bluuebunny/crossref_metadata_2025 huggingface dataset:
Abstract B57: A RCT of a community health worker intervention using HPV self-sampling to increase cervical cancer screening among minority populations
Authors: Carrasquillo Olveen , Koru-Sengul Tulay , McCann Sheila , Amofah Anthony , Kobetz Erin
Published: May 2015

Background: Caribbean immigrants (both Hispanics and Blacks from Haiti) are less likely to be screened for cervical cancer than the general population. One promising approach is outreach strategies that employ Community Health Workers (CHWs). Yet even in well structured CHW programs, many women remain unscreened. In our NCI Community Networks sponsored project, we are testing an approach that combines CHWs with self sampling for the human papilloma virus (HPV) as a screening strategy among such hard to reach populations.

Methods: Using a community based participatory research framework, community we are enrolling 600 Latina, Haitian and African American women ages 30-65 who have not had a Pap smear in the 3 last years into a randomized study. health workers (CHWs). Group one receives culturally tailored CHW led public health outreach and education. Groups 2 and 3 receive a one hour CHW home health education session and individualized navigation by the CHWs to Pap smear screening at community based facilities. Women in group 3 have the option of Pap smear or HPV self sampling. A research assistant blinded to study allocation performs a 6 month follow-up assessment.

Results: In 20 months, CHWs have assessed over 3,000 women for study inclusion. One quarter have been study eligible and we have randomized 417 such women, approximately 40% Hispanic, 40% Haitian and 80% African American. To date, have analyzed 6 month follow-up data on 217 women. Among women randomized to culturally tailored health outreach, 32% reported having had a Pap smear at 6 months. In group 2, 54% have been screened. In groups 3, 87% have been screened. Among women in Group 3 to whom we offered HPV self-sampling or tailored navigation to a Pap Smear, 73% preferred to perform HPV self-sampling.

Conclusions: Using the CBPR framework, we have randomized nearly 70% of our planned “hard to reach” study population into our RCT. Our preliminary data suggest that tailored health outreach and individualized CHW navigation are highly effective. Our data, also make an extremely strong case for HPV self-sampling as a strategy for screening among unscreened minority women.

Citation Format: Olveen Carrasquillo, Tulay Koru-Sengul, Sheila McCann, Anthony Amofah, Erin Kobetz. A RCT of a community health worker intervention using HPV self-sampling to increase cervical cancer screening among minority populations. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr B57. doi:10.1158/1538-7755.DISP13-B57
Abstract B92: HPV and Pap test results among low-income, underserved women: Providing insights into management strategies
Authors: Saraiya Mona , Benard Vicki , Greek April , Steinau Martin , Patel Sonya , Manninen Diane , Sawaya George , Massad Stuart , Unger Elizabeth
Published: May 2015

Objective: Human papillomavirus (HPV) DNA testing combined with cytology (co-testing) has been recommended as a primary cervical cancer screening strategy and will be covered as a preventive service by the Affordable Care Act (ACA). Women with discordant results (HPV positive/cytology negative) present significant management challenges and result in additional costs due to follow-up visits and testing required. The frequency of discordant results in insured populations is at a level that does not negate the benefit of co-testing. However, it is unknown if the frequency of discordant results would be the same for underserved women, who may have more risk factors for HPV infection and cancer precursors.

Methods: The Centers for Disease Control and Prevention's Cervical Cancer (Cx3) Study was conducted at 15 clinics in 6 Federally Qualified Health Centers (FQHCs) across Illinois. Providers at these clinics were given the option of co-testing for routine cervical cancer screening. Clinical high-risk HPV testing was performed using the FDA approved Hybrid Capture 2 assay (HC2: Qiagen). An additional research test to determine type-specific HPV results was performed on residual extracts.

Results: Testing was completed on 2246 underserved women, mean age 45.1 years. The HPV test was positive in 7.2% and cytology abnormalities were detected in 6.0% with discordant results in 4.9% of women. The percentage of HPV positive tests decreased with age, from 10.3% among 30-39 year olds to 4.5% among 50-60 year olds. Among women with negative normal Pap test results who where high risk positive, 14% of the women were positive for HPV 16/18 while the remaining were positive for other high risk types.

Conclusion: The rate of discordant co-testing in this study of underserved women was similar to those reported throughout the U.S. in different populations, including those who are insured. Similarly, the lower percentage of discordant results and those positive for HPV 16/18 may favor a more conservative management strategy than an aggressive strategy of immediate colposcopy.

Citation Format: Mona Saraiya, Vicki Benard, April Greek, Martin Steinau, Sonya Patel, Diane Manninen, George Sawaya, Stuart Massad, Elizabeth Unger. HPV and Pap test results among low-income, underserved women: Providing insights into management strategies. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr B92. doi:10.1158/1538-7755.DISP13-B92
Abstract C15: Inflammation-free survival as a surrogate endpoint for overall survival in patients with metastatic renal cell carcinoma
Authors: Harris Wayne B. , Nickleach Dana C. , Liu Yuan , Kucuk Omer , Master Viraj A.
Published: May 2015

Background: The primary objective of the present study was to determine the degree to which factors other than race or ethnicity contribute to large disparities in clinical outcome for patients treated with targeted therapy for metastatic renal cell carcinoma (mRCC).

Methods: A single institution retrospective study was conducted at the Winship Cancer Institute of Emory University. Inclusion criteria were as follows: (1) diagnosis of mRCC, (2) treatment with at least 1 targeted agent for mRCC and (3) concurrent serum C-reactive protein and albumin levels on at least 3 occasions that were at least 2 weeks apart. Statistical analysis was conducted using SAS V9.3 and R2.15.2. Kinetic risk assessment was performed with the newly devised inflammation intensity index (I3). Univariate and multivariate analyses were also completed.

Results: The median overall survival (OS) for the entire cohort (n=55) was 30.6 months (95% CI 19.8, 49.4) with a median follow up of 27.1 months (95% CI 22.0, 31.3). The median OS for non-Hispanic whites (n=39) was 38.4 months (95% CI 23.7, 49.4) vs. 8.6 months (95% CI 5.0, 25.6) for African Americans (n=14) and Hispanics (n=2) with a log-rank p value of <0.0001. Multivariate analysis demonstrated OS was most closely associated with kinetic risk as defined by the I3 risk assessment tool (type 3 p value <0.001) and nephrectomy status (type 3 p value 0.010), but not race/ethnicity.

Conclusions: Prolonged OS was most closely associated with persistent inflammation free survival and shorter OS with increases in the intensity and duration of systemic inflammation.

Citation Format: Wayne B. Harris, Dana C. Nickleach, Yuan Liu, Omer Kucuk, Viraj A. Master. Inflammation-free survival as a surrogate endpoint for overall survival in patients with metastatic renal cell carcinoma. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr C15. doi:10.1158/1538-7755.DISP13-C15
Abstract C34: Comparing patient navigation and survivorship care plans: How do they relate to healthcare among Hispanic and non-Hispanic cancer survivors?
Authors: Jabson Jennifer M.
Published: May 2015

Purpose: Patient navigation (PN), and survivorship care plans, including follow-up care instructions (FCI) and treatment summaries (TS), have been mandated by national organizations as a strategy to improve healthcare received by cancer survivors, and to reduce disparities among survivor subgroups. Empirical evidence has linked PN, FCI, and TS, with survivors' receipt of cancer-related healthcare including cancer surveillance, cancer screenings, and attendance at medical appointments. However, it is currently unknown if these strategies relate equivalently to receipt of healthcare among ethnically diverse survivors, or if one strategy is more important than another.

Methods: Using data from the 2010 LIVESTRONG online survey of cancer survivors (N=4286), the current study tested the associations between FCI, TS, PN and receipt of cancer surveillance, cancer screening, and attendance at regular medical appointments. Analyses were stratified by survivor ethnicity.

Results: In the full sample, FCI related to attendance at regular medical appointments (OR 1.50, 95% CI 1.07, 2.10), cancer surveillance (OR 1.49 95%CI 1.16, 1.93), and cancer screening (OR 2.40 95%CI 1.80, 3.21). PN was related to attendance at medical appointments (OR 1.50 95%CI 1.07, 2.10) and cancer screening (OR 1.31 95%CI 1.03, 1.67). TS related to attendance at medical appointments (OR 1.48 95%CI 1.07, 2.06). Associations varied by survivor ethnicity. Among non-Hispanic white survivors FCI related to all cancer-related healthcare outcomes, and TS related to attendance at medical appointments. Among Hispanic survivors, FCI related to cancer surveillance (OR 3.52 95%CI 1.12, 1.96).

Conclusions: FCI were consistently associated with survivors' cancer-related healthcare. However, FCI, TS, and PN were not equally associated with cancer-related healthcare for all cancer survivors. This evidence suggests that FCI is a valuable strategy for ensuring survivors receipt of cancer-related healthcare, and this may be especially true for Hispanic survivors' receipt of cancer surveillance.

Citation Format: Jennifer M. Jabson. Comparing patient navigation and survivorship care plans: How do they relate to healthcare among Hispanic and non-Hispanic cancer survivors?. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr C34. doi:10.1158/1538-7755.DISP13-C34
Abstract C39: Docetaxel-induced growth and cell cycle phenotypes in prostate stromal cells
Authors: Gales Dominique , McMcmeans Brionna , Samuel Temesgen
Published: May 2015

Background: Docetaxel (D) is a clinically used front-line chemotherapeutic agent for castration resistant advanced prostate cancer. However, its long-term benefits are limited with most patients eventually progressing because of inherent or acquired drug resistance. The treatment of advanced prostate cancer is a significant challenge and there are no effective treatments that stably suppress the disease. The mechanisms behind resistance to Docetaxel are not fully understood.

Since in vivo Docetaxel cytotoxicity is directed not only to cancer cells, we hypothesize that the response of prostate stromal cells exposed to chemotherapeutic agents could modify drug response or therapeutic outcome in prostate cancer. One of cellular responses to chemotherapy is NF-kB activation and inflammatory signaling. NF-κB activation has been proposed as an important event in PCa development, castration-resistant progression and resistance to chemotherapy.

Objective: In this study, we examined the response of prostate stromal (WPMY- 1) cells to Docetaxel.

Current Results: Cellular proliferation was analyzed by MTT assay. The IC50 of Docetaxel for WPMY-1 cells was 10nM. Cell cycle profiles were assessed by flow cytometry. The analysis showed that Docetaxel (10-100nM) induced prominent G2-M arrest in these stromal cells within 24 hours, especially in the higher dose ranges. Interestingly lower doses of Docetaxel (10nM), in contrast to higher doses, consistently resulted in accumulation of sub-G1 population (28% 10nM vs 6% in 100nM) of cells suggestive of fragmented DNA associated with apoptotic process. We show that Docetaxel exhibits strong anti-proliferative effects on prostate stromal WPMY-1 cells.

Conclusions: These preliminary results show that stromal cells are sensitive to Docetaxel. Why lower doses of the drug induce sub-G1 (apoptotic) accumulation while higher doses preferentially induce G2-M arrest is currently unknown.

Future Steps: We will compare responses to D between prostate cancer cells and stromal cells in individual and co-culture models. NF-kB activity following D treatment or radiation, and the expression of genes in NF-kB pathway in D treated cells will be examined.

Citation Format: Dominique Gales, Brionna McMcmeans, Temesgen Samuel. Docetaxel-induced growth and cell cycle phenotypes in prostate stromal cells. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr C39. doi:10.1158/1538-7755.DISP13-C39
Abstract C51: In vitro cytotoxicity of 3-arylcoumarin derivatives in human prostate (PC3) cancer cell line
Authors: Musa Musiliyu A. , Joseph Moise Y. , Latinwo Lekan M. , Badisa Veera L.
Published: May 2015

Coumarins are classified as a member of the benzopyrone family of compounds with diverse and interesting biological activities. They have been used as therapeutic agents in the treatment of various diseases. In the present study, we evaluated the in vitro cytotoxic activity of 3-arylcoumarins (1-11) in human prostate (PC3) cancer and (WPE1-NA22) normal cell lines at various concentrations (0, 10, 25, 50, 75 and 100 μM) after 48 h treatment using crystal violet dye binding assay. The most active compounds cytotoxicity was examined by cell cycle analysis, reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP) measurement and Bax protein expression. Our findings indicate Result that 8-(acetyloxy)-3-(4-methanesulfonylphenyl)-2-oxo-2H-chromen-7-ylacetate (11) showed cytotoxic activity in PC3 cancer cell line (LD50 = 35.0 μM) and no cytotoxic activity in WPE1-NA22 normal cell line (inactive; LD50 = >100 μM) in comparison to the other synthesized analogs. Furthermore, It caused significant cells arrest (p<0.05) in –G1 phase, increase in ROS production, loss of MMP and increase (up-regulation) of Bax protein expression. These findings suggest that these compounds could serve as new leads for the development of novel synthetic compounds with enhanced anticancer activity.

Grant Support: Research supported by Florida A & M University Title III Program

Citation Format: Musiliyu A. Musa, Moise Y. Joseph, Lekan M. Latinwo, Veera L. Badisa. In vitro cytotoxicity of 3-arylcoumarin derivatives in human prostate (PC3) cancer cell line. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr C51. doi:10.1158/1538-7755.DISP13-C51
Abstract C52: Associations between religion-related factors and breast cancer screening among American Muslims
Authors: Padela Aasim I. , Murrar Sohad , Adviento Brigid , Hosseinain Zahra , Peek Monica , Olopade Olufunmilayo , Curline Farr
Published: May 2015

Background: The limited research of breast cancer screening among different American Muslim groups consistently demonstrates low rates of mammography. There has been no survey of how religion-related factors influence screening patterns in a diverse sample of American Muslims.

Methods: We partnered with the Council of Islamic Organizations of Greater Chicago to survey English-speaking women aged 40 years and older frequenting mosques and community sites. The self-administered survey included several adapted measures of religiosity, fatalism, and discrimination from the literature, and incorporated a pilot measure of Islamic modesty.

Results: 240 women completed the survey with nearly equal numbers of indigenous African Americans (27%), Arab Americans (33%), and South Asians (32%). 77% of the sample reported ever having a mammogram while only 37% had a mammogram within the past 1-2 years. There were no significant differences in rates by race/ethnicity. On multivariate analysis positive religious coping (OR= 0.21, p <0.05) and perceived religious identity-directed discrimination (OR=0.74, p<0.05) were negatively associated with having biennial mammograms, while having a primary care physician (OR=20, p<0.01,) greatly increased the odds of having a mammogram. Ever having a mammogram was positively associated with years of US residence (>20 yrs OR=4.3, p<0.05) and increasing level of educational attainment. Islamic modesty, fatalistic beliefs, breast cancer knowledge, educational attainment, insurance status and were not associated with mammography rates.

Conclusions: Cancer disparity research typically focuses on inequities across ethnic and racial lines, and therefore overlooks the influence of a shared religion upon health behaviors across race and ethnicity. Our survey suggests that religion-related factors such as positive religious coping and perceived religious discrimination influence breast cancer screening patterns among American Muslims. Consequently, programs leveraging shared religious networks, such as mosques and Imams, may be a means to address religious barriers that impede screening across ethnic and racial lines.

Citation Format: Aasim I. Padela, Sohad Murrar, Brigid Adviento, Zahra Hosseinain, Monica Peek, Olufunmilayo Olopade, Farr Curline. Associations between religion-related factors and breast cancer screening among American Muslims. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr C52. doi:10.1158/1538-7755.DISP13-C52
Abstract C68: Global transcriptome sequencing of ethnically diverse formalin-fixed patient samples identifies biomarkers of recurrence in prostate cancer
Authors: Xu Jianpeng , Long Qi , Osunkoya Adeboye O. , Sannigrahi Soma , Johnson Brent A. , Zhou Wei , Gillespie Theresa , Park Jong Y. , Nam Robert K. , Sugar Linda , Stanimirovic Aleksandra , Seth Arun K. , Petros John A. , Moreno Carlos S.
Published: May 2015

Prostate cancer remains the second leading cause of cancer death in American men, but biomarkers that can predict outcome following treatment are urgently needed to identify patients with aggressive disease. In an effort to identify biomarkers of recurrence, we have performed global RNA-sequencing on 106 formalin-fixed, paraffin-embedded (FFPE) prostatectomy samples from 100 patients at three independent sites, and identified a new set of biomarkers of biochemical recurrence composed of a 24-gene panel including 22 protein-coding genes and two non-coding genes. We observed excellent correlation between TaqMan and RNAseq values, as well as for RNAseq between replicate libraries. We validated this 24-gene panel on an independent publicly available dataset of 140 patients and this new panel outperformed previously published markers based on cell proliferation gene sets. In addition, we have identified genes that are differentially expressed between African-American and Caucasian prostate cancer patients, and mitochondrial SNPs that are associated with both race and outcome. We observed a number of genes relevant to prostate cancer biology including ETV5, ZEB1, ZEB2, B2M, FYN, and miR-183 that were differentially expressed between African-American and Caucasian patients. These genes may play a role in the disparities observed in African-American patients who have significantly worse outcomes relative to Caucasian patients with prostate cancer.

Citation Format: Jianpeng Xu, Qi Long, Adeboye O. Osunkoya, Soma Sannigrahi, Brent A. Johnson, Wei Zhou, Theresa Gillespie, Jong Y. Park, Robert K. Nam, Linda Sugar, Aleksandra Stanimirovic, Arun K. Seth, John A. Petros, Carlos S. Moreno. Global transcriptome sequencing of ethnically diverse formalin-fixed patient samples identifies biomarkers of recurrence in prostate cancer. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr C68. doi:10.1158/1538-7755.DISP13-C68
Abstract C72: Estradiol-ERβ signaling axis in disparity of prostate cancer in African American men
Authors: Elmageed Zakaria Y. Abd , Kim Hogyoung , Thomas Raju , Moparty Krishnarao , Abdel-Mageed Asim B.
Published: May 2015

Our study showed that high circulating estrogens and estrogen receptor beta (ERβ) may be implicated in prostate cancer (PCa) progression, and had higher expression level in African American (AA) than Caucasian American (CA) men. However, the underlying mechanisms remain elusive. The objective of this study was to investigate the signaling cross-talk between ERβ; and AR in vitro and in vivo levels. Prostate cancer cells; LNCaP, C4-2B and PC3 were treated with different concentrations and at different time points with 17β-Estradiol (E2) and 5α-dihydrotestosterone (DHT) and examined for cell proliferation by WST assay, promoter activity by luciferase assay, DNA-protein interaction by electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) assay. After E2 or DHT treatment, the translocation of ERβ; and AR in PCa cells was also examined using fluorescence microscope.

Our results show that ERβ; was stimulated by treatment of cells with 10nM DHT and AR was also induced by treating PCa cells with10nM E2. These results were confirmed by promoter activity of truncated psPSA-luc in either PCa cell lines or Cos-7 cells. The predesigned Androgen Response Element (ARE) was bound to the protein's receptor after E2 induction. ChIP experiment corroborated the cross-talk between AR and ERβ; after treating C4-2B cells with 10nM E2 for 30 min up to 1.5 hr. Immunofluorescence depicted colocalization of AR and ERβ; in the nucleus after 30 min from E2 treatment. To our knowledge, this is the first report demonstrating crosstalk between ERβ; and AR signaling in PCa in response to E2 treatment. Our results implicate potential therapeutic application by targeting AR and ERβ; in castration-resistant PCa (CRPC).

Citation Format: Zakaria Y. Abd Elmageed, Hogyoung Kim, Raju Thomas, Krishnarao Moparty, Asim B. Abdel-Mageed. Estradiol-ERβ signaling axis in disparity of prostate cancer in African American men. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr C72. doi:10.1158/1538-7755.DISP13-C72
Abstract C73: Differences in UPR signaling in ER+ breast cancer between African American and Caucasian women
Authors: Eltayeb Ahreej E. , Shajahan-Haq Ayesha N. , Dave Krupesh , Clarke Robert
Published: May 2015

Cancer is one of the leading causes of death amongst ethnic minorities. African American women between the ages of 40 and 50 are associated with higher rate of mortality due to breast cancer compared to Caucasian women. Estrogen receptor positive (ER+) subtype is the most common amongst all races. However, amongst those with ER+ breast cancer, African American women face a higher mortality rate compared to Caucasian women. We hypothesize that this higher mortality in African American women is potentially due to increased drug resistance to anti-estrogen therapy and disease progression to either inherent or acquired resistance to endocrine therapy. Despite the clinical advances with anti-estrogen agent, tamoxifen, many women experience recurrence. We have shown that the endoplasmic reticulum (ER) plays an important role in anti-estrogen sensitivity through the unfolded protein response (UPR), a stress response for cellular self-preservation. The UPR pathway consists of three known pathways that eventually lead to either apoptosis (cell death) or autophagy (“self-eating”); PERK, ATF6 and IRE1a. We will investigate the potential difference between these signaling receptors and downstream signaling proteins affiliated with the UPR pathway between African American and Caucasian American ER+ breast cancer from public databases. Understanding whether the UPR is differently regulated in different ethnic background of women may help uncover why mortality in African American women with ER+ breast cancer has a higher mortality rate.

Citation Format: Ahreej E. Eltayeb, Ayesha N. Shajahan-Haq, Krupesh Dave, Robert Clarke. Differences in UPR signaling in ER+ breast cancer between African American and Caucasian women. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr C73. doi:10.1158/1538-7755.DISP13-C73
Abstract C84: Body size across the lifecourse and risk of breast cancer in African American women, the Carolina Breast Cancer Study
Authors: Robinson Whitney , Tse Chiu Kit , Olshan Andrew F. , Troester Melissa
Published: May 2015

Background: Body size is a modifiable risk factor associated with postmenopausal breast cancer in US White women. However, in African-Americans, there have been fewer studies and relationships are not well established.

Aims and Methods: We investigated the association between breast cancer risk and body size in childhood, young adulthood, and near the time of breast cancer diagnosis using data from the Carolina Breast Cancer Study, a 1993-2001 population-based case-control study of African-American (AA) cases (343 premenopausal, 445 postmenopausal) and controls frequency-matched by age and race. We investigated whether a) self-reported body size at age 10, age 18, age 35, and a year before interview and b) nurse-measured BMI, waist circumference, and waist-to-hip ratio (WHR) at interview were associated with cancer risk. Logistic regression models were adjusted for age, family history of breast cancer, education level, alcohol use, age at menarche, parity, age at first birth, and lactation.

Results: For premenopausal AA women, larger body size tended to be positively associated with cancer risk. The strongest results were for WHR (0.84+ vs <0.77): OR=2.00 [1.28, 3.13]). For postmenopausal women, body size was not significantly associated with risk, but weak inverse associations with higher adiposity were observed for nurse-measured BMI, weight at age 10, and possibly WHR (0.84+ vs <0.77) (OR=1.20 [0.76, 1.89]).

Conclusions: Associations between body size and breast cancer risk varied by menopausal status, measure of adiposity, and timing in the lifecourse. Strikingly, associations were not in the direction expected from the previous literature, which is based predominantly on Caucasian women. In fact, body size associations for premenopausal AA women may be inverse of that observed in Whites.

Impact: African-American women have higher risk of breast cancer at young ages (<40 years), but the causes of this disparity are not well understood. Given that the prevalence of obesity is high among African American women, understanding how body size relates to their risk of premenopausal breast cancer may offer insights for prevention.

Citation Format: Whitney Robinson, Chiu Kit Tse, Andrew F. Olshan, Melissa Troester. Body size across the lifecourse and risk of breast cancer in African American women, the Carolina Breast Cancer Study. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr C84. doi:10.1158/1538-7755.DISP13-C84
Abstract CN01-04: Cancer survivors: Opportunities and challenges in managing comorbidities among disadvantaged populations
Authors: Henderson Tara O.
Published: May 2015

As the treatment of cancer is becoming more successful, there is a growing population of cancer survivors. For patients diagnosed with a cancer prior to the age of 21 years, over 80% will be cured and as a result there are more than 350,000 survivors of childhood cancer currently living in the US. Research in large cohorts of childhood cancer survivors indicate these patients are at significant risk of premature mortality due to late effects and second cancers due to their previous therapy. Recognizing this, in 2003, the Institute of Medicine has recommended lifelong, risk-based long term follow up care focused on monitoring for cancer recurrence, surveillance and early intervention of late effects, and second cancers and education. Despite these recommendations, survivors are not receiving risk based care. There are many barriers to medical care in this vulnerable population. Many of these patients are young adults and not able to secure employment and/or insurance. Our research has indicated that primary care physicians who follow patients in the community are not aware of the risks and surveillance guidelines for these patients. Further, most survivors and their primary care physicians report that they do not have a treatment summary and follow up plan. These issues are likely compounded in disadvantaged populations. Research must be focused on examining risk of late effects and second cancers in minority populations in order to tailor surveillance recommendations. Intervention studies must be designed that are focused on the dissemination of treatment summaries and care plans for survivors not cared for in tertiary care centers, but in the community. Specific education must be in place at the time of cancer care such that patients are aware of their risks and need for long term follow up care. Policy measures must include focused efforts for disadvantaged survivors in order to ensure appropriate health care coverage to meet their significant and specialized health care needs.

Citation Format: Tara O. Henderson. Cancer survivors: Opportunities and challenges in managing comorbidities among disadvantaged populations. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr CN01-04. doi:10.1158/1538-7755.DISP13-CN01-04
Abstract CN03-03: Cancer survivorship and health equity research: Lessons learned from pediatric, adolescent, and young adult survivors
Authors: Casillas Jacqueline
Published: May 2015

Pediatric, adolescent and young adult survivors of childhood cancer are at risk for premature morbidity and mortality due to their cancer treatment at a young age. They require lifetime follow-up care for targeted surveillance for late effects detection and risk-reduction counseling. Yet, disparities in the receipt of and access to high quality survivorship care can exist. In this session, we will

describe outcomes by race/ethnicity in adult survivors of pediatric cancer. We will also characterize risks for disparities in the young adult childhood cancer survivor population. New research paradigms designed to outreach to minority childhood cancer survivors aimed at improving access to risk-based survivorship care will be described

Citation Format: Jacqueline Casillas. Cancer survivorship and health equity research: Lessons learned from pediatric, adolescent, and young adult survivors. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr CN03-03. doi:10.1158/1538-7755.DISP13-CN03-03
Abstract ED03-02: Communication in the context of community-based participatory research
Authors: Estrada John J.
Published: May 2015

Scientists and healthcare providers have begun to recognize that addressing prevention and treatment in the context of health and wellness, requires consideration of complex non-clinical issues not entirely familiar to them. These issues are social, economic, political, and environmental, together known as the Social Determinants of Health. In addition, communities have become more aware of the importance of biological determinants of health. Community-based participatory research (CBPR) is a collaborative approach to address these determinants. This collaborative approach to health care and research equitably involves all partners in the process and recognizes the unique strengths that each partner brings. It aims to combine scientific knowledge with interventions to improve health and ultimately brings social change. CBPR then poses new challenges regarding communication among health care providers, academia and communities. The intervention begins with a brief socio-cultural contextualization of communication between two stakeholders: communities and health professionals. Then the intervention discusses some case studies, challenges, and reflections around communication in the context of CBPR. Finally, the presentation ends with practical recommendations for considering the adoption of methodologies and processes to bring balance to communication between these two communities.

Citation Format: John J. Estrada. Communication in the context of community-based participatory research. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr ED03-02. doi:10.1158/1538-7755.DISP13-ED03-02
Abstract OS01-02: Eliminating Cancer Health Disparities: Can It Be Done?
Authors: Thompson Beti
Published: May 2015

Background: Cancer health disparities continue to be a vexing problem in the United States. As long ago as 1985, the then-Secretary of Health and Human Services noted that the disparities in cancer research and treatment present “an affront to the ideals and genius of American medicine.” Almost three decades letter, the disparities continue. Much has been attempted to reduce these disparities; most recently, a community-based participatory research methodology, where researchers work WITH communities, is being used to reduce disparities. In this presentation, we explore some of the challenges and successes that accompany community engagement in reducing health disparities. Two initiatives that use community-based participatory research are reviewed.

Methods: In the first initiative, ongoing research with communities is described. In the second initiative, cancer prevention activities currently taking place in a predominantly Hispanic region in eastern Washington State are described. A Community Advisory Board (CAB) has been working with researchers to increase colorectal cancer (CRC) screening among Hispanics. Using a pre- post-test design, 947 participants were asked about CRC knowledge and intention to be screened.

Results: Engaging the community in research activities has a positive outcome both in terms of community participation and in screening outcomes. In the CRC study, for example, odds ratios indicate that Hispanics are much less likely to be ever screened for CRC than non-Hispanic Whites (NHW). Further, when given the opportunity to participate in screening, 76 percent of Hispanics given an FOBT screening kit returned the completed kit; others not receiving the kit, significantly increased their intention to be screened.

Discussion: Access to care continues to be a major impediment to the Latino population in terms of cancer prevention behavior. Using community-based participatory research, it is possible to engage members of underserved communities in cancer prevention. With the advent of the Affordable Care Act and complementary interventions to enroll Latinos, it may be possible to remove one of the primary obstacles to the reduction of health disparities.

Citation Format: Beti Thompson. Eliminating Cancer Health Disparities: Can It Be Done?. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr OS01-02. doi:10.1158/1538-7755.DISP13-OS01-02
Abstract PC01-02: Colorectal cancer screening for African Americans: Should we be screening at an earlier age? Con
Authors: Gupta Samir
Published: May 2015

African Americans have the highest colorectal cancer (CRC) incidence and mortality of any racial/ethnic group. Citing the higher age-specific rate of CRC compared to whites that begins after age 45, several medical societies have recommended early age of screening initiation for African Americans at age 40 or 45 years. However, there are several reasons why early screening initiation may be a suboptimal strategy for improving CRC outcomes among African Americans. First, evidence to support effectiveness of early screening initiation for improving CRC outcomes is limited. The highest excess rates of CRC among African Americans occur after age 60, and the most rigorous studies suggest that there are not substantial differences in rates of polyps between African Americans and other groups younger than age 50, making the effectiveness of early initiation uncertain. Second, there are substantial logistical challenges to implementing early age of screening initiation for African Americans, but not other groups. Third, many alternate strategies have been proven to improve CRC screening; if implemented widely these strategies might be more effective than lowering the age of screening initiation. In taking the “Con” position against lowering the screening age, the author will highlight these issues, and make the case that lowering the screening age may not be the optimal strategy for improving CRC outcomes among African Americans.

Citation Format: Samir Gupta. Colorectal cancer screening for African Americans: Should we be screening at an earlier age? Con. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr PC01-02. doi:10.1158/1538-7755.DISP13-PC01-02
Abstract SS01-02: Microbial sulfur metabolism and colorectal cancer risk
Authors: Gaskins H. Rex
Published: May 2015

Both sporadic and IBD-associated colon cancer result from multifactorial interactions among common alleles of polymorphic genes and insults in the intestinal environment. We are examining the extent to which bacterial-derived hydrogen sulfide may serve as a proinflammatory and genotoxic insult that modifies colon cancer risk. Data will be presented which demonstrate that the human colonic mucosa is persistently colonized by bacteria capable of generating sulfide from both inorganic and organic sulfur sources along with evidence that sulfide activates molecular pathways that underlie epithelial inflammation and hyperplasia, a phenotype common to both ulcerative colitis and colorectal cancer. Our published studies will also be summarized, which demonstrate that exogenous sulfide is a potent genotoxin that acts independent of cellular metabolism and mediated by free radicals. These observations highlight the possible role of sulfide as an intestinal insult that, given a predisposing genetic background, may lead to genomic instability or the cumulative mutations characteristic of colorectal cancer.

Citation Format: H. Rex Gaskins. Microbial sulfur metabolism and colorectal cancer risk. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr SS01-02. doi:10.1158/1538-7755.DISP13-SS01-02
Abstract SS02-01: Splice variants associated with African American prostate cancers promote oncogenesis and chemoresistance
Authors: Lee Norman
Published: May 2015

There are striking population disparities in cancer risk and survival outcome borne out of current health statistics. African American (AA) men are approximately 1.6 times more likely to develop prostate cancer (PCa), and 2.4 times more likely to die from this disease compared to their Caucasian American (CA) counterparts. A growing body of biological and genetic evidence suggests that genetic polymorphisms and aberrant gene expression are important influences predisposing or contributing to the disparities of cancer incidence and mortality. Perhaps underappreciated has been the role of alternative splicing in cancer health dis¬parities, and cancer development in general. The expression of specific variants is regulated in a developmentally- and tissue-specific manner. Alternative spliced isoforms from the same gene can pro¬duce proteins with drastically different prop¬erties. We demonstrate that differential alternative splicing takes place for ∼400 genes in PCa specimens of AA compared to CA patients. Many are oncogenes and tumor suppressor genes. In addition, we provide evidence of 4 genes (PIK3CD, FGFR3, TSC2 and RASGRP2) that undergo population-dependent differential splicing where the AA-specific variants are engendered with a more aggressive oncogenic phenotype. Of interest, small molecule inhibitors are clinically available (or being tested clinically) for PIK3CD and FGFR3 in the treatment of various cancers, and we demonstrate in vitro that the AA-specific PIK3CD variant, but not the CA-counterpart, is resistant to small molecule inhibitor CAL-101. Xenograft studies of the splice variants are underway to look at cancer growth, metastasis and response to small molecule inhibitors. Based on our in vitro findings, we hypothesize that the existence of AA-specific splice variants encoding more aggressive oncogenic proteins and/or oncogenic proteins resistant to small molecule inhibitors may account for, in part, the observed cancer health disparities.

Citation Format: Norman Lee. Splice variants associated with African American prostate cancers promote oncogenesis and chemoresistance. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr SS02-01. doi:10.1158/1538-7755.DISP13-SS02-01
Abstract SS03-01: Promise and pitfalls of personalized medicine from a clinical science perspective
Authors: duPont Nefertiti C.
Published: May 2015

Personalized medicine tailors treatment to meet an individual patient's needs and specific disease. While the idea of personalized medicine is not new, advances in biomedical science have evolved to target molecular pathways to reduce toxicity and provide more effective treatment options to patients with many common cancers. For a few cancers, such as breast cancer, biomarker assisted diagnoses and therapy have already replaced the standard “one size fits all” treatment. As our understanding of molecular genetics increases we will be able to offer tailored cancer therapy to more patients, however, the cost of cancer care will continue to be a public policy concern. In this session we will discuss the promise and pitfalls of personalized medicine from a clinical science perspective.

Citation Format: Nefertiti C. duPont{Authors}. Promise and pitfalls of personalized medicine from a clinical science perspective. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr SS03-01. doi:10.1158/1538-7755.DISP13-SS03-01
Endoplasmic Reticulum Stress–Activated Cell Reprogramming in Oncogenesis
Authors: Chevet Eric , Hetz Claudio , Samali Afshin
Published: May 2015

Stress induced by the accumulation of unfolded proteins in the endoplasmic reticulum (ER) is observed in many human diseases, including cancers. Cellular adaptation to ER stress is mediated by the unfolded protein response (UPR), which aims at restoring ER homeostasis. The UPR has emerged as a major pathway in remodeling cancer gene expression, thereby either preventing cell transformation or providing an advantage to transformed cells. UPR sensors are highly regulated by the formation of dynamic protein scaffolds, leading to integrated reprogramming of the cells. Herein, we describe the regulatory mechanisms underlying UPR signaling upon cell intrinsic or extrinsic challenges, and how they engage cell transformation programs and/or provide advantages to cancer cells, leading to enhanced aggressiveness or chemoresistance. We discuss the emerging cross-talk between the UPR and related metabolic processes to ensure maintenance of protein homeostasis and its impact on cell transformation and tumor growth.

Significance: ER stress signaling is dysregulated in many forms of cancer and contributes to tumor growth as a survival factor, in addition to modulating other disease-associated processes, including cell migration, cell transformation, and angiogenesis. Evidence for targeting the ER stress signaling pathway as an anticancer strategy is compelling, and novel agents that selectively inhibit the UPR have demonstrated preliminary evidence of preclinical efficacy with an acceptable safety profile. Cancer Discov; 5(6); 586–97. ©2015 AACR.
64
Cu-DOTATATE PET/MRI for Detection of Activated Macrophages in Carotid Atherosclerotic Plaques
Authors: Pedersen Sune Folke , Sandholt Benjamin Vikjær , Keller Sune Høgild , Hansen Adam Espe , Clemmensen Andreas Ettrup , Sillesen Henrik , Højgaard Liselotte , Ripa Rasmus Sejersten , Kjær Andreas
Published: May 2015

Objective—

A feature of vulnerable atherosclerotic plaques of the carotid artery is high activity and abundance of lesion macrophages. There is consensus that this is of importance for plaque vulnerability, which may lead to clinical events, such as stroke and transient ischemic attack. We used positron emission tomography (PET) and the novel PET ligand [
64
Cu] [1,4,7,10-tetraazacyclododecane-
N
,
N
′,
N
″,
N
‴-tetraacetic acid]-
d
-Phe1,Tyr3-octreotate (
64
Cu-DOTATATE) to specifically target macrophages via the somatostatin receptor subtype-2 in vivo.

Approach and Results—

Ten patients underwent simultaneous PET/MRI to measure
64
Cu-DOTATATE uptake in carotid artery plaques before carotid endarterectomy.
64
Cu-DOTATATE uptake was significantly higher in symptomatic plaque versus the contralateral carotid artery (
P
<0.001). Subsequently, a total of 62 plaque segments were assessed for gene expression of selected markers of plaque vulnerability using real-time quantitative polymerase chain reaction. These results were compared with in vivo
64
Cu-DOTATATE uptake calculated as the mean standardized uptake value. Univariate analysis of real-time quantitative polymerase chain reaction and PET showed that cluster of differentiation 163 (CD163) and CD68 gene expression correlated significantly but weakly with mean standardized uptake value in scans performed 85 minutes post injection (
P
<0.001 and
P
=0.015, respectively). Subsequent multivariate analysis showed that CD163 correlated independently with
64
Cu-DOTATATE uptake (
P
=0.031) whereas CD68 did not contribute significantly to the final model.

Conclusions—

The novel PET tracer
64
Cu-DOTATATE accumulates in atherosclerotic plaques of the carotid artery. CD163 gene expression correlated independently with
64
Cu-DOTATATE uptake measured by real-time quantitative polymerase chain reaction in the final multivariate model, indicating that
64
Cu-DOTATATE PET is detecting alternatively activated macrophages. This association could potentially improve noninvasive identification and characterization of vulnerable plaques.