bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract P1-07-19: Spatial analyses of breast cancer in women 15-49 years-old in Rio Grande do Sul, southern Brazil
Authors: Vianna FSL , Vargas F , Gross LG , Nunes LN , Ashton-Prolla P , Camey SA 
Published: May 2016

Abstract
Breast cancer (BC) rates under 50 years have been increasing over time in several countries. Although the exact impact of BC is not know in low and middle income countries, it's estimated that at least 20% of deaths caused by BC affect women under the ahe of 50 years. In Porto Alegre, the capital of Rio Grande do Sul (RS), Brazil's southernmost state, the incidence of BC in women aged 40-49 years is 165 cases per 100,000, while the mortality rate reaches 25 in 100,000 women. In order to understand BC profile in this age group in the entire state of RS, we established incidence, morbidity and mortality between 2002-2011 through crude and smoothed rates for each municipality. Furthermore, we perform the spatial analysis of these indicators. Incidence data were only available for the state capital, where the rate incidence was 19 and 160 cases per 100,000 women in the age groups of 15-39 and 40-49, respectively. Statewide mortality was 2 and 21 per 100,000 women in the age groups of 15-39 and 40-49, respectively. Hospitalar morbidity associated with BC was 0.6% and 2% in women 15-39 and 40-49 years, respectively. The distribution of morbidity and mortality showed regions with continuously high rates throughout this period with result above 3% and 20 deaths per 100,000 women. In the same areas we did not identified centers specialized in cancer treatment and care. Although there is specific epidemiological surveillance for cancer in Brazil, the coverage is insufficient, especially when it comes to incidence. Morbidity and mortality data showed regions continually affected by high rates, suggesting that specific measures as well as specialized care for women in these regions are necessary. This result is particularly important since current guidelines of the Ministry of Health in Brazil recommend mammographic screening starting at the age of 50 years. The expansion of coverage and access to appropriate treatment is essential for the recognition of risk factors, adoption of effective strategies and reduction of cases and deaths in this group of women. Knowledge of the age distribution of BC cases and BC related deaths is important for the definition of health care policies, which will likely be different in different regions of the world.
Citation Format: Vianna FSL, Vargas F, Gross LG, Nunes LN, Ashton-Prolla P, Camey SA. Spatial analyses of breast cancer in women 15-49 years-old in Rio Grande do Sul, southern Brazil. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P1-07-19.
Abstract P1-08-05: Expression levels of sialyl transfereases and fucosyl transferases in breast cancer and their prognostic significance
Authors: Yu AL , Liao K-H , Chang C-H , Lin Y-C , Fan T-C , Hung J-T , Yeo H-L , Lin R-J , Yu J-C 
Published: May 2016

Abstract
Aberrant expression of fucose or sialic acid containing glycans is prevalent in various cancers, including breast cancer. The addition of fucose and sialic acid to glycans is mediated by fucosyl transferases (FUTs) and sialyl transferases (STs), respectively. To explore the roles of these FUTs and STs in breast cancer, we collected 123 paired breast cancer specimens (tumor tissue and non-tumor tissue) and determined the RNA expression levels of 13 FUTs (FUT1-13) and 13 STs (ST3Gal1-6, ST6Gal1, ST6GalNAc1-4, ST6GalNAc6, ST8Sia1 and ST8Sia4) by q-PCR. The expression of 10 FUTs and 10 STs is significantly higher in tumor tissue than in non-tumor tissue by 1.2-4.09 folds. Notably, expression of FUT1 and ST3Gal1 appeared to be highest in triple negative subtype. Further multivariate Cox regression analysis showed a significant correlation between higher hazard ratios (HRs) for five-year relapse-free survival (RFS) and higher ST3Gal1 expression (N = 16, HR = 2.54, p = 0.02) or lower ST3Gal3 expression (N = 88, HR = 3.44, p &lt; 0.001). As to the joint effects of high expression of ST3Gal1 and low expression of ST3Gal3 (N = 10) compared with low expression of ST3Gal1 and high expression of ST3Gal3 (N = 82), the HR was 5.5 (95% CI = 2.16-14.02, p = 0.0004) for RFS. The two gene additive model displayed a statistically significant HR of 2.33 for RFS (95% CI = 1.48-3.69, p = 0.0003). These results suggest that FUTs and STs play important roles in tumor progression.
Citation Format: Yu AL, Liao K-H, Chang C-H, Lin Y-C, Fan T-C, Hung J-T, Yeo H-L, Lin R-J, Yu J-C. Expression levels of sialyl transfereases and fucosyl transferases in breast cancer and their prognostic significance. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P1-08-05.
Abstract P1-09-04: New Orleans has the highest incidence rates of triple negative breast cancer
Authors: Loch MM , Li X , Hsieh M-C , Chen VW , Wu X-C 
Published: May 2016

Abstract
Background: We previously demonstrated increased incidence rates of triple negative breast cancer (TNBC) in Black women (BW) in New Orleans (NO) and Louisiana (LA) compared with SEER 17. We explored the hypothesis that BW in NO had a higher incidence of TNBC than in BW other metro areas in the SEER Program.
Methods: We analyzed tumor characteristics of invasive female breast cancers diagnosed 2010-12 from SEER, focusing on racial disparities. We compared LA data with SEER 17 and metropolitan areas (Atlanta, Detroit, Los Angeles and San Francisco). Predictors of TNBC were identified in multivariate logistic regression.
Results: Overall incidence rate of TNBC in BW was significantly higher in NO (32 per 100,000) than in the rest of LA (24 per 100,000) and the SEER metro areas combined (23 per100,000). Detroit had the 2nd highest rates (27.3 per 100,000) followed by Los Angeles, San Francisco and Atlanta (23.2, 23, 22.4 respectively). Compared with SEER 17, the rate ratio of TNBC was 38% higher for BW in NO (CI: 1.17-1.61) and 17% higher for BW in Detroit (CI: 1.06-1.29). Compared with other LA metro areas, the rate ratio of TNBC was 44% higher for BW in NO (CI: 1.10-1.91). Young age (&lt;65) and black race predicted TNBC after adjusting for insurance status, tumor size, lymph node status, grade and derived AJCC stage.
Conclusions: The incidence rates and rate ratios of TNBC in BW in NO and LA are not only significantly higher than in SEER 17 but also higher than any other SEER metro area. We will explore this dataset further by analyzing BMI, comorbidities and SES. This disparity in BW in NO has clinical implications and translational research potential as it enables us to broaden the understanding and treatment of this aggressive disease.
Citation Format: Loch MM, Li X, Hsieh M-C, Chen VW, Wu X-C. New Orleans has the highest incidence rates of triple negative breast cancer. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P1-09-04.
Abstract P1-10-11: Prognostic value of non-alcoholic fatty liver disease in stage II/III breast cancer patients who received neoadjuvant chemotherapy
Authors: Yang Y , Lee K-H , Kim T-Y , Han S-W , Oh D-Y , Kim T-Y , Han W , Moon H-G , Park IA , Noh D-Y , Im S-A 
Published: May 2016

Abstract
Background
Metabolic syndrome is associated with various malignancies, including breast cancer. Non-alcoholic fatty liver disease (NAFLD) is a hepatic manifestation of metabolic syndrome. NAFLD is frequently observed during chemotherapy, but its clinical implication is unclear. The purpose of this study is to evaluate the prognostic value of NAFLD in patients with stage II/III breast cancer who received neoadjuvant chemotherapy (NAC Tx).
Methods
The patients with clinical stage II/III breast cancer who received NAC Tx with docetaxel and doxorubicin were enrolled. Treatment sequences were: 3 cycles of NAC Tx → surgery → 3 cycles of adjuvant chemotherapy (AC Tx), or 6 cycles of NAC Tx → surgery, allowing AC Tx at the physician's discretion. NAFLD was determined by ultrasonography (radiologists' decision), non-constrast computed tomography [CT] (the attenuation of liver is less than that of spleen or &lt;49 hounsfield unit [HU]) or contrast CT (the difference between liver and spleen attenuation &lt; -18.5 HU). The presence of NAFLD was evaluated 3 times, at diagnosis, after NAC Tx and after the completion of AC Tx. Improvement of NAFLD was defined as the disappearance of NAFLD after NAC Tx.
Results
Between 2002 and 2008, 269 patients were enrolled. The median age was 45 (range 18-69), and 51.7% and 28.6% were with hormone receptor and HER2 positive tumors, respectively. The median number of NAC Tx was 3 cycles (range 1-6). NAFLD was observed in 33 (12.4%) patients at diagnosis, 52 (19.3%) after NAC Tx and 71 (26.4%) at the completion of AC Tx. The patients with NAFLD at diagnosis showed shorter overall survival than those without NAFLD (HR=2.688, 95% CI 1.259-5.747, P=0.011). The improvement of NAFLD during NAC Tx was observed in 28 (10.4%, group A) and persistence of NAFLD observed in 24 (8.9%, group B). Group A showed better prognosis in both PFS (HR 0.125, 95 % CI 0.016-0.962) and OS (no event), whereas group B showed worse PFS (HR 2.329, 95% CI 1.280-4.237) and OS (HR 3.721, 95% CI 1.727-8.015) compared to the patients without NAFLD at diagnosis.
Conclusions
NAFLD at diagnosis was a poor prognostic marker of OS in patients who received NAC Tx. Improvement of NAFLD during NAC TX was associated with good prognosis in terms of PFS and OS.
Citation Format: Yang Y, Lee K-H, Kim T-Y, Han S-W, Oh D-Y, Kim T-Y, Han W, Moon H-G, Park IA, Noh D-Y, Im S-A. Prognostic value of non-alcoholic fatty liver disease in stage II/III breast cancer patients who received neoadjuvant chemotherapy. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P1-10-11.
Abstract P1-10-12: Biopsychosocial concerns of adolescent young adults (AYA) with breast cancer
Authors: Smith R , Mortimer J , Loscalzo M , Clark K 
Published: May 2016

Abstract
Background: The natural history of breast cancer in the AYAs with breast cancer is reported to be more aggressing than that observed in older women. We wanted to determine the level of biopsychological distress in this population compared with women in other age groups.
Methods: All new patients seen at City of Hope complete a tablet-based self report biopsychosocial screening questionnaire (SupportScreen®). Patients are asked to score a series of problems on a 5-point Likert scale ("not a problem" to "very severe problem") and are asked if they are interested in obtaining help for that problem. Results: To date 1,159 women have undergone screening; 79 pts (6.9%) were age 18-39 yrs (AYA), 807 (69.6%) age 40-64 yrs, and 273 (23.6%) &gt; 65 yrs. The concerns that were unique to the AYA population included: Ability to have children (p=0.001) and physical appearance (p=0.047 for 40-64 yrs and p=0.018 for age &gt; 65 yrs). Older women were more concerned that AYAs or middle aged women about transportation (p=0.008), walking, climbing stairs (p=0.000). Compared to older women, those age 40-64 yrs were more likely to identify feeling anxious or fearful (p=0.032) and managing work, school or home life (p=0.018). In comparison to AYAs, those age 40-64 yrs had more distress related to recent weight change (p=0.034) and difficulty sleeping (p=0.006).
Conclusions: Biopsychosocial concerns change over the continuum of age. Compared to other age groups, the AYA population was more concerned about their ability to have children and their physical appearance. In other domains of distress, they were comparable to women age 40-65 yrs.
Citation Format: Smith R, Mortimer J, Loscalzo M, Clark K. Biopsychosocial concerns of adolescent young adults (AYA) with breast cancer. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P1-10-12.
Abstract P1-15-07: The neuroprotective aminopropyl carbazole, P7C3-A20, prevents paclitaxel-induced pain
Authors: LoCoco PM , Risinger AL , Mooberry SL , Berg KA , Clarke WP 
Published: May 2016

Abstract
Paclitaxel (PTX), a microtubule-targeting anticancer agent, produces a debilitating peripheral neuropathy that is accompanied by neuropathic pain. Currently, there are only marginally effective therapeutic interventions available. Consequently, patients are forced to reduce or discontinue life-saving chemotherapy to cope with the pain. Recently, a newly identified agent, P7C3-A20, was found to be protective in several models of neurodegeneration, including Parkinson's disease and traumatic brain injury. Given that PTX triggers progressive degeneration of peripheral afferent neurons, this study was performed to evaluate the potential neuroprotective efficacy of P7C3-A20 in rodent models of PTX-induced peripheral neuropathy. P7C3-A20 (10 mg/kg) or vehicle (Cremophor EL/DMSO/5% Dextrose; 1:1:3) was administered intraperitoneally (i.p.) to Sprague-Dawley rats (250-300 g) everyday over a 28-day experimental paradigm. Following two days of treatment with P7C3-A20 or vehicle, rats also received 3 injections of PTX (11.7 mg/kg, i.p.) or vehicle (Cremophor EL/DMSO/5% Dextrose; i.p.) administered every other day. Treatment with P7C3-A20 did not alter body weights or leukocyte counts in control or PTX-treated rats. PTX treatment increased sensitivity to mechanical and cold stimulation (allodynia) of the hindpaw, evidence of peripheral neuropathy. Notably, P7C3-A20 treatment prevented the development of allodynia in response to PTX. Immunohistochemical analysis of paw biopsies indicated that P7C3-A20 prevented PTX-mediated degeneration of terminal nerve endings. Collectively, these data suggest that P7C3-A30 prevented the neurotoxic effects of PTX on peripheral sensory neurons. A xenograft tumor model of triple negative breast cancer was then used to determine whether P7C3-A20 diminished the antitumoral efficacy of PTX. MDA-MB-231 tumors were bilaterally implanted into flanks of female athymic nude mice and allowed to grow for 3 weeks prior to treatment. Using the same treatment protocol as the rats, tumor-bearing mice received daily treatment with P7C3-A20 (20 mg/kg, i.p.) or vehicle for 16 days. P7C3-A20 did not alter PTX-mediated inhibition of tumor growth. Furthermore, P7C3-A20 prevented PTX-induced mechanical allodynia in the mice. Taken together, this work indicates that P7C3-A20 prevents PTX-induced neuropathic damage without diminishing its antitumoral efficacy. P7C3-A20 may be an exciting new candidate to prevent peripheral neuropathy in patients undergoing cancer treatment with PTX.
Citation Format: LoCoco PM, Risinger AL, Mooberry SL, Berg KA, Clarke WP. The neuroprotective aminopropyl carbazole, P7C3-A20, prevents paclitaxel-induced pain. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P1-15-07.
Abstract P2-04-01: The role of Jmjd1a in mammary gland development and breast tumor growth
Authors: Qin L , Xu Y , Wu Y , Yu X , Toneff MJ , Liao L , Li Y , Xu J 
Published: May 2016

Abstract
Histone modification alters chromatin architecture and thereby influences gene transcription. Histone methylation status is reversible and counter-regulated by methyltransferases and demethylases. Jmjd1a (also known as KDM3A, TSGA, JMJD1, JHDM2A and JHMD2A) is a histone demethylase. It belongs to JmjC domain-containing protein family and could specifically remove di- and mono- methyl residues from di or mono-methylated histone H3K9 (H3K9me2/me1). Recent studies showed that Jmjd1a plays an important role in embryonic stem cell self-renewal, spermatogenesis, regulation of metabolic gene expression and body weight, sex determination, tumor angiogenesis, and macrophage infiltration. However, its role in mammary gland (MG) development, breast carcinogenesis and breast cancer progression hasn't been systemically investigated. In this study, we found that Jmjd1a is expressed in mouse luminal epithelial cells. Genetic disruption of the Jmjd1a gene significantly slowed down MG development as indicated by retarded MG elongation and decreased ductal density in virgin mice observed at the ages of 4, 6 and 8 weeks. In agreement with the retarded MG development, the expression of Ki67 and cyclinD1 in epithelial cells of MGs from Jmjd1a knockout (KO) mice dramatically reduced compared with that from wild type (WT) mice. H3K9me1 and H3K9me2 levels in the epithelial cells of KO MGs are much higher than that in WT MGs. To assess the role of Jmjd1a in breast cancer progression, we crossbred Tg(Jmjd1a-/-) mice with MMTV-TVA(RCAS-PyMT) mice and obtained Tg(Jmjd1a-/-)×MMTV-TVA(RCAS-PyMT) mice. Infection of the TVA-expressing MG epithelial cells with the RCAS-PyMT virus induced mammary tumors in these mice and MMTV-TVA(RCAS-PyMT) control mice. We found that KO of Jmjd1a slightly accelerated mammary tumor initiation but significantly decreased tumor growth. Ki67 and cyclinD1 expression statistically reduced in KO tumors versus WT tumors. At the molecular level, Jmjd1a expression positively correlated with cyclin D1 expression in mammary epithelial cells and mammary tumors. Knockdown of Jmjd1a in MCF-7 cells significantly reduced cyclin D1 expression, while ectopic expression of Jmjd1a in MCF-7 cells increased cyclin D1 expression. ChIP assay revealed that Jmjd1a is associated with a promoter region of cyclin D1. Co-expression of c-Myc and Jmjd1a boosted the activity of the cyclin D1 reporter. In conclusion, our study indicated that Jmjd1a plays an important role in promoting mammary gland development and breast tumor growth by up-regulating cyclin D1 expression. Targeting Jmjd1a may inhibit breast cancer progression.
Citation Format: Qin L, Xu Y, Wu Y, Yu X, Toneff MJ, Liao L, Li Y, Xu J. The role of Jmjd1a in mammary gland development and breast tumor growth. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P2-04-01.
Abstract P2-05-17: ARGX-111 depletes MET-expressing circulating tumor cells via enhanced ADCC, resulting in inhibition of metastasis
Authors: Morello V , Hultberg A , De Jonge N , Huyghe L , Hanssens V , Brouckaert P , Saunders M , Dreier T , Thibault A , Rolfo C , Aftimos P , Awada A , Michieli P , de Haard H 
Published: May 2016

Abstract
Several lines of experimental evidence suggest that Hepatocyte Growth Factor (HGF) and its receptor MET play an important role in breast cancer progression and drug resistance. To date, targeted MET inhibitors in clinical development have primarily shown cytostatic rather than cytotoxic effects. Development of a cytotoxic MET inhibitor would serve to complement standard breast cancer therapy, especially when administered in the adjuvant/neo-adjuvant setting.
We have developed ARGX-111, a human antibody antagonist of MET function. ARGX-111 blocks both HGF-dependent and -independent signaling, down-regulates tumor cell surface expression of MET and kills MET-overexpressing cells by enhanced antibody-dependent cellular cytotoxicity (ADCC).
ARGX-111 was shown to be more efficacious than an ADCC-inactive control antibody in both HGF-dependent and -independent tumor xenograft models. ADCC reporter assays confirmed the cytotoxic effects of ARGX-111 in patient-derived primary tumor specimens, including MET-expressing breast cancer stem-like cells. In an orthotopic mouse model of metastatic mammary carcinoma (MDA-MB-231), adjuvant or neo-adjuvant treatment with ARGX-111 was significantly more effective in depleting circulating tumor cells (CTCs) and suppressing the development of bone and lung metastases than the ADCC-inactive control.
Taken together, these results provide a rationale for clinical investigation of ARGX-111 in the early breast cancer setting. An ongoing Phase 1 study (NCT02055066) is examining the effects of ARGX-111 on CTCs, alongside the assessment of its safety and efficacy.
Citation Format: Morello V, Hultberg A, De Jonge N, Huyghe L, Hanssens V, Brouckaert P, Saunders M, Dreier T, Thibault A, Rolfo C, Aftimos P, Awada A, Michieli P, de Haard H. ARGX-111 depletes MET-expressing circulating tumor cells via enhanced ADCC, resulting in inhibition of metastasis. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P2-05-17.
Abstract P2-05-23: TWIST1 silences FOXA1 transcription to promote breast cancer progression
Authors: Xu Y , Feng Z , Xu Y , Mo Q , Qin L , Sun T , Wu H , Li Y , Liao L , Xu J 
Published: May 2016

Abstract
TWIST1 promotes epithelial-mesenchymal transition (EMT), invasion and metastasis of breast cancer cells, but the underlying mechanism is still not well understood. We generated mammary gland tumor specific Twist1 knock out mouse model and found that TWIST1 does not affect PyMT-induced mammary tumor initiation and growth but promotes tumor lung metastasis. We identified FOXA1 as a novel direct target of TWIST1 in both mouse and human breast cancer. We further found that TWIST1 inhibits FOXA1 expression through direct binding to its proximal promoter region and recruiting Mi2/nucleosome remodeling and deacetylase (Mi2/NuRD) transcriptional repressor complex. Moreover, TWIST1 also diminished transcriptional activator AP1 binding to FOXA1 promoter. TWIST1 mediated FOXA1 down-regulation is essential for promoting breast cancer migration, invasion and metastasis. FOXA1 significantly inhibits TWIST1 dependent cell migration and invasion capability of MCF7 cells through inhibiting integrin α5, β1 and MMP9 expression. Importantly, TWIST1high FOXA1low correlates with the poorest prognosis in breast cancer patients.
Citation Format: Xu Y, Feng Z, Xu Y, Mo Q, Qin L, Sun T, Wu H, Li Y, Liao L, Xu J. TWIST1 silences FOXA1 transcription to promote breast cancer progression. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P2-05-23.