bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 1360: Reaching minority and low-income women with breast cancer prevention mobile messages: Implications for health promotion and clinical office collaboration.
Authors: Kratzke Cynthia , Vilchis Hugo 
Published: August 2014

Abstract
Background: While growing literature for breast cancer information supports the use of the Internet, little is known about breast cancer prevention and the use of mobile messages especially for women of different ages, race/ethnicity, income, and education levels. Minority and low-income women are more likely to be diagnosed with breast cancer at a later stage. Purpose: We examined differences for breast cancer risk factor knowledge, current channels, and mobile message preferences among Hispanic and non-Hispanic women in southern New Mexico. The study was guided using a conceptual framework of McGuire's Input-Output Persuasion Model. Methods: Women ages 40 and older at an imaging center completed a survey assessing their knowledge of breast cancer risk factors, channels of information, mobile message preferences, and demographics. In bivariate analysis, relationships between age, income, race/ethnicity and education of women and their mobile message preferences were examined. Results: A total of 157 women ages 40 to 91 (mean = 61, SD = 12.07) completed the survey. Breast cancer risk factor knowledge was significantly higher for non-Hispanic (p=.035), women with higher education levels (p=.023) and higher income levels (p=.000). The most common channels were television, magazines, Internet, and brochures. Overall, 87% used cell phones. Cell phone use was more likely among younger women ages 40-59 (p=.017), non-Hispanic women (p=.013), and women with incomes $20,000 or higher (p=.032). Of the cell phone users, 20% preferred breast cancer prevention messages. Breast cancer prevention cell message preferences were more likely among younger women ages 40-59 (p=.001), Hispanic women (p=.000), and women with lower incomes (p=.011). Nearly 47% used text messaging. Of the text users, 36% preferred breast cancer prevention text messages and 37% preferred mammogram appointment text reminders. Text message preferences were more likely among Hispanic women (p=.001). Conclusions: Traditional and mobile messages for breast cancer information are preferred by women. Targeting lower income, Hispanic, and younger women with mobile messages may help to reduce health disparities. Further research is needed for mobile technology use in health promotion. Health promotion specialists may partner with clinical offices to develop and target breast cancer prevention mobile messages for improved mammography adherence, patient education, and best practices in managing screening appointments.
Citation Format: Cynthia Kratzke, Hugo Vilchis. Reaching minority and low-income women with breast cancer prevention mobile messages: Implications for health promotion and clinical office collaboration. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1360. doi:10.1158/1538-7445.AM2013-1360
Abstract 1380: In vivo evidence for prior manipulation therapy-induced metastasis of primary osteosarcoma.
Authors: Wang Jir-You , Wu Po-Kuei , Chen Chih-Hsueh , Yen Chuen-Chuan , Hung Giun-Yi , Hung Shih-Chieh , Chen Wei-Ming , Liu Chien-Lin , Chen Tain-Hsiung 
Published: August 2014

Abstract
Our previous clinical study demonstrated that manipulation therapy (MT) on osteosarcoma (OS) patients prior to diagnosis resulted in poor prognosis after surgical treatment. This study was aimed to provide in vivo evidence of MT-induced metastasis in primary osterosarcoma. Eight-week-old male GFP-labeled human OS cells-transferred nude mice were randomly allocated into 2 groups, namely, MT (+) and MT (-) groups. MT was conducted with repeated massage on tumor site twice a week for 7 or 15 weeks. The parameters evaluated were x-ray diagnosis, micro-PET/CT scan, histopathology and serum metalloproteinase 9 (MMP9) level. The results showed that MT (+) mice showed a decreased body weight (30.5±0.65g) and an increased tumor volume (8.3±1.18 mm3) compared to MT (-) group with body weight (35.8±0.40g, p&lt;0.0001) and tumor volume (3.9±1.34mm3, p=0.038), respectively. There was an increased signal intensity over lymph node region of hind limb by micro-PET/CT and the GFP-labeled human OS cells were detected in the lung and bilateral lymph nodes in MT (+) group, while there were no such findings in MT (-) group. The serum MMP9 level was higher in MT (+) group (27.1±1.29 ng/ml) than in MT (-) group (17.8±1.97 ng/ml, p=0.048). Taken previous clinical observation and the present in vivo evidence together, we conclude that physicians should pay more attention on those patients who seek MT before diagnosis or during treatment for osteosarcoma.
Citation Format: Jir-You Wang, Po-Kuei Wu, Chih-Hsueh Chen, Chuen-Chuan Yen, Giun-Yi Hung, Shih-Chieh Hung, Wei-Ming Chen, Chien-Lin Liu, Tain-Hsiung Chen. In vivo evidence for prior manipulation therapy-induced metastasis of primary osteosarcoma. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1380. doi:10.1158/1538-7445.AM2013-1380
Abstract 1385: PPARδ promotes mammary tumorigenesis through mTOR activation.
Authors: Glazer Robert I. , Yuan Hongyan , Upadhyay Geeta , Yin Yuzhi , Kopelovich Levy 
Published: August 2014

Abstract
Background: Peroxisome proliferator-activated receptorδ (PPARδ) regulates a multitude of physiological processes associated with glucose and lipid metabolism, inflammation and proliferation. One or more of these processes are potential risk factors for the ability of PPARδ agonists to promote tumorigenesis in the mammary gland. In the present study, we describe a new transgenic mouse model in which activation of PPARδ by endogenous or synthetic ligands results in mammary neoplasia.
Methods: Transgenic mice were generated in which expression of PPARδ was directed to the mammary gland under the control of the MMTV long terminal repeat.
Results: Multiparous MMTV-PPARδ mice presented with infiltrating ductal carcinomas after a latency of 12 months. When transgenic animals were maintained on a diet supplemented with the PPARδ ligand GW501516, rapid progression to ductal and alveolar hyperplasia, dysplasia and ductal carcinoma in situ occurred within three months, and multifocal ductal carcinomas occurred after 5 months. Histopathological changes occurred in concert with a marked increase in phosphatidylcholine (PC) and lysoPC levels. Gene array profiling revealed an inflammatory, invasive, metabolic and proliferative signature denoted by enhanced expression of Saa1/2, S100a8, Klk6/7, Acsl4 and Plac1, and increased mTOR signaling. Treatment with the mTOR inhibitor, everolimus, dramatically reversed many of the histopathological and gene expression abnormalities.
Conclusion: MMTV-PPARδ mice demonstrate a direct role for PPARδ in breast tumorigenesis that is linked to several previously unknown signaling processes. These findings suggest a rationale for new therapeutic approaches to prevent and treat this disease.
Supported by 1N01CN43302-WA19 and 1P30CA51008
1st Choice Category: TB1 Cell Culture and Animal Models of Cancer
Citation Format: Robert I. Glazer, Hongyan Yuan, Geeta Upadhyay, Yuzhi Yin, Levy Kopelovich. PPARδ promotes mammary tumorigenesis through mTOR activation. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1385. doi:10.1158/1538-7445.AM2013-1385
Abstract 1386: Development and application of a syngeneic breast tumor preclinical model to study anticancer efficacy and cardiac safety of doxorubicin and dexrazoxane.
Authors: Gonzalez-Berrios Yanira , Dickey Jennifer S. , Aryal Baikuntha P. , Rosen Elliot T. , Herman Eugene H. , Mog Steven , Nakamura Asako J. , Redon Christophe E. , Baxa Ulrich , Parekh Palak , Mason Karen P. , Bonner William , Rao Ashutosh 
Published: August 2014

Abstract
Doxorubicin is a chemotherapeutic drug that causes oxidative stress-mediated cardiotoxicity. To prevent oxidative stress and help to mitigate the cardiotoxic effects of doxorubicin, the iron chelator dexrazoxane is clinically used. However, iron chelators and other antioxidants have not completely succeeded in mitigating this effect and do not protect against iron-independent oxidative damage. One limitation to the development of new cardioprotectants is the lack of physiologically-relevant animal models to simultaneously study antitumor activity and cardioprotection. Therefore, we optimized a syngeneic rat model and examined the mechanisms by which oxidative stress affects the safety and efficacy outcome. Immune-competent spontaneously hypertensive rats (SHRs) were implanted with the SHR-derived, breast tumor cell line, SST-2. Tumor growth and cytokine responses (IL-1A, MCP-1, TNF-α) were observed two weeks post-implantation. In order to demonstrate the utility of SHR/SST-2 model for monitoring both anticancer efficacy and acute cardiotoxicity, we studied cardiotoxic doxorubicin alone and in combination with dexrazoxane. As predicted, significant tumor reduction, DNA damage, and cardiomyopathy were demonstrated by doxorubicin. Treatment with the cardioprotectant dexrazoxane increased the pro-survival autophagy marker LC3-II and decreased caspase-3 in the heart, as a single agent and in combination with doxorubicin. Histopathology and transmission electron microscopy demonstrated apoptosis, autophagy, and necrosis in tumor and heart. Our results demonstrate the advantage of the immune-proficient SHR/SST-2 model to study anticancer agents and simultaneously address anticancer efficacy and cardiac safety.
Citation Format: Yanira Gonzalez-Berrios, Jennifer S. Dickey, Baikuntha P. Aryal, Elliot T. Rosen, Eugene H. Herman, Steven Mog, Asako J. Nakamura, Christophe E. Redon, Ulrich Baxa, Palak Parekh, Karen P. Mason, William Bonner, Ashutosh Rao. Development and application of a syngeneic breast tumor preclinical model to study anticancer efficacy and cardiac safety of doxorubicin and dexrazoxane. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1386. doi:10.1158/1538-7445.AM2013-1386
Abstract 139: Alcohol and breast cancer subtypes in a Spanish cohort.
Authors: Gago-Dominguez Manuela , Redondo Carmen M. , Enguix Manuel , Fernandez Maite Peña , Martinez Maria Elena , Munoz Victor , Carracedo Angel , Gude Francisco , Castelao Jose Esteban 
Published: August 2014

Abstract
Background Although alcohol intake is an established risk factor for overall breast cancer, few studies have looked at the relationship between alcohol use and breast cancer risk by subtype of breast cancer.
Materials and Methods A population-based study was conducted in Galicia, Spain. A total of 1211 Spanish women diagnosed with operable invasive breast cancer between 1997 and 2010 and 550 controls participated in the study. Data on demographics, breast cancer risk factors, and clinico-pathological characteristics were collected. The four major breast cancer subtypes [hormone-receptor-positive, HER2-negative (luminal A); hormone-receptor-positive, HER2-positive (luminal B); hormone-receptor-negative, HER2-negative (triple-negative); and hormone-receptor-negative, HER2-positive (HER2 over-expressing)] were compared on their clinico-pathological characteristics and risk factor profiles, particularly alcohol intake and reproductive variables.
Results With the exception of Her2 overexpressing, the risk of all subtypes of breast cancer increased with increasing alcohol intake (luminal A: OR=2.32, 95%CI:1.43-3.77; luminal B: OR=2.03, 95%CI 1.01-4.06, and triple negative: OR=2.36, 95%CI 1.11-5.00). The association of alcohol with breast cancer was similar among women who drank wine exclusively and other drinkers. The alcohol-breast cancer association appeared to be more pronounced among lobular breast cancers (OR= 2.70, 95% CI:1.33-5.52) than among ductal type breast cancers (OR= 2.09, 95%CI:1.33-3-01). It has been suggested that the association of alcohol intake with breast cancer may be stronger in women who are current or past users of hormone replacement therapy compared with never users, or among non-ovariectomized compared to ovariectomized women, we found no such differences.
Conclusions To our knowledge, no prior study has examined the association of breast cancer with alcohol intake according to breast cancer subtypes and the type of wine consumed in Spanish women. Our findings indicate that breast cancer risk increased with increasing alcohol intakes for three out of the four major subtypes of breast cancer and that the risk was similar in women who drank wine, beer and/or liquor exclusively or in mixture.
Citation Format: Manuela Gago-Dominguez, Carmen M. Redondo, Manuel Enguix, Maite Peña Fernandez, Maria Elena Martinez, Victor Munoz, Angel Carracedo, Francisco Gude, Jose Esteban Castelao. Alcohol and breast cancer subtypes in a Spanish cohort. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 139. doi:10.1158/1538-7445.AM2013-139
Abstract 1391: Cellular and molecular bases of susceptibility to estrogen-induced mammary cancer in the rat.
Authors: Ding Lina , Zhao Yang , Warren Christopher , Shull James 
Published: August 2014

Abstract
Known breast cancer risk factors include a family history of breast cancer, cumulative exposure to endogenous and exogenous estrogens and breast mammographic density. Although several genes have been identified that significantly impact risk when mutated or aberrantly expressed, the genetic determinants of responsiveness to estrogens and mammographic density remain poorly defined. We are using the ACI rat model of 17β-estradiol (E2)-induced mammary cancer to identify genetic and environmental determinants of susceptibility to mammary cancer. When treated continuously with physiologic levels of E2, female ACI rats develop mammary carcinoma at an incidence approaching 100%. The mammary cancers that develop in E2 treated ACI rats express estrogen receptor-α (ERα) and progesterone receptor (PgR) and are dependent upon E2 for continued growth. By contrast, Brown Norway (BN) rats are highly resistant to E2-induced mammary cancer. The purpose of this study was to compare the impact of E2 treatment on mammary gland biology in susceptible ACI and resistant BN rats. Dramatic differences in numerous cellular and molecular responses to E2 were observed when these two inbred rat strains were compared. Whereas the mammary epithelium of susceptible ACI rats exhibited a marked proliferative response to E2, the epithelium of resistant BN rats exhibited responses associated with differentiation to secretory epithelium. Strain differences in expression of multiple genes associated with mammary epithelial cell proliferation and differentiation were observed. Specifically, Areg, Pgr, Wnt4 and Tnfsf11 were highly expressed in mammary glands of E2 treated ACI rats, relative to treated BN rats, whereas Lcn2, Spp1, Cd44, Mmp7 and Mmp9 were highly expressed in mammary glands of BN rats, relative to ACI rats. This study provides novel insight into the molecular bases of inherited susceptibility to E2-induced mammary cancer. We further propose that the observed strain differences in mammary gland responsiveness to E2 represent phenotypes that underlie variation in mammographic density in humans and may have the potential to serve as biomarkers that predict breast cancer risk.
Citation Format: Lina Ding, Yang Zhao, Christopher Warren, James Shull. Cellular and molecular bases of susceptibility to estrogen-induced mammary cancer in the rat. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1391. doi:10.1158/1538-7445.AM2013-1391
Abstract 1392: Role of mutant p53 for anti-TGF-β therapy in isogenic basal-like breast cancer models.
Authors: Lugo Fernando P. , Lin Shu , Bandyopadhyay Abhik , Yang Junhua , Sun Lu-Zhe 
Published: August 2014

Abstract
Breast cancer remains as one of the most common cancers worldwide accounting for 450,000 deaths. During cancer progression, transforming growth factor-β (TGF-β) signaling in tumor cells is often converted from tumor suppression to tumor promotion. However, how this oncogenic switch occurs is not well understood. Tripe-negative breast cancer (TNBC) is a breast cancer subtype, which is frequently associated with p53 mutation and lacks specific molecular targets for therapeutic intervention. TGF-β signaling has been shown to be oncogenic in TNBC models. Therefore, we tested the hypothesis that mutation of p53 may cause the oncogenic switch of TGF-β and thus serve as a biomarker for anti-TGF-β therapy.
In an effort to create isogenic models resembling the transformation of normal breast epithelial cells into TNBC, oncogenic H-Ras V12, human telomerase reverse transcriptase (hTERT), and mutant p53 R175H (mP53) or vector control were sequentially introduced into untransformed human breast epithelial MCF-10A cells. These generated cell lines were orthotopically introduced into the mammary fat pads of female nude mice and tumor burden was monitored. Mice were divided into two groups receiving a TGF-β type I receptor (RI) kinase inhibitor or PBS as control. Harvested lungs were analyzed for metastasis with GFP fluorescent imaging and quantitative PCR for tumor cell specific genes.
Mice inoculated with the transformed MCF-10A cells containing mp53 (10A/mp53) displayed greater tumor burden and lung metastasis incidence than the vector control counterparts. Systemic treatment with the TGF-β inhibitor resulted in a decrease in metastasis in the mice inoculated with 10A/mp53 representing disruption of TGF-β’s oncogenic role. In contrast, inhibition of TGF-β signaling in mice inoculated with 10A/pp290 vector control displayed greater lung metastasis incidence, likely due to the disruption of TGF-β tumor suppressive effects. Our results indicate that the mp53 may serve as a biomarker for the oncogenic switch of TGF-β pathway and anti-TGF-β therapy for the inhibition of TNBC-induced metastasis.
Citation Format: Fernando P. Lugo, Shu Lin, Abhik Bandyopadhyay, Junhua Yang, Lu-Zhe Sun. Role of mutant p53 for anti-TGF-β therapy in isogenic basal-like breast cancer models. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1392. doi:10.1158/1538-7445.AM2013-1392
Abstract 1394: Stable knockdown of osteoprotegerin increases cell proliferation and metastasis in breast cancer cells.
Authors: Weichhaus Michael , Segaran Prabu , Le Andrew , Geerts Dirk , Connelly Linda 
Published: August 2014

Abstract
Human breast cancer cells express and secrete osteoprotegerin (OPG, also called TNFRSF11B), a negative regulator for osteoclast differentiation. Previous in vitro data indicated that OPG expression promotes survival of breast cancer cells by inhibiting the apoptotic effect of TRAIL, through direct interaction of OPG with TRAIL. We generated stably transfected OPG-knockdown (KD) MDA-MB-231 breast cancer cells, using OPG shRNA clones, to examine the effect of OPG expression on primary tumor growth and metastasis in vivo. Positive selection of successfully transfected clones revealed that OPG KD cells expressed 60% less OPG (mRNA and protein) than control shRNA cells. OPG expression in control shRNA cells was not different from wild-type (wt) cells. Cell proliferation showed a small decrease after TRAIL challenge of KD cells compared to control and wt cells, assessed by MTT-assay, suggesting this was not a significant interaction. We decided to investigate the impact of OPG KD on tumor growth and metastasis using the chick embryo in vivo model. In brief, fertilized white leghorn chicken eggs were incubated for 10 days, after which the chorioallantoic membrane (CAM) was inoculated with 3 million KD or control cells. After an additional 7 days incubation, the primary tumor and a portion of the distant CAM were excised and measured for weight and the presence of human DNA, respectively. Primary tumor weight of KD cells was 31% higher than primary tumors from control cells. Moreover detection of human DNA in the distant CAM was 58% higher in eggs incubated with KD cells than in eggs incubated with control cells. Cell growth experiments in vitro showed that cell proliferation of KD cells was 40% higher compared to control and wt cells, as measured by trypan exclusion method. For validation in human cancer patients we mined a public microarray database, detailing gene expression in primary breast tumors. In agreement with our experimental data, high OPG gene expression in breast tumors was correlated with better prognosis. Contrary to the current understanding of OPG expression in breast cancer cells, our data indicates that OPG expression in breast cancer cells inhibits growth, the ability to metastasize and may promote survival in breast cancer patients.
Citation Format: Michael Weichhaus, Prabu Segaran, Andrew Le, Dirk Geerts, Linda Connelly. Stable knockdown of osteoprotegerin increases cell proliferation and metastasis in breast cancer cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1394. doi:10.1158/1538-7445.AM2013-1394