bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract B39: Administrative tools to promote cancer health disparities research partnerships
Authors: O'Connell Mary A. , Thompson Beti , Loest Helena , Anderson Jennifer 
Published: December 2010

Abstract
For the past eight years New Mexico State University (NMSU) a minority-serving institution, and the Fred Hutchinson Cancer Research Center (FHCRC), a comprehensive cancer center, have increased the cancer research, training and outreach programs at NMSU through partnership activities. The institutional differences in missions, values and cultures presented challenges that were overcome by proactive planning, administrative energy and committees with bi-institutional representation. A number of surveys, handbooks, guidelines and policy statements were developed and used by the administrative team and committees that would be useful as templates or guides to other groups developing networks or partnerships that involve multiple organizations. The success of the partnership is documented in part by the publications written and subsequent grants awarded by the partnering scientists; as well as the number of students trained and their career paths in cancer research. These data will be presented chronologically. To provide the administrative tools that facilitated these activities, we have created a web portal from which these materials can be downloaded (http://cancer.nmsu.edu/). Examples of documents available in pdf format will be presented, these include (1) materials for local workshops on cancer health disparities; (2) surveys for student tracking and surveys for pre and post knowledge tests; (3) the career development templates for proposals from junior investigators, and the evaluation forms for use by the mentoring committee to monitor junior investigators progress; (4) the scoring sheets for use by the proposal reviewers; (5) conflict resolution policy for partnership projects; and (6) handbooks for student training.
Citation Information: Cancer Epidemiol Biomarkers Prev 2010;19(10 Suppl):B39.
Abstract B42: Short-term cancer research experiences for medical students: Goals and outcomes
Authors: Bhatt Ananta , Cho May , Beech Derrick , Marshall Dana 
Published: December 2010

Abstract
Over the last five years, we have implemented an NIH-R25-funded program that exposes minority medical students to cancer research. Our goals are to increase awareness of our medical students in regards to the various research opportunities available in cancer research and to access how this program has impacted their medical education and future goals. Through the students evaluation and documentation we gained an understanding of 1) overall evaluation of the program and its strengths and weaknesses, 2) impact of this program in the students residency selection, and 3) impact of this program on their choice of a career, both clinical and research, in the field of oncology. The R25 has been successful in increasing the number of minority students who participate in cancer research, present their research at regional and national meetings, and publish articles in peer reviewed medical journals. Overall, the experiences of the students in this program suggest that this program has been a positive part of their medical education. This program provides minority students at Meharry Medical College an opportunity to learn and participate in cancer research and attracts trainees to cancer research. The true success of this program will be determined in future after following the students to see if the experiences from this program impacted their career choice in cancer research.
Citation Information: Cancer Epidemiol Biomarkers Prev 2010;19(10 Suppl):B42.
Abstract B43: Assessment of an educational video and brochure in four languages: Cantonese, Hmong, Vietnamese, and English for biospecimen contributions
Authors: Dang Julie H. T. , Chen Moon S. 
Published: December 2010

Abstract
Background: Racially specific biospecimens increase the likelihood of developing personalized treatment approaches for cancer patients in comparison to utilizing biospecimens that may have originated from individuals of a different race than the patient. Thus increasing the proportion of biospecimens from Asian Americans would increase the likelihood of having biospecimens that may be more applicable to cancer treatments for Asian American cancer patients. We have not found any reliable data on the proportion of biospecimens derived from Asian Americans in any database due to a variety of factors. However, we assume that the proportion is relatively low. Therefore to increase contributions among Asian Americans, particularly for English-limited patients, we are developing a video and accompanying brochure in Cantonese, Hmong, Vietnamese and English for Asian Americans that explain the need for biospecimens and recruit them to donate biospecimens for cancer research.
Objectives: To test the feasibility of an in-language biospecimen education video and brochure intervention to increase biospecimen contributions among Asian Americans
Methods: By mid-August, our educational video and brochure in Cantonese, Hmong, Vietnamese, and English will have been professionally produced. Our assumption is that respondents will use the language that they will be most comfortable in. Thus, respondents who view the video and ask for the brochure in one of the Asian language are presumed to be less acculturated than those who view the video and ask for the English language brochure. By mid-September, we shall have pilot-tested it with multiple Asian Americans both in a group and in individualized settings. In particular, Chinese, Hmong, and Vietnamese UC Davis Cancer Center patients undergoing cancer surgery will be given the educational video to view and the brochure to read prior to surgery and prior to receiving the biorespository consent form.
Results: We anticipate presenting data by language and report responses on the basis of the extent to which respondents learned more about biospecimens and whether their new knowledge about biospecimen would now predispose them to more likely contribute biospecimens. We shall report on the extent to which the educational materials increased knowledge and willingness to contribute biospecimens for research.
Conclusions: Increasing the proportion of Asian American biospecimens for cancer research will increase the likelihood of more personalized cancer therapies for Asian Americans. Our pilot study is among the first to empirically assess the potential of in-language video and brochures to increase biospecimen contributions by Asian Americans.
Citation Information: Cancer Epidemiol Biomarkers Prev 2010;19(10 Suppl):B43.
Abstract B44: GMaP/BMaP Region 3: Coming together to eliminate cancer disparities in the South and Puerto Rico
Authors: Meade Cathy , Scarinci Isabel , Muñoz-Antonia Teresita 
Published: December 2010

Abstract
Background: The Transdisciplinary Geographic Management Program (GMaP) and Minority Biospecimen/Biobanking Geographic Management Program (BMaP) for Region 3 is designed to develop a systematic and comprehensive strategy for building a state-of-the-art network for the support and efficient management of cancer health disparities research, training, and outreach in the five Southeastern states and Puerto Rico. The overall goal of the GMaP/BMaP-3 Network is to eliminate racial/ethnic cancer health disparities by identifying factors associated with such disparities, developing culturally-relevant approaches to address these factors, and disseminating evidence-based interventions across the cancer control continuum and across the continuum of the socio-ecological model. Specific to biobanking the ultimate goal of this network is to create unique, centralized, public resources for multi-ethnic biobanking/biospecimens. These goals are being accomplished in three phases: 1) network establishment, 3) needs/assets assessment, and 3) implementation plan.
Methods: We first established a working infrastructure for a GMaP/BMaP hub in the southeast United States and Puerto Rico as a collaborative partnership among the following institutions: H. L. Moffitt Cancer Center and Research Institute, University of Alabama at Birmingham Comprehensive Cancer Center, Tulane University, Xavier University of Louisiana, University of Mississippi, Tuskegee University, Morehouse School of Medicine, Emory University - Winship Cancer Center, and Ponce School of Medicine. Although the partners have worked closely together in all aspects of the project, we established specific cores in order to obtain an in-depth examination of specific areas in cancer disparities: clinical trials, advanced/emerging technologies, biomedical informatics, communication/dissemination, and evaluation. Given the importance of biospecimen/biobanking (BMaP), additional cores were established specific to this topic: collection, processing, storage and analysis of biospecimen; community and sociocultural beliefs; ethical, legal, and policy. Once the network was established, we designed a comprehensive needs/assets assessment of current strengths, weaknesses, capabilities, needs and interest in cancer health disparities in our participating institutions, CRCHD programs, and targeted communities with regard to research, training, and infrastructure development.
Results: A draft of the Comprehensive Assessment Tool (CAT) specific to our region has being developed through a participatory and methodic process with active involvement of all partnering institutions.
Conclusions: The data obtained from the needs assessment will inform the planning, nature, and extent of activities associated with the development of an operational plan to prioritize cancer research and biobanking activities in the Southeast US and PR.
Citation Information: Cancer Epidemiol Biomarkers Prev 2010;19(10 Suppl):B44.
Abstract B47: Potential role for RNF8 in breast cancer development
Authors: Anduro-Corona Ivan , Thompson Patricia , Buckmeier Julie , Martínez María Elena , Gutiérrez-Millán Luis Enrique 
Published: December 2010

Abstract
Background: Women of Mexican descent have a higher mortality and higher proportion of triple negative or basal-like breast cancers with BRCA like features and a higher population burden of BRCA mutations. Basal-like breast cancer subtype is associated with an elevated Ki67 index and extensive genomic instability. This increase in the Ki67 index indicates cell proliferation and perhaps greater cell DNA damage. In another report it was shown that knockdown of ring finger 8 (RNF8), an E3 ubiquitin-protein ligase, by siRNA inhibited focus formation at double strand break sites suggesting that RNF8 is an important regulator of the DNA repair system. We hypothesized that loss of RNF8 would be associated with more aggressive tumors such as those having high Ki67 levels. We are investigating the hypothesis that RNF8 is a tumor suppressor gene and acts as a novel regulatory protein of BRCA1 expression in human breast cancers.
Methods: We tested whether 37 formalin fixed paraffin embedded human breast cancers taken from a population of Mexican women enriched for basal-like cancers show altered RNF8 and Ki67 mRNA expression compared to median expression as reference value.
Results: Copy number differences in tumors for Ki67 and RNF8 mRNA were observed. The average differences in copy number for Ki67 between low and high expressing tumors was 8.8 fold and for RNF8 the average copy number differences between high and low expressors were 5.5 fold. When we compared the relationship between RNF8 and Ki67 expression within individual tumors, RNF8 expression was positively associated with Ki67 gene expression (p=0.04). Tumors that were high RNF8 were significantly more likely to also be high for Ki67. We found a non-significant but similar direction between RNF8 and cyclin B1 (p=0.08) but no relationship between RFN8 and cyclin D1 gene expression (p=0.318). This suggests that RNF8 is overexpressed in the tumors that are undergoing high mitoses.
Conclusion: This is the first report demonstrating differential expression of RNF8 in a series of human breast cancers and a positive association between Ki67 and RNF8 levels. This finding is counter to our hypothesis that RNF8 acts as a tumor suppressor and that we would observe loss of gene expression. Interestingly, a recent study found that among BRCA deficient backgrounds, the involvement of an alternative DNA repair pathway that is prone to more mistakes involving p53 binding protein (53BP1), which interacts with RNF8 in cells, modifies susceptibility of the BRCA1 deficient background to carcinogenesis. Our findings may suggest that among some breast tumors overexpression of this altered DNA repair pathway including activation of RNF8 made contribute to the genomic instability in more aggressive tumors. Additional studies to assess the relationship between 53BP1 and RNF8 in these tumors are ongoing.
Citation Information: Cancer Epidemiol Biomarkers Prev 2010;19(10 Suppl):B47.
Abstract B48: Do the gut flora play a role in the high incidence of colon cancer in African Americans?
Authors: Brim Hassan , Lee Edward , Zoetendal Erwin , Nelson Karen , Torralba Mannolito , Smoot Duane , Ashktorab Hassan , Sears Cynthia 
Published: December 2010

Abstract
Colonic adenomatous polyps are common tumors occurring in 50% of Western populations with 10% risk of malignant progression. To date, the environmental exposures proposed to promote the development of colorectal cancer (CRC) have been primarily dietary agents. However, the local environment to which the colonic mucosa is exposed is created by the bacterial microbiota of the colon and their metabolic products that include toxins. African Americans are known to have a higher incidence of colon cancer than other groups.
We analyzed the gut flora from African Americans patients by both 16S rDNA sequencing and HIT (Human Intestinal Tract) Chip. Our findings reflected a high prevalence of Bacteroidetes and Clostridia groups with the Bacteroidetes slightly more represented in patients with colon polyps than healthy ones. While Bifidobacteria were not detected at all in all samples, Lactobacilliwere present at a very low frequency. Both bacteria are referred to as “good bacteria” and are generally associated with healthy colon. Helicobacter bacteria, associated with gastric cancer, were also detected in all analysed samples. Bacteroides fragilis and relatives were present in all samples at a high frequency. It is noteworthy that an enterotoxigenic Bacteroides fragilis have been found to trigger colon polyps formation in Min mice through a pSTAT3 pathway. A tissue microarray immunohistochemistry experiment on colon adenoma and matched normals revealed a strong expression of pSTAT3 both in colonic epithelial cells and in colonic immune cells in adenoma samples but not as much in normal ones. These findings highlight the presence of a possible ETBF-like induction mechanism in the analysed samples.
Enzyme immunoassay for the detection of antibodies against ETBF toxin would confirm such findings and a metagenomic analysis of the analysed samples would shed light on predominant bacterial functions in adenoma patients that might play a role in colon oncogenic transformation in this population.
Citation Information: Cancer Epidemiol Biomarkers Prev 2010;19(10 Suppl):B48.
Abstract B50: Telomerase expression is upregulated in response to severe oxidative stress
Authors: Uzamere Theodor U. 
Published: December 2010

Abstract
Overcoming cancer health disparities is one of the best opportunities available for lessening the burden of cancer. Telomerase is an enzyme predominantly associated with its ability to extend the ends of chromosomes, or telomeres, and is expressed in 90% of all cancers. Recent findings suggest that telomerase has multiple cellular functions completely independent of its catalytic ability. Some of these functions help promote cell survival in response to severe oxidative stress which in turn should aid in the ongoing battle against cancer health disparities. Telomerase expression has been implicated in aiding a cell's response to double strand strand breaks in DNA, mitochondria dysfunction, inhibition of apoptosis, and the promotion of cell proliferation. The protein component of telomerase, TERT, is thought to specifically enhance cell viability in response to the hypoxic microenvironment of a tumor. These protective roles of TERT could be vital in promoting cell survival during severe hypoxia. Telomerase expression is upregulated by the kinase Akt, which is in turn induced by the neuregulin/ErbB signaling pathway. Neuregulin is a glycoprotein that is necessary for smooth muscle and neuronal development. Neuregulin activates the ErbB tyrosine kinase family, which promotes cell survival, proliferation, and differentiation. Recently, neuregulin has been shown to be upregulated in response to serve hypoxia, and may reduce the inflammation response to oxidative stress. The mechanism of neuregulin expression protection is unclear, though microarray data shows that neuregulin expression decreases the expression of several pro-inflammatory cytokines. Based on these facts, our hypothesis states that neuregulin can regulate the expression of telomerase during severe oxidative stress, and that telomerase expression promotes cell survival during hypoxia. The addition of physiologic levels of neuregulin was able to induce telomerase expression, indicating that telomerase activation could play an important role in the cellular response to oxidative stress.
Citation Information: Cancer Epidemiol Biomarkers Prev 2010;19(10 Suppl):B50.
Abstract B51: Neuregulin induces telomerase expression in response to oxidative stress
Authors: Uzamere Theodor , Butts DeMario , Sharif Wallace 
Published: December 2010

Abstract
Telomerase is an enzyme that can extend the ends of chromosomes and is aberrantly expressed in 90% of all cancers. Recent findings suggest that telomerase has cellular functions independent of its catalytic ability to elongate the telomere. Telomerase expression has been implicated in aiding cellular response to double strand breaks in DNA, to mitochondria dysfunction, inhibition of apoptosis, and the promotion of cell proliferation. The protein component of telomerase, TERT, can specifically enhance cell viability in response to the hypoxic microenvironment of a tumor. Telomerase expression is upregulated by the kinase Akt, which is induced by the neuregulin/ErbB signaling pathway. Neuregulin is a glycoprotein that is necessary for smooth muscle and neuronal development. Neuregulin activates the ErbB tyrosine kinase family, which promotes cell survival, proliferation, and differentiation. Recently, neuregulin has been shown to be upregulated in response to severe hypoxia, and may reduce the inflammation response to oxidative stress. The mechanism of neuregulin expression protection is unclear, though microarray data shows that neuregulin expression decreases the expression of several pro-inflammatory cytokines. We hypothesize that neuregulin can regulate the expression of telomerase during severe oxidative stress, and that telomerase expression promotes cell survival during hypoxia. We examined telomerase expression in differentiated rat neuroblastoma cell and observed a significant increase in telomerase expression in response to the addition of physiological levels of neuregulin. Surprisingly, treatment with the oxidizing agent diidopropyl flourosphophate (DFP) had no effect on telomerase expression in these cells. The neuregulin-mediated telomerase expression did confer a mild survival benefit in this cell line. These results could strengthen the link between neurodegeneration and cancer.
Citation Information: Cancer Epidemiol Biomarkers Prev 2010;19(10 Suppl):B51.
Abstract B59: A novel mechanism in tumor development and progression
Authors: Osman Mahasin A. 
Published: December 2010

Abstract
Cancer is a progressive disease that can culminate in acquisition of metastatic potential by tumor cells and directly contributes to patient mortality. An understanding of the involved genetic elements and their cellular networks offer an exceptional opportunity for defining potentially relevant and effective targets for improving cancer therapy. IQGAP1 is a widely conserved effector of CDC42 GTPase and has emerged as a potential oncogene associated with diverse human cancers, however, its role in tumor development and progression remains unclear. Here we discuss a novel mechanism by which IQGAP1 generates neoplastic lesions and promotes progression to metastasis.
Our work shows that IQGAP1 binds mTOR and regulates cell homeostasis. Expression of the N-terminal domain, which binds mTOR, enhances insulin secretion, enlarges the cell size and arrests cytokinesis whereas expression of the C-terminal domain that binds and activates CDC42GTPase, accelerates the cell cycle and decreases the cell size. Expression of full-length or the C-terminal domain also increases serine phosphorylation of IQGAP1 and generates transformed phenotypes that are sensitive to rapamycin and PI3K-Akt1 inhibitors.
These findings suggested that IQGAP1 serves as a phosphorylation-sensitive conformational switch to modulate cell proliferation. Indeed, treatment with EGF increases IQGAP1 phosphorylation and the phosphomimetic, but not the phosphodefective, mutant generates transformed phenotypes and promotes cell invasion. In response to EGF, IQGAP1 attenuates mTORC1 signaling and activates Akt1, which may provide an in vivo mechanism by which it generates neoplastic transformation and progression to metastasis. Thus our work has uncovered a novel pathway CDC42-IQGAP1 -mTORC1 -Akt1 in tumor development and progression that may yield new approaches for cancer detection and treatment.
Citation Information: Cancer Epidemiol Biomarkers Prev 2010;19(10 Suppl):B59.
Abstract B60: NR4A2: A novel therapeutic target in triple negative breast cancer
Authors: Williams Christopher C. , Llopis Shwan D. 
Published: December 2010

Abstract
Despite the lack of an increased rate of breast cancer occurrence among African American women, African American women suffer greater mortality due to breast cancer as compared with other ethnic groups. Recent studies suggest that the increase in mortality is likely multifactorial, however the elevated occurrence of triple negative (ER-/PR-/HER2-) breast cancer may be a key factor in decrease survival among African American women. Since the lack of ER and HER2 make these patients ineligible for hormonal therapy or Her2 targeted therapies such as trastuzumab, patients are often relegated to cytotoxic chemotherapeutic strategies. As such, it is imperative to identify therapeutic targets which can be exploited to design highly selective, less toxic regimens which are effective in treating triple negative breast cancer. The NR4A (NR4A1, NR4A2, and NR4A3) orphan nuclear receptors have the potential to serve as distinct, specific pharmacological targets which can directly affect apoptosis in triple negative breast cancer cells. Breast tumor microarrays demonstrate that NR4A2 is highly expressed in the nucleus of normal, but not malignant breast epithelial cells. shRNA-mediated silencing of NR4A2 in triple negative breast cancer cells leads to increased proliferation in vitro and in breast cancer xenograft models. In vitro studies also revealed that shRNA silencing of NR4A2 expresssion mediated partial resistance to doxorubicin, while overexpression of NR4A2 leads to cell cycle arrest. Additionally, gene expression arrays show that overexpression of NR4A2 induces expression of angiogenic factors, as well as causes suppression of markers associated epithelial-mesenchymal transition. Taken together, these studies suggest that NR4A2 is a viable pharmacological target in triple negative breast cancer. Targeting triple negative breast cancer may prove an effective means to address the disparity in survival rates of African American women as compared to other ethnicities.
Citation Information: Cancer Epidemiol Biomarkers Prev 2010;19(10 Suppl):B60.