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Associated Risk Factors and Preventive Practices among Confirmed Cases of Cervical Cancer in a Hospital-based Retrospective Study
at the University of Santo Tomas Hospital
A Research Proposal Submitted to theUniversity of Santo Tomas
Faculty of Medicine and SurgeryDepartment of Clinical Epidemiology
In Partial Fulfilment of the RequirementsFor Clinical Epidemiology
Co-author: Dr. Ervin Nucum
Submitted by:Calupitan, Carmela Angeline E.
Cambe, Joy Christine P.Diploma, Suzette P.
Malig, Melody Anne C.Panday, Emilia Socorro O.
Batch 2011
II. Research Proposal / Protocol
Introduction
Cervical cancer is the second most commonly diagnosed cancer and the leading cause
of cancer-related deaths among women in the Philippines (Widdice and Kahn, 2006). Human
papillomavirus is identified as the causative agent but is not sufficient to cause the neoplastic
transformation. Studies (Misra et al, 2009, Domingo et al, 2008, Herbert & Coffin, 2008, Abdul et
al, 2008) identified cofactors which include young age at first intercourse, high parity, multiple
sexual partners and chronic pelvic inflammatory disease.
Cancer of viral origin is preventable by vaccines targeted on the causative organism, as
has been proven effective for hepatocellular carcinoma by hepatitis B vaccine (Chang, 2009).
This became the premise of the vaccines being formulated in targeting specific types of HPV
(Zwaveling, 2002 and Kenter, 2009). Moreover, HPV vaccination with screening is cost-effective
and reduces 70% of cervical cancer cases (Goldie et al, 2004 and Schiffman, 2007). Both the
bivalent and quadrivalent vaccines are used locally.
This study aims to review and summarize the cofactors associated with cervical cancer
in Filipino women and discuss the impact of prophylactic HPV vaccination.
Significance of Study
The sexual knowledge and attitudes of the Filipinos contribute to increasing the risk for
HPV infection and cervical cancer. Different surveys reveal significant risk behaviors and low
knowledge of the Filipinos about sexually transmitted infections. Also, women in occupations
with low socioeconomic status are less likely to have access to health promotion programs.
With this regard, the clinician is tasked to review the risk factors associated with cervical
cancer to his or her patients. Assessment to the over-all health risk factor of the patient could be
given and a prophylactic HPV vaccination could be advised to reduce the risk. Through
education, safe sexual practices could be implemented. Finally, knowledge on the risk factors
could further prevent the development and/or progression of the disease.
2
III. Objectives of the Study
This study aims to review and summarize the cofactors associated with cervical cancer in
Filipino women and discuss the potential impact of prophylactic human papillomavirus
vaccination; specifically:
To identify the relationship of cervical cancer development with age.
To identify the relationship of cervical cancer development with occupation.
To identify the relationship of cervical cancer development with reproductive factors, i.e.
parity, age at marriage or first intercourse, number of sexual partners, contraceptive use.
To identify the relationship of cervical cancer development and sexually transmitted
diseases and other co-morbid conditions.
To identify the association of prophylactic HPV vaccination with cervical cancer.
IV. Methodology
Study Design: Retrospective Cohort
Setting of the Study: Hospital-based
Study Subjects
Women aged between 14 and 65 years who have confirmed cases of cervical cancer.
Inclusion criteria: Medical records of women who have confirmed cervical cancer with
the following data present or available: women from the ages of 14-65, age of first intercourse,
occupation, socioeconomic status, obstetrical history (parity), social history (smoking, alcohol),
cervical screening tested positive (VIA, PAP), immunizations, co-morbid conditions.
Exclusion criteria: Non-confirmed cases of cervical cancer and those records having
incomplete data.
Sample Size
Medical records of confirmed cases of cervical cancer from the Department of Obstetrics
and Gynecology that meet the inclusion criteria are to be obtained (Sample size is to be
determined based on the available data from Benavides Cancer Institute and Department of
Obstetrics and Gynecology).
3
Study Procedure/Interventions
Convenience sampling will be utilized in gathering medical records. All the data pertinent
to the study are to be identified and tallied.
Outcome Measurements
To estimate the risk of cervical cancer associated with various HPV types and the other
risk factors, odds ratios (ORs) will be calculated and 95% confidence intervals (CIs) as
approximations of relative risks by using unconditional logistic regression (Breslow & Day,1980)
The odds ratio for HPV will be adjusted only for age (categorized in six age groups: 14-
19 years , 20-29 years ,30-39 years, 40-49 years, 50-59 years, 60-65 years. Various measures
will be examined including of demographic, socioeconomic status, age, marital status will
occupation i.e. overseas Filipino worker (OFW), educational attainment, smoking, age of first
intercourse, parity, gynecological factors, number of sexual partners, use of contraceptives will
be collected for multivariate analysis. Multiple regression will be conducted to adjust for any
confounding variables (Appendix A).
V. Review of Related Literature
Cervical Cancer
Among women worldwide, cancer of the cervix uteri is the second most common cancer
(after breast cancer) and the third leading cancer mortality (after lung and breast cancer).
Squamous cell carcinoma (SCC) is the predominant histological type accounting for three-
fourths of all cervical cancers. Adenocarcinoma and adenosquamous cell carcinoma represent
10–15%, and other or unspecified histology represent the remaining 10–15%. Cervical cancer is
usually caused by a sexually transmitted virus called the human papilloma virus (HPV). But
most HPV infections will not lead to cancer.
Saslow, et. al. (2002) confirmed that cervical cancer screening should begin
approximately three years after the onset of vaginal intercourse. Screening should begin no
later than 21 years of age. In the United States, cervical cancer in women less than 19 years of
age is rare. Mount, et al. (1999) provided the highest reported prevalence (3.77 percent) of
squamous intraepithelial lesions (SIL) among 10,296 cytology smears from patients aged 10 to
4
19 years, 18 percent of SILs were high grade, and no cases of invasive cancer were detected.
The National Cancer Institute’s Surveillance, Epidemiology, and End Results (SEER) program
reported that the incidence rate of invasive cervical cancer was 0/100,000/year for ages 10 to
14 years; 0/100,000/year for ages 15 to 19 years and 1.7/100,000/year for ages 20 to 24 years
from 1995 to 1999.
However, it is critical that adolescents who may not need a cervical cytology test obtain
appropriate preventive health care, including assessment of health risks, contraception, and
prevention counseling, screening and treatment of sexually transmitted diseases. The need for
cervical cancer screening should not be the basis for the onset of gynecologic care. Although
the process of cervical screening is a method of secondary prevention, making screening for
cervical cancer priority in routine check ups for women within the target population will provide
for a great health education opportunity and provide clinical approach to raising awareness on
the risks of cervical cancer will enable women of a wide age range.
Precancerous conditions of the cervix are identified as cells that appear to be abnormal,
but are not cancerous at the present time. However, the appearance of these abnormal cells
may be the first evidence of cancer that develops years later. Precancerous changes of the
cervix usually do not cause pain and, in general, do not cause any symptoms. Squamous
intraepithelial lesions (SIL) is a term that refers to abnormal changes in the cells on the surface
of the cervix.
According to the University of Chicago Medical Center, statistics from the National
Cancer Institute (NCI) states that changes in these cells can be divided into two categories:
Low-grade SIL-refers to early changes in the size, shape, and number of cells that form the
surface of the cervix. They may go away on their own, or, with time, may grow larger or become
more abnormal, forming a high-grade lesion. These precancerous low-grade lesions may also
be called mild dysplasia or cervical intraepithelial neoplasia 1 (CIN 1). These early changes
most often occur in women between the ages of 25 and 35, but can appear at any age. High-
grade SIL-means there are a large number of precancerous cells, and, like low-grade SIL, these
precancerous changes involve only cells on the surface of the cervix. The cells often do not
become cancerous for many months, perhaps years. High-grade lesions may also be called
moderate or severe dysplasia, CIN 2 or 3, or carcinoma in situ. They develop most often in
women between the ages of 30 and 40, but can occur at any age.
5
If detected prior to invasion, a variety of treatment options are available that result in
almost certain cure. The most widely cited evidence of the contribution of cytologic screening to
the reduction in cervical cancer mortality is the long-term decline in deaths from cervical cancer
in the United States coincident with the introduction of the Pap smear. In actuality, death rates
had begun to decline prior to widespread use of Pap smears, perhaps due to an increase in the
hysterectomy rate, trends in the underlying epidemiology of disease, and other factors.
HPV Infection and Cervical Cancer
According to Sauvageau et al (2007), the most common sexually transmitted infection is
caused by Human papilomavirus (HPV). At least 50% of sexually active women have been
infected with genital HPV at some time in their life, 82% were prevalent in adolescents and
young adults. Cervical cancer was reportedly caused by approximately 15 virus genotypes of
HPV. In a study by Wheeler et al (2009) in a population of US women, the most common HPV
genotypes detected in invasive cancers were HPV type 16 (53.2%), HPV 18 (13.1%), and HPV
45 (6.1%), whereas in situ cancers revealed HPV 16 (56.3%), HPV 31 (12.6%), and HPV 33
(8.0%). It is noted that HPV types 16 and 18 caused the majority of these cancers.
In 1995, the International Agency for Research on Cancer (IARC) evaluated all relevant
data on the carcinogenicity of HPV and concluded that there was sufficient evidence to
categorize HPV types 16 and 18 as human carcinogens but that the existing evidence was
limited or inadequate for the other HPV types. At that time, odds ratios (ORs) for HPV types 31,
33, and 35 and invasive cervical carcinoma had been reported for only the three types as a
group from case–control studies in Spain and Colombia and in Brazil. A polymerase chain
reaction (PCR)-based assay capable of detecting 33 HPV types was used and ORs for the most
common HPV types were estimated for both squamous cell carcinomas and adenocarcinomas.
The role of other risk factors after controlling for the strong effect of HPV has been examined in
a few studies. These are the main results of a hospital-based, case–control study conducted in
Manila, Philippines, which has a population with intermediate rates for cervical cancer (age-
adjusted incidence rate 25 per 100 000). (Ngelangel etal, 1998).
6
Age and Cervical Cancer
Cervical cancer in women over 60 years of age accounts for 24% of new cases and 40%
of deaths from this disease. Misra et al (2009) reported that the frequency of cytopathologic
abnormalities was increased with advancing age. Maximum frequency was observed in older
women beyond 40 years of age. Yet in regions where older women have been aggressively
screened, their death rates have declined; however, less than 50% of women over 65 years of
age have been screened for cervical cancer (Balducci et al, 1998).
The earliest identified etiologic step in cervical cancer development is infection of young
women with specific types of venereally transmissible human papillomaviruses (HPVs). Cervical
HPV infections often lead to low grade squamous intraepithelial lesions (mildly abnormal Pap
smears). Human papillomavirus infections and their associated lesions are extremely common
among young, sexually active women. The infections typically resolve spontaneously even at
the molecular level within months to a few years. Uncommonly, HPV infections and/or low grade
lesions persist and progress to high grade lesions. The risk factors for progression are mainly
unknown but include HPV type and intensity, cell-mediated immunity, reproductive factors,
nutrition, and co-infection with other pathogens. Except for advancing age, no epidemiologic risk
factors have been found for the next step between high grade intraepithelial lesions and
invasive cancer. Based on worldwide research, the steps in cervical carcinogenesis appear to
be fundamentally the same everywhere, with a central role for HPV infection. (Schiffman et al,
2006).
Occupation and Cervical Cancer
Cervical cancer remains an important health problem for women. Few published studies
have examined cervical cancer with respect to a woman's occupation. Mortality data from the
National Occupational Mortality Surveillance System were used to calculate the proportion of
deaths from cervical cancer according to occupation. Standardized death certificate data for
almost 2 million deaths among women in 27 states covering the period 1985-1990 showed
elevated risk with service and apparel manufacturing workers. Data showed a difference in
cervical cancer mortality by occupational group. Women in occupations with low socioeconomic
status are less likely to have access to health promotion programs (Burnett et al, 1997).
7
Reproductive factors and Cervical cancer (Age at first intercourse, Parity, Number of
sexual partners, Contraceptive use)
Parity
For decades, high parity has been suspected of being associated with an increased risk
of cervical cancer. Confounding with sexual behavior specifically with age at first sexual
intercourse, was, however, thought to account for the apparent adverse effect of multiparity.
Nevertheless, results of a few case-control studies of cervical carcinoma confirmed an
independent role for high parity after allowance for several indicators of sexual habits: the risk of
cervical cancer was increased by more than two-fold in women who had four children or more
compared with those who had one or none. (Munoz et al, 2002)
According to Munoz et al. (2002) assessed the effect of the number of full-term
pregnancies and other reproductive variables on the probability of being HPV-DNA-positive,
compared the 255 control women positive for HPV DNA with the 1661 HPV-DNA-negative
control women. It was found out that nulliparous women were more likely to be HPV positive
than each category of parous women, but among parous women, no trend in HPV positivity was
seen according to the number of full-term pregnancies. No consistent relation emerged among
controls between HPV positivity and age at first full-term pregnancy or number of abortions.
Parazzini et al (1989) found that the number of births has an independent and relevant
role in invasive cervical cancer. The risk increased markedly with increasing parity and was over
four-fold in women with five or more births, compared with nulliparous ones. There was also an
effect of earlier first birth on cervical cancer risk, which could be largely explained in terms of
higher parity among women who had their first child earlier. In contrast, no important influence
of reproductive variables was observed on preinvasive cervical neoplasms. It is unlikely that the
association observed between parity and invasive cervical cancer is incidental. The magnitude
of the association by itself suggests that it cannot be totally accounted for by bias alone. This
was supported by Misra et al (2009), in which the frequency of both squamous intraepithelial
lesions and cervical cancer showed a progressive rise with increasing parity and more
pronounced and statistically significant between para 2, and 3 &above (p<0.10).
8
Age at Marriage
The relationship of squamous intraepithelial lesions (SIL) and cervical cancer with age at
marriage showed varying results in the study of Misra et al (2009). Women married between
ages 21 to 30 years showed to be at a higher risk for SIL, while women married beyond 30
years were at increased risk of cervical cancer. SIL was highest among women ages 21 to 30
years at marriage since the maximum number of smears were taken from this group, with
smears taken five to 20 years after consummation.
Other Reproductive Factors
The case-control study of Brinton et al (1987) involving 418 women with invasive
squamous cell cervical cancer and 704 population controls enabled evaluation of risk factors for
this relatively rare cancer. Consistent with an infectious etiology was a pronounced effect of
multiple sexual partners, with those reporting 10 or more partners being at a significant threefold
excess risk. Early first intercourse also was associated with some residual effect on risk,
although the relationship was not linear, nor the explanation readily apparent. Those with
multiple births were at significantly elevated risks, even after adjustment for sexual parameters.
Menstrual and hygiene factors, including use of tampons, vaginal deodorants, and douching
products, were not consistently related to risk. Histories of specific infections involving the
genital tract were poor predictors of risk, since few women provided positive responses, but
those with nonspecific diseases were at a significant twofold excess risk.
Oral Contraceptive Pills and Cervical Cancer
Since use of exogenous steroid hormones became more widespread in the 1960s,
concern has been raised about the safety of such treatment in patients with neoplastic diseases.
Risk of invasive squamous cervical cancer and ISC for women who tested positive for HPV
DNA is increased three-fold if they have used oral contraceptives for 5 years or longer. Because
the prevalence of oral contraceptive use and other risk correlates varied between countries,
odds ratios among ever users of oral contraceptives showed some heterogeneity between
studies (Moreno et al, 2002).
9
Sexually Transmitted Diseases, Co-morbid conditions and Cervical Cancer
HPV is a necessary cause of cervical cancer, but it is not a sufficient cause. Other
cofactors are necessary for progression from cervical HPV infection to cancer. Co-infection with
Chlamydia trachomatis and herpes simplex virus type-2, immunosuppression, and certain
dietary deficiencies are among these cofactors. Genetic and immunological host factors and
viral factors other than type, such as variants of type, viral load and viral integration, are likely to
be important but have not been clearly identified (Muñoz et.al., 2006).
Four sexually transmitted diseases were identified to be associated with SIL and cervical
carcinoma in 36,484 screened women in India by Misra et al (2009). Trichomonas vaginalis
infection was found to be the most prevalent STD while Herpes simplex virus and HPV were
highly associated with SIL and carcinoma.
In a case-control study by Abdul et al (2009), women with chronic pelvic inflammatory
diseases were at a statistically significant (p<0.05) higher risk of developing cervical dysplasia
than women without chronic PID, with a prevalence rate of 140/1000 or 14% for Cervical
Intraepithelial Neoplasia. Only 10% of these women were aware of both cervical cancer and
Pap smear.
OFWs and Cervical Cancer
The sexual knowledge and attitudes of the Filipinos contribute to increasing the risk for
HPV infection and cervical cancer. Different surveys reveal significant risk behaviors and low
knowledge of the Filipinos about sexually transmitted infections (STI). In 2002, freelance Filipino
female sex workers admitted having an average of 5 partners per week with only 30%
consistent condom use. Most avoid the use of condoms as they ascribe condom use to a lot of
myths. These sex workers likewise claim to have little or no knowledge on STI.
Condom use is equally low among high-risk male individuals. According to a multicenter
population based survey by Ramos-Jimenez et al, (2000) condom usage is very low among
Filipino male sex workers, seafarers and truckers, and its primary usage is as a contraceptive
and not as protection against STI.
10
Overseas Filipino workers (OFW) are also considered vulnerable to STI. These
individuals admit to engage in casual sex brought about by factors, such as homesickness,
desire for sexual contact, economic pressure to engage in paid sex, and vulnerability to sex
trafficking. In most instances, they fail to use condoms. (Ngelangel et.al., 1998)
Smoking and Cervical Cancer
According to the meta-analysis done by (Haverkos et al, 2002) on cigarette smoking and
cervical disease, they concluded that the cigarette smoking has a role in cervical cancer
progression. A multifactorial hypothesis involving a virus–tar interaction was proposed as one of
the etiologies of cervical cancer.
The rates and occurrence of cervical and lung cancer and women smoking throughout
the world were compared. For example, smoking prevalence among US women (by state)
ranged from 11.4% to 29.5%, and worldwide, the range was 1.0–39.2%. The range of the
incidence of lung and cervical cancer also varied widely. Worldwide, there were generally higher
rates of cervical cancer incidence than lung cancer incidence per 100,000 men or women, but in
the US, the opposite was true. In the US, there was a positive correlation between female
smoking prevalence and cervical cancer that was not statistically significant (r-value = +0.203).
In Europe, there was a negative correlation between women smoking and cervical cancer (r
value = –0.305).Worldwide, there was a significant negative correlation between percent of
female smoking prevalence and incidence rates of cervical cancer (r-value = –0.250). Female
smoking prevalence and female lung cancer incidence were significantly and positively
correlated in the US (r-value = +0.523), Europe (r-value = +0.503) and worldwide (r-value =
+0.399).
They recommended that since smoking represents a risk factor for cervical cancer
through confounding or a direct causative mechanism, all women should be encouraged to
abstain from smoking and limit exposure to passive smoke because of the well documented
health risks associated with the use of tobacco products.
11
VI. Data Analysis
*Please refer to statistical analysis.
VII. Ethical Considerations
Confidentiality on the personal data of all the cases is maintained. All the data to be
obtained is only for the purpose of the study.
VIII. Time Schedule (Gantt Chart)
ActivityOutp
ut Date Gantt Chart
Start
Completion
June
July
Aug
Sep
Oct
Nov
Dec
Jan
Feb
Mar
Apr
May
Jun
Jul
Aug
Sept
Oct
Making of New Proposal
New Proposal
June Nov
2009 2009
IRS Approval
Dec
Jan 2010
Coordination with Dept
2009
Data Gathering
Medical Records
Feb Aug
2010 2010
Data Analysis
Medical Records
Aug Sept
2010 2010
Final writing of Paper
Sept Oct
2010 2010
12
IX. Budget
Personnel Php 2,500.00
Research Subject Compensation N/A
Maintenance and Operational Expenses N/A
Equipment and Testing Services N/A
Miscellaneous 2,500.00
TOTAL 5,000.00
X. Bibliography
Abdul MA, Shittu SO, Randawa JA, Shehu MS. (2009). The cervical smear pattern in patients with chronic pelvic inflammatory disease. Niger J Clin Pract. Sep;12(3):289-93. PubMed PMID: 19803028.
Alterman T, Burnett C, Peipins L, Lalich N, Halperin W. (1997). Occupation and Cervical Cancer: An Opportunity for Prevention. Journal of Women's Health, 6(6): 649-657. doi:10.1089/jwh.1997.6.649.
Balducci L, Lyman G, Ershler W, Coprehensive geriatric oncology (1998)
Haverkos H, Soon G, Steckley SL, Pickworth W (2003) Cigarette smoking and cervical cancer: Part I: a meta-analysis Biomedicine & Pharmacotherapy 57 (2003) 67–77
Khan SA, Rogers MAM, Khurana KK, Meguid MM, Numann PJ, (1998). Estrogen Receptor Expression in Benign Breast Epithelium and Breast Cancer Risk (1998) Journal of the National Cancer Institute; 90(1)
Misra JS, Srivastana S, Singh U, Srivastana AN. (2009). Risk factors and strategies for control of carcinoma cervix in India Hospital based cytological screening experience of 35 years. Indian Journal of Cancer; 46(2), 155-159.
Moreno V, Bosch FX, Muñoz N, Meijer CJLM, Keerti V Shah KV, Walboomers JMM, Herrero R,Franceschi S.(2002). Effect of oral contraceptives on risk of cervical cancer in women with
human papillomavirus infection: the IARC multicentric casecontrol study. Lancet; 359: 1085–192
Munoz N, Castellsague X, de Gonzalez AB, Gissmann L. (2006). HPV in the etiology of human cancer. Vaccine; 24 (Suppl 3):S3/1-S3/10.
Muñoz N, Franceschi S, Bosetti C, Moreno V, Herrero R, Smith S, Shah KV, Meijer CJ, Bosch
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FX, (2002) Role of parity and human papillomavirus in cervical cancer: the IARC multicentric case-control study International Agency for Research on Cancer (IARC) Multicentric Cervical Cancer Study Group The Lancet Vol 359
Ngelangel CA, Munoz N, Bosch FX, Limson GM, Festin MR, Deacon J, et al. Causes of cervical cancer in the Philippines: a case control study. (1998) J Natl Cancer Inst; 90: 43-9.
Parazzini FC, La Vecchia, Negri E, Cecchetti G, Fedele ML (1989). Reproductive factors and the risk of invasive and intraepithelial cervical neoplasia. Br. J. Cancer 59, 805-809
Ramos-Jimenez P, Lee R, Lim-Nalian M, Gomez M, Chiong ER. Sexual risk behavior of men: a multi-city population-based survey in the Philippines. 13th International Conference on AIDS; (2000) July 9-14; Durban, South Africa: Abstract no. MoOrD213.
Sauvageau C, Duval B, Gilca V, Lavoie F, Ouakki M (2007). Human Papilloma Virus vaccine and cervical cancer screening acceptability among adults in Quebec, Canada. BMC Public Health, 7:304 doi:10.1186/1471-2458-7-304
Schiffman MH, Brinton LA, The epidemiology of cervical carcinogenesis (2006) Cancer Volume 76
Wheeler CM, Hunt WC, Joste NE, Key CR, Quint WGV, Castle PE. (2009). Human Papillomavirus Genotype Distributions: Implications for Vaccination and Cancer Screening in the United States. J Natl Cancer Inst;101: 475 – 487
XI. Appendices
14
Research Study Design
15
Medical Records of Cervical Cancer Positive Patients
Current Age
HPV VaccinationScreening History
Statistical Analysis
Age at First Intercourse
Parity
Occupation
No. of Sexual Partners
Contraceptive Use
Co-morbid Conditions
Curriculum Vitae
Calupitan, Carmela Angeline E.
2921 Banga 1st, Plaridel, Bulacan
09174191716
Current Position: Post Graduate Student
Educational Background:
Tertiary: University of Santo Tomas 2003-2007
College of Science
España, Manila
Bachelor of Science in Biology
Secondary: Holy Spirit Academy of Malolos 2000-2003
Sta. Isabel, Malolos, Bulacan
Primary: Zensville Montessori School 1993-1999Paltao, Pulilan, Bulacan
16
Cambe, Joy Christine
Unit 921 University Tower 1
Moret St. Sampaloc, Manila
(905) 339-5278
Current Position: Post Graduate Student
Educational Background:
Tertiary: New York Medical College MPH 2005-2007
State University of New York BS 2001-2005
Binghamton University
Secondary: Nyack High School 1997-2001
Primary: Valley Cottage Elementary School 1990-1997
17
Diploma, Suzette P.
Permanent address: Carlatan, San Fernando City, La Union
City address: Galleria Suites, 945 P. Noval St., Sampaloc, Manila
0917-827-9580
Current Position: Post Graduate Student
Educational Background:
Tertiary: University of Santo Tomas 2003-2007
College of Science
España, Manila
Bachelor of Science in Biology
Secondary: Saint Louis College Science High School 1999-2003
San Fernando City, La Union
Primary: Lorma Grade School 1993-1999
San Fernando City, La Union
18
Melody Anne C. Malig
Unit A, Mansions
1249 Dos Castillas St., Sampaloc, Manila
09158243792
Current Position: Post Graduate Student
Educational Background:
Tertiary: Philippine Women’s University 2002 – 2006
B.S. Pharmacy
Secondary: Sto. Nino Academy 1998 - 2002
Primary: Country Springs Elementary 1992 - 1998
19
Panday, Emilia Socorro O.
Permanent address: #1 Almeda St., Concepcion Pequeña, Naga City, Cam. Sur
City address: #1141 Miguelin Street, Sampaloc, Manila
0920-920-5035
Current Position: Post Graduate Student
Educational Background:
Tertiary: University of Santo Tomas 2003-2007
Faculty of Pharmacy
España, Manila
Bachelor of Science in Pharmacy
Secondary: Saint Joseph School 1999-2003
Naga City, Camarines Sur
Primary: Saint Joseph School 1993-1999
Naga City, Camarines Sur
20
