genotypes of CYP1A2*1D or CYP1A2*1F was also observed in the study. Since
CYP1A2 is induced by smoking and is involved in the metabolic activation of
heterocyclic amines and procarcinogens (Landi et al. 1999; Bofetta et al. 2008),
there is a strong interaction of smoking with polymorphic CYP1A2 genotypes in
enhancing the risk to lung cancer. Other studies have also provided evidence for
interaction of CYP1A1 and 1B1 genotypes with tobacco chewing in enhancing the
susceptibility to lung cancer (Shah et al. 2008a, b). Apart from lung cancer, an
elevated risk was also observed in smokers who carried variant alleles of
CYP1A2*1D and CYP1A2*1F in pancreatic cancer (Li et al. 2006).
The Gallbladder cancer is a deadly malignancy which exhibits considerable
differences in prevalence among certain ethnicities and geographic regions. The
areas which are the most affected regions are the Indo-Gangetic plains of India,
Mapuche Indians in Chile and South America (Sharma et al. 2017). A meta-analysis
showed that GSTM1 deletion and NAT2 slow acetylator status were significantly
associated with bladder cancer and an interaction with smoking was only observed
for the NAT2 polymorphisms (García-Closas et al. 2005). Studies have also been
carried out in the Indian population to study the role of genetic variations in the
development of gall bladder cancer. A case-control genome-wide association study
of gallbladder cancer cases and controls of Indian descent observed genome-wide
significant associations for ABCB1 and ABCB4 genes which suggests the importance of hepatobiliary phospholipid transport in the pathogenesis of gallbladder
cancer in Indian populations (Mhatre et al. 2017). Another study performed in a
north Indian population showed significant associations of the SNPs in TERT
(rs2736100C > A, CLPTM1L rs401681C > T and CASC8 rs6983267G > T) with
gallbladder cancer risk (Yadav et al. 2018). Several other studies by Mittal and
co-workers have also reported the association of polymorphisms in several genes
with risk of gallbladder cancer in north Indian population. Genetic polymorphisms
of IL-1 (Vishnoi et al. 2008), Complement receptor 1 (Srivastava and Mittal 2009),
OGG1 and XRCC1 (Srivastava et al. 2009), ERCC2, MSH2, and OGG1 (Srivastava
et al. 2010a), Caspase-8 (Srivastava et al. 2010b), CYP7A1 (Srivastava et al. 2010c),
ADRβ3 T190C (Rai et al. 2014), and TERT-CLPTM1L and 8q24 (Yadav et al.
2018) were reported to be associated with gallbladder cancer risk. In an another
gene–environment study in north Indian population, usage of tobacco (smoking or
nonsmoking) by gallbladder cancer patients showed a significant increase in cancer
risk with CYP1A1 Msp1 polymorphism (Pandey et al. 2008).
Studies conducted on HNSCC reported an association between tobacco use and
genetic variations of CYP1A1 (Singh et al. 2009). Amount of tobacco use also
influences the outcome of such interaction as a study in a Japanese population
reported that the risk associated with CYP1A1*2A genotype is inversely proportional to the amount of tobacco use (Sato et al. 1999; Tanimoto et al. 1999) and Sato
et al. (2000) observed that the risk was highest in the group with the lowest cigarette
dose level. Variant genotypes of CYP1B1*2 were found to interact with cigarette
smoking while no such significant interaction was reported with CYP1B1*3 or
CYP1B1*4 (Li et al. 2005; Singh et al. 2008b). However, contrasting reports are
also available with Ko et al. (2001) reporting that variant genotypes of CYP1B1*3
10 Interactions of Environmental Risk Factors and Genetic Variations: Association. . .
225
CYP1A2 is induced by smoking and is involved in the metabolic activation of
heterocyclic amines and procarcinogens (Landi et al. 1999; Bofetta et al. 2008),
there is a strong interaction of smoking with polymorphic CYP1A2 genotypes in
enhancing the risk to lung cancer. Other studies have also provided evidence for
interaction of CYP1A1 and 1B1 genotypes with tobacco chewing in enhancing the
susceptibility to lung cancer (Shah et al. 2008a, b). Apart from lung cancer, an
elevated risk was also observed in smokers who carried variant alleles of
CYP1A2*1D and CYP1A2*1F in pancreatic cancer (Li et al. 2006).
The Gallbladder cancer is a deadly malignancy which exhibits considerable
differences in prevalence among certain ethnicities and geographic regions. The
areas which are the most affected regions are the Indo-Gangetic plains of India,
Mapuche Indians in Chile and South America (Sharma et al. 2017). A meta-analysis
showed that GSTM1 deletion and NAT2 slow acetylator status were significantly
associated with bladder cancer and an interaction with smoking was only observed
for the NAT2 polymorphisms (García-Closas et al. 2005). Studies have also been
carried out in the Indian population to study the role of genetic variations in the
development of gall bladder cancer. A case-control genome-wide association study
of gallbladder cancer cases and controls of Indian descent observed genome-wide
significant associations for ABCB1 and ABCB4 genes which suggests the importance of hepatobiliary phospholipid transport in the pathogenesis of gallbladder
cancer in Indian populations (Mhatre et al. 2017). Another study performed in a
north Indian population showed significant associations of the SNPs in TERT
(rs2736100C > A, CLPTM1L rs401681C > T and CASC8 rs6983267G > T) with
gallbladder cancer risk (Yadav et al. 2018). Several other studies by Mittal and
co-workers have also reported the association of polymorphisms in several genes
with risk of gallbladder cancer in north Indian population. Genetic polymorphisms
of IL-1 (Vishnoi et al. 2008), Complement receptor 1 (Srivastava and Mittal 2009),
OGG1 and XRCC1 (Srivastava et al. 2009), ERCC2, MSH2, and OGG1 (Srivastava
et al. 2010a), Caspase-8 (Srivastava et al. 2010b), CYP7A1 (Srivastava et al. 2010c),
ADRβ3 T190C (Rai et al. 2014), and TERT-CLPTM1L and 8q24 (Yadav et al.
2018) were reported to be associated with gallbladder cancer risk. In an another
gene–environment study in north Indian population, usage of tobacco (smoking or
nonsmoking) by gallbladder cancer patients showed a significant increase in cancer
risk with CYP1A1 Msp1 polymorphism (Pandey et al. 2008).
Studies conducted on HNSCC reported an association between tobacco use and
genetic variations of CYP1A1 (Singh et al. 2009). Amount of tobacco use also
influences the outcome of such interaction as a study in a Japanese population
reported that the risk associated with CYP1A1*2A genotype is inversely proportional to the amount of tobacco use (Sato et al. 1999; Tanimoto et al. 1999) and Sato
et al. (2000) observed that the risk was highest in the group with the lowest cigarette
dose level. Variant genotypes of CYP1B1*2 were found to interact with cigarette
smoking while no such significant interaction was reported with CYP1B1*3 or
CYP1B1*4 (Li et al. 2005; Singh et al. 2008b). However, contrasting reports are
also available with Ko et al. (2001) reporting that variant genotypes of CYP1B1*3
10 Interactions of Environmental Risk Factors and Genetic Variations: Association. . .
225