Leung Chun-on, Paul. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1995. / Includes bibliographical references (leaves 149-167). / Content Page / Acknowledgments --- p.7 / Chapter / Chapter Chapter1 --- Introduction --- p.8 / Chapter Chapter2 --- Literature Review --- p.13 / Chapter 2.1 --- Anatomy of the cervix --- p.13 / Chapter 2.2 --- Classification --- p.14 / Chapter 2.2.1 --- Cervical intraepithelial neoplasia (CIN) --- p.14 / Chapter 2.2.2 --- Cervical cancer --- p.17 / Chapter 2.2.3 --- Incidence and screening --- p.21 / Chapter 2.2.4 --- Etiology / Chapter 2.2.4.1 --- Sexual and reproductive factors --- p.23 / Chapter 2.2.4.2 --- Smoking as a risk factor --- p.23 / Chapter 2.2.4.3 --- Male partner contribution --- p.24 / Chapter 2.2.4.4 --- Human papillomaviruses and cervical cancer --- p.24 / Chapter 2.2.4.5 --- Oral contraceptive pills --- p.27 / Chapter 2.2.4.6 --- Oncogenes and tumour suppresser genes --- p.28 / Chapter 2.2.4.7 --- Oncogenes and cervical cancer --- p.35 / Chapter 2.3 --- Immunohistochemical technique in cancer study / Chapter 2.3.1 --- Principle of immunostaining --- p.39 / Chapter 2.3.2 --- Fixation --- p.40 / Chapter 2.3.3 --- Section preparation --- p.41 / Chapter 2.3.4 --- The choice of antibodies --- p.41 / Chapter 2.3.5 --- Enzyme labels --- p.42 / Chapter 2.3.6 --- Blocking endogenous enzymes --- p.43 / Chapter 2.3.7 --- Blocking background staining --- p.43 / Chapter 2.3.8 --- Dilution preparation --- p.44 / Chapter 2.3.9 --- The Avidin-Biotin technique --- p.44 / Chapter 2.3.10 --- Control --- p.47 / Chapter 2.3.11 --- Antigen retrieval --- p.47 / Chapter 2.3.12 --- Cell counting and scoring --- p.49 / Chapter 2.4 --- The application of Polymerase Chain Reaction Single-Strand Conformation Polymorphism(PCR-SSCP) in cancer study --- p.52 / Chapter Chapter3 --- Materials and Methods --- p.56 / Chapter 3.1 --- Materials --- p.56 / Chapter 3.2 --- Methods --- p.61 / Chapter 3.2.1 --- Specimens collection --- p.61 / Chapter 3.2.2 --- Antibodies preparation --- p.63 / Chapter 3.2.3 --- Immunohistochemical staining and antigen retrieval procedures --- p.63 / Chapter 3.2.4 --- Cell counting and scoring --- p.68 / Chapter 3.2.5 --- PCR-SSCP analysis for myc gene mutation --- p.70 / Chapter 3.2.5.1 --- DNA extraction --- p.70 / Chapter 3.2.5.2 --- PCR --- p.72 / Chapter 3.2.5.3 --- Preparing the single strand DNA --- p.73 / Chapter 3.2.5.4 --- Electrophoresis --- p.73 / Chapter 3.2.5.5 --- Gel drying and scanning --- p.77 / Chapter 3.2.6 --- Statistical analysis --- p.77 / Chapter Chapter 4 --- Result --- p.78 / Chapter Chapter 5 --- Discussion --- p.126 / Chapter Chapter 6 --- Conclusions --- p.144 / Reference --- p.148

Ip Toi Yan. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (leaves 81-105). / Abstracts in English and Chinese. / CONTENTS --- p.i-iii / ACKNOWLEDGEMENT --- p.iv / ABSTRACT --- p.v-vi / Chapter Chapter One --- INTRODUCTION --- p.1-2 / Chapter Chapter Two --- LITERATURE REVIEW --- p.3-37 / Chapter 2.1 --- Epidemiology and Etiology of Cervical and Endometrial Cancers --- p.3-4 / Chapter 2.1.1 --- Epidemiology and Etiology of Cervical cancer --- p.4 / Chapter 2.1.1.1 --- Incidence and Mortality --- p.4-6 / Chapter 2.1.1.2 --- Etiology --- p.6-8 / Chapter 2.1.2 --- Epidemiology and Etiology of Endometrial Cancer --- p.9 / Chapter 2.1.2.1 --- Incidence and Mortality --- p.9-11 / Chapter 2.1.2.2 --- Rick Factors --- p.11-14 / Chapter 2.2 --- Pathology of Cervical and Endometrial Cancers --- p.14 / Chapter 2.2.1 --- Pathology of Cervical Cancer --- p.14-15 / Chapter 2.2.1.1 --- Macroscopic Appearance --- p.15 / Chapter 2.2.1.2 --- Histology --- p.15-18 / Chapter 2.2.2 --- Staging of Cervical Cancer --- p.19-21 / Chapter 2.2.3 --- Pathology of Endometrial Cancer --- p.21 / Chapter 2.2.3.1 --- Macroscopic Appearance --- p.22 / Chapter 2.2.3.2 --- Histology --- p.22-24 / Chapter 2.2.4 --- Staging of Endometrial Cancer --- p.24-25 / Chapter 2.2 --- Introduction to Microsatellite Instability (MI) --- p.25 / Chapter 2.3.1 --- DNA structure --- p.25-27 / Chapter 2.3.2 --- Microsatellite --- p.27-28 / Chapter 2.3.3 --- Mismatch Repair (MMR) --- p.28-29 / Chapter 2.3.4 --- Microsatellite Instability (MI) --- p.30-33 / Chapter 2.3.5 --- Microsatellite Instability in various cancers --- p.33-37 / Chapter Chapter Three --- MATERIALS AND METHODS --- p.38-50 / Chapter 3.1 --- Materials --- p.38 / Chapter 3.1.1 --- Patients and Specimens --- p.38-39 / Chapter 3.1.2 --- Chemicals and Reagents --- p.39 / Chapter 3.1.2.1 --- Chemicals --- p.39-40 / Chapter 3.1.2.2 --- Solution --- p.40-41 / Chapter 3.1.2.3 --- Microsatellite Markers --- p.42 / Chapter 3.1.3 --- Major Equipment --- p.43 / Chapter 3.2 --- Methodology --- p.43 / Chapter 3.2.1 --- DNA Extraction --- p.43-45 / Chapter 3.2.2 --- DNA Amplification --- p.45 / Chapter 3.2.2.1 --- End-labeling of Primer --- p.45 / Chapter 3.2.2.2 --- Polymerase Chain Reaction (PCR) --- p.46 / Chapter 3.2.3 --- Electrophoresis of PCR Products and Autoradiography --- p.46-49 / Chapter 3.2.4 --- Determination Of Microsatellite Instability (MI) --- p.49 / Chapter 3.3 --- Statistical Analyses --- p.50 / Chapter Chapter Four --- Result --- p.51-66 / Chapter 4.1 --- Microsatellite Instability in Cervical Cancer --- p.51 / Chapter 4.1.1 --- Prevalence of MI in Cervical Cancer --- p.51 -54 / Chapter 4.1.2 --- MI and Age in Cervical Cancer --- p.55 / Chapter 4.1.3 --- MI and Histological Type in Cervical Cancer --- p.55-56 / Chapter 4.1.4 --- MI and Histologic Grades in Cervical Cancer --- p.56-57 / Chapter 4.1.5 --- MI and Clinical stage in Cervical Cancer --- p.57-58 / Chapter 4.1.6 --- MI and Clinical Status in Cervical Cancer --- p.58-59 / Chapter 4.2 --- Microsatellite Instability in Endometrial Cancer --- p.59 / Chapter 4.2.1 --- Prevalence of MI in Endometrial Cancer --- p.59-62 / Chapter 4.2.2 --- MI and Age Groups in Endometrial Cancer --- p.63 / Chapter 4.2.3 --- MI and Histological Type in Endometrial Cancer --- p.63-64 / Chapter 4.2.4 --- MI and Histologic Grades in Endometrial Cancer --- p.64-65 / Chapter 4.2.5 --- MI and Clinical stage of Endometrial Cancer --- p.65 / Chapter 4.2.6 --- MI and Clinical Status in Endometrial Cancer --- p.66 / Chapter Chapter Five --- Discussion --- p.67-77 / Chapter 5.1 --- MI detection --- p.67-71 / Chapter 5.2 --- MI of Cervical Cancer --- p.71 -74 / Chapter 5.3 --- MI of Endometrial Cancer --- p.74-77 / Chapter Chapter Six --- Conclusions --- p.78-80 / Reference --- p.81-112 / Appendix --- p.113-114

Aim: To explore potential methods of increasing cervical screening coverage. Methods: Cervical screening defaulters in Dumfries and Galloway were identified in 2012, split into a control (N=64) and 7 intervention groups who were offered multiple screening options including self-collecting a vaginal sample at home. Self-samples were tested for high-risk human papillomavirus (HPV). A total of 3323 were invited to request a kit and 492 were sent a kit directly. Women who declined screening were asked to complete a questionnaire. Colposcopy referrals from defaulters were audited to identify changes over time. Defaulters attending the hospital smear clinic were questioned to ascertain barriers to cervical screening. Results: Among seven intervention groups the proportion responding varied between 32% (25%-38%) and 14% (11%-17%) compared to 6% among controls. One hundred and thirty women were HPV positive on self-sample, 8 of whom had CIN2+ diagnosed. A significantly higher number of defaulters were referred to colposcopy in June-December 2012 (n=51) than in the same period in 2011 (n=17; OR=3.8, 2.1-6.9). Defaulting was more commonly attributed to practical (112/155=72%) than attitudinal barriers (23/115=15%) (RR=4.9, 3.3-8.0). Conclusions: Practical barriers are often the cause of women not attending for cervical screening and offering more options, particularly the option of self- sampling at home, increases screening coverage.

Introduction: Cervical cancer is the fourth most common malignancy diagnosed in women worldwide. It results from cellular transformation by the high-risk human papillomavirus (HPV) oncogenes E6 and E7, which accounts for more than 99% of diagnosed cases. HPV links its life cycle to epithelial proliferation and differentiation, which requires the cells to remain active in cell cycle. p63 modulates epithelial development as well as proliferation, differentiation and DNA damage response (DDR), which makes it an important target for HPV oncoproteins to allow viral replication and survival in infected cells. Methods: In this study, small interfering RNAs targeting E7 oncoprotein and p63 in the HPV16 positive cervical cancer cell line CaSki were used. Western blotting, proliferation assays, apoptosis assays and cell cycle analysis were applied to examine the effects of E7 and p63 depletion on cell fate. Overexpression of different types of HPV-E7 was performed in the N/Tert-1 keratinocyte cell line to study the effect of E7 overexpression on p63 level. Results: E7 drives the expression of p63 at both transcript and protein levels in cervical cancer cell lines. Downregulation of E7 is accompanied by a remarkable inhibition of cell proliferation and cell cycle arrest in the G0/G1 phase. Depletion of E7 is associated with a significant reduction in p63 expression which is not due to impaired proliferation or induced differentiation. Downregulation of p63 is associated with delayed DDR in cervical cancer cells following treatment with ionising radiation. High-risk HPV E7s are more potent in inducing p63 upregulation and increasing the proliferation rates in keratinocytes. Conclusion: This work for the first time demonstrated that E7 modulates the expression of p63, which regulates DNA damage repair pathways, that promotes efficient and rapid repair of the DNA damage following ionising radiation treatment in cervical cancer cells. Tumour recurrence due to resistance to radiotherapy is common, mostly due to promoted DNA repair ability of cancer cells to reduce radiation-induced toxicity and increase cell survival in response to ionising radiation. These findings might be the key to the development of radioresistance in cervical cancer. The HPV E7-p63 axis may be a novel therapeutic target to enhance radio-sensitivity in HPV-transformed tumours.

Poon Kin-yan. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (leaves 119-147). / Abstracts in English and Chinese. / ACKNOWLEDGMENT --- p.i / ABSTRACT --- p.iii / ABBREVIATIONS --- p.viii / TABLE OF CONTENTS --- p.x / Chapter CHAPTER I --- INTRODUCTION --- p.1 / Chapter 1.1 --- Cervical Intraepithelial Neoplasia (CIN) and Cervical Cancer --- p.1 / Chapter 1.1.1 --- Epidemiology --- p.3 / Chapter 1.1.1.1 --- Descriptive Epidemiology --- p.4 / Chapter 1.1.1.2 --- Risk Factors --- p.7 / Chapter 1.1.2 --- Pathology --- p.22 / Chapter 1.1.2.1 --- Macroscopic Appearance --- p.22 / Chapter 1.1.2.2 --- Symptoms and Diagnosis --- p.23 / Chapter 1.1.2.3 --- Staging Classification --- p.25 / Chapter 1.1.2.4 --- Histopathology --- p.29 / Chapter 1.2 --- Microsatellite Instability (MSI) --- p.35 / Chapter 1.2.1 --- Microsatellite --- p.35 / Chapter 1.2.2 --- Mismatch Repair --- p.37 / Chapter 1.2.3 --- Microsatellite Instability (MSI) --- p.38 / Chapter 1.2.4 --- MSI in Various Cancers --- p.42 / Chapter 1.2.5 --- The Role of MSI in Carcinogenesis --- p.49 / Chapter 1.2.6 --- MSI as a Diagnostic / Prognostic Tool --- p.50 / Chapter CHAPTER II --- AIMS OF THE STUDY --- p.53 / Chapter CHAPTER III --- MATERIALS AND METHODS --- p.56 / Chapter 3.1 --- Materials --- p.56 / Chapter 3.1.1 --- Patients and Specimens --- p.56 / Chapter 3.1.2 --- Microsatellite Markers --- p.57 / Chapter 3.2 --- Methods --- p.59 / Chapter 3.2.1 --- Preparation of OCT-embedded Specimen Sections --- p.59 / Chapter 3.2.2 --- Microdissection of Epithelial Cells and Neoplastic Cells from Specimen Sections --- p.60 / Chapter 3.2.3 --- DNA Extraction --- p.60 / Chapter 3.2.3.1 --- Normal Blood --- p.61 / Chapter 3.2.3.2 --- Dissected Cells --- p.62 / Chapter 3.2.4 --- DNA Amplification --- p.64 / Chapter 3.2.4.1 --- End-labeling of Primers --- p.64 / Chapter 3.2.4.2 --- Polymerase Chain Reaction --- p.65 / Chapter 3.2.5 --- Denaturing Polyacrylamide Gel Electrophoresis --- p.66 / Chapter 3.2.6 --- Autoradiography --- p.67 / Chapter 3.2.7 --- Determination of MSI --- p.67 / Chapter 3.2.8 --- HPV Detection --- p.68 / Chapter 3.2.9 --- Statistical Analysis --- p.69 / Chapter CHAPTER IV --- RESULTS --- p.70 / Chapter 4.1 --- Incidence of MSI in Cervix --- p.70 / Chapter 4.1.1 --- Incidence of MSI in Normal Cervix --- p.70 / Chapter 4.1.2 --- Incidence of MSI in CIN --- p.70 / Chapter 4.1.3 --- Incidence of MSI in Cervical Carcinoma --- p.71 / Chapter 4.1.4 --- Correlation of MSI-positive with the Evolution of Cervical Neoplasm --- p.77 / Chapter 4.2 --- Correlation of MSI-positive with Clinicopathological Characteristics in Cervical Carcinoma --- p.77 / Chapter 4.2.1 --- MSI and Age --- p.80 / Chapter 4.2.2 --- MSI and Clinical Stage --- p.80 / Chapter 4.2.3 --- MSI and Histological Grade --- p.80 / Chapter 4.2.4 --- MSI and Clinical Status --- p.81 / Chapter 4.3 --- Comparison between Two Panels of Microsatellite Markers used in MSI Detection --- p.84 / Chapter 4.4 --- Human Papilloma Virus (HPV) Infection in Cervical Neoplasm --- p.89 / Chapter 4.4.1 --- HPV Infection and Typing in CIN and Cervical Carcinoma --- p.89 / Chapter 4.4.2 --- Correlation of MSI-positive with HPV Infection in Cervical Carcinoma --- p.94 / Chapter CHAPTER V --- DISCUSSION --- p.96 / Chapter 5.1 --- MSI Detection --- p.96 / Chapter 5.1.1 --- Techniques in MSI Assays --- p.98 / Chapter 5.1.2 --- Choice of Microsatellite Markers --- p.101 / Chapter 5.1.3 --- Diagnostic Criteria of MSI --- p.105 / Chapter 5.2 --- The Role of MSI in the Carcinogenesis of Cervical Neoplasm --- p.107 / Chapter 5.3 --- The Clinical Significant of MSI in Cervical Carcinoma --- p.111 / Chapter 5.4 --- The Interaction between HPV Infection and MSI in Cervical Carcinoma --- p.113 / Chapter CHAPTER VI --- CONCLUSION --- p.116 / REFERENCES --- p.119

Made available in DSpace on 2014-06-11T19:30:52Z (GMT). No. of bitstreams: 0 Previous issue date: 2001Bitstream added on 2014-06-13T20:21:20Z : No. of bitstreams: 1 azevedo_gc_dr_botfm.pdf: 1468738 bytes, checksum: 5d4e12fc75c354ee245a948583564151 (MD5) / Este trabalho experimental propõe uma nova e eficiente técnica para in-trodução de parafuso no processo articular cervical, com menor risco. Utilizando um novo dispositivo e determinando o comprimento efetivo médio do parafuso. Foram usadas cinco colunas cervicais de esqueleto humano de C3 a C7, num total de 25 vértebras e 50 perfurações. Foram selecionados dois grupos de vértebras: um de C3 a C6, outro de C7. No primeiro grupo, o ponto inicial do parafuso situou-se a 2 mm. mediais e caudais do ponto central do processo articular, dirigindo-se a ponta do parafuso a 21,5º no sentido cranial. No outro grupo, o ponto inicial foi localizado a 2mm. da linha média vertical, logo abaixo da superfície articular superior, dirigindo-se a ponta do parafuso a 16,5º no sentido caudal. Em ambos os grupos, o parafuso foi desviado lateralmente a 42,5º. Concluímos que a nossa técnica é eficiente e segura porque: 1) utiliza um dispositivo que mede o ângulo de introdução do parafuso, bloqueando-o após a ultrapassagem da cortical anterior, introduzindo somente o comprimento ideal para cada processo articular, diminuindo o risco de lesão; 2) não causa lesão da artéria vertebral e da raiz nervosa; 3) apresenta baixa incidência de violação da superfície articular, 7,5% nas vértebras C3 a C6 e 0% nas C7; 4) apresenta um comprimento efetivo do parafuso de 10,7 mm. para ambos os grupos vertebrais oferecendo boa fixação óssea e boa margem de segurança, em relação às estruturas anatômicas importantes. / This experimental paper presents a new and efficient technique to insert a screw in the cervical lateral mass with the less risk of damaging the vertebral artery, the nerve root and the articular facet. This procedure is carried out by using a new device which measures the screw insertion angle and lock the screw after it goes through the posterior cortical area. This paper also aims at determining the effective screw length to be used in this technique. Five human lower cervical spines from C3 to C7 - were used. Two holes were made in both sides of these 25 vertebrae. Therefore 50 holes were made. Two vertebrae groups were selected: C3-C6 and C7. In the C3-C6 group the start point of the screw was placed in a medial and caudal position 2mm. in relation to the central point of the articular prossece; the screw tip was directed to the half of the lateral vertebral line at a 21,5° angle in the cranial direction; for the C7 vertebrae the screw initial point was placed at a 2 mm. medial position in the vertical mean line just below the upper articular level; the screw tip was directed to the half of the lateral vertebral line at a 16,5° angle in the caudal direction. In both vertebral groups the screw was laterally deviated at a 42,5° angle. The conclusion is that this new technique is efficient and safe because: 1) it utilizes a new device to guide and measure the screw insertion and lock the screw after it goes through the posterior cortical area; the in-sertion is thus adequate for each specific lateral mass and decreases the risk of damage to the vertebral artery and to the nerve root; in fact it did not occur in both vertebral groups; 2) it presents a low rate of articular facet violation; 3) it presents a 10,7 mm. screw length which is effective for both vertebral groups; 4) therefore there occurs a good bone fixation and the important anatomic structures are preserved.

Master of Science - Science / DWNN-deficient Chinese Hamster Ovary cells have been found to be resistant to staurosporine-induced apoptosis. The human DWNN gene is located on chromosome 16p21, with 18 exons and is 36 kb long. It is alternatively spliced at exon 16 and makes two major mRNA transcripts, 1.1 and 6.1 kb, encoding 13 kDa and 200 kDa proteins respectively. The purpose of the study was to elucidate the possible role of DWNN in cervical cancer and apoptosis, to establish tissue distribution and expression levels of DWNN at protein and mRNA levels in cervical cancer. In situ hybridization studies showed elevated levels of the three mRNA transcripts in cervical cancer as compared to the normal tissues. The transcripts were localized in the nuclei of invaded stroma, moderately differentiated islands of tumours, dysplastic epithelium and some infiltrating lymphocytes. Immunocytochemistry showed that DWNN proteins were highly expressed in the dysplastic epithelium, dysplastic endocervical glands, moderately and well differentiated islands of tumours and the invaded stroma. Image analysis indicated elevated expression levels in the islands of tumours. Apoptosis detection by TUNEL revealed high apoptotic levels in the invaded stroma and moderately differentiated islands of tumours and this significantly correlated with DWNN localization. Proliferation assay using Ki67 antibody was found to be indirectly directly proportional to DWNN expression. Antiapoptotic Bcl-2 expression levels were found to be inversely proportional to the expression levels of DWNN. The up-regulated levels of DWNN in cervical cancers in contrast to normal tissues suggest DWNN to be proapoptotic, as there were elevated levels of apoptosis in the same sites where there were high levels of DWNN expression and Bcl-2 was down-regulated in the same sites. DWNN expression significantly correlated with apoptotic levels and was indirectly proportional to ki67 in human cervical cancers. Real Time PCR also confirmed the up-regulation in levels of DWNN in cervical cancer. This study suggests that the DWNN gene may be involved in apoptosis. Further characterization of this gene could lead to its manipulation as a diagnostic marker and a potential therapeutic target for cancer treatment.

MMed(Obstetrics and Gynaecology) / Introduction Against the high background rate of HIV among our antenatal clinic attendees, 30.3% in Gauteng in 2007, and the importance of cancer of the cervix as a health issue; this study was undertaken to determine the rate of abnormality found in cervical smears performed on HIV positive women attending the postnatal clinic at Johannesburg Hospital. The degree of abnormality and where possible its management, was reviewed. Secondly it was determined whether the immune status, namely the WHO clinical stage, CD4 cell count and viral load, correlated with the Pap smear results. Lastly patients were also analyzed according to the treatment received for HIV and their Pap smear results. Patients and Methods The study is a retrospective record review. All the patients who attended the postnatal clinic (PNC) between October 2005 and the end of July 2006, who had a Pap smear, were included. Follow-up test results were collected to the end of June 2007. A total of 324 patients attended the clinic in the study time period, of which 248 (76.5%) had a Pap smear done and 76 (23.5%) did not. iv Results The main results of interest were as follows – 131 patients (52.8%) had normal Pap smears, 64(25.8%) had LGSIL, 32 (12.9%) had HGSIL, 10 (4.0%) had ASCUS and 11 (4.4%) had Pap smears that could not be classified. In total 47.2% of the Pap smears were abnormal. There was one case of malignancy developing after an abnormal Pap smear. Patients with abnormal Pap smears tended to have a lower mean CD4 cell count while the viral load and WHO Stage did not appear to have an impact on the final analysis of the Pap smears. Conclusion The rates of cervical abnormality in HIV sero-positive patients attending the Johannesburg Hospital postnatal clinic are much higher (47.2%) than would be expected in the general population (10%), with a significant portion requiring follow-up investigation and management. It is however preferable to deal with cervical cytological abnormalities comprehensively during the screening phase rather than trying to manage a potential increase in cervical cancer cases.

Thesis (M.Sc. (Medical Laboratory Sciences)) -- University of the North, 1986 / Refer to the document

OBJETIVOS: El objetivo de este trabajo es evaluar la validez de la citología convencional y la colposcopía como pruebas de detección precoz de displasia moderada, severa, carcinoma in situ o carcinoma invasivo de cérvix. MÉTODOS: Se realizó un estudio tranversal de tipo retrospectivo. La población estuvo conformada por pacientes que requirieron ser sometidas a CONO LEEP durante el periodo 2012 a 2015 en el INMP. Se realizó una revisión las historias clínicas para obtener una muestra siguiendo los criterios de inclusión y exclusión. Para poder evaluar la validez de ambas pruebas, se realizó el cálculo de la sensibilidad, especificidad, valor predictivo positivo y valor predictivo negativo de las pruebas. Para ello se tomó como punto de corte a la displasia moderada (NIC II) o una lesión mayor para considerar un resultado positivo. Para comparar ambas pruebas, se realizó una comparación del área bajo la curva de ROC (AUC) de dichas pruebas. RESULTADOS: La citología presenta una sensibilidad de 39.66%, una especificidad de 91.38%, un valor predictivo positivo de 82.14%, un valor predictivo negativo de 60.23%. La colposcopía presenta una sensibilidad de 77.59%, una especificidad de 63.79%, un valor predicitivo positivo de 68.18% y un valor predictivo negativo 74%. El área bajo la curva de ROC de la colposcopía con un valor de 0.7201 fue mayor al área bajo la curva de ROC de la citología con valor de 0.6892, lo que sugiere una mejor capacidad de discriminación de la enfermedad. CONCLUSIONES: La citología y la colposcopía son pruebas con utilidad clínica para la detección de displasia moderada, displasia severa, carcinoma in situ y carcinoma invasor. La citología presenta una baja sensibilidad por el alto índice de falsos negativos posiblemente por una baja calidad en el procedimiento de la prueba. Palabras clave: Citología cervical, colposcopía, lesiones intraepiteliales de alto grado, validez diagnóstica. / --- OBJECTIVES: To assess the validity of Pap smear and colposcopy as screening tests for moderate dysplasia, severe dysplasia, carcinoma in situ or cervical cancer. METHODS: A cross-sectional retrospective study was performed. The population consisted of patients who required treatment under LEEP conization in the period 2012-2015. A review of medical records was conducted to obtain a sample by following the criteria of inclusion and exclusion. The estimation of sensitivity, specificity, positive and negative predictive value of the tests were performed in order to assess the validity of both tests. For this purpose it was taken as a cutpoint to moderate dysplasia (CIN II) or a greater injury to consider a positive result. To compare both tests, a comparison of the area under the ROC curve (AUC) of such tests was developed. RESULTS: Sensibility, specificity, positive predictive value and negative predictive value of Pap smear were 39.66%, 91.38%, 82.14%, 60.23% respectively. Sensibility, specificity, positive predictive value and negative predictive value of colposcopy were 77.59%, 63.79%, 68.18%, 74% respectively. The area under ROC curve of colposcopy was 0.7201 was greater than the area under ROC curve of cytology which had a value of 0.6892, suggesting a better ability of discrimination of the disease. CONCLUSIONS: Pap smear and colposcopy are clinically useful tests for detecting moderate dysplasia, severe dysplasia, carcinoma in situ and invasive carcinoma. Cytology has a low sensitivity for the high rate of false negatives possibly because of a low quality in the test procedure. Keywords: Pap smear, colposcopy , high-grade intraepithelial lesions , diagnostic validity. / Tesis