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1.
Cancer Epidemiol Biomarkers Prev ; 22(6): 1030-6, 2013 Jun.
Article in English | MEDLINE | ID: mdl-23576691

ABSTRACT

Studies have shown that Whites have a higher colorectal cancer survival rate than Blacks. However, it is unclear whether racial disparities result from unequal access to medical care or factors other than health care access or both. This study assessed whether non-Hispanic Whites (NHW) and non-Hispanic Blacks (NHB) differ in colon cancer survival in an equal-access health care system and examined whether racial differences varied by demographic and tumor characteristics. The study included 2,537 Military Health System patients diagnosed with colon cancer between 1998 and 2007. Median follow-up time was 31.4 months. Cox models estimated HRs and 95% confidence intervals (CI) for race, overall and stratified by age at diagnosis, sex, and tumor stage. No difference in overall survival (OS) between NHWs and NHBs was observed in general. However, among patients younger than 50 years old, NHBs experienced significantly worse OS than NHWs (HR: 2.03, 95% CI: 1.30-3.19). Furthermore, stratification by sex and tumor stage showed that this racial disparity was confined to women (HR: 2.87; 95% CI: 1.35-6.11) and patients with distant stage disease (HR: 2.45; 95% CI: 1.15-5.22) in this age group. When medical care is equally available to NHWs and NHBs, similar overall colon cancer survival was observed; however, evidence of racial differences in survival was apparent for patients younger than 50 years old. This study suggests that factors other than access to care may be related to racial disparities in colon cancer survival among younger, but not older, patients.


Subject(s)
Adenocarcinoma/mortality , Colonic Neoplasms/mortality , Ethnicity/statistics & numerical data , Health Services Accessibility , Health Status Disparities , Racial Groups , Adenocarcinoma/ethnology , Aged , Aged, 80 and over , Colonic Neoplasms/ethnology , Female , Follow-Up Studies , Humans , Male , Middle Aged , Prognosis , Risk Factors , Socioeconomic Factors , Survival Rate
2.
Cancer Causes Control ; 23(6): 951-8, 2012 Jun.
Article in English | MEDLINE | ID: mdl-22527173

ABSTRACT

PURPOSE: Recent research, although inconsistent, indicates that socioeconomic status (SES) may be associated with hormone receptor (HR) status. This study aims to examine the association between SES and breast cancer HR status within and across racial/ethnic groups stratified by age at diagnosis and tumor stage. METHODS: The study subjects were 184,602 women with incident breast cancer diagnosed during 2004-2007 and identified from the National Cancer Institute's Surveillance, Epidemiology and End Results program. Log-binomial regression assessed the risk of having breast tumors that were (1) HR-negative versus HR-positive and (2) HR-unknown versus HR-known between women who, at the time of diagnosis, were residing in high or medium poverty areas compared to low poverty areas. RESULTS: High poverty areas tended to have a greater prevalence of HR-negative tumors compared to more affluent areas. Although not always significant, this was observed among non-Hispanic white and Hispanic women regardless of age-tumor stage category, and only among young, non-Hispanic black women and non-Hispanic Asian/Pacific Islander women with regional and distant stage. High poverty areas also tended to have a greater prevalence of HR-unknown tumors compared to more affluent areas. Furthermore, significant trends between HR status and poverty level varied by race/ethnicity, age, and tumor stage. CONCLUSIONS: Poverty may be related to breast cancer negative and unknown HR status. These findings suggest the effects of non-genetic factors on biochemical features of breast cancer, as well as imply a clinical importance to improve HR measurement or recording for low socioeconomic breast cancer patients.


Subject(s)
Breast Neoplasms/epidemiology , Breast Neoplasms/metabolism , Receptors, Estrogen/metabolism , Breast Neoplasms/ethnology , Ethnicity , Female , Humans , Middle Aged , Registries , Risk Factors , SEER Program , Socioeconomic Factors , United States/epidemiology
3.
Cancer Prev Res (Phila) ; 5(3): 435-43, 2012 Mar.
Article in English | MEDLINE | ID: mdl-22246618

ABSTRACT

Serous uterine cancer is not a feature of any known hereditary cancer syndrome. This study evaluated familial risk of cancers for patients with serous uterine carcinoma, focusing on Lynch syndrome malignancies. Fifty serous or mixed serous endometrial carcinoma cases were prospectively enrolled. Pedigrees were developed for 29 probands and tumors were assessed for DNA mismatch repair (MMR) abnormalities. Standardized incidence ratios for cancers in relatives were estimated. A second-stage analysis was undertaken using data from Gynecologic Oncology Group (GOG)-210. Incidence data for cancers reported in relatives of 348 patients with serous and mixed epithelial and 624 patients with endometrioid carcinoma were compared. Nineteen of 29 (65.5%) patients in the single-institution series reported a Lynch-related cancer in relatives. Endometrial and ovarian cancers were significantly overrepresented and a high number of probands (6 of 29, 20.7%) reported pancreatic cancers. None of the probands' tumors had DNA MMR abnormalities. There was no difference in endometrial or ovarian cancer incidence in relatives of serous and endometrioid cancer probands in the case-control study. Pancreatic cancers were, however, significantly more common in relatives of patients with serous cancer [OR, 2.39; 95% confidence interval (CI), 1.06-5.38]. We identified an excess of endometrial, ovarian, and pancreatic cancers in relatives of patients with serous cancer in a single-institution study. Follow-up studies suggest that only pancreatic cancers are overrepresented in relatives. DNA MMR defects in familial clustering of pancreatic and other Lynch-associated malignancies are unlikely. The excess of pancreatic cancers in relatives may reflect an as yet unidentified hereditary syndrome that includes uterine serous cancers.


Subject(s)
Colorectal Neoplasms, Hereditary Nonpolyposis/etiology , Cystadenocarcinoma, Serous/complications , Neoplastic Syndromes, Hereditary/genetics , Uterine Neoplasms/complications , Aged , Aged, 80 and over , DNA Mismatch Repair/genetics , Female , Follow-Up Studies , Humans , Middle Aged , Pedigree , Prognosis , Prospective Studies
4.
Breast Cancer Res ; 13(2): R42, 2011 Apr 06.
Article in English | MEDLINE | ID: mdl-21470416

ABSTRACT

INTRODUCTION: Studies suggest that high circulating levels of prolactin increase breast cancer risk. It is unclear if genetic variations in prolactin (PRL) or prolactin receptor (PRLR) genes also play a role. Thus, we examined the relationship between single nucleotide polymorphisms (SNPs) in PRL and PRLR, serum prolactin levels and breast cancer risk in a population-based case-control study. METHODS: We genotyped 8 PRL and 20 PRLR tag SNPs in 1965 breast cancer cases and 2229 matched controls, aged 20-74, and living in Warsaw or Lódz, Poland. Serum prolactin levels were measured by immunoassay in a subset of 773 controls. Odds ratios (ORs) and 95% confidence intervals (CIs) for genotype associations with breast cancer risk were estimated using unconditional logistic regression, adjusted for age and study site. Geometric mean prolactin levels were estimated using linear regression models adjusted for age, study site, blood collection time, and menstrual cycle day (premenopausal women). RESULTS: Three SNPs were associated with breast cancer risk: in premenopausal women, PRLR rs249537 (T vs. C per-allele OR 1.39, 95% CI 1.07 - 1.80, P = 0.01); and in postmenopausal women, PRLR rs7718468 (C vs. T per-allele OR 1.16, 95% CI 1.03 - 1.30, P = 0.01) and PRLR rs13436213 (A vs. G per-allele OR 1.13 95% CI 1.01 - 1.26, P = 0.04). However, mean serum prolactin levels for these SNPs did not vary by genotype (P-trend > 0.05). Other SNPs were associated with serum prolactin levels: PRLR rs62355518 (P-trend = 0.01), PRLR rs10941235 (P-trend = 0.01), PRLR rs1610218 (P-trend = 0.01), PRLR rs34024951 (P-trend = 0.02), and PRLR rs9292575 (P-trend = 0.03) in premenopausal controls and PRL rs849872 (P-trend = 0.01) in postmenopausal controls. CONCLUSIONS: Our data provide limited support for an association between common variations in PRLR and breast cancer risk. Altered serum prolactin levels were not associated with breast cancer risk-associated variants, suggesting that common genetic variation is not a strong predictor of prolactin-associated breast cancer risk in this population.


Subject(s)
Breast Neoplasms/genetics , Polymorphism, Single Nucleotide , Prolactin/blood , Prolactin/genetics , Receptors, Prolactin/genetics , Adult , Aged , Breast Neoplasms/blood , Breast Neoplasms/epidemiology , Case-Control Studies , Female , Genotype , Humans , Middle Aged , Poland , Postmenopause/genetics , Premenopause/genetics , Risk Factors
5.
Virology ; 411(1): 1-8, 2011 Mar 01.
Article in English | MEDLINE | ID: mdl-21227476

ABSTRACT

Earlier studies indicated that transgenic (tg) mice engineered to express prion protein (PrP) lacking the glycophosphatidylinositol (GPI⁻/⁻) membrane anchor formed abnormal proteinase-resistant prion (PrPsc) amyloid deposits in their brains and hearts when infected with the RML strain of murine scrapie. In contrast, RML scrapie infection of normal mice with a GPI-anchored PrP did not deposit amyloid with PrPsc in the brain or the heart. Here we report that scrapie-infected GPI⁻/⁻ PrP tg mice also deposit PrP and transmissible infectious material in the gut, kidneys, and islets of Langerhans. Similar to previously reported amyloid deposits in the brain and heart, amyloid deposits were found in the gut; however, no amyloid deposited in the islets. By high-resolution electron microscopy, we show PrP is located primarily in α cells and also ß cells. Islets contain abundant insulin and there is no abnormality in glucose metabolism in infected GPI⁻/⁻ PrP tg mice.


Subject(s)
Glycosylphosphatidylinositols/deficiency , Prion Diseases/veterinary , Prions/metabolism , Rodent Diseases/pathology , Amyloid/analysis , Animal Structures/pathology , Animals , Female , Male , Mice , Mice, Transgenic , Prion Diseases/pathology , Prion Proteins
6.
J Nutr Educ Behav ; 43(5): 308-15, 2011.
Article in English | MEDLINE | ID: mdl-20965787

ABSTRACT

OBJECTIVE: Examine the relationship of family meals to children's consumption of fruit and vegetables as well as soda and chips. Additionally, to assess the relationship between viewing TV during family meals and children's diet. DESIGN: Cross-sectional study that used a questionnaire completed by parents. SETTING: Thirteen schools in San Diego, California. PARTICIPANTS: Seven hundred ninety-four children and their parents. ANALYSIS: Ordinal regression assessed associations between children's intake of fruit, vegetables, soda, and chips with family meal frequency and TV viewing during family meals. RESULTS: Children who consumed breakfast, lunch, or dinner with their family at least 4 days per week ate fruit and vegetables 5 or more times a week 84%, 85%, and 80%, respectively. Of those children who ate breakfast, lunch, or dinner with their family at least 4 days per week, 40%, 44%, and 43% consumed soda and chips 5 or more times a week, respectively. Children who ate breakfast with their families at least 4 times a week were more likely to consume fruit and vegetables, and children whose TV was never or rarely on during family meals were less likely to consume soda and chips (P = .04 and P < .001, respectively). CONCLUSIONS: Interventions geared at increasing the frequency of eating breakfast as a family and decreasing the amount of TV watched during family meals are needed, especially among acculturating Latino families.


Subject(s)
Family/ethnology , Feeding Behavior/ethnology , Hispanic or Latino/statistics & numerical data , Television/statistics & numerical data , California , Child , Cross-Sectional Studies , Female , Humans , Male , Surveys and Questionnaires
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