Aimwadee Kiatsukasem (Ami) 11-02

Cigarettes (tobacco smoke) link to oral leukoplakia(white sore patches

disease) cause from epigenetics
Abstracts
This experiment will prove that smoke tobacco effect a cellular model of oral
leukoplakia which cause white sores/ patch. Also, there are a link between oral leukoplakia to
CYP1A1 and CYP1B1 metabolizing enzymes which cause the change in CYP1A1 and
CYP1B1 genes. It can be conclude that tobacco is link to epigenetic alterations

Introduction
epigenetic is define as the effect of external or environments factors that work to
switch on and off call expression which bring about cellular and physiological phenotypic
traits. The term also refer to the change themselves, it is functionally relevant changes to the
genome that do not involve a change in the nucleotide sequence. They also control the gene
expression through the action of repressor proteins that attach to DNA. The change that cause
fom epigenetic last through cells life and also last for reproduction which may cause
mutation of gene.
Cigarettes or tobacco smoke has tobacco which is a green leafy plant grow by number
of chemicals. Chemicals in cigarettes and it smoke have been known as cause of cancer and
other serious health problems. Many of the chemicals are poisonous and from the statistics, If
a person ate one pack of cigarettes, he/she would die. The rates of cigarette smoking vary
throughout the world and changing considerably since cigarettes were first widely used in the
mid-19th century.The smoking rates contine to declined in the developed world while
continue to rise in developing nations. Cigarettes is the main cause of terrible disease that
lead to numerous death every years. For examples, lung cancer, COPD(chronic obstructive
pulmonary disease), heart disease and one disease thatmainly focus in this experiment is oral
leukoplakia.
Oral leukoplakia (OL) is a disease that cause a white patch or plaque that cannot be
rubbed off, it is not associated with any physical or chemical agent except tobacco. The study
suggest that cancer is more likely to occur in individuals with people who have leuloplakia
than the individuals who do not have this condition. The people who are idopathic
leukoplakia is consider to be a premalignant lesion.The gene that cause the OL named
CYP1A1 and CYP1B1 which belongs to the cytochrome P450 superfamily of enxymes. The
cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in
drug metabolism and synthesis of cholesterol and other lipids. Mutations in this gene have
been associated with leukoplakia. Therefore it is thought that the enzyme also metabolizes a
signaling molecule involved in oral leukoplakia development.

Method
In this experiment we divided 1000 participant by gender first; 500 males and 500
females by each 100 males and female didnt smoke as a control group. Then divided people
who smoke both males and females by amount of cigarattes they have per day in to four
groups, each will have 100 males and females. The group will be divided as least than half
pack per day, more than half pack but least than 1 pack per day, more than one but least than
two pack per day and more than two pack per day. By classified participaint like this will
determined gender and amount they smoke as a factor of how different they may have or not
have oral leukoplakia.
In previous research states that age is also a factor for this disease by saying that
approximately 80 percent of patients are older than 40 years. Therefore in this experiment, all
the paticipant will age above 40 and reseacher will give out survey about their health and how
long have they been smoking. This will help decreased the external factor that may cause an
error. This experiment will last for 3 years by follow up paticipant health every 6 month to
see the change and did they have sore patch or not. Then classified participant who have
disease and follow up until their have kids to see does the sore patch cause the mutation in
CYP1A1 and CYP1B1 gene or not. We will take cell samples and quantify the DNA
methylation of the CYP1A1 and CYP1B1 gene.

Implications
if the study is sucess, it will prove that mutation of CYP1A1 and CYP1B1 gene is the
cause of oral leukoplakia disease and may transfer from parent to their kids. In futher study it
can be used to determined the gene and be able to clear out this gene for oral leukoplakia
patient to cure the dieseae and avoid pass down mutated gene.

Reference
G., W., D., S., M., & B. (2008, July 1). Effects of tobacco smoke on gene expression
and cellular pathways in a cellular model of oral leukoplakia. US National Library of
Medicine National Institutes of Health, 100(11). doi:10.1158/1940-6207.CAPR-08-0007
from https://www.ncbi.nlm.nih.gov/pubmed/19138943
Harris, C. (2015, March 31). Oral Leukoplakia (A. D. Meyers, Ed.). Retrieved
December 11, 2016, from http://emedicine.medscape.com/article/853864-overview#a6