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I AM IIT DELHI STUDENT.I AM DOING M.SC IN MATHEMATICS

Thesis submitted to Indian institute of technology Delhi In partial fulfillment of the requirement for the

Degree of

MASTER OF SCIENCE IN “MATHEMATICS”

By VINEET SINGH 2010MAS7115 ANUPAM SINGH 2010MAS7127

Under the guidance of DR.S.DHARMARAJA

TABLE OF CONTENTS

ABSTRACT                                                                                                              IV NOMENCLATURE                                                                                                    V CHAPTER 1. INTRODUCTION                                                                          1 1.1 What is cervical cancer								 1 1.2 Cervical cancer magnitude of the problem					 1 1.3 Natural History of Cervical Cancer						 2

1.4 Burden of cervical cancer in India 						 4

1.5 Literature Review									 6 1.6 Objective										 7 CHAPTER 2. SCREENING METHODS                                                               9 2.1 Cervical Cancer Screening                                                                                    9 2.2 Visual inspection VIA and VILI Testing                                                            10

2.3 Human Papilloma Virus (HPV) DNA testing                                                     11 CHAPTER 3.TREATMENT OF CERVICAL CANCER IN INDIA                   13 3.1 Treatment of Cervical Cancer                                                                              13

3.2 Stages of Cervical Cancer                                                                                    16 CHAPTER 4.MODEL FORMULATION                                                                 17 4.1 A description of mathematical terms                                                                    17 4.2 Model Formulation                                                                                               18 CHAPTER 5. CONCLUSIONS AND FUTURE WORK                                          24 5.1 Conclusion									 24 5.2 future work									 24 REFERENCES                                                                                                           26

LIST OF FIGURES

Figure 1.1 new cervical cancer cases worldwide in 2000. Figure 1.2 global burden of cervical cancer Figure 1.3. Natural history of HPV Infections Figure 1.4. District wise comparison of age-adjusted incidence of cervical cancer (per 100,000 populations) Figure 2.1. Screening and Treatment Procedures for a Female Patient in Colsubsidio.

Figure 4.1 Transition diagram of Colombian women’s Figure 4.2 Transition diagram for Indian women’s

NOMENCLATURE

Nomenclature ASCUS: Atypical Squamous Cells of Undetermined CIN     Cervical Intraepithelial Neoplasia CCSP : Cervical Cancer Screening Programme FIGO    International Federation of Gynecology and Obstetrics HPV    HUMAN PAPILLOMA VIRUS

VILI : Visual Inspection with Lugol's Iodine	Hyst    Hysterectomy HSIL   High Squamous Intraepithelial Lesion LSIL  Low Squamous Intraepithelial Lesion

LEEP   Loop electrosurgical excision procedure MDP   Markov Decision Process PAP : Papanicolaou POMDP Partially observable Markov decision PHC : Primary Health Center RCC : Regional Cancer Center VIA : Visual Inspection with Acetic Acid

	CHAPTER 1.INTRODUCTION

1.1	What is cervical cancer?

The cervix is the lower part of the uterus (womb). It is sometimes called the uterine Cervix. The body of the uterus (the upper part) is where a baby grows. The cervix Connects the body of the uterus to the vagina (birth canal). The part of the cervix closest to the body of the uterus is called the endocervix. The part next to the vagina is the exocervix (or ectocervix). The 2 main types of cells covering the cervix are squamous cells (on the exocervix) and glandular cells (on the endocervix). The place where these 2 cell types meet is called the transformation zone. Most cervical cancers start in the transformation zone. Most cervical cancers begin in the cells lining the cervix. These cells do not suddenly change into cancer. Instead, the normal cells of the cervix first gradually develop precancerous changes that turn into cancer.

1.2	Cervical cancer: Magnitude of the problem Cervical cancer continues to have a major impact on women worldwide, particularly women in developing countries. The most recent compilation of global data indicates that an estimated 466,000 new cases of cervical cancer occur annually among women worldwide (see Figure 1.1) nearly 80 percent of cases are in developing countries, where screening programs are not well established or are minimally effective. In developing countries, cervical cancer incidence is second only to breast cancer and it is the leading cause of cancer deaths among women. Worldwide (see Figure 1.2), cervical cancer takes the lives of 231,000 women annually, with over 80 percent of these deaths occurring in developing countries.

Figure 1.1 Figure 1.2

1.3	Natural History of Cervical Cancer

Although the incidence of and mortality from cervical cancer have declined substantially over the last four decades worldwide .cervical cancer continues to be a leading cause of cancer death in women. Cervical cancer rates are highest in less developed countries, including those of Latin America, sub-Saharan Africa, and Southeast Asia, and lowest in industrialized nations. This disproportionate burden of cervical cancer is due largely to the absence of well-organized screening programs. There are more than 100 types, or strains, of HPV. Only some of these strains cause cervical cancer. Although an oncogenic HPV infection is a necessary factor for developing cervical cancer, the immune system naturally eliminates most HPV infections. An HPV infection can progress to precancerous abnormal cells, called cervical intraepithelial neoplasia (CIN).There are three levels of CIN. Each level refers to the thickness of the skin covering the affected cervix: CIN I refers to mild cell changes; CIN II refers to moderate cell changes; CIN III refers to severe cell changes. Within each of these stages the disease may progress to the next state, or the immune system may naturally eliminate it (i.e., it regresses). Regression is more common; however, the chance of the immune system eliminating the disease is effectively zero once the HPVinfection reaches cancerous levels. Cervical cancer has four stages denoted by FIGO I–IV (Fédération Internationale de Gynécologieetd’ Obstétrique). These stages indicate how far the cancer has spread, where FIGO IV represents the most severe and invasive form of cervical cancer. Strictly speaking, one is said to have cancer in FIGO I–IV states and to have precancerous abnormal cells in CIN I–III states. There are two other systems of classification. According to the Cervical Intraepithelial Neoplasia(CIN) system, mild to moderate dysplasia are classified as CIN1, intermediate dysplasia as CIN2, and severe dysplasia and carcinoma in situ are together classified as CIN3. The Bethesda system simplifies it further, by classifying CIN1 as Low Grade Squamous Intraepithelial Lesion (LSIL), and both CIN2 and CIN3 as High Grade Intraepithelial Lesion (HSIL). Low-grade SIL refers to early changes in the size, shape, and number of cells that form the surface of the cervix. Some low-grade lesions go away on their own. However, with time, others may grow larger or become more abnormal, forming a high-grade lesion. Precancerous low-grade lesions also may be called mild dysplasia or cervical intraepithelial Neoplasia (CIN 1). Such early changes in the cervix most often occur in women between the ages of 25 and 35 but can appear in other age groups as well.

For reasons that are not fully understood, approximately 5% to 10% of women infected with high-risk types of HPV develop persistent infections. Evidence shows that these women have an increased risk of developing high-grade precancerous lesions, and, if the lesions are not treated, cervical cancer. It is not possible to predict in which women precursor lesions will progress to cancer, because the environmental and host immunological factors associated with progression to cancer are also not fully understood. Figure 1.3. Natural history of HPV Infections