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Year : 2012  |  Volume : 49  |  Issue : 1  |  Page : 144--162

Indian studies on genetic polymorphisms and cancer risk

A Bag1, NS Jyala2, N Bag3,  
1 Institute of Allied Health (Paramedical) Services, Education and Training, Department of Biochemistry, Government Medical College, Haldwani, Uttarakhand, India
2 Department of Biochemistry, Government Medical College, Haldwani, Uttarakhand, India
3 Plantation Management and Studies, Sikkim University, Gangtok, Sikkim, India

Correspondence Address:
A Bag
Institute of Allied Health (Paramedical) Services, Education and Training, Department of Biochemistry, Government Medical College, Haldwani, Uttarakhand


Genetic influences on cancer development have been extensively investigated during the last decade following publication of human genome sequence. The present review summarizes case-control studies on genetic polymorphisms and cancer risk in Indians. It is observed that the most commonly studied genes in the Indian population included members of phase I and phase II metabolic enzymes. Other than these genes, genetic polymorphisms for cell cycle and apoptosis-related factors, DNA repair enzymes, immune response elements, growth factors, folate metabolizing enzymes, vitamin/hormone receptors, etc., were investigated. Several studies also evidenced a stronger risk for combined genotypes rather than a single polymorphism. Gene-environment interaction was also found to be a determining factor for cancer development in some experiments. Data for single polymorphism and single cancer type, however, was insufficient to validate an association. It appears that much more experiments involving larger sample size, cross-tabulating genetic polymorphisms and environmental factors are required in order to identify genetic markers for different cancers in Indian populations.

How to cite this article:
Bag A, Jyala N S, Bag N. Indian studies on genetic polymorphisms and cancer risk.Indian J Cancer 2012;49:144-162

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Bag A, Jyala N S, Bag N. Indian studies on genetic polymorphisms and cancer risk. Indian J Cancer [serial online] 2012 [cited 2020 Jul 7 ];49:144-162
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Publication of the human genome sequence led to a stupendous growth in the field of biomarker studies. Search for genetic associations with various diseases, including cancers, got momentum with an aim to identify preventive/prognostic markers. Mostly, cancer cases are diagnosed at advanced stages and existing treatments are successful for only a fraction of the patients. Hence, cancer markers that can be used as tools for early diagnosis and prognosis are urgently required.

Because genetic alterations have an unquestionable influence on cancer development and treatment outcome, gene-based markers are expected to have a significant impact on cancer management. The most common genetic alterations are single nucleotide polymorphisms (SNPs). SNP(s) account for >90% of the variations in human genome, and the remaining 10% of these variations include chromosomal aberrations, DNA copy number and microsatellites. [1] Because of their preponderance in human genome (approximately one in every 1000 base pairs), SNP(s) in candidate genes have been widely explored for cancer risk.

The scientific community in India has shown a great concern toward the identification of genetic markers for cancer development as well as chemotherapeutic outcome. The Indian Genome Variation Database (IGVdb) consortium was established in 2003, with the objectives to build a database on SNPs and repeat polymorphisms of biomedically important genes in Indian subpopulations, and constructing haplotype maps. The information is expected to contribute in the steeply growing field of pharmacogenetics. Indian studies on genetic association with cancer are summarized in this article.

We identified studies related to the association of different genetic polymorphisms with the risk of various types of cancers in Indians. Selected articles followed a case-control design. Studies were identified through PubMed, published before October 2010. For each study, we extracted the first author, year of publication, population, size of study population, genetic polymorphisms and the reported results. We used the term ND (not defined) when specific information was not obvious either in text or in an abstract (and when only abstracts of these articles could be collected). Similarly, only OR values were mentioned in Tables for those articles in which the 95% confidence intervals were not mentioned in abstracts. For no association (NS), OR values were not included in the extract. We found that majority of the experiments followed the polymerase chain reaction (PCR) (for null genotypes) and PCR followed by Restriction fragment length polymorphism, and few used the DNA sequencing and PCR coupled Single strand conformation polymorphism for the detection of SNP.

 Genetic Polymorphisms and Cancer Risk

A total of 137 studies were included in this review. The genes included in these studies were grouped according to their broad functions and represented in separate Tables [Table 1], [Table 2], [Table 3], [Table 4] and [Table 5]. The first group includes xenobiotic metabolizing enzymes. Mostly, carcinogens undergo activation by phase I enzymes often as an oxidation reaction. Then, metabolites are detoxified by phase II metabolic enzymes. [2] Hence, polymorphisms in genes controlling carcinogen metabolism are hypothesized to influence a person's risk for cancer. Cytochrome P450 enzyme super-family (CYP) constitutes the majority of phase I enzymes, and glutathione S-transferases (GSTs), sulfotransferases (SULTs), N-acetyltransferases (NATs) and UDP glycosyltransferases (UGTs) are the main phase II enzymes. The most commonly studied metabolic genes in Indian populations were found to be members of the CYP and GST superfamilies.{Table 1}{Table 2}{Table 3}{Table 4}{Table 5}

[Table 1] represents the case-control studies on genetic polymorphisms of carcinogen metabolizing enzymes for cancer association. It is found that CYP1A1 was the most commonly studied CYP gene. In the present article, its polymorphisms are named following the nomenclature system recommended in CYP1A1 enzyme, previously known as aryl hydrocarbon hydroxylase, is a major phase I metabolizing enzyme involved in the metabolic activation of pro-carcinogens to carcinogens. Hence, CYP1A1 polymorphisms got adequate attention as a putative biomarker for cancer susceptibility. Unlike majority of the CYPs that are expressed mainly in human liver, CYP1A1 is expressed predominantly in the extrahepatic tissues, e.g. lung, breast, ovarian follicles, etc. A number of studies have been carried out on the association between CYP1A1 variants with lung cancer risk worldwide, although findings of these studies remain largely contradictory. [3] We found four studies on CYP1A1 polymorphisms in Indian populations [4],[5],[6],[7] that depict significant associations with lung cancer. However, a meta- analysis could not be carried out at this stage as the number of studies and their total population size were too less to validate CYP1A1 and lung cancer risk in Indians. Both m1 (T3698C) and m2 (A2454G) polymorphisms demonstrated a significant association with different cancers. CYP2E1 is responsible for the activation of many low-molecular weight carcinogens. [2] Because CYP2E1 is expressed in human lung, CYP2E1 can be a good candidate gene to be studied for lung cancer. This gene has been observed to be significantly associated with gastrointestinal tract (GIT) cancer in the Kashmiri population. [8],[9] CYP17, which mediates in sex steroid synthesis, has been found to be significantly associated with prostate cancer [10],[11] in North Indian populations. Sporadic studies involving other CYP genes were also observed [Table 1]. CYP1B1 with an important role in hormonal carcinogenesis or CYP2D6 with a high number of variant alleles could not be noted in Indian studies.

Oxidative stress has often been implicated in carcinogenesis. GST is a superfamily of multifunctional enzymes that facilitates detoxification reactions and thus plays an important role in the cellular defense system against oxidative stress. Thus, a decrease in the level of GST enzymes is expected to increase the risk of cancer formation. Structural homozygous deletions in these genes represent null genotype with total loss of enzyme function, and have been widely tested for cancer link. From [Table 1], it is found that the GSTT1 null genotype was associated with different types of cancers except in two cases where it was responsible for reduced risk of oral [12] and gall bladder cancers. [13] The Ile105Val form of GSTP1 isoform has been linked to head and neck cancers, with 105 Val allele as the risky genotype. [2] Significant risk for Val/Val genotype has been reported in Indian populations for few cancer types, but not for all [Table 1].

Acetylating polymorphisms are investigated for cancer development as many carcinogens are metabolized by acetylation in the liver. Two NAT isozymes, NAT1 and NAT2, are responsible for both O-acetylation (activation) and N-acetylation (usually detoxification) of aromatic and heterocyclic amine carcinogens in humans. [2] Only few studies could be identified on NAT polymorphisms for the Indian population. Only one study [14] reported a significant association of a NAT2 genotype with acute myeloid leukemia (AML).

Cytosolic SULT1A1 is responsible for both activation and inactivation of different carcinogens. Probably SULT1A1 Arg213His has an important role in tobacco-related cancers. [15] Kotnis et al. [15] found a significant risk for this polymorphism, with multiple primary neoplasms in the upper aerodigestive tract including lung. A seven-fold risk of head and neck cancer has been reported in smokers with UGT1A7 low activity polymorphism in a single study noted here. [16] The human epoxide hydrolase 1 (EPHX1) is involved in the metabolism of environmental and tobacco carcinogens. [17] Two polymorphisms, Tyr113His and His139Arg, have been studied for cancer association. Both these polymorphisms were found to be protective as well as risk factors for esophageal cancer. [17],[18]

Polymorphisms of genes related to cell cycle, apoptosis and cancer risk have been summarized in [Table 2]. Tumor suppressor gene p53 has been found to be inactivated in half of human cancers. [19] Because of its critical role in cell cycle control, apoptosis and cellular senescence, it has become one of the most sought after genes for carcinogenesis study. Inherited germline mutations in this gene have been evidenced to promote cancer in mice and humans, and a loss of function can transform normal cells to tumor cells with the help of other mutant cell cycle genes. [20] Most commonly studied polymorphism with cancer link is a G>C polymorphism in codon 72, which leads to Arg>Pro substitution. Pro/Pro genotype poorly suppresses cellular transformation in comparison with Arg/Arg, [21] and has been suspected as the risk genotype. Although few, investigations on Indian populations reported higher cancer risk for Arg homozygous genotype [22],[23],[24] rather than as low-risk genotype and in one case for Pro/Pro genotype. [25] Inhibition of p73 function by mutant p53 abrogates apoptosis. [26] Only one study was noted on p73 mutation. [27] Common cyclin D1 (CCND1) plays a critical role in the transition from G1 to S phase of the cell cycle. [28] Overexpression of CCND1 has commonly been observed in human cancers with diverse histological origin. [29] A870G polymorphism of this gene has been reported for its significant association with cervical cancer. [28],[30] Although MDM2 is an important oncoprotein and inactivates p53 tumor suppressor activity, [31] only one study was observed in the Indian population. [27] Apoptotic gene caspase-9-1263A/G polymorphism was found to have reduced the risk for prostate and bladder cancer. [32],[33] A single study noted a significant association for each of antiapoptotic Bcl2, cell death receptors Fas, tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) receptors and signaling molecule H-Ras [Table 2].

DNA-repair enzymes are required for removal of DNA damage caused due to endogenous metabolic processes or because of exposure to environmental carcinogens. Aberrant functions of these enzymes are obvious to promote carcinogenesis. Genes involved in the base excision repair (BER) and nucleotide excision repair (NER) pathways have been extensively studied worldwide for cancer risk. XRCC1, a major member in the BER pathway, is encoded by X-ray repair cross-complementary 1 (XRCC1) and involved in single-strand break repair. It has been studied for three polymorphisms in Indians, Arg399Gln, Arg194Trp and Arg280His. All three polymorphisms have been found to be associated with increased cancer risk, reduced cancer risk or for no risk at all [Table 3]. Highly polymorphic excision cross-complementary gene encodes ERCC2/xeroderma pigmentosum type D (XPD) protein, a member of the NER pathway, also acts as part of transcription factor complex, TFIIH. [34] XPD Lys751Gln has been extensively studied for cancer risk. Indian studies described a significant association between different types of cancers and XPD, and XPC, another NER gene xeroderma pigmentosum type C. BER gene apurinic/apyrimidinic endonuclease (APE1) has been identified as a protective factor for Asp148Gln polymorphism. [35],[36] Polymorphisms of human 8-oxoguanine glycosylase 1 (OGG1), MSH2 and APEX1 have also been found to be associated with different types of cancer risk in some cases [Table 3].

[Table 4] summarizes the Indian studies on immune response genes and cancer association. Chronic inflammation contributes to transformation of a normal cell to a malignant one. [37] Interleukin-1 receptor antagonists (IL-1RN) and IL-1β are pro-inflammatory cytokine genes whose polymorphisms can affect inflammatory diseases, including cancer. Although limited, studies show involvement of polymorphisms of these genes with cancers of the digestive system. [38],[39] IL-6 is known to play a major role in the proliferation of tumor cells, [40] and has been studied for -174G/C polymorphism. [40],[41],[42] IL-10, which influences immune response and immune evasion of tumor cells, [43] was studied for two polymorphisms, and associations were found for prostate [43] and bladder [44] cancer.

TNFα and -β pro-inflammatory cytokines are known to contribute in both tumor progression and destruction based on their concentrations. [45] -308G/A polymorphism of TNFα was largely found to be strongly associated with breast [46] cancer and cervical cancer, [47],[48] although in a limited number of studies. Cyclooxygenase-2 (COX-2) influences carcinogenesis through regulation of angiogenesis, apoptosis and cytokine expression. [49] Cancer association was found for its polymorphisms among Indians. Other gene cytokine receptors CCR5δ32, complement receptor 1 (CR1), toll-like receptors (TLRs) and interferon (IFNγ) were also described for cancer association, although in isolated studies. [50],[51],[52],[53]

Epidermal growth factors (EGF) influence cell cycle progression, apoptosis, angiogenesis and metastasis. [54] A61G of EGF, 497Arg/Lys of EGFR (EGF receptor) and SNPs of tumor growth factor β1 (TGFβ1) were studied for cancer risk [Table 5]. Estrogen receptor (ER), progesterone receptor (PR) and androgen receptor (AR) were also studied and found to be associated with breast and prostate cancer. [55],[56],[57],[58],[59] Extracellular matrix (ECM) degradation enzymes were demonstrated as risk factor. [60],[61],[62] Vitamin-D is antiproliferative and is reported to induce apoptosis in human bladder tumor cells in vivo.[63] Fok-I polymorphism of its receptor (VDR) was found to be associated with prostate and bladder cancer. [63],[64] Methylenetetrahydrofolate reductase (MTHFR), a folate metabolizing enzyme, is involved in DNA synthesis, DNA repair and DNA methylation. [65] Its polymorphisms were largely found to be reduced risk factors. [66],[67] ABCB1-encoded P-glycoprotein efflux pump and adenosine triphosphate-binding cassette transporter ABCG8 were evidenced as risk factors. [68],[69]


Because high-penetrance gene mutations are known to cause only <5% of all cancers (mostly hereditary), [70],[71] it is widely believed that genes with relatively small effects could have a significant contribution in cancer development. It is believed that cumulative effects of polymorphisms in low-penetrance genes affecting gene-environment and gene-gene interactions may influence the risk of cancer development. [71] Hence, low-penetrance common alleles with minor allele frequency (MAF) >5% have frequently been chosen in genetic association studies. A large sample size is required in order to get statistically significant power in these kinds of association studies [72] as these alleles contribute only modestly toward the risk for cancers. It has been found that, often, the case-control studies are published with small sample size, which may, sometimes, generate a false-positive association. To overcome these limitations, genome-wide association studies (GWAS) that scan the genomes of thousands of people at a time [73] for common SNPs associated with a trait, e.g. cancer or other diseases, are currently being studied. However, metaanalysis on existing data of published case-control studies could also be considered as a strong tool to validate a polymorphism for true cancer risk. In the present review on Indian studies, it was seen that the available data on a particular polymorphism in association with a specific cancer type was not sufficient to carry out metaanalysis.

Further, we think that other than the discussed genes, polymorphisms of oxidative stress genes, especially human manganese superoxide dismutase (MnSOD), can be a good choice for investigating cancer association. MnSOD, one of the major antioxidant enzymes, catalyzes the dismutation of superoxide radicals (O 2 - ) to hydrogen peroxide (H 2 O 2 ) and oxygen in mitochondria and thus constitutes first-line defense against reactive oxygen species in the mitochondria. A change in the level of O 2 - and of H2 O2 in mitochondria modulates the molecular mechanisms of apoptosis, cellular adhesion and cell proliferation and thus plays a key role in cancer development. [74] Hence, it is conceivable that structural and/or functional polymorphisms of the MnSOD gene could influence carcinogenesis process.

Other than tobacco, alcohol-related cancers are also a major problem in Indians. Alcohol consumption enhances the risk of mouth, tongue, pharynx, larynx, esophagus and liver cancer. Except in liver cancer, in all these alcohol-related cancers, smoking may cause a multiplicative effect. [75] Hence, studies can be extended to identify the association between polymorphic alcohol-metabolizing enzymes with cancer risk in Indians. A Glu487Lys change in aldehyde dehydrogenase-2 (ALDH2), which has been reported to be prevalent in East Asian populations, [76],[77] and is related to high serum levels, [78] can be of particular interest. Further, association studies for ovarian cancers in Indian women were found to be lacking. CYP3A4 plays an important role in estrogen oxidation. A promoter polymorphism in CYP3A4 has been shown to be associated with ovarian cancer risk. [79] This polymorphism, along with other polymorphic steroid-metabolizing enzymes, can be studied.

Interestingly, a considerable number of Indian studies observed much higher association between cancer and combined genotypes rather than a single polymorphism. Few prominent examples include the findings of Singh et al.,[80] which demonstrated a much greater risk (4.47; 95% CI, 1.62-12.31; P=0.002) for HNSCC in the patients carrying a combination of GSTM1 null, GSTT1 null and GSTP1 (Ile105Ile) than in those carrying individual variations [Table 1]. While Srivastava et al. [81] found no association of GSTT1, GSTM1 null alleles with bladder cancer risk separately [Table 1], a combination of these null genotypes and GSTP1 risk genotypes demonstrated a several-fold increased risk (OR 7.29; 95% CI 2.81-18.93). Again, Soya et al. [82] observed that a combination of GSTM1 and GSTT1 had a significantly increased risk (OR 4.6; 95% CI 1.3-15.6) for UADT cancer, and GSTT1 null genotype along with GSTP1 polymorphic variants had further increased the risk (OR 5.3; 95% CI 2.0-13.6). Risk for hepatocellular carcinoma was increased by 35.96-times for a combination of Arg280His and Arg194Trp of XRCC1, a higher value than that of single polymorphism. [83] All these findings indicate the need for combined genotype analysis rather than a single polymorphism study in order to reveal any genetic association with cancer.

Again, lifestyle factors such as food habits, smoking, alcohol consumption, etc. are known to influence genes to develop cancer. Perhaps one of the most significant gene-environment interactions was observed by Mittal et al. [84] They found a highly significant risk for GSTP1 gene polymorphism in combination with tobacco exposure (OR 24.06; 95% CI 4.80-120.42) and bladder cancer. While Malik et al. [85] found no association for OGG1 Ser326Cys with gastric cancer in the Kashmiris, they observed a highly significant risk for smokers and high-salted tea drinkers (OR 8.975 and OR 14.778, respectively).


Germline mutations are important as they can be used as tools to predict a person's risk for cancer as well as can be used to understand the underlying mechanism of carcinogenesis. Hence, more association studies for more candidate genes involving a larger sample size and more variables, such as polymorphisms in linkage disequilibrium, gene-gene interactions and environmental exposures, are required to reveal a true genetic association for cancer.


The authors are grateful to the State Biotechnology Department, Uttarakhand, for the research grant.[153]


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112Singh H, Sachan R, Devi S, Pandey SN, Mittal B. Association of GSTM1, GSTT1, and GSTM3 gene polymorphisms and susceptibility to cervical cancer in a North Indian population. Am J Obstet Gynecol 2008;198:303.e1-303.e6.
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115Kesarwani P, Singh R, Mittal RD. Association of GSTM3 intron 6 variant with cigarette smoking, tobacco chewing and alcohol as modifier factors for prostate cancer risk. Arch Toxicol 2009;83:351-6.
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119Jain M, Kumar S, Lal P, Tiwari A, Ghoshal UC, Mittal B. Association of genetic polymorphisms of N-Acetyltransferase 2 and susceptibility to esophageal cancer in North Indian population. Cancer Invest 2007;25:340-6.
120Malik MA, Upadhyay R, Modi DR, Zargar SA, Mittal B. Association of NAT2 gene polymorphisms with susceptibility to esophageal and gastric cancers in the Kashmir Valley. Arch Med Res 2009;40:416-23.
121Srivastava DS, Mittal RD. Genetic polymorphism of the N-acetyltransferase 2 gene, and susceptibility to prostate cancer: A pilot study in North Indian population. BMC Urol 2005;5:12.
122Pachouri SS, Sobti RC, Kaur P, Singh J, Gupta SK. Impact of polymorphism in sulfotransferase gene on the risk of lung cancer. Cancer Genet Cytogenet 2006;171:39-43.
123Chacko P, Rajan B, Mathew BS, Joseph T, Pillai MR. CYP17 and SULT1A1 gene polymorphisms in Indian breast cancer. Breast Cancer 2004;11:380-8.
124Sobti RC, Kaur P, Kaur S, Singh J, Janmeja AK, Jindal SK, et al. Effects of cyclin D1 (CCND1) polymorphism on susceptibility to lung cancer in a North Indian population. Cancer Genet Cytogenet 2006;170:108-14.
125Jain M, Kumar S, Lal P, Tiwari A, Ghoshal UC, Mittal B. Role of BCL2 (ala43 th r), CCND1 (G870A) and FAS(A-670G) polymorphisms in modulating the risk of developing esophageal cancer. Cancer Detect Prev 2007;31:225-32.
126Jiang J, Wang J, Suzuki S, Gajalakshmi V, Kuriki K, Zhao Y, et al. Elevated risk of colorectal cancer associated with the AA genotype of the cyclin D1 A870G polymorphism in an Indian population. J Cancer Res Clin Oncol 2006;132:193-9.
127Kordi Tamandani DM, Sobti RC, Shekari M. Association of Fas-670 gene polymorphism with risk of cervical cancer in North Indian population. Clin Exp Obstet Gynecol 2008;35:183-6.
128Pal R, Gochhait S, Chattopadhyay S, Gupta P, Prakash N, Agarwal G, et al. Functional implication of TRAIL -716 C/T promoter polymorphism on its in vitro and in vivo expression and the susceptibility to sporadic breast tumor. Breast Cancer Res Treat 2011;126:333-43.
129Sreeja L, Syamala VS, Syamala V, Hariharan S, Raveendran P, Vijayalekshmi R, et al. Prognostic importance of DNA repair gene polymorphisms of XRCC1 Arg399Gln and XPD Lys751Gln in lung cancer patients from India. J Cancer Res Clin Oncol 2008;134:645-52.
130Pachouri SS, Sobti RC, Kaur P, Singh J. Contrasting impact of DNA repair gene XRCC1 polymorphisms Arg399Gln and Arg194Trp on the risk of lung cancer in the north-Indian population. DNA Cell Biol 2007;26:186-91.
131Sobti RC, Singh J, Kaur P, Pachouri SS, Siddiqui EA, Bindra HS. XRCC1 codon 399 and ERCC2 codon 751 polymorphism, smoking, and drinking and risk of esophageal squamous cell carcinoma in a North Indian population. Cancer Genet Cytogenet 2007;175:91-7.
132Srivastava A, Srivastava K, Pandey SN, Choudhuri G, Mittal B. Single-nucleotide polymorphisms of DNA repair genes OGG1 and XRCC1: Association with gallbladder cancer in North Indian population. Ann Surg Oncol 2009;16:1695-703.
133Mitra AK, Singh N, Singh A, Garg VK, Agarwal A, Sharma M, et al. Association of polymorphisms in base excision repair genes with the risk of breast cancer: A case-control study in North Indian women. Oncol Res 2008;17:127-35.
134Chacko P, Rajan B, Joseph T, Mathew BS, Pillai MR. Polymorphisms in DNA repair gene XRCC1 and increased genetic susceptibility to breast cancer. Breast Cancer Res Treat 2005;89:15-21.
135Mandal RK, Gangwar R, Mandhani A, Mittal RD. DNA repair gene X-ray repair cross-complementing group 1 and xeroderma pigmentosum group D polymorphisms and risk of prostate cancer: A study from North India. DNA Cell Biol 2010;29:183-90.
136Gangwar R, Mittal B, Srivastava S, Singh H, Mittal RD. Genetic variants of DNA repair gene XPC modulating susceptibility to cervical cancer in North India. Oncol Res 2010;18:329-35.
137Mitra AK, Singh N, Garg VK, Chaturvedi R, Sharma M, Rath SK. Statistically significant association of the single nucleotide polymorphism (SNP) rs13181 (ERCC2) with predisposition to Squamous Cell Carcinomas of the Head and Neck (SCCHN) and Breast cancer in the North Indian population. J Exp Clin Cancer Res 2009;28:104.
138Srivastava K, Srivastava A, Mittal B. Polymorphisms in ERCC2, MSH2, and OGG1 DNA repair genes and gallbladder cancer risk in a population of Northern India. Cancer 2010;116:3160-9.
139Upadhyay R, Malik MA, Zargar SA, Mittal B. OGG1 Ser326Cys polymorphism and susceptibility to esophageal cancer in low and high at-risk populations of northern India. J Gastrointest Cancer 2010;41:110-5.
140Upadhyay R, Jain M, Kumar S, Ghoshal UC, Mittal B. Potential influence of interleukin-1 haplotype IL-1 beta-511*T-IL-1RN*1 in conferring low risk to middle third location of esophageal cancer: A case-control study. Hum Immunol 2008;69:179-86.
141Konwar R, Chaudhary P, Kumar S, Mishra D, Chattopadhyay N, Bid HK. Breast cancer risk associated with polymorphisms of IL-1RN and IL-4 gene in Indian women. Oncol Res 2009;17:367-72.
142Singh H, Sachan R, Goel H, Mittal B. Genetic variants of interleukin-1RN and interleukin-1beta genes and risk of cervical cancer. BJOG 2008;115:633-8.
143Bid HK, Manchanda PK, Mittal RD. Association of interleukin-1Ra gene polymorphism in patients with bladder cancer: case control study from North India. Urology 2006;67:1099-104.
144Gupta R, Sharma SC, Das SN. Association of TNF-alpha and TNFR1 promoters and 3' UTR region of TNFR2 gene polymorphisms with genetic susceptibility to tobacco-related oral carcinoma in Asian Indians. Oral Oncol 2008;44:455-63.
145Srivastava K, Srivastava A, Pandey SN, Kumar A, Mittal B. Functional polymorphisms of the cyclooxygenase (PTGS2) gene and risk for gallbladder cancer in a North Indian population. J Gastroenterol 2009;44:774-80.
146Pandey S, Mittal RD, Srivastava M, Srivastava K, Mittal B. Cyclooxygenase-2 gene polymorphisms and risk of cervical cancer in a North Indian population. Int J Gynecol Cancer 2010;20:625-30.
147Vishnoi M, Pandey SN, Modi DR, Kumar A, Mittal B. Genetic susceptibility of epidermal growth factor +61A>G and transforming growth factor beta1-509C>T gene polymorphisms with gallbladder cancer. Hum Immunol 2008;69:360-7.
148Saha A, Gupta V, Bairwa NK, Malhotra D, Bamezai R. Transforming growth factor-beta1 genotype in sporadic breast cancer patients from India: Status of enhancer, promoter, 5'-untranslated-region and exon-1 polymorphisms. Eur J Immunogenet 2004;31:37-42.
149Chakraborty A, Mishra AK, Soni A, Regina T, Mohil R, Bhatnagar D, et al. Vitamin D receptor gene polymorphism(s) and breast cancer risk in North Indians. Cancer Detect Prev 2009;32:386-94.
150Jain M, Kumar S, Ghoshal UC, Mittal B. Association of ECRG2 TCA short tandem repeat polymorphism with the risk of oesophageal cancer in a North Indian population. Clin Exp Med 2008;8:73-8.
151Srivastava K, Srivastava A, Mittal B. Angiotensin I-converting enzyme insertion/deletion polymorphism and increased risk of gall bladder cancer in women. DNA Cell Biol 2010;29:417-22.
152Surekha D, Vishnupriya S, Sailaja K, Nageswara Rao D, Raghunadharao D. Influence of Apolipoprotein E gene polymorphism on the risk for breast cancer. Int J Hum Genet 2008;8:277-82.
153Jiang J, Gajalakshmi V, Wang J, Kuriki K, Suzuki S, Nakamura S, et al. Influence of the C161T but not Pro12Ala polymorphism in the peroxisome proliferator-activated receptor-gamma on colorectal cancer in an Indian population. Cancer Sci 2005;96: 507-12.