Elimination of Cancer Health Disparities through the Acceleration of HPV Vaccines and Vaccinations: A Simplified Version of the President's Cancer Panel Report on HPV Vaccinations.

The human papillomavirus (HPV) is a major public health concern affecting both females and males. HPV is associated with cervical, anal, head and neck cancers. About 99% of all cervical cancers are related to HPV. HPV vaccines, Gardasil, Cervarix, and Gardasil 9 are used in the primary prevention of HPV related cancers. Gardasil and Gardasil 9 are available for use in both females and males ages 9 to 26, while Cervarix is available for females ages 9 to 25. Gardasil 9 was approved by the FDA for prevention against additional HPV types. Despite the availability of this preventative measure against cervical cancer, the rate of HPV vaccination in the United States remains lower than that of other industrialized nations. The purpose of this study is to elucidate mechanisms to help increase the HPV vaccination rate by using education as a tool; by simplifying the president report so that lay person can understand the information presented in the report. Through the quantitative examination of the data from the states with the lowest and highest vaccination rates, using SPSS statistical analysis; we analyzed several factors involved with the low uptake of the vaccines. The results collected show that socioeconomic status, misconceptions about HPV, and misconceptions about the safety of the vaccines were identified as possible obstacles to the effective uptake of HPV vaccinations. The proposals made by the President's Cancer Panel to accelerate the uptake of vaccines include, increasing coverage of the vaccines through government-sponsored programs, and the Affordable Care Act; increasing accessibility to vaccines through pharmacies, schools, and clinics; and disseminating more information on HPV to healthcare providers, parents, caregivers, and patients. Allowing greater accessibility to the vaccines for all populations regardless of income, education, and eliminating misconceptions of the vaccines would play a significant role in eliminating cancer.

Type II Endometrial Cancer Overexpresses NILCO: A Preliminary Evaluation.

OBJECTIVE: The expression of NILCO molecules (Notch, IL-1, and leptin crosstalk outcome) and the association with obesity were investigated in types I and II endometrial cancer (EmCa). Additionally, the involvement of NILCO in leptin-induced invasiveness of EmCa cells was investigated. METHODS: The expression of NILCO mRNAs and proteins were analyzed in EmCa from African-American (n = 29) and Chinese patients (tissue array, n = 120 cases). The role of NILCO in leptin-induced invasion of Ishikawa and An3ca EmCa cells was investigated using Notch, IL-1, and leptin signaling inhibitors. RESULTS: NILCO molecules were expressed higher in type II EmCa, regardless of ethnic background or obesity status of patients. NILCO proteins were mainly localized in the cellular membrane and cytoplasm of type II EmCa. Additionally, EmCa from obese African-American patients showed higher levels of NILCO molecules than EmCa from lean patients. Notably, leptin-induced EmCa cell invasion was abrogated by NILCO inhibitors. CONCLUSION: Type II EmCa expressed higher NILCO molecules, which may suggest it is involved in the progression of the more aggressive EmCa phenotype. Obesity was associated with higher expression of NILCO molecules in EmCa. Leptin-induced cell invasion was dependent on NILCO. Hence, NILCO might be involved in tumor progression and could represent a new target/biomarker for type II EmCa.

Endometrial carcinoma with ectopic human chorionic gonadotropin expression.

•Aggressive course and treatment resistance characterize ectopic human chorionic gonadotropin.•Recurrence of endometrial cancer with ectopic hCG was treated with brachytherapy and EMACO.•The serum hCG level can serve as a marker in tumors with ectopic hCG expression.

Molecular cues on obesity signals, tumor markers and endometrial cancer.

Tumor markers are important tools for early diagnosis, prognosis, therapy response and endometrial cancer monitoring. A large number of molecular and pathologic markers have been described in types I and II endometrial cancers, which has served to define the main oncogenic, epidemiological, genetic, clinical and histopathological features. Ongoing attempts to stratify biological markers of endometrial cancer are presented. However, data on changes in tumor marker profiles in obesity-related endometrial cancer are scarce. Obesity is a pandemic in Western countries that has an important impact on endometrial cancers, albeit through not very well-defined mechanisms. Although endometrial cancer is more common in Caucasian women, higher mortality is found in African Americans who also show higher incidence of obesity. Here, we describe how obesity signals (estrogen, leptin, leptin induced-molecules, Notch; cytokines and growth factors) could affect endometrial cancer. Leptin signaling and its crosstalk may be associated to the more aggressive and poor prognosis type II endometrial cancer, which affects more postmenopausal and African-American women. In this regard, studies on expression of novel molecular markers (Notch, interleukin-1 and leptin crosstalk outcome) may provide essential clues for detection, prevention, treatment and prognosis.

Physician and provider education for improving health and eliminating disparities.

The Sixth Annual Primary Care and Prevention Conference and the Eleventh Annual HeLa Women's Health Conference was held on September 11-13, 2006 in Atlanta, Georgia. The reports in this supplement of Ethnicity & Disease provide a sample of the presentations made during the primary care and women's health sessions.

Improving health, eliminating disparities: finding solutions for better health care for all populations.

The Fourth Annual Primary Care and Prevention Conference was held October 25-27, 2004 in Atlanta, Georgia to address inequalities in primary care health outcomes and to develop strategies to improve the health status among under-served communities throughout the country. The Ninth Annual HeLa Women's Health Conference was conducted concurrently during the conference's Tuesday, October 26 sessions and were designed for those in obstetrics/gynecology. The reports herein provide a sample of the rich presentations and scientific knowledge imparted by a faculty of more than 100 who addressed disparities across disease states (heart disease and stroke; cancer; diabetes, chronic kidney disease, and obesity; infectious disease; mental health and mental disorders; environmental health/injury and violence; respiratory diseases; and substance abuse, tobacco use) and within focused areas (adult health; maternal, child and adolescent health; health policy and practice; and social and community health).

Maternal blood lead effects on infant intelligence at age 7 months.

A sample of 7-month-old African-American infants, exposed to maternal blood lead levels less than 5 microg/dL, were assessed with the Fagan test of Infant Intelligence. The results indicate significant effects on memory and cognitive functioning. Specifically, infants who scored in the upper 5th to 15th percentile of novelty preference scores had lower lead values than those scoring in the lower 5th or 15th percentile. Of note, is the finding that no infant who scored in the upper percentile range was ever classified as having high maternal blood lead levels. These results are in accord with previous studies that report relationships between low-level lead exposure and nonoptimal infant development.

PTEN/MMAC1 mutations correlate inversely with an altered p53 tumor suppressor gene in gynecologic tumors.

OBJECTIVE: This study was conducted to evaluate the different mutations of p53 and compare p53 expression in gynecologic tumors in African American and Chinese women. METHOD: Tumor samples were collected from Atlanta, Ga, hospitals and National Taiwan University Hospital, Taiwan. Samples were examined for different mutations using electrophoretic variants after single-stranded conformational analysis (SSCA). Cell lines obtained from the American Type Culture Collection were also used. RESULTS: Mutations were identified in the gene for the tumor protein p53 at codons 156, 157, 176, 183, 246, and 248 at sites predicted to disrupt DNA binding. Collectively, an altered p53 status was found in about 28% of all tumors with similar frequencies observed between the African American and Chinese women. African American or Chinese women did not have common polymorphism. CONCLUSION: This study showed that in mutations in the PTEN/MMAC1 gene correlated inversely with an altered p53 status. Similar findings were found in 2 tumor cell lines examined. As p53 changes are associated with late stage cancers, we favor the possibility that in certain tumor subtypes, PTEN/MMAC1 genes alteration may be useful clinically in the evaluation of the tumor.