SCHOOL of cancer (Shi et al., 2015). According to




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Breast cancer is the common type of
cancer that usually affects women all around the world with an amount of 1.7
million new cases diagnosed in 2012 and is the leading cause of cancer-related
mortality (Ferlay et al., 2014). Usually, consumption of alcoholic beverages is
related to female breast cancer (Chiara et al., 2014). Alcohol is one of the
substances that promote carcinogenesis and leads to the formation of cancer
(Shi et al., 2015). According to World Health Organization (WHO), the
International Agency for Research on Cancer (IARC) has been confirmed that the
consumption of alcoholic beverages can cause cancers of the oral cavity,
pharynx, larynx, liver and female breast due to its carcinogenicity.

The components in alcoholic beverage
are important to be known due to the effect of carcinogenicity (Schwab, 2011).
Polycyclic aromatic hydrocarbon (PHA’s) is a hydrocarbon organic compound which
can be found in dark hard liquors while N-nitrosoamine is a chemical compound
which can be detected in beers. It can reach to the breast tissue and induce
faster cell division which may lead to breast cancer  (Schwab, 2011). For instance, PHA’s
containing substances lead to an enhanced risk of cancer by increasing estrogen
level in women (Bostrom et al., 2002).

The association of the mechanism of
alcohol with human cancer can be determined by observing the effect of alcohol
on RNA polymerase. According to Sporn & Suh (2000), carcinogenesis is the
accumulation of somatic mutations in a single cell line which will cause
neoplastic changes frequently. However, the development of carcinogenesis can be
controlled physiologically and pharmacologically at preneoplastic stages by
chemoprevention (Sporn & Suh, 2000). Chemoprevention has the ability to
reduce cancer load, while the use of tamoxifen and raloxifene can be used as
the agents during chemoprevention to control breast cancer among women (Bozovic
et al., 2012).



2.1 Composition of alcohol

Alcoholic drinks consist of
naturally occurring or naturally produced chemical substances which include the
micronutrients and macronutrients (Boyle et al., 2013). Macronutrients such as
ethanol, carbohydrates, protein and fats are required in the specific amount
for human health and growth whereas micronutrients of beers and wines contain
essential components like minerals of calcium, potassium, copper, iron and
magnesium as well as vitamins required only in a small amount by the body
(Boyle et al., 2013). However, it is necessary to determine the recommended
quantity of alcohol which is safe to be consumed without suffering from breast
cancer. There are a few guidelines about the amount and the standard unit of
alcohol wise to drink per day (Jones, 2016). Men should not drink more than 3
to 4 units of alcohol per day while women should not drink more than 2 to 3
units of alcohol per day (Jones, 2016).


2.2 Mechanism of breast cancer associated with alcohol

According to Wright, Mcmanaman,
& Repine (1999), ethanol can be converted to acetate easily by a two-step
reaction. It is metabolized by alcohol dehydrogenase (ADH), producing
acetaldehyde and followed by the second stage of turning acetaldehyde into
acetate by molybdenum hydroxylase enzymes, xanthine oxidoreductase (XOR) or
aldehyde oxidase (AOX). Acetaldehyde can also be converted to acetate by
aldehyde dehydrogenase (ALDH) without forming reactive oxygen species (ROS).
However, both XOR and AOX have the ability to generate ROS. ROS are radicals,
ions or molecules which have a single unpaired electron in their outermost
shell of electron arrangement and have been recognized as signaling molecules
in different pathways of regulating both cell survival and cell death (Azad,
Chen, & Gibson, 2009). Examples are superoxide anion (), hydroxyl radical (•OH) and
hydrogen peroxide () that are the products of partial
reduction of oxygen. Metabolism of alcohol will increase the toxicity level in
the liver and lead to a higher amount of ROS, thus inducing DNA damage which
will result in DNA modification and the breaking of strands. In the case of
breast cancer, the development of breast cancer is associated with high levels
of •OH modified DNA. •OH is one of the major constituents for breast
carcinogenesis as it is able to create •OH adduction products, single strand or
double strand breakage, base deletions by modifying DNA (Wright, Mcmanaman,
& Repine, 1999).


Based on a newer research of
Dumitrescu & Shields (2005), alcohol consumption may cause breast cancer
through the disruption of estrogen metabolism and response. Alcohol intrudes
the estrogen pathways in multiple ways, affects hormone levels and influences
the estrogen receptors. Studies have been done on female rats by feeding them
with drinking water containing 12% ethanol (Dumitrescu & Shields, 2006).
The studies show that the rats have developed mammary tumours faster at a
median of 8 months compared to the controls fed with only drinking water at a
median of 14.2 months. Estrogen replacement has been practiced for many years
to prevent osteoporosis and reverse the hypoestrogenic symptoms of menopause.
However, alcohol alters circulating estrogen levels in females, giving an
impact of an undesirable direction of estrogen replacement. The combination of
estrogen replacement and alcohol is managed to elevate the breast cancer risk
to a higher level than either one alone.


2.3 Alcohol and folate

There is a significant interaction
between alcohol and folate as alcohol acts as a folate antagonist (Al-Sader, 2009).
Folate functions to help in preventing from certain spinal cord birth defects,
including spina bifida with the consumption of a right amount before and during
pregnancy (Lindblad, et al., 2005). In the study of Al-Sader (2009), a low intake of folate with at
least 15g/day of alcohol consumption led to a higher risk for breast cancer
while a high intake with at least 600 microgram/day of folate could reduce the
risk for breast cancer. There are possible mechanisms explaining why folate
deficiency and alcohol consumption might give rise to the risk for breast
cancer. Folate will be converted to its active form of tetrahydrofolic acid
(THF) that acts as a carrier compound to carry methyl group (5-methyl THF) and
causes global hypomethylation which is linked to genome mutation. Besides,
alcohol gives an impact on the folate transport and metabolism, interfering its
supply to tissues. It then disrupts the gene expression and causes DNA
breakage, which are critical risk factors to develop breast cancer.

2.4 Alcohol and smoking

A study from British Journal of
Cancer (2002) has shown that smoking was closely related to breast cancer
especially when combined together with the consumption of alcohol. Data
indicated that the relative risk of breast cancer was enhanced by 7.5% when
smokers drank alcohol. This interaction was considered complex as acetaldehyde
was also one of the by-products of burning tobacco. The body’s system could not
handle or work more quickly to control the damage caused by the by-products
because both drinking and smoking created a large amount of acetaldehyde.
Acetaldehyde and other toxins would destruct DNA and thus yield a higher chance
to develop breast cancer. In addition, alcohol was believed that it could allow
cancer-causing tobacco chemicals to diffuse into body’s cells and tissues more


2.5 Chemoprevention

Based on Sporn & Suh (2000), tamoxifen, raloxifene and
4-hydroxyphenylretinamide (fenretinide) were known to act as the effective
agents for the prevention of breast cancer in women of varying degrees of risk.
Estrogen was recognized as the promoting agent for carcinogenesis, however,
both tamoxifen and raloxifene were the estrogen receptor antagonists in women
breast that could bind to the estrogen receptors of ER-? and ER-?. Besides, fenretinide
which was a synthetic retinoid acted as a differentiating agent for
tracheobronchial and mammary epithelium or an effective drug to prevent from
experimental breast cancer. Fenretinide and tamoxifen could also work
synergistically to suppress mammary carcinogenesis in rats.



In 2006, breast cancer was the most
important cancer among population regardless of sex in Peninsular Malaysia.
There were 3525 female breast cancer cases (about 16.5 % of cancer cases
registered). The age pattern in 2006 showed a peak Age-specific Incidence Rate
at the 50-59 age group. The overall ASR was 39.3 per 100,000 population. The
incidence of breast cancer was highest among Chinese (ASR: 46.4), followed by
Indian (ASR: 38.1) and Malay (ASR: 30.4) (National Cancer Registry, 2006).
            The International Agency for
Research on Cancer (IARC) has listed both ethanol and its major metabolite,
acetaldehyde, as a carcinogen in humans. The risk of breast cancer was
increased 40-45 % for women which consumed alcohol. Women who drink alcohol
more than 5 gram/day have the risk of breast cancer 50% higher. This indicates
that moderate levels consumption increased the breast cancer risk. Some
researchers showed that no relation between age of starting drinking alcohol to
breast cancer. Other researchers reviewed relationship duration of alcohol
consumption to breast cancer. After consuming alcohol in 40 years, the risk of
breast cancer was increasing significantly (Bowlin et al., 1997).



Breast cancer is one of the common
types of cancer that affects women all around the world. Alcohol is related to
breast cancer because it can increase certain hormones, including oestrogen
which acts as the fuel for the development of breast cancer, make the cells in
the mouth and throat to absorb other cancer-causing chemicals more easily and
can be broken down into acetaldehyde which is a toxic chemical that is able to
allow cancer to develop by damaging DNA. Women who usually drink alcoholic
drinks have a higher risk of breast cancer compared to women who do not drink
at all.



Alcohol, tobacco and breast cancer – collaborative
reanalysis of individual data from 53 epidemiological studies, including 58 515
women with breast cancer and 95 067 women without the disease. (2002). British Journal of Cancer, 87(11),
1234-1245. doi:10.1038/sj.bjc.6600596

Al-Sader, H. (2009). Alcohol and Breast Cancer: The
Mechanisms Explained. Journal of Clinical Medicine Research.

Azad, M. B., Chen, Y., & Gibson, S. B. (2009).
Regulation of Autophagy by Reactive Oxygen Species (ROS): Implications for
Cancer Progression and Treatment. Antioxidants
& Redox Signaling, 11(4), 777-790. doi:10.1089/ars.2008.2270

Bostrom C. E., Gerde P., Hanberg A., Jenstrom B., Johansson
C., Kyrklund T., Rannug A., Tornqvist M., Victorin K., & Westerholm R.
(2002). Cancer risk assessment, indicators, and guidelines for polycyclic
aromatic hydrocarbons in the ambient air website Online. Accessed 8th December
2017. Available from World Wide Web:

Bowlin S. J., Leske M. C., Varma A., Nasca P., Weinstein A.,
Caplan L. (1997). Breast Cancer Risk and Alcohol Consumption: Results from
Large Case-Control Study. International
Journal Epidemiology, 26(5), 915-923. 

Boyle, P., Boffetta, P., Lowenfels A. B., Burns, H.,
Brawley, O., Zatonski, W. & Rehm, J. (2013) Alcohol: Science, Policy and
Public Health, United Kingdom: Oxford University Press. P.50

Bozovic-Spasojevic, I., Azambuja, E., McCaskill-Stevens, W.,
Dinh, P., & Cardoso, F. (2012). Chemoprevention for breast cancer. Cancer Treatment Reviews, 38(5),
329-339. doi:10.1016/j.ctrv.2011.07.005

Chiara Scoccianti & Isabelle Romieu (2014). Female
Breast Cancer and Alcohol Consumption: A review of the literature. American Journal of Preventive Medicine, 46(3),
16-25. doi:10.1016/j.amepre.2013.10.031.

Dumitrescu, R. G., & Shields, P. G. (2006). Alcohol and
Breast Cancer Risk. Alcohol, Tobacco and
Cancer, 119-139. doi:10.1159/000095020

10.     Ferlay J., Soerjomataram I, Ervik M,
Dikshit R., Eser S. & Mathers C. (2014). Cancer Incidence and Mortality Worldwide. Accessed on 25 Nov 2017:

11.     G. Shi, Q. Zhang, D. Levy & S.
Zhong (2015). Exploring common mechanism
of alcohol-associated breast and liver cancers. (Suppl. P301A)(2015).

12.     Jones, C. R. (2016) Sport and
Alcohol: An ethical perspective, New York: Routledge.  P.172

13.     Lindblad, B., Zaman, S., Malik, A.,
Martin, H., Ekström, A. M., Amu, S., . . . 1 Norman, M. (2005). Folate, vitamin
B12, and homocysteine levels in South Asian women with growth-retarded fetuses.
Acta Obstetricia et Gynecologica Scandinavica,
84(11), 1055-1061. doi:10.1111/j.0001-6349.2005.00876.x

14.     Meadows, G.G.; Zhang, H. (2015).
Effects of Alcohol on Tumor Growth, Metastasis, Immune Response, and Host
Survival. Alcohol Res 37, 311–322.

15.     National Cancer Registry. (2006). Malaysia Cancer Statistics Data and Figure
Peninsular Malaysia. 

16.     Schwab, M. (2011) Encyclopedia of Cancer 3rd Edition.
Heidelberg: Springer. P.123

17.     Sporn, M. B., & Suh, N. (2000).
Chemoprevention of cancer. Carcinogenesis,
21(3), 525-530. doi:10.1093/carcin/21.3.525

18.     WHO. International Agency for
Research in Cancer. IARC monograph on the evaluation of carcinogenic risks to
humans. Accessed on 25 Nov 2017:

19.     Wright, R. M., Mcmanaman, J. L.,
& Repine, J. E. (1999). Alcohol-induced breast cancer: a proposed
mechanism. Free Radical Biology and
Medicine, 26(3-4), 348-354. doi:10.1016/s0891-5849(98)00204-4




should write all of the names in ref, (but can use in citation)