various types of cancers in individuals who consume alcohol. One such gene is
alcohol dehydrogenase (ADH) which is involved in the metabolism of alcohol. A
study by Hashibe et al. (2008) analyzed six ADH variants in more than 3800
individuals with aerodigestive cancer and over 5200 controls. One variant each in
ADH1B and ADH7 was significantly protective against aerodigestive cancer specifically in individuals who were alcohol drinkers, and most strongly in those who had
higher alcohol intake. Individuals with the protective variant in ADH1B are known
to metabolize alcohol up to 100 times faster than those without it, suggesting that
lower exposure to alcohol is protective against the disease.
10.5 Conclusions
Environmental risk factors such as tobacco (in the form of smoking or chewing) or
alcohol use increase the cancer risk in cases carrying the variant genotypes of phase I
and phase II XMEs compared to those not exposed to these risk factors. Cancer is
caused by certain changes in genes that control the functions of the cell related to
growth and division. Cancer-causing gene mutations either occur over the course of
a lifetime or are inherited from parents. Studies suggest that genetic variations in
genes metabolizing tobacco and alcohol interact with these environmental risk
factors and increase the cancer risk clearly stating the significance of gene–environment interactions. The studies indicate that gene–environment studies have a higher
power than only environmental studies. The applications of gene–environment
studies range from searching for new causes of disease (when the effects of the
tested genes, environmental exposures or both are unknown), or exploring the
mechanisms of cellular action of established environmental factors, such as smoking. Such studies need to assemble large data sets and large well-characterized
populations in order to test complex gene–environment interaction pathways. This
will help in improving accuracy and precision in the assessment of both genetic and
environmental influences leading to well-informed recommendations for cancer
prevention.
References
Accort NA, Waterbor JW, Beall C et al (2005) Cancer incidence among a cohort of smokeless
tobacco users (United States). Cancer Causes Control 16:1107–1115
Altieri A, La Vecchia C, Negri E (2003) Fluid intake and risk of bladder and other cancers. Eur J
Clin Nutr 57:S59–S68
Andre K, Schraub S, Mercier M et al (1995) Role of alcohol and tobacco in the aetiology of head
and neck cancer: a case-control study in the Doubs region of France. Eur J Cancer B Oral Oncol
5:301–309
Asthana S, Patil RS, Labani S (2016) Tobacco-related cancers in India: a review of incidence
reported from population-based cancer registries. Indian J Med Paediatr Oncol 37:152–157
Bagnardi V, Rota M, Botteri E et al (2015) Alcohol consumption and site-specific cancer risk: a
comprehensive dose-response meta-analysis. Br J Cancer 112:580–593
Bofetta P, Hecht S, Grey N et al (2008) Smokeless tobacco and cancer. Lancet Oncol 9:667–675
228
M. Ruwali and R. Shukla
alcohol dehydrogenase (ADH) which is involved in the metabolism of alcohol. A
study by Hashibe et al. (2008) analyzed six ADH variants in more than 3800
individuals with aerodigestive cancer and over 5200 controls. One variant each in
ADH1B and ADH7 was significantly protective against aerodigestive cancer specifically in individuals who were alcohol drinkers, and most strongly in those who had
higher alcohol intake. Individuals with the protective variant in ADH1B are known
to metabolize alcohol up to 100 times faster than those without it, suggesting that
lower exposure to alcohol is protective against the disease.
10.5 Conclusions
Environmental risk factors such as tobacco (in the form of smoking or chewing) or
alcohol use increase the cancer risk in cases carrying the variant genotypes of phase I
and phase II XMEs compared to those not exposed to these risk factors. Cancer is
caused by certain changes in genes that control the functions of the cell related to
growth and division. Cancer-causing gene mutations either occur over the course of
a lifetime or are inherited from parents. Studies suggest that genetic variations in
genes metabolizing tobacco and alcohol interact with these environmental risk
factors and increase the cancer risk clearly stating the significance of gene–environment interactions. The studies indicate that gene–environment studies have a higher
power than only environmental studies. The applications of gene–environment
studies range from searching for new causes of disease (when the effects of the
tested genes, environmental exposures or both are unknown), or exploring the
mechanisms of cellular action of established environmental factors, such as smoking. Such studies need to assemble large data sets and large well-characterized
populations in order to test complex gene–environment interaction pathways. This
will help in improving accuracy and precision in the assessment of both genetic and
environmental influences leading to well-informed recommendations for cancer
prevention.
References
Accort NA, Waterbor JW, Beall C et al (2005) Cancer incidence among a cohort of smokeless
tobacco users (United States). Cancer Causes Control 16:1107–1115
Altieri A, La Vecchia C, Negri E (2003) Fluid intake and risk of bladder and other cancers. Eur J
Clin Nutr 57:S59–S68
Andre K, Schraub S, Mercier M et al (1995) Role of alcohol and tobacco in the aetiology of head
and neck cancer: a case-control study in the Doubs region of France. Eur J Cancer B Oral Oncol
5:301–309
Asthana S, Patil RS, Labani S (2016) Tobacco-related cancers in India: a review of incidence
reported from population-based cancer registries. Indian J Med Paediatr Oncol 37:152–157
Bagnardi V, Rota M, Botteri E et al (2015) Alcohol consumption and site-specific cancer risk: a
comprehensive dose-response meta-analysis. Br J Cancer 112:580–593
Bofetta P, Hecht S, Grey N et al (2008) Smokeless tobacco and cancer. Lancet Oncol 9:667–675
228
M. Ruwali and R. Shukla