Skip to main content
Download PDF
Download ePub

Apolipoprotein A1 -75 G/A and +83 C/T polymorphisms and renal cancer risk

Lipids in Health and Disease volume 14, Article number: 143 (2015) Cite this article

Abstract

Background

Apolipoprotein A1 (ApoA1) is the major apoprotein constituent of high-density lipoprotein that can play important roles in tumor invasion and metastasis. The objective of the present study was to evaluate the association of two genetic variants (−75 G/A and +83 C/T) of APOA1 with predisposition to renal cancer.

Methods

A total of 432 subjects, including 216 pathologically-proven renal cancer cases and 216 age- and gender-matched healthy controls, were recruited into this hospital-based case–control study. Genotyping of the APOA1 was performed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) combined with gel electrophoresis, and then confirmed by direct sequencing.

Results

Patients with renal cancer had a significantly higher frequency of APOA1 -75 AA genotype [odds ratio (OR) = 2.10, 95 % confidence interval (CI) = 1.18, 3.75; P = 0.01] and APOA1 -75 A allele (OR =1.40, 95 % CI = 1.05, 1.87; P = 0.02) than controls. When stratifying by the distant metastasis status, patients with distant metastasis had a significantly higher frequency of APOA1 -75 AA genotype genotype (OR =2.20, 95 % CI = 1.04, 4.68; P = 0.04).

Conclusion

This study is, to our knowledge, the first to examine prospectively an increased risk role of APOA1 -75 AA genotype and APOA1 -75 A allele in renal cancer susceptibility.

Introduction

Renal cancer is the predominant form of malignancy of the kidney and represents 3–4 % of all cancers [1]. In 2015, an estimated 61,560 new cases of kidney and renal pelvis cancers will be diagnosed in the United States [1]. An estimated 14,080 Americans are expected to die from the disease in 2015 [1]. The crude incidence rates of renal cell carcinoma were 7.1 and 3.1 per 100,000 population for men and women respectively in Japan in 1997 [2]. The crude incidence rates of renal cell carcinoma were increased from 4.5 to 5.6 per 100,000 population in China between 1989 and 2008 [3, 4]. Many epidemiological studies have found that environmental factors, such as smoking, diesel exhaust, and various dioxins, may be involved in the development of sporadic renal cancer [5–8]. Although many subjects are exposed to these risk factors during their lifetime, only some of them develop renal cancer, which suggests that genetic susceptibility may play a role in the etiology of renal cancer [9]. The impact of genetic background on renal cancer is still unclear.

Apolipoprotein A1 (ApoA1) is the major apoprotein constituent of high-density lipoprotein (HDL) that can play important roles in tumor invasion and metastasis [10, 11]. Recent findings revealed the crucial roles of ApoA1 in inflammation, tumor growth, angiogenesis, invasion and metastasis [12–14]. APOA1 gene, located on the 11q23-q24, encodes apoA1 [11, 15]. There are several single-nucleotide polymorphisms (SNPs) in the APOA1 gene [16]. Two SNPs (−75 G/A and +83 C/T) of APOA1 play an important role in lipid metabolism [17–19]. It has also been found that APOA1 -75 G/A and +83 C/T genotypes were associated with susceptibility to breast cancer and lymph node metastases occurrence, respectively [20].

To our best knowledge, no reports concerning the role of APOA1 -75 G/A and +83 C/T genotypes on renal cancer risk have been reported yet. We hypothesized that APOA1 -75 G/A and +83 C/T genotypes were associated with renal cancer risk. To test this hypothesis, we performed a prospective hospital-based case–control study to evaluate the association of the APOA1 -75 G/A and +83 C/T genotypes with predisposition to renal cancer.

Materials and methods

Study population

A total of 432 subjects, including 216 pathologically-proven renal cancer cases and 216 age- and gender-matched healthy controls, were recruited into this hospital-based case–control study between February 2012 and December 2014 in the West China Hospital of Sichuan University [21]. All renal cancer cases were histopathologically confirmed. We extracted the following information: tumor grade, tumor classification, lymph node invasion status, distant metastasis status and the pathology of renal cancer. In order to confirm that healthy controls were healthy and free of cancer, volunteers underwent various tests that included physical exams, questionnaires about their health and history, chest X-rays, blood and urine tests for various tumor markers, abdominal ultrasound, gastric endoscopy, and colon enema. The patient or their families/surrogates were interviewed. The Institutional Ethical Committee of the West China Hospital of Sichuan University approved all parts of the study, and informed consent according to the Declaration of Helsinki was obtained from all participants or their families/surrogates.

DNA extraction and genotyping

Genomic DNA was isolated from 20 g/L ethylenediaminetetraacetic acid (EDTA) or sodium citrate anticoagulated 3–5 ml venous blood by the commercially available Qiagen kit (QIAGEN Inc., Valencia, CA, USA) and stored at 4 °C. Genotyping of the APOA1 was performed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Based on the GenBank reference sequence, the PCR primers designed for the APOA1 -75 G/A and +83 C/T were as follows: 5ʹ-AGG GAC AGA GCT GAT CCT TGA ACT CTT AAG-3ʹ (forward) and 5ʹ-TTA GGG GAC ACC TAG CCC TCA GGA AGA GCA-3ʹ (reverse). The restriction endonuclease enzyme MspI digested the amplified PCR products overnight. Electrophoresis in a 3 % agarose gel followed by ethidium bromide staining and ultraviolet illumination allowed detection of the alleles. The presence of the MspI restriction stie at −75 bp (G allele) and at +83 bp (C allele) in the 433 bp product resulted in four fragments of 45, 66, 113 and 209 bp (Fig. 1). The absence of the restriction site at −75 bp (A allele) resulted in three fragments of 45, 179 and 209 bp (Fig. 1). The absence of the restriction site at +83 bp (T allele) created a larger fragment of 254 bp instead of two fragments of 45 and 209 bp (Fig. 1). For quality control, two independent observers randomly chose 44 samples (22 cases and 22 controls) by computer-generated number scheme. They performed double sampling PCR-RFLP and found no differences, and then confirmed by direct sequencing from Qiagen cleaned up DNA.

Fig. 1
figure 1

Electrophoresis in a 3 % agarose gel after the Mspl digested in renal cancer cases and healthy controls

Full size image

Statistical analysis

Data are presented as percentages for categorical variables or as means ± standard deviation (SD). Differences between categorical variables were evaluated using Pearson x 2 test, while those between continuous variables were assessed by Student’s t test. The existence of differences in genotypic frequencies between groups was assessed by means of Pearson x 2 test and calculating the odds ratio (OR) with the 95 % confidence intervals (CI). A P-value was considered significant at a level of < 0.05. The Statistical Analysis System software (Version 9.1; SAS Institute Inc., Cary, NC, USA) was used for all statistical tests.

Results

Characteristics of participants

Healthy volunteers and cancer patients were not significantly different in terms of age distribution and gender (Table 1). For renal cancer cases, the tumor grade, tumor classification, lymph node invasion status, distant metastasis status and pathology were presented in a separate paper [21].

Table 1 General characteristics of renal cancer cases and healthy controls
Full size table

APOA1 -75 G/A polymorphisms and renal cancer

Patients with renal cancer had a significantly higher frequency of APOA1 -75 AA genotype [odds ratio (OR) = 2.10, 95 % confidence interval (CI) = 1.18, 3.75; P = 0.01] and APOA1 -75 A allele (OR =1.40, 95 % CI = 1.05, 1.87; P = 0.02) than controls (Table 2). When stratifying by the distant metastasis status, patients with distant metastasis had a significantly higher frequency of APOA1 -75 AA genotype genotype (OR =2.20, 95 % CI = 1.04, 4.68; P = 0.04) (Table 3). When stratifying by the tumor grade, tumor classification, lymph node invasion status and pathology, no significant differences were found (Table 3).

Table 2 Genotype and allele frequencies of APOA1 gene polymorphisms (−75 G/A and +83 C/T) among renal cancer cases and healthy controls
Full size table
Table 3 Stratification analysis of APOA1 -75 G/A polymorphisms in renal cancer cases
Full size table

APOA1 + 83 C/T polymorphisms and renal cancer

We did not find any association between APOA1 + 83 C/T polymorphisms and renal cancer risk (Table 2).

Discussion

Many studies have suggested that genetic susceptibility may play a role in the etiology of renal cancer. The DKK3 polymorphisms were associated with renal cancer and that the DKK2 rs17037102 polymorphism might be a predictor for survival in patients with renal cancer after radical nephrectomy [22]. We recently found that IL-6 -174 CC genotype was associated with an increased risk for renal cancer [21]. The functional -31G/C polymorphism in the promoter of survivin might influence the susceptibility and progression of renal cancer in the Chinese population [23]. The polymorphisms of the CYP1B1 gene at codons 119 and 432 might be risk factors for renal cancer, especially in the male population [7]. The CYP1A1 polymorphisms might play an important role in the etiology of renal cancer [24]. The polymorphisms of catechol-O-methyltransferase in men were associated with renal cancer [25]. The R allele of paraoxonase-1 gene Q192R polymorphism might protect against renal cancer [26]. Two SNPs in AGTR1 might be a candidate pathway in renal cancer etiology [27]. Polymorphisms in genes of the renin-angiotensin-aldosterone system (AGTR1 and AGT) influenced renal cell cancer susceptibility [27]. A common variant, rs35252396, at 8q24.21 was associated with renal cell cancer [28].

The APOA1 gene polymorphisms were also associated with many other diseases. It has been found that the APOA1 -75 G/A polymorphism was associated with gallstone disease [29]. The APOA1 -75 G/A and +83 C/T genotypes were also associated with susceptibility to breast cancer and lymph node metastases occurrence, respectively [20]. A pilot study found that APOA1 polymorphisms (−75 G/A and +83 C/T) might be susceptibility to myocardial infarction in a north Indian population [19]. The individuals with the APOA1 -75 A allele were likely to have a lower risk of coronary artery disease as a result of its effect on higher serum concentrations of ApoA1 and HDL-C [30]. The APOA1 -75G/A promoter polymorphism was associated with cognitive performance in multiple sclerosis [31]. It has been found that the APOA1 polymorphisms (−75 G/A and +83 C/T) could be as risk factors for hypertension and obesity in a Brazilian elderly cohort [32]. The APOA1 -75 A allele was associated with an increased risk for Alzheimer’s disease [33]. The APOA1 -75 AA genotype was associated with a higher acute lung injury risk after cardiopulmonary bypass surgery [34].

The exact biological mechanism of the association between the APOA1 -75G/A polymorphisms and the risk of renal cancer is still unclear. ApoA1 can play important roles in tumor growth, angiogenesis, invasion and metastasis [12–14]. Expression of ApoA1 is associated with colonic adenocarcinoma progression, and thus ApoA1 is a potential marker of the aggression [35]. It has also been found that APOA1 -75 G/A and +83 C/T genotypes were associated with susceptibility to breast cancer and lymph node metastases occurrence, respectively [20]. A recent fascinating study reveals an overall protective ability of HDL, specifically APOA1, to induce tumor suppression through both innate and adaptive immune processes in multiple animal tumor models [36]. Tabet et al. demonstrated that HDL’s anti-inflammatory properties were conferred, in part, through HDL-micro-RNA (miR)-223 delivery and translational repression of ICAM-1 in endothelial cells [37]. However, the miR221/222 cluster increases the aggressiveness of tumors in epithelial cancers, through repression of tumor suppressors and through induction of cell motility [38]. APOA1 allelic variety may have an impact on angiogenesis [39]. APOA1 binding protein (AIBP) positively regulates cholesterol efflux from endothelial cells and that effective cholesterol efflux is critical for proper angiogenesis [39]. AIBP is highly expressed in human renal cancer and in 83 % of cancers in general [39]. But there is no study about the interaction of AIBP and the APOA1 alleles. Further research on the possible interaction of AIBP and the APOA1 alleles is necessary.

Some shortcomings of this study should be mentioned. First of all, potential selection bias might have been present, because this is a hospital based case control study and the subjects may not be representative of the general population. Second, this study is limited by its size and lack of replication. Finally, further research on the biological mechanism of the association between the APOA1 -75G/A polymorphisms and the risk of renal cancer is necessary.

In conclusion, to our best knowledge, up to now this study is the first to examine prospectively an increased risk role of APOA1 -75 AA genotype and APOA1 -75 A allele in renal cancer susceptibility.

References

  1. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2015. CA Cancer J Clin. 2015;65:5–29.

    Article  PubMed  Google Scholar 

  2. Marumo K, Satomi Y, Miyao N, Hasegawa M, Tomita Y, Igarashi T, et al. Japanese Society of Renal C: The prevalence of renal cell carcinoma: a nation-wide survey in Japan in 1997. Int J Urol. 2001;8:359–65.

    Article  CAS  PubMed  Google Scholar 

  3. Chen W, Zheng R, Zeng H, Zhang S, He J. Annual report on status of cancer in China, 2011. Chin J Cancer Res. 2015;27:2–12.

    Article  PubMed Central  PubMed  Google Scholar 

  4. Chen WQ, Zheng RS, Zeng HM, Zhang SW, Zhao P, He J. Trend analysis and projection of cancer incidence in China between 1989 and 2008. Zhonghua Zhong Liu Za Zhi. 2012;34:517–24.

    PubMed  Google Scholar 

  5. Kroeger N, Klatte T, Birkhauser FD, Rampersaud EN, Seligson DB, Zomorodian N, et al. Smoking negatively impacts renal cell carcinoma overall and cancer-specific survival. Cancer. 2012;118:1795–802.

    Article  PubMed  Google Scholar 

  6. Theis RP, Dolwick Grieb SM, Burr D, Siddiqui T, Asal NR. Smoking, environmental tobacco smoke, and risk of renal cell cancer: a population-based case–control study. BMC Cancer. 2008;8:387.

    Article  PubMed Central  PubMed  Google Scholar 

  7. Sasaki M, Tanaka Y, Okino ST, Nomoto M, Yonezawa S, Nakagawa M, et al. Polymorphisms of the CYP1B1 gene as risk factors for human renal cell cancer. Clin Cancer Res. 2004;10:2015–9.

    Article  CAS  PubMed  Google Scholar 

  8. McLaughlin JK, Gao YT, Gao RN, Zheng W, Ji BT, Blot WJ, et al. Risk factors for renal-cell cancer in Shanghai, China. Int J Cancer. 1992;52:562–5.

    Article  CAS  PubMed  Google Scholar 

  9. Cao Q, Qin C, Ju X, Meng X, Wang M, Zhu J, et al. Chromosome 11q13.3 variant modifies renal cell cancer risk in a Chinese population. Mutagenesis. 2012;27:345–50.

    Article  CAS  PubMed  Google Scholar 

  10. Segrest JP, Li L, Anantharamaiah GM, Harvey SC, Liadaki KN, Zannis V. Structure and function of apolipoprotein A-I and high-density lipoprotein. Curr Opin Lipidol. 2000;11:105–15.

    Article  CAS  PubMed  Google Scholar 

  11. Breslow JL, Ross D, McPherson J, Williams H, Kurnit D, Nussbaum AL, et al. Isolation and characterization of cDNA clones for human apolipoprotein A-I. Proc Natl Acad Sci U S A. 1982;79:6861–5.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  12. Clarke CH, Yip C, Badgwell D, Fung ET, Coombes KR, Zhang Z, et al. Proteomic biomarkers apolipoprotein A1, truncated transthyretin and connective tissue activating protein III enhance the sensitivity of CA125 for detecting early stage epithelial ovarian cancer. Gynecol Oncol. 2011;122:548–53.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  13. Moore LE, Fung ET, McGuire M, Rabkin CC, Molinaro A, Wang Z, et al. Evaluation of apolipoprotein A1 and posttranslationally modified forms of transthyretin as biomarkers for ovarian cancer detection in an independent study population. Cancer Epidemiol Biomarkers Prev. 2006;15:1641–6.

    Article  CAS  PubMed  Google Scholar 

  14. Charet JC, Watine J, Marre A, Charet P. Prognostic value of serum levels of cholesterol and apolipoprotein A1 in pulmonary cancer. Ann Biol Clin (Paris). 1997;55:52.

    CAS  Google Scholar 

  15. Arinami T, Hirano T, Kobayashi K, Yamanouchi Y, Hamaguchi H. Assignment of the apolipoprotein A-I gene to 11q23 based on RFLP in a case with a partial deletion of chromosome 11, del(11)(q23.3----qter). Hum Genet. 1990;85:39–40.

    Article  CAS  PubMed  Google Scholar 

  16. Karathanasis SK. Apolipoprotein multigene family: tandem organization of human apolipoprotein AI, CIII, and AIV genes. Proc Natl Acad Sci U S A. 1985;82:6374–8.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  17. Saha N, Tay JS, Low PS, Humphries SE. Guanidine to adenine (G/A) substitution in the promoter region of the apolipoprotein AI gene is associated with elevated serum apolipoprotein AI levels in Chinese non-smokers. Genet Epidemiol. 1994;11:255–64.

    Article  CAS  PubMed  Google Scholar 

  18. Wang XL, Badenhop R, Humphrey KE, Wilcken DE. New MspI polymorphism at +83 bp of the human apolipoprotein AI gene: association with increased circulating high density lipoprotein cholesterol levels. Genet Epidemiol. 1996;13:1–10.

    Article  PubMed  Google Scholar 

  19. Dawar R, Gurtoo A, Singh R. Apolipoprotein A1 gene polymorphism (G-75A and C + 83 T) in patients with myocardial infarction: a pilot study in a north Indian population. Am J Clin Pathol. 2010;134:249–55.

    Article  CAS  PubMed  Google Scholar 

  20. Hamrita B, Ben Nasr H, Gabbouj S, Bouaouina N, Chouchane L, Chahed K. Apolipoprotein A1–75 G/A and +83 C/T polymorphisms: susceptibility and prognostic implications in breast cancer. Mol Biol Rep. 2011;38:1637–43.

    Article  CAS  PubMed  Google Scholar 

  21. Liu Z, Wang Z, Xiao Y, Lu Y, Lu Y. Association between the interleukin-6 gene polymorphisms and renal cancer risk. Immunol Lett. 2015;164:125–8.

    Article  CAS  PubMed  Google Scholar 

  22. Hirata H, Hinoda Y, Nakajima K, Kikuno N, Yamamura S, Kawakami K, et al. Wnt antagonist gene polymorphisms and renal cancer. Cancer. 2009;115:4488–503.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  23. Qin C, Cao Q, Li P, Ju X, Wang M, Chen J, et al. Functional promoter -31G > C variant in survivin gene is associated with risk and progression of renal cell cancer in a Chinese population. PLoS One. 2012;7:e28829.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  24. Chen J, Cheng M, Yi L, Jiang CB. Relationship between CYP1A1 genetic polymorphisms and renal cancer in China. Asian Pac J Cancer Prev. 2011;12:2163–6.

    PubMed  Google Scholar 

  25. Tanaka Y, Hirata H, Chen Z, Kikuno N, Kawamoto K, Majid S, et al. Polymorphisms of catechol-O-methyltransferase in men with renal cell cancer. Cancer Epidemiol Biomarkers Prev. 2007;16:92–7.

    Article  CAS  PubMed  Google Scholar 

  26. Uyar OA, Kara M, Erol D, Ardicoglu A, Yuce H. Investigating paraoxonase-1 gene Q192R and L55M polymorphism in patients with renal cell cancer. Genet Mol Res. 2011;10:133–9.

    Article  CAS  PubMed  Google Scholar 

  27. Deckers IA, van den Brandt PA, van Engeland M, van Schooten FJ, Godschalk RW, Keszei AP, et al. Polymorphisms in genes of the renin-angiotensin-aldosterone system and renal cell cancer risk: interplay with hypertension and intakes of sodium, potassium and fluid. Int J Cancer. 2015;136:1104–16.

    Article  CAS  PubMed  Google Scholar 

  28. Gudmundsson J, Sulem P, Gudbjartsson DF, Masson G, Petursdottir V, Hardarson S, et al. A common variant at 8q24.21 is associated with renal cell cancer. Nat Commun. 2013;4:2776.

    Article  PubMed  Google Scholar 

  29. Dixit M, Choudhuri G, Saxena R, Mittal B. Association of apolipoprotein A1-C3 gene cluster polymorphisms with gallstone disease. Can J Gastroenterol. 2007;21:569–75.

    PubMed Central  PubMed  Google Scholar 

  30. Liao B, Cheng K, Dong S, Liu H, Xu Z. Effect of apolipoprotein A1 genetic polymorphisms on lipid profiles and the risk of coronary artery disease. Diagn Pathol. 2015;10:102.

    Article  PubMed Central  PubMed  Google Scholar 

  31. Koutsis G, Panas M, Giogkaraki E, Karadima G, Sfagos C, Vassilopoulos D. An APOA1 promoter polymorphism is associated with cognitive performance in patients with multiple sclerosis. Mult Scler. 2009;15:174–9.

    Article  CAS  PubMed  Google Scholar 

  32. Chen ES, Mazzotti DR, Furuya TK, Cendoroglo MS, Ramos LR, Araujo LQ, et al. Apolipoprotein A1 gene polymorphisms as risk factors for hypertension and obesity. Clin Exp Med. 2009;9:319–25.

    Article  CAS  PubMed  Google Scholar 

  33. Vollbach H, Heun R, Morris CM, Edwardson JA, McKeith IG, Jessen F, et al. APOA1 polymorphism influences risk for early-onset nonfamiliar AD. Ann Neurol. 2005;58:436–41.

    Article  CAS  PubMed  Google Scholar 

  34. Tu J, Zhang B, Chen Y, Liang B, Liang D, Liu G, et al. Association of apolipoprotein A1–75 G/A polymorphism with susceptibility to the development of acute lung injury after cardiopulmonary bypass surgery. Lipids Health Dis. 2013;12:172.

    Article  PubMed Central  PubMed  Google Scholar 

  35. Tachibana M, Ohkura Y, Kobayashi Y, Sakamoto H, Tanaka Y, Watanabe J, et al. Expression of apolipoprotein A1 in colonic adenocarcinoma. Anticancer Res. 2003;23:4161–7.

    CAS  PubMed  Google Scholar 

  36. Zamanian-Daryoush M, Lindner D, Tallant TC, Wang Z, Buffa J, Klipfell E, et al. The cardioprotective protein apolipoprotein A1 promotes potent anti-tumorigenic effects. J Biol Chem. 2013;288:21237–52.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  37. Tabet F, Vickers KC, Cuesta Torres LF, Wiese CB, Shoucri BM, Lambert G, et al. HDL-transferred microRNA-223 regulates ICAM-1 expression in endothelial cells. Nat Commun. 2014;5:3292.

    Article  PubMed Central  PubMed  Google Scholar 

  38. Chistiakov DA, Sobenin IA, Orekhov AN, Bobryshev YV. Human miR-221/222 in Physiological and Atherosclerotic Vascular Remodeling. Biomed Res Int. 2015;2015:354517.

    Article  PubMed Central  PubMed  Google Scholar 

  39. Fang L, Choi SH, Baek JS, Liu C, Almazan F, Ulrich F, et al. Control of angiogenesis by AIBP-mediated cholesterol efflux. Nature. 2013;498:118–22.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

Download references

Acknowledgements

Thanks are expressed to all coinvestigators, local project coordinators, research assistants, laboratory technicians, and secretaries/administrative assistants.

Funding

This research received no specific grant from any funding agency in the public, commercial, nor for-profit sectors.

Author information

Author notes

    Authors and Affiliations

    1. Department of Urology, West China Hospital, Sichuan University, No 37, Guo Xue Xiang, Chengdu, 610041, China

      ZhiHong Liu, LiangYou Tang, Liang Jiang, YuJie Wang, RuoChen Zhang, Qiang Wei & YiPing Lu

    2. Department of Urology, The Second people’s Hospital of Sichuan, Chengdu, 610041, China

      YingMing Xiao

    Authors
    1. ZhiHong Liu
      View author publications

      You can also search for this author in PubMed Google Scholar

    2. YingMing Xiao
      View author publications

      You can also search for this author in PubMed Google Scholar

    3. LiangYou Tang
      View author publications

      You can also search for this author in PubMed Google Scholar

    4. Liang Jiang
      View author publications

      You can also search for this author in PubMed Google Scholar

    5. YuJie Wang
      View author publications

      You can also search for this author in PubMed Google Scholar

    6. RuoChen Zhang
      View author publications

      You can also search for this author in PubMed Google Scholar

    7. Qiang Wei
      View author publications

      You can also search for this author in PubMed Google Scholar

    8. YiPing Lu
      View author publications

      You can also search for this author in PubMed Google Scholar

    Corresponding author

    Correspondence to YiPing Lu.

    Additional information

    Competing interests

    The authors declare that they have no competing interests.

    Authors’ contributions

    ZHL, YMX and YPL carried out the molecular genetic studies and drafted the manuscript. LYT and LJ carried out the genotyping. YJW, RCZ and QW participated in the design of the study and performed the statistical analysis. ZHL, YMX, LYT, LJ, YJW, RCZ, QW and YPL conceived of the study, and participated in its design and coordination and helped to draft the manuscript. All authors read and approved the final manuscript.

    ZhiHong Liu and YingMing Xiao, are joint first authors.

    ZhiHong Liu and YingMing Xiao contributed equally to this work.

    Rights and permissions

    Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

    Reprints and Permissions

    About this article

    Check for updates. Verify currency and authenticity via CrossMark

    Cite this article

    Liu, Z., Xiao, Y., Tang, L. et al. Apolipoprotein A1 -75 G/A and +83 C/T polymorphisms and renal cancer risk. Lipids Health Dis 14, 143 (2015). https://doi.org/10.1186/s12944-015-0132-0

    Download citation

    • Received:

    • Accepted:

    • Published:

    • DOI: https://doi.org/10.1186/s12944-015-0132-0

    Keywords

    • Apolipoprotein A1
    • Renal cancer
    • Gene polymorphism

    Lipids in Health and Disease

    ISSN: 1476-511X