Patient navigation to increase colorectal cancer screening among Latino Medicare enrollees: a randomized controlled trial.

PURPOSE: Latino Medicare enrollees report suboptimal rates of colorectal cancer screening (CRCS) despite Medicare policies designed to improve CRCS access for older persons. Patient navigation (PN) may address many underlying barriers to CRCS, yet little is known about the effectiveness of PN to increase CRCS adherence among Latino Medicare enrollees. METHODS: Using a randomized controlled trial study design, we evaluated tailored PN delivered outside of primary care settings as an intervention to increase CRCS adherence in this population. Intervention participants (n = 135) received tailored PN services which included education, counseling, and logistical support administered in their language of choice. Comparison participants (n = 168) received mailed cancer education materials. We compared CRCS rates between interventions and used multivariable logistic regression to assess the odds of CRCS adherence for PN versus comparison groups after adjusting for covariates of interest. RESULTS: More navigated than non-navigated participants became CRCS adherent during the study period (43.7 vs. 32.1%, p = 0.04). The odds of CRCS adherence were significantly higher for PN relative to comparison participants before and after adjusting for covariates (unadjusted OR 1.64, p = 0.04; adjusted OR 1.82, p = 0.02). Higher CRCS adherence rates were observed primarily in the uptake of endoscopic screening methods. CONCLUSION: This study demonstrates that PN delivered outside of the primary care environment is modestly effective in increasing CRCS adherence among Latino Medicare enrollees. This intervention strategy should be further evaluated as a complement to primary care-based PN and other care coordination strategies to increase adherence with CRCS and other evidence-based screenings among older Latinos.

Detection of chromosomal aberrations by fluorescence in situ hybridization in cervicovaginal biopsies from women exposed to diethylstilbestrol in utero.

Epidemiologic studies have associated estrogens with human neoplasms such as those in the endometrium, cervix, vagina, breast, and liver. Perinatal exposure to natural (17beta-estradiol [17beta-E(2)]) and synthetic (diethylstilbestrol [DES]) estrogens induces neoplastic changes in humans and rodents. Previous studies demonstrated that neonatal 17beta-E(2) treatment of mice results in increased nuclear DNA content of cervicovaginal epithelium that precedes histologically evident neoplasia. In order to determine whether this effect was associated with chromosomal changes in humans, the frequencies of trisomy of chromosomes 1, 7, 11, and 17 were evaluated by the fluorescence in situ hybridization (FISH) technique in cervicovaginal tissue from 19 DES-exposed and 19 control women. The trisomic frequencies were significantly elevated in 4 of the 19 (21%) DES-exposed patients. One patient presented with trisomy of chromosomes 1, 7, and 11, while trisomy of chromosome 7 was observed in one patient. There were two patients with trisomy of chromosome 1. Trisomy of chromosomes 1, 7, 11, and 17 was not observed in the cervicovaginal tissue taken from control patients. These data suggest that DES-induced chromosomal trisomy may be an early event in the development of cervicovaginal neoplasia in humans.

Cervical cancer among Vietnamese women: efforts to define the problem among Houston's population.

INTRODUCTION: Asian American/Pacific Islanders (AAPIs) in the United States (US) continue to bear a disproportionate burden of cancer. This report focuses on the interviews with local health-care delivery providers, directors, administrators, and community outreach liaisons in the Vietnamese community in Houston, Texas. METHODS: The Center for Minority Health (CMRH) at the University of Texas M.D. Cancer Center interviewed 17 leaders, as defined above, to identify factors that have a negative impact on screening practices among Vietnamese women. RESULTS: The results show that some of the barriers to cervical cancer screening include: lack of knowledge, lack of female physicians, language barriers, lack of insurance, and embarrassment. Interviews established that "prevention" is a Western concept that the Vietnamese community has not yet adopted. Vietnamese women used their churches, community physicians (licensed or not), circle of friends, and families for their health information. Many patients used herbs as alternative or complementary therapies. CONCLUSION: Cultural factors play a vital role in limiting Vietnamese women in the use of cervical screening. Further research needs to focus on identifying specific barriers and how they can be overcome.

"5 A Day" achievement badge for urban boy scouts: formative evaluation results.

BACKGROUND: Certain cancers are more common among African Americans (AA). Fruit and vegetables (F&V) reduce cancer risk, but Americans, and African Americans in particular, do not meet the "5 A Day" goal. Scouting organizations, particularly urban Boy Scout groups that target inner-city youth, provide promising channels for nutritional behavioral change programs. METHODS: Focus groups were conducted with urban Boy Scouts and their parents to identify factors influencing F&V consumption and evaluate potential intervention activities. Twenty-four-hour dietary recalls were collected from 85 area Boy Scouts. A national data set was used to obtain values for F&V consumption by African American and European American (boys age 0-16). RESULTS: Vegetable preferences were low and a negative peer influence for vegetables was reported. The group has limited food-preparation skills, but both parents and scouts reported that F&V were available in their homes. Use of goal setting and use of problem-solving techniques were limited. The local scouts' mean F&V intake was 3.2 servings per day. Ethnic differences in F&V consumption were identified in the national data. CONCLUSIONS: Based on these results and previous interventions in schools, an overall structure for the intervention was developed to include eight weekly troop sessions and two camping sessions, parent newsletters, seven weekly home badge assignments, and ten comic books.

During development, 17alpha-estradiol is a potent estrogen and carcinogen.

Neonatal administration of estradiol-17beta (E2-17beta) increases the nuclear DNA content in the mouse reproductive tract. Similar responses have been demonstrated for synthetic estrogens such as diethylstilbestrol. One of the questions raised regarding environmental estrogens such as organochlorines is whether they are potent enough to result in abnormal changes such as those demonstrated by both natural and synthetic estrogens. To test this hypothesis, female BALB/c mice were treated neonatally (days 1-5) with either E2-17beta or estradiol-17alpha (E2-17alpha), an inactive stereoisomer in adult reproductive tissues. We also proposed whether neonatal administration of (E2-17alpha) was tumorigenic and whether the effects were age dependent. To answer these questions, one set each of 10 day-old treated and control mice received short-term secondary administration of E2-17beta, E2-17alpha, or cholesterol. Cervicovaginal tracts from intact BALB/c mice were examined histologically and by flow cytometry at 70 days of age and by histology alone at 18 to 22 months of age. The results include several important findings: a) like E2-17beta, neonatal E2-17alpha treatment induced persistent vaginal cornification, hypospadias, vaginal concretions, and hyperproliferation in nearly 100% of the animals regardless of the secondary treatment for most groups; b) neonatal E2-17alpha treatment increased the nuclear DNA content of cervicovaginal epithelium at one-half both the level (mean DNA index of 1.02 vs 1.04) and incidence (22 vs 46% of the animals) of E2-17beta; c) short-term secondary treatment with E2-17alpha, unlike E2-17beta, did not significantly augment the increase in DNA content (13% for E2-17alpha vs 37 and 56% for control and E2-17beta, respectively); and d) neonatal administration with E2-17alpha induced adenosquamous tumors in the reproductive tract in 25% of the animals. Therefore, the biological effects (estrogenic potency) of E2-17alpha may be age dependent.

Dietary fiber, Hispanics, and breast cancer risk?

The cancer rates of immigrant populations in the United States must be taken into account when looking at the importance of diet and culture as it relates to cancer prevention. Unfortunately, some nutrition studies targeted toward nontraditional white populations have not adequately confronted the issue of cultural meaning in efforts to gather dietary data accurate enough to support nutritional analyses, identify marginal diets, or relate risk to dietary patterns. The study presented here resolves many of the culturally specific issues utilizing awareness, attention, and judicious combination of culturally sensitive qualitative and quantitative research techniques. The importance of such a study in an Hispanic population is based on the fact that the age-adjusted rate of breast cancer in countries such as Mexico is among the lowest in the world. In addition, although one of the fastest-growing minority groups in the United States, Hispanic women living in this country have been shown to have the lowest incidence of the mortality rates from this disease across most geographic regions of the United States. Therefore, one might speculate that dietary factors, which have been shown to play a role in breast cancer prevention, may account for this difference. It is well recognized that the traditional Hispanic diet is rich in protective nutrients such as dietary fiber. It is known that through complex mechanisms, dietary fiber works to reduce the amount of estrogens in the body. Research also indicates that it is the level of endogenous estrogen in the body that may influence the onset of breast cancer. In order to better understand how dietary factors may be associated with breast cancer in Hispanic women, it is important that one develop the proper tools to discern any potential differences. Therefore, we developed an approach to obtaining dietary fiber information from a small cohort of 22 Houston-area Hispanic women as a vanguard study for a larger breast cancer prevention trial. Two separate dietary assessment instruments were utilized, a three-day food record and the Southwest Food Frequency Questionnaire. The mean intake of dietary fiber was 16 g/day according to the food record and 21 g/day according to the SWFFQ. Fruits, vegetables, breads, cereals, and beans provided for most of the participants' dietary fiber intake. These results support evidence that the Hispanic population's dietary fiber intake is higher than that for other groups, and this may help explain the lower incidence of breast cancer among some Hispanic populations.

Molecular genetic analysis of clear cell adenocarcinomas of the vagina and cervix associated and unassociated with diethylstilbestrol exposure in utero.

BACKGROUND: Prenatal exposure to the synthetic estrogen diethylstilbestrol (DES) is associated with the subsequent development of clear cell adenocarcinoma of the lower reproductive tract in young women, and data concerning the molecular genetic alterations involved in the etiology of this tumor type have not previously been reported. Such knowledge would be of potential value by providing insight into the molecular mechanisms of hormonal carcinogenesis in general, as well as by suggesting molecular markers for risk assessment in the estrogen-exposed population. METHODS: A total of 24 samples of clear cell adenocarcinoma of the vagina or cervix, 16 associated with exposure in utero to DES and 8 with no history of DES exposure, were obtained as archival fixed and embedded tissue specimens. DNA was purified from these tissues and used to examine a number of biologically plausible molecular genetic endpoints for tumor specific alterations. RESULTS: No evidence was found for mutations in the K-ras or H-ras protooncogenes, the Wilms' tumor (WT1) tumor suppressor gene, or the estrogen receptor gene. Sporadic overexpression of the p53 tumor suppressor gene was detected in some tumor cell nuclei by immunohistochemistry, but in the absence of detectable p53 gene mutation. Genetic instability as manifested by somatic mutation of microsatellite repeats was widespread in these tumors, with evidence of microsatellite instability in all DES-associated tumors examined, and in 50% of those tumors not associated with DES exposure. CONCLUSIONS: These data are consistent with the hypothesis that the induction of genomic instability may be an important mechanism of DES-induced carcinogenesis.

Effects of estrogenic chemicals on development.

The sum of the evidence supports the necessity to continue to investigate the developmental effects of estrogenic and antiestrogenic compounds when exposure occurs early in life. Additional studies will answer questions relevant to the molecular definition of the developmental or carcinogenic effects of estrogens such as hormone-induced gene alterations. These studies also support the need to use the neonatal mouse model to demonstrate the consequences of reproductive and nonreproductive stem-cell exposure to estrogenic compounds.

Improved prediction of survival in advanced adenocarcinoma of the ovary by immunocytochemical analysis and the composition adjusted receptor level of the estrogen receptor.

Conventional cytosol estrogen receptor analysis is not a significant prognostic variable in serous ovarian carcinoma. Although the use of immunocytochemical receptor analysis for estrogen does provide prognostically useful information in enhanced accuracy of predicting survival in patients with ovarian cancer, its usefulness can still be improved. Surgical samples from ovarian carcinomas are heterogeneous in tissue composition. Immunocytochemical receptor analysis allows for the specific assessment of the tumorous portions of a histological specimen. However, it is limited by its dependence on staining intensity as the determining factor. Biochemical receptor analysis does provide objective information concerning the number of receptor molecules present in a given sample, but the value is not adjusted for histological composition of the tumor section. Therefore, we have attempted to combine the advantages of both methods. By adjusting the conventional receptor analysis for the percentage of tumor present in the specimen, we have eliminated the tissue heterogeneity as a confounding variable. The resulting value is named Composition Adjusted Receptor Level or CARL. A prospective study was performed on the estrogen receptor concentrations in 61 ovarian cancers. Minimum follow-up was 8 years. For the percentage of tumor in the specimen, a highly significant correlation of the assessment of the two pathologists was observed. Stage (P < 0.05) and grade (P < 0.05) as well as cell type (P < 0.05) were found to be significant prognostic variables. In an attempt to eliminate the confounding influences of these variables, the CARL of the estrogen receptor was assessed with regard to its prognostic significance in 32 grade 2 and 3 serous carcinomas of the ovary, stage III and IV. A linear correlation between CARL and survival was found above a threshold estrogen receptor concentration of 15 fmol/mg cytosol protein using a correlation of the Cox proportional hazards model (P < 0.02). Our data suggest that (a) the assessment of the percentage of tumor in a given sample is not significantly observer dependent, (b) CARL is a significant predictor of survival in serous ovarian carcinoma, and (c) a CARL should be determined for the analysis of any cytosol receptor in solid tumors.

In vivo induction of increased DNA ploidy of mouse cervicovaginal epithelium by neonatal estrogen treatment.

The purpose of this study was to test the hypothesis that exposure to natural estrogen early in the development of hormone-dependent tissue induces a change in nuclear DNA content. Female BALB/c mice were treated neonatally with daily s.c. injections of either 25 micrograms of 17 beta-estradiol (E2) in 0.02 ml of sesame oil (vehicle) or vehicle alone for 5 days. Treatment was begun either within 15 h of birth or 6 days after birth. One set each of 10-day-old E2-treated and control mice received s.c. pellet implants containing 15 mg of E2 and cholesterol (10% E2 and 90% cholesterol), a second set received implants containing 25 mg of cholesterol alone, and a third set did not receive implants. Cervicovaginal tracts from intact BALB/c mice were examined histologically and by flow cytometry at 21, 40, 70, 180, or 240 days of age. The results obtained include several important findings: 1) neonatal E2 treatment in BALB/c mice causes an increase in nuclear DNA content in cervicovaginal epithelium; 2) short-term administration of secondary exogenous E2 reduces the latency period for the appearance of increased nuclear DNA content in neonatally E2-treated cervicovaginal epithelium; 3) increased nuclear DNA content can indicate abnormal cervicovaginal epithelium before histological abnormalities become evident; and 4) there is a sensitive period for neonatal E2 induction of increased nuclear DNA content in the cervicovaginal epithelium. These findings support other reports of the carcinogenic potential of estrogen in vivo. Therefore, increased DNA ploidy may be an important early detectable event in estrogen-induced carcinogenesis.