucose metabolism in breast cancer occurrence. Int J Cancer 2012;130:921-9.  Back to cited text no. 43
Alokail MS, Al-Daghri NM, Al-Attas OS, Hussain T. Combined effects of obesity and Type 2 diabetes contribute to increased BC risk in premenopausal women. Cardiovasc Diabetol 2009;8:33.  Back to cited text no. 44
Jernström H, Barrett-Connor E. Obesity, weight change, fasting insulin, proinsulin, C-peptide, and insulin-like growth factor-1 levels in women with and without breast cancer: The rancho bernardo study. J Womens Health Gend Based Med 1999;8:1265-72.  Back to cited text no. 45
Kaaks R, Lundin E, Rinaldi S, Manjer J, Biessy C, Soderberg S, et al. Prospective study of IGF-I, IGF-binding proteins, and BC risk, in Northern and Southern Sweden. Cancer Causes Control 2002;13:307-16.  Back to cited text no. 46
Gunter MJ, Hoover DR, Yu H, Wassertheil-Smoller S, Rohan TE, Manson JE, et al. Insulin, insulin-like growth factor-I, and risk of breast cancer in postmenopausal women. J Natl Cancer Inst 2009;101:48-60.  Back to cited text no. 47
Ikeda Y, Suehiro T, Nakamura T, Kumon Y, Hashimoto K. Clinical significance of the insulin resistance index as assessed by homeostasis model assessment. Endocr J 2001;48:81-6.  Back to cited text no. 48


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

  [Table 1], [Table 2], [Table 3], [Table 4]

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