bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract P4-03-03: Microenvironment induced DDR2 mediates stromal-cancer interactions and metastasis growth in breast cancer
Authors: Kleer CG , Martin EE , Anwar T , Arellano-Garcia C , Lama A , Medhora N , Chen Y-C , Yoon E , Ge C , Franceschi R , Gonzalez ME 
Published: March 2017

Abstract
This abstract was not presented at the symposium.
Abstract P4-03-09: Human breast cancer biopsies induce eosinophil recruitment and enhance adjacent cancer cell proliferation
Authors: Spencer BL , Szalayova G , Ogodnik A , Rincon M , James T 
Published: March 2017

Abstract
Previous research has demonstrated that chronic inflammation facilitates cancer progression and spread to other sites. The effect of acute inflammation in the microenvironment of the tumor that develops as a result of standard biopsy procedures has not been studied in detail. Recent studies demonstrated that acute inflammation in mouse models from a mammary biopsy increases the frequency of distal cancer metastasis. Core needle biopsies are the standard procedure for breast cancer diagnosis, but there have been no studies detailing the inflammatory response from the biopsy. The purpose of this study is to determine if core needle biopsies in breast cancer patients trigger an inflammatory response, determine the type of inflammatory response that occurs and study the potential effect of acute inflammatory response on tumor cells remaining. The biopsy wound site was identified in primary tumor resection samples from breast cancer patients. The inflammatory response adjacent and distant to the biopsy were studied via histology and immunohistochemistry. Tumor cell proliferation was studied as well. Our study demonstrated that diagnostic core needle biopsies trigger inflammatory cell recruitment at the site, and those cells remain over long periods of time. An unexpected increase in eosinophils were found to accumulate at the biopsy site. The biopsy also was shown to increase proliferation adjacent to the wound site. Overall, core needle biopsies used for breast cancer diagnosis induce a unique inflammatory environment at the site of the biopsy as well as the closely surrounding cells. Inflammation induced by the biopsy could lead to tumor cell progression or metastasis in breast cancer. These findings may be important for the clinical management of breast cancer.
Citation Format: Spencer BL, Szalayova G, Ogodnik A, Rincon M, James T. Human breast cancer biopsies induce eosinophil recruitment and enhance adjacent cancer cell proliferation [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P4-03-09.
Abstract P4-03-12: Cancer-associated fibroblasts release exosomal microRNAs that dictate an aggressive phenotype in breast cancer
Authors: Condorelli G , Elvira D , Danilo F , Giuseppina R , Martina N , Assunta A , Alessandra A , Cristina Q , Salvatore P , Rienzo A , Renato T 
Published: March 2017

Abstract
This abstract was not presented at the symposium.
Abstract P4-03-13: Obesity and breast cancer: The adipocyte-macrophage interaction as a mediator of metastasis
Authors: Connelly L , Yadav N , Barcikowski A , Imaizumi Y , Jacobs A 
Published: March 2017

Abstract
Obese individuals with breast cancer have a poorer prognosis and higher risk of metastatic disease vs. non-obese patients. Prior research has largely focused on defining the interactions between adipocytes and tumor cells, but other cell types may also play a role. Adipose tissue in obese individuals is characterized by a significant infiltration of macrophages. We have therefore investigated the adipocyte-macrophage interaction as a possible mechanism whereby obesity promotes breast cancer metastasis.
We performed co-culture with both human and murine cells to determine whether adipocytes influence the expression of metastasis-promoting signals in macrophages. For the human system we co-cultured primary breast adipocytes with THP-1 macrophages. For the murine system we co-cultured 3T3-L1 differentiated adipocytes with J774.1 macrophages. We then assayed the mRNA levels and protein expression of metastasis-promoting genes.
In both systems we found that co-culture with adipocytes increased the expression of Vascular Endothelial Growth Factor A (VEGF-A) in macrophages. In examining a potential mechanism, we also show that media collected from cultured adipocytes (adipocyte-conditioned media) activates the transcription factor Egr-1 in macrophages. Since Egr-1 is a known regulator of VEGF-A expression, this is a potential mechanism whereby VEGF-A transcription is up-regulated. Treatment of human macrophages with Interleukin-6, Leptin and Insulin induced VEGF-A levels to a similar degree as co-culture, identifying these as adipocyte-derived signals that can possibly mediate this effect.
In summary we have found that the interaction between adipocytes and macrophages leads to the up-regulation of the pro-angiogenic signal VEGF-A in macrophages. Therefore this represents a potential mechanism whereby obesity could promote breast cancer metastasis.
Citation Format: Connelly L, Yadav N, Barcikowski A, Imaizumi Y, Jacobs A. Obesity and breast cancer: The adipocyte-macrophage interaction as a mediator of metastasis [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P4-03-13.
Abstract P4-03-15: Joint influence by paracrine adipocyte signals and metabolic conditions on breast cancer
Authors: Rosendahl AH , Bergqvist M , Lettiero B , Kimbung S , Borgquist S 
Published: March 2017

Abstract
Background: The growing global population of overweight and obese people represents a pressing public health concern. A higher percentage of body fat is linked to an altered metabolic state and an increased risk of chronic metabolic disorders and cancer. Although, the mechanistic explanations for how obesity affects the development, progression and prognosis of cancer is incompletely mapped.
Purpose: To investigate the joint influence by adipocytes and metabolic pressure on breast cancer cell expansion.
Experimental Design: In vitro differentiated 3T3-L1 adipocytes were exposed to metabolic glucoselow/high and insulinlow/high pressure in order to mimic normal, pre-diabetic, overt diabetic and late diabetic conditions. Adipocyte-conditioned medium was collected and paracrine effects by adipocyte-derived factors on estrogen receptor (ER)-positive (T47D, MCF-7) and ER-negative (MDA-MB-231) breast cancer cell proliferation, molecular adaptations, and cell motility were subsequently analyzed using sulforhodamine B, Western immunoblotting and migration assays.
Results: Under normal metabolic conditions, adipocytes stimulated the growth of ER+ (1.1-2.0-fold; P&lt;0.001) and to a greater extent, ER- breast cancer cells (3.1-fold; P&lt;0.001), compared with controls. The joint effects by adipocyte paracrine signals and higher metabolic pressure (overt or late diabetic conditions), further enhanced the proliferative response in both ER+ and ER- cells (1.3-3.5-fold; P&lt;0.01), compared with controls. Furthermore, adipocyte-derived factors induced morphological changes, protrusion extensions and cell migration in the low invasive T47D cells. Additional acquisition of molecular epithelial-mesenchymal transition features were observed in breast cancer cells following co-culturing with adipocyte-derived factors.
Conclusion: These study results support the hypothesis that paracrine signals by adipocytes significantly stimulate the proliferation and induction of a more motile phenotype of human breast cancer cells, which is further enhanced under obesity-associated metabolic conditions.
Citation Format: Rosendahl AH, Bergqvist M, Lettiero B, Kimbung S, Borgquist S. Joint influence by paracrine adipocyte signals and metabolic conditions on breast cancer [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P4-03-15.
Abstract P4-03-17: Tartrate-resistant acid phosphatase (TRACP) modulates breast cancer pre-metastatic niche
Authors: Dai M-S , Wu C-C , Chen L-C , Chen C-M , Chao T-Y 
Published: March 2017

Abstract
Background: Tartrate-resistant acid phosphatase (TRACP or ACP5) is a metalloprotein enzyme that belongs to the acid phosphatase family and is mainly expressed by osteoclasts. It is a classic marker for bone resorption and osteoclast differentiation. TRACP expression is a useful serum marker for extensive bone metastasis. Recent studies have reported that TRACP promotes the invasion and distant metastasis of melanoma and breast cancer cells through the modulation of focal adhesion kinase (FAK) phosphorylation and epithelial cell migration. Therefore, TRACP has received considerable attention as a newly discovered proinvasion metastasis driver associated with different malignancies. Additionally, TRACP overexpression is indicative of the poor prognoses cancer patients and suggests that TRACP may have an important role in promoting tumor metastasis. Its detail mechanism in modulating cancer metastasis remains unknown. We have previously demonstrated the serum TRCAP 5a is a valuable marker in assessing disease activity, severity or systemic macrophage (inflammatory) burden. It has recently been found that up-regulation of TRACP promoted cancer cell invasion and lung metastasis, whereas TRACP knockdown inhibited these processes.
Aims: No studies have previously addressed the question of extracellular effects of TRAP. The aim of this study was to evaluate if TRACP binds to and is endocytosed by cancer cells. We also aim to determine if extracellular TRACP affect oncogenesis or cancer progression, alter the cancer cell expressions of angiogenesis or adhesion molecules, or direct the treatment resistance or cancer prognosis.
Results: Knockdown of TRACP significantly attenuated FoxM1-enhanced invasion and lung metastasis. Extracellular TRACP in culture media influenced the tumor invasion upon endocytosis. Significant increased invasion/migration was observed upon higher concentrations of TRACP. Tumor growth was significantly enhanced when the tumor xenografting previously primed with polarized M2Ø or TRACP protein, by enhanced metalloproteinase (MMP-9) and angiogenic factor (VEGF-A) expression
Conclusions: TRACP or M2Ø-secreted TRACP could promote cancer growth and modulated the tissue and microenvironment and create pre-metastatic condition by cell adhesion/angiogenesis signaling alteration. TRACP-targeting strategy is plausible in breast cancer metastasis treatment.
Citation Format: Dai M-S, Wu C-C, Chen L-C, Chen C-M, Chao T-Y. Tartrate-resistant acid phosphatase (TRACP) modulates breast cancer pre-metastatic niche [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P4-03-17.
Abstract P4-07-11: MicroRNA-367a promotes tumor growth and stemness potential by targeting FBXW7 in breast cancer
Authors: Xiao G , Zhang J , Sun X , Qin S , Zhang B , Liu D , Liu J , Ren H 
Published: March 2017

Abstract
Increasing studies showed that MicroRNAs (miRNAs)participate in the carcinogenesis and progression of breast cancer, but the specific mechanism of miRNAs in breast cancer needs to be furtherexplored. in this study, wefound that miR-367a was significantly up-regulated in breast cancer tissue samples and cell lines, compared to paired normal tumor-adjacent samples and MCF-10A. meanwhile, Kaplan–Meier analysis demonstrated high miR-367a expression was evidently correlated with poor prognostic features of breast cancer. overexpression of miR-367a remarkably promoted proliferation, cell cycle,inhibited apoptosis ratios and stem-like capacity of breast cancer cells in vitro, whilesilencing the expression of miR-367a dramaticallyreversed these cellular events .in addition,In vivo studies showed that knockdown of miR-367a inhibited tumor growth of breast cancer ,moreover, F-box and WD repeat domain-containing 7 (FBXW7) was identified as a direct target genes of miR-367a, as miR-367a directly bound to the 3'untranslated region of FBXW7 . Notably, alterations of FBXW7 levels abrogated the effects of miR-367a on breast cancer cell proliferation, cell cycle, apoptosis and stemness potential. In conclusion,evidence from this study demonstrated that miR-367amay serve as a novel prognostic indicator for breast cancer patients andexerts tumor promotion,at least in part, by inhibiting FBXW7.
Key words: miR-367a, FBXW7, breast cancer, tumor growth, stem-like capacity.
Citation Format: Xiao G, Zhang J, Sun X, Qin S, Zhang B, Liu D, Liu J, Ren H. MicroRNA-367a promotes tumor growth and stemness potential by targeting FBXW7 in breast cancer [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P4-07-11.
Abstract P4-10-02: Transmembrane protein 33 (TMEM33) induces apoptosis via UPR signaling and autophagy in breast cancer cells
Authors: Clarke R , Hu R , Zhang X , Hilakivi-Clarke L , Kasid U 
Published: March 2017

Abstract
Breast cancer is the most common cancer diagnosed in women. Endoplasmic reticulum stress (EnR stress) and the related unfolded protein response (UPR) are activated in breast cancer cells and can promote cell survival and endocrine resistance. TMEM33 is a novel transmembrane protein that resides in the endoplasmic reticulum (EnR) and has been shown to activate the PERK and IRE1α branches of the UPR. However, the underlying mechanism of action of this EnR resident protein TMEM33 and the cellular functions that it regulates remain largely unknown. In this study, we show that overexpression of TMEM33 induces robust cell death in breast cancer cells. TMEM33 overexpression strongly activates UPR associated pro-death JNK-p53 signaling. We also observed a significant inhibition of the downstream survivin, which blocks cell death activation by binding to caspases and inhibiting their activation. We further show that the blockage of JNK activation with either an inhibitor or overexpression of survivin, protects cells against TMEM33 induced apoptosis. In addition, we show that TMEM33 overexpression induces autophagy in breast cancer cells. Inhibition of autophagy with using either the inhibitor chloroquine or knockdown of the Atg5 gene, further sensitizes breast cancer cells to the effects of TMEM33 overexpression. Cell death induced by TMEM33 is also decreased by overexpression of the autophagy gene Beclin 1. The findings in this study demonstrate that the novel EnR resident protein TMEM33 induces cell death by activating IRE1α-JNK-p53-survivin signaling in breast cancer cells. Concurrently, autophagy is also activated by TMEM33, and functions as a pro-survival mechanism. Cell fate reflects the balance between the pro-death and pro-survival activities as regulated by TMEM33.
Citation Format: Clarke R, Hu R, Zhang X, Hilakivi-Clarke L, Kasid U. Transmembrane protein 33 (TMEM33) induces apoptosis via UPR signaling and autophagy in breast cancer cells [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P4-10-02.
Abstract P4-10-03: Pterostilbene enhances TRAIL-induced apoptosis in TRAIL-resistant triple negative breast cancer cells
Authors: Wu Y-C , Wang H-C , Chen C-J , Liu L-C , Way T-D 
Published: March 2017

Abstract
Triple-negative breast cancer (TNBC) is refractory to commonly used chemotherapeutic agents, as a result it leads to relatively poor prognosis. TNF-related apoptosis-inducing ligand (TRAIL) is currently in clinical trials as a treatment for cancer. Unfortunately, patients develop resistance to the TRAIL, therefore, agents that can sensitize cells to TRAIL are urgently needed. Pterostilbene (PTER), a natural dimethylated analog of resveratrol, is known to have diverse pharmacologic activities. In the present study, we investigated whether PTER affect TRAIL-induced apoptosis and its mechanism in TRAIL-resistant TNBC cells. First, our results indicated that PTER induced apoptosis in TNBC BT-20 cells. Next, we found that PTER enhanced TRAIL-induced apoptosis in TRAIL-resistant TNBC BT20 and MDA-MB-468 cells. We demonstrated that PTER induced both death receptor (DR)-5, DR4 and decreased decoy receptor (DcR)-2 expression. PTER also decreased the expression of anti-apoptotic proteins survivin, Bcl-xL and c-FLIPS/L, but had minimal effect on the expression of Bcl-2. PTER caused the cleavage of bid protein and enhanced the expression of pro-apoptotic Bax. Moreover, we found that PTER induced DR4 and DR5 expression through the reactive oxygen species (ROS) –mediated activation of extracellular signal-regulated kinase 1/2 (ERK 1/2) and p38 mitogen activated protein kinase (p38 MAPK). Overall, our results show that PTER can potentiate TRAIL-induced apoptosis through the ROS–mediated activation of ERK 1/2 and p38 MAPK leading to DR4 and DR5 induction and down-regulation of anti-apoptotic proteins.
Citation Format: Wu Y-C, Wang H-C, Chen C-J, Liu L-C, Way T-D. Pterostilbene enhances TRAIL-induced apoptosis in TRAIL-resistant triple negative breast cancer cells [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P4-10-03.
Abstract P4-13-01: Prospective association between breast cancer risk and an individual dietary index based on the British Food Standards Agency nutrient profiling system
Authors: Deschasaux M , Julia C , Zelek L , Kesse-Guyot E , Gourlet V , Lécuyer L , Méjean C , Ducrot P , Peneau S , Latino-Martel P , Fézeu L , Fassier P , Hercberg S , Touvier M 
Published: March 2017

Abstract
Background: The Food Standards Agency Nutrient Profiling System (FSA-NPS) constitutes the basis for the Five-Colour Nutrition Label suggested in France to be put on the front-of-pack of food products. At the individual level, a dietary index (FSA-NPS DI) has been derived and validated and corresponds to a weighted mean of all FSA-NPS scores of foods usually consumed by the individual, reflecting the nutritional quality of his/her diet. Our aim was to investigate the association between the FSA-NPS DI and breast cancer risk in a large cohort.
Methods: This prospective study included 46,864 women aged over 35y from the NutriNet-Santé cohort (2009-2015) who completed at least three 24h dietary records during the first 2y of follow-up (median follow-up: 4.0y). 555 incident breast cancers were diagnosed. FSA-NPS DI was computed for each subject using the following nutrient content for 100g of each foods and beverages consumed: energy, total sugar, saturated fatty acid, sodium, fruits and vegetables (%), fibres and proteins. Higher values of the FSA-NPS DI correspond to a lower nutritional quality of the diet. Associations were characterized by multivariate Cox proportional hazards models.
Results: The FSA-NPS DI was directly associated with breast cancer risk (HR1-point increment=1.06 (1.02-1.11), P-trend=0.005; HRQ5vs.Q1=1.52 (1.11-2.08), P-trend=0.002). These associations were similar after the exclusion of cases diagnosed during the first year of follow-up.
Conclusions: In this prospective study, a higher FSA-NPS individual score was associated with an increased breast cancer risk. These results suggested that unhealthy food choices may be associated with a 52% increase in breast cancer risk (FSA-NPS DI ≥7.7 (Q5) vs. &lt;4.1 (Q1)), supporting the public health relevance of developing front-of-pack nutrition labels based on this score.
Citation Format: Deschasaux M, Julia C, Zelek L, Kesse-Guyot E, Gourlet V, Lécuyer L, Méjean C, Ducrot P, Peneau S, Latino-Martel P, Fézeu L, Fassier P, Hercberg S, Touvier M. Prospective association between breast cancer risk and an individual dietary index based on the British Food Standards Agency nutrient profiling system [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P4-13-01.
Abstract P4-20-04: Young women with breast cancer in Mexico: A report of the pilot phase of the “Mujer Joven y Fuerte” prospective cohort
Authors: Villareal-Garza CM , Platas A , Castro-Sánchez A , Miaja M , Bargalló-Rocha E , Martinez-Cannon BA , Vega Y , Fonseca A , Ramos-Elias P , Márquez-Perez CJ , Bukowski A , Goss P , St. Louis J , Chapman J-A , Partridge A , Meneses A , Mohar A 
Published: March 2017

Abstract
Background: Despite high rates of breast cancer in young women from low-and-middle-income countries (LMICs), their needs and concerns are not systematically studied or addressed. Understanding the characteristics of young women with breast cancer (YWBC) and the issues they face is of great relevance to the medical community, in order to tailor clinical interventions and supportive care for this unique and understudied patient population. The Mexican cohort “Mujer Joven y Fuerte” (Young and Strong Woman) has the goal of comprehensively characterizing and assessing the needs of YWBC in Mexico using patient- and physician-based surveys. Methods: A prospective cohort of newly diagnosed YWBC was established in November 2014 at two Mexican cancer centers in Mexico City and Monterrey. Eligible women answer web-based surveys on relevant topics including physical activity, genetics, psychosocial needs, and fertility. Clinicians complete pre-specified surveys using the US NIH BOLD Task Force common data elements registering clinical/pathologic characteristics and outcomes. Patients are evaluated at diagnosis, after 6 months, and annually for 5 years. Sub-studies assessing changes in cognition, sexual function and satisfaction, quality of life and depression/anxiety are being conducted, and biologic samples are stored for future research. Results: 96 YWBC with median age at diagnosis of 34 (21-41 y) were accrued to our pilot phase. 26% were single and 25% childless. 43% had higher education and 28% were employed. 90% presented with a self-detected mass. Clinical stage at diagnosis was distributed as follows: stage 0: 2%; I: 15%; IIA: 13%; IIB: 17%; III: 47%, and stage IV: 6%. The most frequent molecular subtype was HR+/HER2- (47%), followed by HER2+ (26%) and triple negative (21%). First follow-up results will be available shortly. Conclusions: To our knowledge, this represents the first prospective cohort of YWBC in Latin America. We are expanding this project to other centers in the region. Our findings will help develop culturally tailored interventions aimed at improving the psychosocial and medical outcomes of this vulnerable patient population.
Citation Format: Villareal-Garza CM, Platas A, Castro-Sánchez A, Miaja M, Bargalló-Rocha E, Martinez-Cannon BA, Vega Y, Fonseca A, Ramos-Elias P, Márquez-Perez CJ, Bukowski A, Goss P, St. Louis J, Chapman J-A, Partridge A, Meneses A, Mohar A. Young women with breast cancer in Mexico: A report of the pilot phase of the “Mujer Joven y Fuerte” prospective cohort [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P4-20-04.
Abstract P5-02-02: Combined use of elastography and color doppler ultrasound for the evaluation of breast masses detected at screening ultrasound in women with dense breasts
Authors: Lee SH , Chang JM , Cho N , Yi A , Choi SH , Kook SH , Youk JH , Son EJ , Chung J , Cha ES , Koo HR , Park JS , Chu AJ , Ko KH , Choi HY , Ryu EB , Han W , Moon WK 
Published: March 2017

Abstract
This abstract was withdrawn by the authors.