Carcinogenesis Of Cervical Cancer Research Articles

Genotypes and prevalence of HPV single and multiple concurrent infections in women with HSIL

The contribution of human papillomavirus (HPV) types to the carcinogenesis of cervical cancer has been established for a long time. However, the role of phylogenetically related and rare variants remains uncertain, as well as the influence of concurrent multiple HPV genotypes infection. We aimed at studying the prevalence of several HPV genotypes infecting women with single versus concurrent multiple HPV genotypes infection with a HSIL diagnosis in a cervical cytology. We conducted a cross-sectional study using Thin-Prep(®) liquid-based cervical cytology specimens with the diagnosis of high-grade squamous intraepithelial lesion (HSIL), in which HPV genotype was sequentially tested. Genotypes were determined with a PapilloCheck(®) system, a DNA-Chip for the type-specific identification of 18 high-risk and six low-risk types of HPV. Of the total study population, 176 cases had a diagnosis of HSIL and positive HPV genotyping result, being HPV16 the most prevalent genotype (48.86%; 95%CI: 41.58-56.19) followed by HPV31 (14.20%; 95%CI: 9.75-20.18). Concurrent multiple HPV genotypes were detected in 36.93% (95%CI: 30.15-44.27) of the patients. The prevalence of the 10 most common HPV genotypes detected varied significantly according to the presence of single vs. concurrent multiple HPV genotypes (P = 0.022). Moreover, women with concurrent multiple HPV genotypes were on average 3.53 (95%CI: 0.43-6.64) years younger than women with single genotype infection. Our results suggest that women with multiple genotype HPV infection differ in terms of age and distribution of the most prevalent HPV genotypes. Additionally, we provide further evidence of the predominance of HPV16 in HSIL lesions of the uterine cervix.

Cyclooxygenase-2 expression in cervical cancer.

Cyclooxygenase (COX) or prostaglandin H2 synthase is the first enzyme that catalyzes the first two steps in the biosynthesis of prostaglandins from arachidonic acid. The aim of the study was to determine the expression level of COX-2 in patients with cervical cancer and compare it with that in the control group with no cervical pathology. The study included 76 patients divided into two groups: the control group--30 patients without histopathological changes and the group A--46 patients with cervical cancer, FIGO stage IB-IIA. Histopathological and immunohistochemical analyses were performed in these two groups of patients. In the control group, the expression of COX-2 was not confirmed compared to the group A of 26 (56.52%) patients. The expression of COX-2 showed a statistically significant difference in the presence oflymphocytic stromal infiltration (p = 0.0053). The expression of COX-2 was more pronounced in the stromal tissue without lymphocytic infiltration (80% vs. 20%). A higher expression of COX-2 in cervical carcinoma without stromal lymphocytic infiltration suggests a possible paradoxical effect of COX-2 in immunosuppression. Frequent COX-2 expression in the subgroup with poor prognostic histological parameters in the group A indicates the importance of COX-2 expression in the carcinogenesis of cervical cancer.

A polymorphism in the 3’ untranslated region of Hypoxia-Inducible Factor-1 alpha confers an increased risk of cervical cancer in a Chinese population

Cervical cancer is a multifactorial disease involving a complex interplay between genetic and environmental factors. An important role of HIF-1α in cervical cancer carcinogenesis has been studied by multiple researches. We hypothesized that there is a possible association between HIF-1α gene polymorphisms and the risk of cervical cancer in Chinese women. In a case-control study of 518 cervical cancer patients and 553 cancer-free controls, we genotyped three single-nucleotide polymorphisms (SNPs) (rs11549465, rs11549467 and rs2057482) of HIF-1α using the TaqMan SNP Genotyping Assays and assessed its associations with the cervical cancer risk. Besides, 17 cervical cancer tissues were used to assess the expression of the mature mRNA expression of HIF-1α by real-time quantitative reverse transcription PCR. We found that a significantly increased risk of cervical cancer was associated with the CC genotype of rs2057482 in the 3´-untranslated region (3'-UTR) of HIF-1α (odds ratio (OR), 1.44; 95% confidence interval (CI), 1.11-1.88), compared with the CT/TT genotypes. Moreover, the carriers of CT/TT genotypes had significantly decreased HIF-1α mRNA expression levels compared to those with CC genotype. No association was observed between the two polymorphisms (rs11549465, rs11549467) and cervical cancer risk. So that, our results provided the first insight into rs2057482 polymorphism of in the 3´-untranslated region of HIF-1α contributed to the risk of cervical cancer in a Chinese population and thus may serve as a reliable predictive factor of cervical cancer.

Human Papillomavirus and Epstein-Barr virus co-infection in Cervical Carcinoma in Algerian women

BackgroundDespite the fact that the implication of human papillomavirus (HPV) in the carcinogenesis and prognosis of cervical cancer is well established, the impact of a co-infection with high risk HPV (HR-HPV) and Epstein-Barr virus (EBV) is still not fully understood.MethodsFifty eight randomly selected cases of squamous cell carcinomas (SCC) of the uterine cervix, 14 normal cervices specimens, 21 CIN-2/3 and 16 CIN-1 cases were examined for EBV and HPV infections. Detection of HR-HPV specific sequences was carried out by PCR amplification using consensus primers of Manos and by Digene Hybrid Capture. The presence of EBV was revealed by amplifying a 660 bp specific EBV sequence of BALF1. mRNA expression of LMP-1 in one hand and protein levels of BARF-1, LMP-1 and EBNA-1 in the other hand were assessed by RT-PCR and immunoblotting and/or immunohischemistry respectively.ResultsHR-HPV infection was found in patients with SCC (88%), low-grade (75%) and high grade (95%) lesions compared to only 14% of normal cervix cases. However, 69%, 12.5%, 38.1%, and 14% of SCC, CIN-1, CIN-2/3 and normal cervix tissues, respectively, were EBV infected. The highest co-infection (HR-HPV and EBV) was found in squamous cell carcinoma cases (67%). The latter cases showed 27% and 29% expression of EBV BARF-1 and LMP-1 oncogenes respectively.ConclusionThe high rate of HR-HPV and EBV co-infection in SCC suggests that EBV infection is incriminated in cervical cancer progression. This could be taken into account as bad prognosis in this type of cancer. However, the mode of action in dual infection in cervical oncogenesis needs further investigation.

HPV16 E6/E7 induces EMT via Twist and promotes carcinogenesis and metastasis of cervical cancer

HPV16 E6/E7 induces EMT via Twist and promotes carcinogenesis and metastasis of cervical cancer

No association of functional variant in pri-miR-218 and risk of congenital heart disease in a Chinese population

BackgroundMiR-218 plays an important role in heart development in zebrafish. pri-miR-218 rs11134527 variant is associated with cervical cancer carcinogenesis. Therefore, we hypothesized that single nucleotide polymorphism (SNPs) in pri-miR-218 might influence susceptibility to sporadic congenital heart disease (CHD). Methods and resultsWe conducted a case–control study of CHD in a Chinese population to test our hypothesis by sequencing and genotyping pri-miR-218 in 1116 CHD cases and 1219 non-CHD controls. We identified one SNP rs11134527 located in pri-miR-218 sequence. Logistic regression analyses showed that there was no significant association in genotype and allele frequencies of pri-miR-218 rs11134527 A/G polymorphism between CHD cases in overall or various subtypes and the control group. However, real-time PCR analysis showed that rs11134527 allele G significantly increased mature miR-218 expression. In vitro binding assays further revealed that the rs11134527 variant affects miR-218-mediated regulation of Robo1. ConclusionsThis is the first study to investigate the relationship between miR-218 and CHD cases. Our results demonstrate that the functional variant rs11134527 in pri-miR-218 has no major role in genetic susceptibility to sporadic CHD, at least in the population studied here.

Human Papillomavirus Infection and the Multistage Carcinogenesis of Cervical Cancer

This short review outlines our understanding of cervical cancer precursors, concentrating on the central etiologic role of persistent human papillomavirus infection. The stages of cervical carcinogenesis are better understood than for most other major cancers, providing a successful cancer etiology and prevention model.

The role of human papillomavirus in oral squamous cell carcinoma: myth and reality

As the traditional risk factors for oral squamous cell carcinoma, especially tobacco, decline, new potential causative agents become the focus of research. Since the discovery of human papillomavirus (HPV) and its importance in carcinogenesis in cervical cancer, a lot of research has been undertaken to define its role in different types of cancer. In the present study, we evaluate the role of high-risk HPV types in initiation and progression of oral squamous cell carcinoma (OSCC) using a systematic review of the current literature. A literature research with the search term "HPV oral squamous cell carcinoma" was performed via PubMed. Results were screened systematically for relevance and classified into the following categories: molecular biology, genetics, clinical aspects, and prevalence. Articles were then further analyzed to assess quality. The literature research led to 527 results, with an overall HPV prevalence of 30.1 % in OSCCs. The most frequently identified subtypes were HPV-16 and HPV-18 (25.4 and 18.1 %, respectively). Prognostic relevance of HPV was discussed controversially. HPV detection via polymerase chain reaction is the most established method today. Molecular changes according to carcinogenic pathways described for cervix carcinoma were not routinely found in OSCC. In general, no definite role of high-risk HPV is currently deducible from the literature. High-risk subtypes 16 and 18 are present in the genome in approximately one third of OSCC. Its role as a causative agent is less clear than the role in oropharyngeal tumors. The infection might not be the cause of carcinogenesis in a significant number of patients but may become proportionally more important with the decrease of the classical risk factors of tobacco and alcohol.

Peroxiredoxin 3 is a novel marker for cell proliferation in cervical cancer

Although peroxiredoxin 3 (Prx3) has been reported to be involved in cervical cancer (CC) carcinogenesis, the significance of Prx3 in CC progression remains unclear. The present study was conducted to investigate the expression features of Prx3 to better understand the mechanism of tumor growth and invasion. Sixty-eight patients with invasive squamous cervical cancer were included in the present study. The status of human papillomavirus (HPV) infection was detected by hybridization and quantitative real-time polymerase chain reaction (qRT-PCR). Immunohistochemistry was performed on paraffin-embedded sections using monoclonal antibodies against Prx3 and Ki67. All samples were positive for high-risk HPV, among which fifty-six samples were positive for HPV16, seven for HPV18 and five for HPV33. The expression of HPV16 E6/E7 was significantly higher in cancer areas compared to the adjacent normal epithelial tissuses. The positive cells for Prx3 and Ki67 were significantly higher in cancer cells compared to normal epitheliums and the staining pattern of Prx3 was consistent with that of Ki67 (Pearson's correlation coefficient was 0.801, P= 0.000). The upregulation of Prx3 might be a protective response to oxidative stress in the cancer microenvironment. The expression consistency of Prx3 and Ki67 suggests Prx3 to be a potential marker for cell proliferation of CC.

17β-Oestradiol activates proteolysis and increases invasion through phosphatidylinositol 3-kinase pathway in human cervical cancer cells

Despite evidence that oestrogen may play an important role in the carcinogenesis of cervical cancer, its action and mechanism in cervical cancer invasion are not well defined. The invasion induced by 17β-oestradiol (E2) was measured by invasion assay. Real-time polymerase chain reaction (PCR), Western blot, enzyme-linked immunosorbent assay (ELISA) and gelatin zymography were used to study the role of E2 on metastasis-related proteases. The signal pathway was also investigated. E2 was found to significantly enhance the invasion of cervical cell lines including HeLa, CaSki and SiHa cells, but not C33A cells. Moreover, E2 10(-8)M increased the expression and activation of matrix metalloproteinases (MMP-2 and MMP-9) in HeLa and CaSki cells, as shown by real-time PCR, Western blot, ELISA and gelatin zymography. The expression of tissue inhibitor of metalloproteinases (TIMP-1 and TIMP-2) was decreased significantly by E2. Pretreatment with GM6001 10 μM (total MMP inhibitor) or SB-3CT 20 μM (specific gelatinase inhibitor) blocked the pro-invasive effect of E2. E2 was found to induce invasion via the phosphatidylinositol 3-kinase (PI3K) signalling pathway. E2 may contribute to cervical cancer metastasis through activation of proteolysis and increased invasion via the PI3K pathway.

The Immunoexpression of Heparanase 2 in Normal Epithelium, Intraepithelial, and Invasive Squamous Neoplasia of the Cervix

Heparanase 2 (HPSE2) is expressed in various tissues, including the brain, intestine, prostate, breast, and endometrium. The aim of this study was to investigate the role of HPSE2 in cervical carcinogenesis, which has not been clarified to date. The immunoexpression of HPSE2 in normal and neoplastic cervical squamous epithelia was determined using a semiquantitative (SQ) method and an index of expression (IE) method, using Image Lab Software. A total of 230 cervical tissue samples were analyzed and segregated into the following diagnostic groups: normal (27.4%), cervical intraepithelial neoplasia 1 (CIN 1, 15.2%), CIN 2 (16.5%), CIN 3 (15.2%), and invasive neoplasia (25.7%). The mean HPSE2 expression in the normal group was significantly lower than that of the other groups individually or combined (p < .001, for all combinations). The immunoexpression via the SQ method was significantly greater in the CIN 3 group compared with that in the CIN 1 group (p = .02). The mean immunoexpression of the high-grade squamous intraepithelial lesion groups was significantly greater than those of the normal and low-grade squamous intraepithelial lesion groups (p < .001) and lower compared with that of the invasive neoplasia group (p < .001). There were no statistically significant differences in the immunoexpression of HPSE2 among the different clinical states within the invasive neoplasia group. The SQ method produced a greater sensitivity and specificity than did the index of expression method. There was a progressive increase in the mean HPSE2 immunoexpression according to the severity of the cervical lesion from the low-grade squamous intraepithelial lesion group to the invasive neoplasm group, whereas the normal group displayed the lowest level of expression. This is a novel study concerning HPSE2 in the cervix and cervical cancer carcinogenesis.

HPV16 E6/E7 induced EMT is Twist dependent and can promote carcinogenesis and metastasis of cervical cancer

Objective: Human papillomaviruses (HPVs) are recognized as the etiological agent of cervical cancer that local invasion is the major way to metastasis. P53 and retinoblastoma proteins are well-characterized targets of the HPV16 E6/E7 oncoproteins. However, recent studies figured out that the alterations of additional pathways are equally important for transformation. Meanwhile, cancer-associated epithelial to mesenchymal transition (EMT) has been focused and considered as a critical phenomenon in invasion and metastasis such as breast cancer and prostate cancer these days, but little items involve in cervical cancer.

Genetic polymorphism of urokinase‐type plasminogen activator is interacting with plasminogen activator inhibitor‐1 to raise risk of cervical neoplasia

To evaluate the impact of plasminogen activator (PA) system genes, including urokinase plasminogen activator (uPA), uPA receptor (uPAR), and plasminogen activator inhibitor-1 (PAI-1) gene polymorphisms in patients with the cervical neoplasia. In total, 336 blood samples were collected from healthy women and 136 patients with cervical neoplasia to analyze the gene polymorphisms of representative PA system genes. There was no significant association between cervical neoplasia cases and gene polymorphisms of uPA, uPAR and PAI-1 genes as well as to the carcinogenesis of cervical if the cervical neoplasia cases were stratified to HSILs and invasive cancer cases. However, we found a mutual interaction between uPA/PAI-1 genes, which women carrying the uPA/PAI-1 CC/4G4G allele had a 1.70-fold higher risk (OR = 1.70; 95% CI 1.04-2.79) of cervical neoplasia compared with those carrying the CC/4G5G allele. Individuals with uPA/PAI-1 CC/4G5G allele were in high susceptibility for cervical neoplasia. The combined polymorphism of uPA/PAI-1 might diminish the ability of PAI-1 to inhibiting cervical cancer carcinogenesis when PAI-1 alone as the role of inhibitor.

Metabolic risk factors and cervical cancer in the metabolic syndrome and cancer project (Me–Can)

BackgroundLittle is known about the association between metabolic risk factors and cervical cancer carcinogenesis. Material and methodsDuring mean follow-up of 11years of the Me–Can cohort (N=288,834) 425 invasive cervical cancer cases were diagnosed. Hazard ratios (HRs) were estimated by the use of Cox proportional hazards regression models for quintiles and standardized z-scores (with a mean of 0 and a SD of 1) of BMI, blood pressure, glucose, cholesterol, triglycerides and MetS score. Risk estimates were corrected for random error in the measurements. ResultsBMI (per 1SD increment) was associated with 12%, increase of cervical cancer risk, blood pressure with 25% and triglycerides with 39%, respectively. In models including all metabolic factors, the associations for blood pressure and triglycerides persisted. The metabolic syndrome (MetS) score was associated with 26% increased corrected risk of cervical cancer. Triglycerides were stronger associated with squamous cell carcinoma (HR 1.48; 95% CI, 1.20–1.83) than with adenocarcinoma (0.92, 0.54–1.56). Among older women cholesterol (50–70years 1.34; 1.00–1.81), triglycerides (50–70years 1.49, 1.03–2.16 and ≥70years 1.54, 1.09–2.19) and glucose (≥70years 1.87, 1.13–3.11) were associated with increased cervical cancer risk. ConclusionThe presence of obesity, elevated blood pressure and triglycerides were associated with increased risk of cervical cancer.

A Single Nucleotide Polymorphism in EXO1 Gene Is Associated With Cervical Cancer Susceptibility in Chinese Patients

The aim of this study was to investigate the association of Exonuclease1 (EXO1) genetic polymorphism and the development of cervical carcinoma. This study was conducted with 126 patients diagnosed with cervical cancer and 278 people with no cancer history. The polymerase chain reaction-based restriction fragment length polymorphism was used to evaluate the K589E and C908G gene polymorphisms. Unconditional logistic regression analysis was used to estimate the association between the genotypes and the risk for cervical cancer. This is the first study on the role of EXO1 K589E (rs1047840) and EXO1 C908G (rs10802996) polymorphisms in cervical cancer in a Chinese population. Our results indicated that the EXO1 K589G polymorphism were significantly associated with the risk for cervical cancer. Compared with the G allele EXO1 K589E, the A allele increased the risk for cervical cancer (adjusted odds ratio, 1.67; 95% confidence interval, 1.13-2.45). By contrast, we have not found a significant association between the EXO1 C908G polymorphism and cervical cancer risk (P = 0.791). These findings indicate that the SNPs of EXO1 K589E may contribute to cervical cancer carcinogenesis in Chinese populations. A larger population study will need to be carried out to further validate the potential association of EXO1 genetic polymorphism and cervical carcinoma.

Expression of CHOP in Squamous Tumor of the Uterine Cervix

BackgroundHigh-risk human papillomavirus (HR-HPV) infection and abnormal p53 expression are closely involved in carcinogenesis of squamous cell carcinoma (SqCC) of uterine cervix. Recent studies have suggested that virus-induced endoplasmic reticulum (ER) stress modulates various cell survival and cell death signaling pathways. The C/EBP homologous protein (CHOP) is associated with ER stress-mediated apoptosis and is also involved in carcinogenesis of several human cancers. We hypothesized that CHOP is involved in the carcinogenesis of uterine cervical cancer in association with HR-HPV and/or p53.MethodsImmunohistochemistry was used to analyze CHOP and p53 protein expression of tissue sections from 191 patients with invasive cancer or preinvasive lesions of the uterine cervix (61 cases of SqCC, 66 cases of cervical intraepithelial neoplasia [CIN] III, and 64 cases of CIN I).ResultsCHOP was expressed in 59.4% of CIN I, 48.5% of CIN III, and 70.5% of SqCC cases. It was also significantly more frequent in invasive SqCC than in preinvasive lesions (p=0.042). Moreover, CHOP expression significantly correlated with HR-HPV infection and p53 expression (p=0.009 and p=0.038, respectively).ConclusionsOur results suggest that CHOP is involved in the carcinogenesis of the uterine cervix SqCC via association with HR-HPV and p53.

A Genetic Variant in the Promoter Region of Toll-Like Receptor 9 and Cervical Cancer Susceptibility

The Toll-like receptors (TLRs) are important for the innate immune system by recognizing pathogen-associated molecular patterns expressed in infectious agents. E6 and E7 protein from HPV16 suppress the host immune response by regulating the TLR9 transcript. Therefore, we hypothesized that a single nucleotide polymorphism in TLR9 may contribute to cervical cancer. We genotyped TLR9 -1486T/C (rs187084) in a case-control study of 712 cervical cancer cases and 717 cancer-free controls in Chinese women. Logistic regression analyses showed that the rs187084 heterozygote TC was associated with a significantly increased risk of cervical cancer (adjusted OR=1.28, 95% CI=1.01-1.62), compared with the TT genotype. Although the variant homozygote was associated with a nonsignificantly increased cervical cancer risk, the TC/CC genotypes contributed to the risk of cervical cancer in the dominant genetic model (adjusted OR=1.24, 95% CI=1.01-1.53). The findings indicate that TLR9 -1486T/C (rs187084) may contribute to cervical cancer carcinogenesis.

Aberrant promoter methylation and inactivation of PTEN gene in cervical carcinoma from Indian population

PTEN, a tumor-suppressor gene located on chromosome 10q23.3 is implicated in multiple tumors including cervical carcinoma. We examined 135 cervical cancer specimens for PTEN gene expression and promoter methylation using methylation-specific PCR and immunohistochemistry and also studied the mutation in PTEN gene through PCR-single-stranded conformational polymorphism. PTEN expression and its methylation status were also correlated with clinicopathologic parameters. The results showed an abnormal band on exon 5 and exon 9 of the PTEN gene. In PTEN gene, 61% specimen showed methylation. PTEN methylation was found in 39% cases of stage I, 60% of stage II, and 75% of stages III-IV. The correlation between PTEN methylation and clinical stage was found to be statistically significant (P=0.003). Nuclear PTEN expression was detected in 84 of 135 (62%) cases of cervical carcinoma, and the remaining 51 of 135 (38%) cases were observed as expressional loss. The loss of PTEN expression was significantly correlated clinical stage (P=0.001). Loss of PTEN expression was observed in 34 (41%) cases among 83 methylation positive cases, whereas among 52 methylation-negative cases, only 13 (25%) cases were seen as immunostaining negative with the statistically significant value (P=0.05). Promoter methylation and loss of PTEN expression occur frequently in carcinoma of uterine cervix. Our results suggest that PTEN plays an important role in the carcinogenesis of cervical cancer.

Study on the distribution of HPV subtypes in Uighur people living in the Karsay township, Moyu county, Xinjiang

To study the distribution of human papilloma virus (HPV) subtypes in Uyghur people from the high risk region of cervical cancer in Xinjiang. 21 subtypes of HPV from 400 cases of men's swabs of penile and 400 cases of women's cervix swabs were detected, using flow-through hybridization and gene chip technology. (1) The positive rate of HPV among the 400 women cases was 14.25%, with HPV16 the most common type. In women whose HPV was positive, the positive rate of HPV16 was 66.67%. The ranking of frequencies on the HPV subtypes in women were:HPV16, 58, 39, 18, 33, 52, 43, 66, CP8304, HPV6 and 11. (2) Among the 400 male cases, the positive rate of HPV was 8.00%, with HPV16 the most common type. In men whose HPV was positive, the rate of HPV16 was 44.44%. The ranking of HPV subtypes in men were HPV16, 43, 33, 39, 6 (HPV39 and 6 are equivalent) and 53. (3) Both wives and husbands were infected by different subtypes of HPV, the positive rate was relatively low among men whose wife's HPV were positive. However, the HPV positive rate was relatively low among women whose husband's HPV were positive. The concordance infection rate of women and men were 7.02% and the concordance infection rate of men and women were 9.38%. The HPV positive rates were relatively low in both men and women living in the region with high risk of cervical cancer in Xinjiang. However, the positive rate of high risk types HPV and HPV16 in both men and women were relatively high. Uyghur men seemed to have played a certain role related to the carcinogenesis of cervical cancer. HPV16 was the main type in both men and women in Xinjiang.

Abstract PR-11: HPV vaccine adherence in urban youth

Abstract Background: Human papillomavirus (HPV) is the most common sexually transmitted disease among adolescent females in the United States, with 29.5% of sexually active 14-19 year olds infected at any given time. Persistent infection with cancer causing types of HPV is also a necessary step in the cervical cancer carcinogenesis process. HPV vaccines have been licensed in the United States since 2006; however, relatively modest proportions of the vaccine-eligible population have elected to receive the HPV vaccine. Further, among those who initiate HPV vaccination, a majority fail to complete the three-dose regimen needed for maximum protection. Methods: Data from the clinical data repository at the University of Maryland Medical Center was queried to identify women that initiated HPV vaccination between August 2006 (when UMMC began offering the HPV vaccine) and August 2010. Statistical analyses were conducted to assess vaccine adherence in the study population. The association of age and race with vaccination adherence was also assessed. Results: During the time period of interest, 9,658 women potentially eligible women between 9-26 years were seen at the UMMC outpatient practices. Of those, 2,641 women (27.3% of the target group) initiated HPV vaccination. African-American women comprised 2/3 of those who initiated vaccination. Among those women that initiated vaccination, 39.1% completed a single dose, 30.1% completed 2 doses, and 30.78 completed the recommended 3-dose regimen. Age was related to vaccine adherence, with women 18 and older being least likely to complete more than a single dose (p=0.001). African-American women were less likely than Caucasian women to complete the three-dose regimen (p&amp;lt;0.001). Conclusions: Despite strong efficacy data for the HPV vaccines, relatively small proportions of eligible women have elected to uptake the vaccine as primary prevention for cervical cancer. Further, of those who initiate vaccination, significant proportions fail to complete the recommended three-dose regimen. Young adult women are the least likely to complete the three-dose regimen as are women in minority groups. The public health consequence of this is that significant numbers of women remain unprotected or underprotected. Evidence-based interventions are needed to foster both vaccine uptake and adherence for optimal prevention cervical cancer. Interventions that address barriers for minority women and young adult women are needed. Technological innovations such as text messaging may offer an effective method to address these issues. This talk is also presented as Poster B103. Citation Information: Cancer Prev Res 2010;3(12 Suppl):PR-11.