Skip to main content

XAB2 tagSNPs contribute to non-small cell lung cancer susceptibility in Chinese population



XPA-binding protein 2 (XAB2) interacts with Cockayne syndrome complementation group A (CSA), group B (CSB) and RNA polymerase II to initiate nucleotide excision repair. This study aims to evaluate the association of XAB2 genetic variants with the risk of non-small cell lung cancer (NSCLC) using a tagging approach.


A hospital-based case-control study was conducted in 470 patients with NSCLC and 470 controls in Chinese population. Totally, 5 tag single nucleotide polymorphisms (SNPs) in XAB2 gene were selected by Haploview software using Hapmap database. Genotyping was performed using iPlex Gold Genotyping Asssy and Sequenom MassArray. Unconditional logistic regression was conducted to estimate odd ratios (ORs) and 95 % confidence intervals (95 % CI).


Unconditional logistic regression analysis showed that the XAB2 genotype with rs794078 AA or at least one rs4134816 C allele were associated with the decreased risk of NSCLC with OR (95 % CI) of 0.12 (0.03–0.54) and 0.46 (0.26–0.84). When stratified by gender, we found that the subjects carrying rs4134816 CC or CT genotype had a decreased risk for developing NSCLC among males with OR (95 % CI) of 0.39 (0.18–0.82), but not among females. In age stratification analysis, we found that younger subjects (age ≤ 60) with at least one C allele had a decreased risk of NSCLC with OR (95 % CI) of 0.35 (0.17–0.74), but older subjects didn’t. We didn’t find that XAB2 4134816 C > T variant effect on the risk of NSCLC when stratified by smoking status. The environmental factors, such as age, sex and smoking had no effect on the risk of NSCLC related to XAB2 genotypes at other polymorphic sites.


The XAB2 tagSNPs (rs794078 and rs4134816) were significantly associated with the risk of NSCLC in Chinese population, which supports the XAB2 plays a significant role in the development of NSCLC.

Peer Review reports


Worldwide, lung cancer harbored the highest incidence and mortality rates among all malignant cancers [1, 2]. Non-small cell lung cancer (NSCLC), as the most common type of lung cancer, accounts for 75–80 % of all lung cancer cases [3]. The development of lung cancer was greatly affected by the environmental factors, such as cigarette smoking, alcohol drinking and air pollutants [46]. However, evidence has showed that the genetic variants of cancer-related genes are associated with lung risk, which the important role of genetic factors in the development of lung cancer [79].

Nucleotide excision repair (NER) is the major DNA repair pathway to remove bulky DNA lesions induced by UV light and environmental carcinogens [10]. NER has two subpathways, global genome NER (GG-NER) and transcription coupling NER (TC-NER). TC-NER is involved in a rapid removal of the damages on the transcribed strands of active genes and a resumption of transcription [1113]. TC-NER is initiated by arresting RNA polymerase II at DNA lesion site on transcript strand. In the initiation of transcription coupling repair, the TC-NER specific proteins Cockayne syndrome complementation group A (CSA) and group B (CSB) are thought to play an important role in removing the stalled RNA polymorase II and recruiting other DNA repair proteins [14]. Many studies have demonstrated that the decreased expression of CSA and CSB in lung cancer and the genetic variants in these two genes were associated with the lung cancer risk [1518].

Xeroderma pigmentosum group A (XPA)-binding protein 2 (XAB2), which located at 19p13.2, was first identified as an interacting protein with XPA and hence found to interact with CSA, CSB and RNA polymerase II to participant to TC-NER and transcription [17, 19, 20]. In vitro, when cells treated with DNA-damaging agents, enhanced interaction of XAB2 with RNA polymerase II or XPA was observed, which suggesting DNA damage-responsive activity of the XAB2 [19].

Due to the important role of XAB2 in the TC-NER, we proposed that the genetic variants in XAB2 genes might contribute to the risk of lung cancer. To verify this proposal, we conducted this case-control study to evaluate the role of XAB2 tagSNPs in the development of NSCLC.


Study population

The study population has been described previously [21]. Briefly, this hospital-based case-control study consisted of 470 patients with NSCLC and 470 cancer-free controls. All subjects were unrelated Han Chinese. All patients with newly diagnosed, and previously untreated primary lung cancer were recruited between January 2008 and December 2012 at Tangshan Gongren Hospital (Tangshan, China). The exclusive criteria included previous cancer and previous radiotherapy or chemotherapy. The controls were randomly selected from cancer-free individuals living in the same region during the same period as the cases were collected. The selection criteria included no prior history of cancer. Controls were frequency matched to the cases by age (±5 years) and sex. At recruitment, informed consent was obtained from each subject who was then interviewed for detailed information on demographic characteristics and lifetime history of tobacco use. The study was approved by Ethics Committee of Hebei United University (Approval No. 12–002).

Tag SNPs selection and genotyping

Based on the Han Chinese in Beijing (CHB) population data from HapMap database, we used Haploview 4.2 program to select candidate tag SNPs with an r2 threshold of 0.80 and minor allele frequency (MAF) greater than 1 %. For XAB2 gene, we extended the 5′- and 3′-untranslated regions (UTR) to include the 5′-UTR and 3′-UTR most SNP. As a result, 5 tagSNPs (2 in 5′ UTR, 2 in intron, 1 in exon region) in XAB2 were included, which represent the common genetic variants in Chinese population. Genotyping was performed at Bomiao Tech (Beijing, China) using iPlex Gold Genotyping Asssy and Sequenom MassArray (Sequenom, San Diego, CA, USA). Sequenom’s MassArray Designer was used to design PCR and extension primers for each SNP. The information on assay conditions and the primers are available upon request. Genotyping quality control consisted of no-temple control samples for allele peaks and verifying consistencies in genotype calls of 2 % randomly selected duplicate sample. In addition, we excluded individuals and SNPs based on genotyping quality (<90 % call rate).

Statistical analysis

The χ2 test was used to examine differences in demographic variables and the distribution of genotype between patients and controls. Hardy-Weinberg equilibrium (HWE) for each SNP in controls was examined using Pearson goodness-of-fit χ2 test. The association of each tag SNP with the risk of NSCLC was estimated by odds ratios (ORs) and 95 % confidential intervals (95 % CI) using unconditional logistic regression adjusted by sex, age, and smoking status. Smokers were considered current smokers if they smoked up to 1 year before the date of cancer diagnosis for NSCLC patients or before the date of the interview for controls. The number of pack-years smoked was determined as an indication of cumulative cigarette-dose level [pack-year = (cigarettes per day/20) × (years smoked)]. Light and heavy smokers were categorized by using the 50th percentile pack-year value of the controls as the cut points (i.e., ≤25 and >25 pack-years). Statistical analysis was performed using the SPSS version16.0 (SPSS Inc, Chicago, IL). A P value of < 0.05 was considered as statistically significant. Gene-smoking interaction was analyzed by GxEscan (


Subject characteristics

The demographic characteristics of all participants are presented in Table 1. The distribution of gender and age among NSCLC cancer cases and healthy controls were not significantly different (P = 0.832 for gender, and P = 0.470 for age). There were also no significant differences in the distribution of smoking status between cases and controls. However, the heavy smokers (≥25 pack-year) accounted for 63.4 % in cases and only 49.2 % in controls, which suggested that cigarette smoking was a prominent contributor to the risk of lung cancer. Among ever-smokers, 46,8 % (96) and 41.8 % (79) are former smokers in lung cancer cases and controls, respectively. Of 470 NSCLC patients, 37.9 % (178) were adenocarcinoma, 50.6 % (238) was squamous cell carcinoma, and 11.5 % (54) were other types, including large cell carcinoma (n = 49) and mixed cell carcinoma (n = 5).

Table 1 Distributions of select characteristics in cases and control subjects

Selected SNPs and risk of developing NSCLC

The position and minor allele frequency (MAF) of the 5 selected tag SNPs in XAB2 gene were presented in Table 2. For all selected SNPs, the distributions of genotype frequencies in controls were close to those expected under Hardy Weinberg Equilibrium (HWE) (P > 0.05 for all).

Table 2 Primary information of tag SNPs inXAB2gene

The observed genotype frequencies in participants and the association of genotypes with the NSCLC were presented in Table 3. Of all selected SNPs in XAB2 genes, two SNPs were identified to be associated with the risk of NSCLC. For XAB2 rs794078 G > A polymorphism, we found that AA genotype carriers had a significantly decreased risk for developing NSCLC (OR = 0.12; 95 % CI = 0.03–0.54) in comparison to those with GG genotype. For XAB2 rs4134816 T > C polymorphism, just one CC genotype was found among all individuals, so we combined CT with CC genotype together for further analysis. Our data showed that the subjects with rs4134816 CT or CC genotype had a decreased risk of NSCLC compared with those carrying TT genotype with OR (95 % CI) of 0.46 (0.26–0.84). We didn’t find that any other selected SNPs were associated with the risk of NSCLC.

Table 3 Genotype frequencies of XAB2 and their association with non-small cell lung cancers

Stratification analysis of the XAB2 polymorphisms and the risk of NSCLC

We then performed stratification analysis to evaluate the effect of environmental factors on the association of XAB2 polymorphisms with the risk of NSCLC (Table 4). In dominant model, we found that the subjects carrying rs4134816 CC or CT genotype had a decreased risk for developing NSCLC among males with OR (95 % CI) of 0.39 (0.18–0.82), but not among females. When stratified by gender, we observed a positively significant interaction between rs4134816 genotypes and gender on decreasing NSCLC risk (P = 0.034). Our data also showed that younger subjects (age ≤ 60) with at least one C allele had a decreased risk of NSCLC with OR (95 % CI) of 0.35 (0.17–0.74), but older subjects didn’t. However, there was no gene-environment interaction observed (P = 0.094). We didn’t find that XAB2 4134816 C > T variant effect on the risk of NSCLC when stratified by smoking status. The environmental factors, such as age, sex and smoking had no effect on the risk of NSCLC related to XAB2 genotypes at other polymorphic sites (Table 4).

Table 4 Association of XAB2 tagSNPs with NSCLC risk stratified by selected variables


In this case-control study in a Chinese population, we found that two tag SNPs (rs794078 and rs4134816) in XAB2 were associated with significantly decreased risk of development non-small cell lung cancer. These findings indicated that XAB2 genetic variants might contribute to the susceptibility of lung cancer.

Nucleotide excision repair is the main mechanism for removing the bulky DNA adduct from damage DNA for preventing carcinogens-induced mutagenesis [22, 23]. Several animal models, where individual NER genes were disrupted, had showed the importance of the integrity of NER pathway in preventing lung cancer [24, 25].

TC-NER, as one of important sub-pathways in NER, only repairs the lesions in the transcribed strand in active genes. There are several major proteins involved in TC-NER in human cells, including CSA, CSB, XPA and XAB2. Studies have showed that the deficient of these nucleotide excision repair proteins contributed to the risk of various cancers. Animal experiments showed that the CSB played an important role in the cellular response to stress and CSB−/− mice were increased susceptible to chemically induced skin cancer [26]. A case-control study also found 12.2 and 12.5 % reduced RNA transcriptional levels of CSA and CSB in lung cancer patients than controls [27].

XAB2 is a key factor in TC-NER, which is composed of 855 amino acids and contains 15 tetratricopeptide repeat motifs. By interacting with CSA, CSB, RNA polymerase II and XPA, XAB2 conducted the multiple functions in the process of transcription and TC-NER [19, 20]. Microinjection of specific antibodies against XAB2 inhibits transcription and TC-NER, suggesting the key role of XAB2 in the process of transcription and TC-NER [20]. Knockdown of XAB2 in HeLa cell resulted in a hypersensitivity to killing by UV light and a decreased recovery of RNA synthesis [19]. Over expression of XAB2 was observed in HL60 cells treated with inhibited all-trans retinoic acid (ATRA) and inhibited XAB2 expression by small interfering RNA (siRNA) increased ATRA-sensitive cellular differentiation, which indicated that XAB2 was associated with the cellular differentiation [28].

Studies have demonstrated that the polymorphisms, which located in NER genes or regulatory sequences, may affect DNA repair capacity and further increase likelihood of cancer development. In the present study of NSCLC in Chinese, we used a relatively comprehensive selection of SNPs and found the significant effects of XAB2 variants on the risk of lung cancer. This is the first study to investigate the association of XAB2 polymorphisms with the risk for developing cancer. There were several studies to evaluate the role of XAB2 genetic variants in complex autoimmune disease. For example, Briggs et al. conducted a case-control study to evaluate the correlation between XAB2 rs4134860 T > C variant and the risk of multiple sclerosis (MS) and found an increased risk of MS among rs4134860 CC genotype carriers [29]. In this lung cancer case-control study, we didn’t find any association of XAB2 rs4134860 T > C polymorphism with the risk of NSCLC. In another study, researchers analyzed the impact of several polymorphisms in DNA repair genes on the prognosis of colorectal cancer patients and didn’t find the association of XAB2 rs794078 G > A variant with the cancer prognosis [30]. In present study, individuals carrying XAB2 rs794078 AA genotype had 88 % decreased risk of NSCLC.

As we know, the magnitude of the effect of smoking far outweighed all other factors leading to lung cancer [31, 32]. Many studies have demonstrated that the strong association of smoking with lung cancer risk [5, 33, 34]. Therefore, we further analyzed the role of XAB2 polymorphisms in the development of NSCLC stratified by smoking status. We observed that a 49 % protective effect for XAB2 rs4134816 variant was evident only for non-smokers, but not for smokers. The exact mechanism of how cigarette-smoking effects on DNA repair capacity posted by XAB2 polymorphism is unknown. One possible explanation may be that the protective effect of XAB2 variant allele might be evident in non-smokers with low levels of oxidative damage. Similar pattern of genetic effects have been observed for DNA repair gene XRCC1 (X-ray repair cross-complementation group 1) at low smoking exposure, but not at high smoking exposure [35].

When stratified by gender, our study showed a 61 % protective effect of XAB2 rs4134816 C genotype among men, but not among women. Genetic variants in NER genes are associated with variability of lung cancer risk. Letkova and his colleagues investigated the polymorphisms of selected DNA repair genes, including XPC, XPD, hOGG1 and XRCC1, and found the different risks of developing lung cancer when stratified by gender, which further supporting our current findings [36]. Our present study also found that a 65 % protective effect for XAB2 rs4134816 T > C genetic variant among subjects aged 60 years or younger. Using Cox proportional hazard model, Gauderman et al. estimated the age-specific genetic incidence rate and found that the estimated proportion of lung cancer patients with high-risk allele exceeds 90 % for cases with onset at age 60 years or less and decreases to approximately 10 % for cases with onset at age 80 years or older. These findings suggested the contribution of age in the development of cancer [37]. The numbers of subjects in several of subgroups were very small, so some caution is needed when interpreting these findings.

Our study has its limitation. Due to the moderate sample size and the lack of related phenotypic and functional assays, large studies and functional evaluations are still need to be conducted in the future.


In conclusion, we have genotyped 5 tag SNPs in XAB2 gene in this NSCLC case-control set. We found the evidence of significant association with the risk of NSCLC for two tag SNPs (rs794078 and rs4134816) in XAB2 gene in Chinese population. These results further supported that XAB2 play a significant role in the development of NSCLC.


XAB2 :

XPA-binding protein 2


Minor allele frequency


Odds ratio


Confidence interval


Single nucleotide polymorphism


  1. Horak J, Sobota J, Burda J. Angiographic diagnostics of splenic tumours (author’s transl). Cesk Radiol. 1975;29(5):348–55.

    CAS  PubMed  Google Scholar 

  2. Bunn Jr PA. Worldwide overview of the current status of lung cancer diagnosis and treatment. Arch Pathol Lab Med. 2012;136(12):1478–81.

    Article  PubMed  Google Scholar 

  3. Kurkcuoglu N, Alaybeyi F. Topical capsaicin for psoriasis. Br J Dermatol. 1990;123(4):549–50.

    Article  CAS  PubMed  Google Scholar 

  4. Jemal A, Bray F, Center MM, Ferlay J, Ward E, Forman D. Global cancer statistics. CA Cancer J Clin. 2011;61(2):69–90.

    Article  PubMed  Google Scholar 

  5. Hecht SS. Lung carcinogenesis by tobacco smoke. Int J Cancer. 2012;131(12):2724–32.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  6. Dresler C. The changing epidemic of lung cancer and occupational and environmental risk factors. Thorac Surg Clin. 2013;23(2):113–22.

    Article  PubMed  Google Scholar 

  7. Liu L, Wu J, Wu C, Wang Y, Zhong R, Zhang X, et al. A functional polymorphism (−1607 1G2G) in the matrix metalloproteinase-1 promoter is associated with development and progression of lung cancer. Cancer. 2011;117(22):5172–81.

    Article  CAS  PubMed  Google Scholar 

  8. Ke J, Zhong R, Zhang T, Liu L, Rui R, Shen N, et al. Replication study in Chinese population and meta-analysis supports association of the 5p15.33 locus with lung cancer. PLoS One. 2013;8(4):e62485.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  9. Yang IA, Holloway JW, Fong KM. Genetic susceptibility to lung cancer and co-morbidities. J Thorac Dis. 2013;5 Suppl 5:S454–62.

    PubMed  PubMed Central  Google Scholar 

  10. Scharer OD. Nucleotide excision repair in eukaryotes. Cold Spring Harb Perspect Biol. 2013;5(10):a012609.

    Article  PubMed  PubMed Central  Google Scholar 

  11. Hanawalt PC, Spivak G. In: Dizdaroglu M, Karakaya AE, editors. Advances in DNA Damage and Repair. New York: Kluwer Academic/Plenum Publishers; 1999. p. 169–79.

    Chapter  Google Scholar 

  12. Mellon I. Transcription-coupled repair: a complex affair. Mutat Res. 2005;577(1–2):155–61.

    Article  CAS  PubMed  Google Scholar 

  13. Hanawalt PC, Spivak G. Transcription-coupled DNA repair: two decades of progress and surprises. Nat Rev Mol Cell Biol. 2008;9(12):958–70.

    Article  CAS  PubMed  Google Scholar 

  14. van den Boom V, Jaspers NG, Vermeulen W. When machines get stuck--obstructed RNA polymerase II: displacement, degradation or suicide. Bioessays. 2002;24(9):780–4.

    Article  PubMed  Google Scholar 

  15. Leng S, Bernauer A, Stidley CA, Picchi MA, Sheng X, Frasco MA, et al. Association between common genetic variation in Cockayne syndrome A and B genes and nucleotide excision repair capacity among smokers. Cancer Epidemiol Biomarkers Prev. 2008;17(8):2062–9.

    Article  CAS  PubMed  Google Scholar 

  16. Lehmann AR. DNA repair-deficient diseases, xeroderma pigmentosum, Cockayne syndrome and trichothiodystrophy. Biochimie. 2003;85(11):1101–11.

    Article  CAS  PubMed  Google Scholar 

  17. Fousteri M, Mullenders LH. Transcription-coupled nucleotide excision repair in mammalian cells: molecular mechanisms and biological effects. Cell Res. 2008;18(1):73–84.

    Article  CAS  PubMed  Google Scholar 

  18. Reddy JK, Rao S, Moody DE. Hepatocellular carcinomas in acatalasemic mice treated with nafenopin, a hypolipidemic peroxisome proliferator. Cancer Res. 1976;36(4):1211–7.

    CAS  PubMed  Google Scholar 

  19. Kuraoka I, Ito S, Wada T, Hayashida M, Lee L, Saijo M, et al. Isolation of XAB2 complex involved in pre-mRNA splicing, transcription, and transcription-coupled repair. J Biol Chem. 2008;283(2):940–50.

    Article  CAS  PubMed  Google Scholar 

  20. Nakatsu Y, Asahina H, Citterio E, Rademakers S, Vermeulen W, Kamiuchi S, et al. XAB2, a novel tetratricopeptide repeat protein involved in transcription-coupled DNA repair and transcription. J Biol Chem. 2000;275(45):34931–7.

    Article  CAS  PubMed  Google Scholar 

  21. Yu X, Rao J, Lin J, Zhang Z, Cao L, Zhang X. Tag SNPs in complement receptor-1 contribute to the susceptibility to non-small cell lung cancer. Mol Cancer. 2014;13:56.

    Article  PubMed  PubMed Central  Google Scholar 

  22. Dreij K, Seidel A, Jernstrom B. Differential removal of DNA adducts derived from anti-diol epoxides of dibenzo[a, l]pyrene and benzo[a]pyrene in human cells. Chem Res Toxicol. 2005;18(4):655–64.

    Article  CAS  PubMed  Google Scholar 

  23. Lage C, de Padula M, de Alencar TA, da Fonseca Goncalves SR, da Silva VL, Cabral-Neto J, et al. New insights on how nucleotide excision repair could remove DNA adducts induced by chemotherapeutic agents and psoralens plus UV-A (PUVA) in Escherichia coli cells. Mutat Res. 2003;544(2–3):143–57.

    Article  CAS  PubMed  Google Scholar 

  24. Hollander MC, Philburn RT, Patterson AD, Velasco-Miguel S, Friedberg EC, Linnoila RI, et al. Deletion of XPC leads to lung tumors in mice and is associated with early events in human lung carcinogenesis. Proc Natl Acad Sci U S A. 2005;102(37):13200–5.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  25. Melis JP, Wijnhoven SW, Beems RB, Roodbergen M, van den Berg J, Moon H, et al. Mouse models for xeroderma pigmentosum group A and group C show divergent cancer phenotypes. Cancer Res. 2008;68(5):1347–53.

    Article  CAS  PubMed  Google Scholar 

  26. van der Horst GT, van Steeg H, Berg RJ, van Gool AJ, de Wit J, Weeda G, et al. Defective transcription-coupled repair in Cockayne syndrome B mice is associated with skin cancer predisposition. Cell. 1997;89(3):425–35.

    Article  PubMed  Google Scholar 

  27. Cheng L, Spitz MR, Hong WK, Wei Q. Reduced expression levels of nucleotide excision repair genes in lung cancer: a case-control analysis. Carcinogenesis. 2000;21(8):1527–30.

    Article  CAS  PubMed  Google Scholar 

  28. Ohnuma-Ishikawa K, Morio T, Yamada T, Sugawara Y, Ono M, Nagasawa M, et al. Knockdown of XAB2 enhances all-trans retinoic acid-induced cellular differentiation in all-trans retinoic acid-sensitive and -resistant cancer cells. Cancer Res. 2007;67(3):1019–29.

    Article  CAS  PubMed  Google Scholar 

  29. Briggs FB, Goldstein BA, McCauley JL, Zuvich RL, De Jager PL, Rioux JD, et al. Variation within DNA repair pathway genes and risk of multiple sclerosis. Am J Epidemiol. 2010;172(2):217–24.

    Article  PubMed  PubMed Central  Google Scholar 

  30. Kim JG, Chae YS, Sohn SK, Moon JH, Kang BW, Park JY, et al. IVS10 + 12A > G polymorphism in hMSH2 gene associated with prognosis for patients with colorectal cancer. Ann Oncol. 2010;21(3):525–9.

    Article  CAS  PubMed  Google Scholar 

  31. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Personal habits and indoor combustions. Volume 100 E. A review of human carcinogens. IARC Monogr Eval Carcinog Risks Hum. 2012;100(Pt E)):1–538.

    Google Scholar 

  32. de Groot P, Munden RF. Lung cancer epidemiology, risk factors, and prevention. Radiol Clin North Am. 2012;50(5):863–76.

    Article  PubMed  Google Scholar 

  33. Schwartz AG, Prysak GM, Bock CH, Cote ML. The molecular epidemiology of lung cancer. Carcinogenesis. 2007;28(3):507–18.

    Article  CAS  PubMed  Google Scholar 

  34. Jassem E, Szymanowska A, Sieminska A, Jassem J. Smoking and lung cancer. Pneumonol Alergol Pol. 2009;77(5):469–73.

    PubMed  Google Scholar 

  35. Stern MC, Umbach DM, van Gils CH, Lunn RM, Taylor JA. DNA repair gene XRCC1 polymorphisms, smoking, and bladder cancer risk. Cancer Epidemiol Biomarkers Prev. 2001;10(2):125–31.

    CAS  PubMed  Google Scholar 

  36. Letkova L, Matakova T, Musak L, Sarlinova M, Krutakova M, Slovakova P, et al. DNA repair genes polymorphism and lung cancer risk with the emphasis to sex differences. Mol Biol Rep. 2013;40(9):5261–73.

    Article  CAS  PubMed  Google Scholar 

  37. Gauderman WJ, Morrison JL. Evidence for age-specific genetic relative risks in lung cancer. Am J Epidemiol. 2000;151(1):41–9.

    Article  CAS  PubMed  Google Scholar 

Download references


This study was supported by National Natural Science Foundation of China (81272613 to X. Zhang), Program for New Century Excellent Talents in University (NCET-11-0933 to X. Zhang), A Foundation for the Author of National Excellent Doctoral Dissertation of PR China (FANEDD) (201274 to X. Zhang), Science Fund for Distinguished Young Scholars of Hebei Scientific Committee (2012401022 to X. Zhang), and Leader talent cultivation plan of innovation team in Hebei province (LJRC001 to X. Zhang).

Author information

Authors and Affiliations


Corresponding authors

Correspondence to Juxiang Yuan or Xuemei Zhang.

Additional information

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

NP drafted the article; NP, JY, LC and YL analyzed the data; JW, QS, JY and ZZ collected clinical data; XZ contributed to the research plan, approved the data and the final version of the manuscript. All authors read and approved the final manuscript.

Rights and permissions

Open Access  This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made.

The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder.

To view a copy of this licence, visit

The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Pei, N., Cao, L., Liu, Y. et al. XAB2 tagSNPs contribute to non-small cell lung cancer susceptibility in Chinese population. BMC Cancer 15, 560 (2015).

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: