Currently, there are no resources to support culturally and linguistically diverse (CALD) women with breast cancer to make decisions about undergoing breast reconstruction (BR). This study evaluated the usability and acceptability of decision aids (DAs) for Vietnamese- and Arabic-speaking women. This two-phase qualitative recruited Vietnamese- (Phase 1) and Arabic-speaking (Phase 2) adult (age ≥ 18 years) women who were diagnosed with breast cancer and could read Vietnamese/Arabic. Women participated in either think-aloud telephone interviews (Phase 1) or semi-structured telephone interviews (Phase 2) and provided feedback on the DA. Interviews were audio-recorded, translated, and transcribed from Vietnamese/Arabic to English, and inductive thematic analysis was undertaken. Additionally, Arabic-speaking women completed the Preparation for Decision Making (PrepDM) scale in Round 2. Twenty-five women were recruited in two phases (Phase 1: Vietnamese-speaking women, n = 14; Phase 2: Arabic-speaking, n = 11). Three themes were developed in Phase 1: (1) DA content and reception; (2) linguistic attributes and cultural appropriateness; and (3) factors that improve the DAs’ impact. Three themes were developed in Phase 2: (1) varying perceptions of DA content; (2) linguistic and cultural suitability of information; and (3) impact of DA on decision making. Women from both phases identified areas for improvement: minimising the use of medical terminology, considering the cultural taboos associated with the word ‘breast’, and addressing remaining information gaps. Both language DAs were generally perceived as acceptable and useful in providing information about BR options and prompting women’s reflections about the suitability of BR as part of their treatment. The mean PrepDM score for Arabic-speaking women in Round 2 was 4.8/5 (SD = 0.3). Further work is needed to ensure that culturally adapted DAs take into account the myriad of information needs and health literacy levels. The key role of healthcare professionals in shared decision making among CALD populations should also be considered.

Introduction: Atypical or B3 lesions comprise a heterogeneous group of uncertain malignant potential. B3 lesions diagnosed on core biopsy are usually recommended for diagnostic open biopsy. Identifying factors which could allow conservative management of B3 lesions would be helpful in avoiding unnecessary surgery.The aim of this study was to identify the upgrade rate to malignancy for B3 core biopsy lesions and to compare characteristics of lesions which were malignant and benign at excision. Method: This retrospective study used data from BreastScreen New South Wales (NSW), Australia, of women who were diagnosed with B3 lesions on needle biopsy from 2011 to 2019. Results: During the study period, 1927 B3 lesions were included. The upgrade rate to malignancy was 26.4%. Of the malignant lesions on excision, 29.6% were invasive and 69.2% were in situ. The rates of upgrade to invasive cancer and DCIS varied substantially with the core biopsy lesion type.Lesions with atypia on core biopsy had significantly higher upgrade rates to malignancy at 34.7% compared to 13.6% for lesions without atypia (p < 0.0001). Lesions with malignant pathology were significantly larger than those with benign pathology (difference = 5.1 mm (95% CI 2.7–7.5 mm), p < 0.001). Conclusions: The overall upgrade rate of B3 lesions to malignancy was 26.4%. The majority of the lesions were upgraded to DCIS instead of invasive cancer. Upgrade rates varied by lesion type. Lesions with atypia had significantly higher upgrade rates to cancer compared to lesions without atypia. Malignant lesions were significantly larger than benign lesions.

Cancer-associated fibroblasts (CAFs) represent an important component of the tumour microenvironment and are implicated in disease progression. Two outstanding questions in cancer biology are how CAFs arise and how they might be targeted therapeutically. The calcium signal also has an important role in tumorigenesis. To date, the role of calcium signalling pathways in the induction of the CAF phenotype remains unexplored. A CAF model was generated through exogenous transforming growth factor beta 1 (TGFβ1) stimulation of the normal human mammary fibroblast cell line, HMF3S (HMF3S-CAF), and changes in calcium signalling were investigated. Functional changes in HMF3S-CAF calcium signalling pathways were assessed using a fluorescent indicator, gene expression, gene-silencing and pharmacological approaches. HMF3S-CAF cells demonstrated functionally altered calcium influx pathways with reduced store-operated calcium entry. In support of a calcium signalling switch, two voltage-gated calcium channel (VGCC) family members, CaV1.2 and CaV3.2, were upregulated in HMF3S-CAFs and a subset of patient-derived breast CAFs. Both siRNA-mediated silencing and pharmacological inhibition of CaV1.2 or CaV3.2 significantly impaired CAF activation in HMF3S cells. Our findings show that VGCCs contribute to TGFβ1-mediated induction of HMF3S-CAF cells and both transcriptional interference and pharmacological antagonism of CaV1.2 and CaV3.2 inhibit CAF induction. This suggests a potential therapeutic role for targeting calcium signalling in breast CAFs.

INTRODUCTION:This study aims to report on the surgical and radiotherapy patterns of breast cancer care in New South Wales (NSW) and Australian Capital Territory (ACT) in Australia, to identify factors that impact on utilisation of evidence-based treatment and to report on the overall survival (OS) rate and the influencing factors on OS.METHODS:Cancer registry data linked to hospital records for all patients with breast cancer diagnosis in NSW and ACT between 2009 and 2014 were used to calculate rates of breast conserving surgery (BCS), mastectomy, sentinel lymph node biopsy (SLNB), axillary lymph node dissection (ALND) and radiotherapy. Multivariate analysis used to identify factors that led to variations in care. 5-year OS was calculated and cox regression model assessed factors that influenced survival.RESULTS:Data for 30,337 patients were analysed. BCS and mastectomy rates were 64% and 36%, respectively. The SLNB, ALND and ALND after SLNB rates were 61.5%, 32.1% and 6.4%, respectively. Radiotherapy was utilised in 63%. Younger age, socio-economic disadvantage, longer distance to a radiotherapy facility and overseas place of birth were factors that predicted for increased rates of mastectomy and ALND. Radiotherapy was more likely to be utilised in later years of diagnosis, patients between 40-69 years old, and those who lived in major cities and closer to a radiotherapy facility. 5-year OS was 80.5%. Older patients, the socioeconomically disadvantaged and those advanced tumours had worse survival.CONCLUSION:Variations in breast cancer care continue to exist in certain patient groups that we identified. Targeted strategic planning and further research to identify other drivers of existing disparities remain a priority.

Therapy of hormone receptor positive breast cancer (BCa) generally targets estrogen receptor (ER) function and signaling by reducing estrogen production or by blocking its interaction with the ER. Despite good long-term responses, resistance to treatment remains a significant issue, with approximately 40% of BCa patients developing resistance to ET. Mutations in the gene encoding ERα, ESR1, have been identified in BCa patients and are implicated as drivers of resistance and disease recurrence. Understanding the molecular consequences of these mutations on ER protein levels and its activity, which is tightly regulated, is vital. ER activity is in part controlled via its short protein half-life and therefore changes to its stability, either through mutations or alterations in pathways involved in protein stability, may play a role in therapy resistance. Understanding these connections and how ESR1 alterations could affect protein stability may identify novel biomarkers of resistance. This review explores the current reported data regarding posttranslational modifications (PTMs) of the ER and the potential impact of known resistance associated ESR1 mutations on ER regulation by affecting these PTMs in the context of ET resistance.

BACKGROUND:The rates of breast reconstruction in Australian patients of culturally and linguistically diverse (CALD) backgrounds are currently unknown. This retrospective study determined the rate of breast reconstruction in women who had mastectomy as treatment for breast cancer at public hospitals in South Western Sydney Local Health District (SWSLHD) - a culturally diverse health district in New South Wales, Australia - and compared the rate of reconstruction in the CALD and non-CALD populations.METHODS:The demographic and clinical data of all female patients who had mastectomy with or without reconstruction for treatment of breast cancer at the five public hospitals in SWSLHD between January 2006 and December 2015 were obtained from the clinical information department of each hospital and from electronic medical records.RESULTS:The average rate of reconstruction in SWSLHD was 9.4% for 2006-2015. Although the reconstruction rate was higher among English-speaking women (9.9%) compared to women from a CALD background (8.6%), the difference was not statistically significant (P = 0.57). The type (autologous versus implant) and timing (immediate versus delayed) of reconstruction did not differ between groups (P = 0.19 and P = 0.22, respectively). The Index of Relative Socio-Economic Disadvantage was not significantly associated with reconstruction (P = 0.74). However, younger patients were more likely to have reconstruction (P < 0.0001) and patients with adjuvant therapy were more likely to have a delayed reconstruction (P = 0.01).CONCLUSION:This study found a low breast reconstruction rate in public hospitals in SWSLHD. The reconstruction rate did not differ between CALD or English-speaking patients, or between patients from diverse socio-economic backgrounds.

The plasticity of the tumour microenvironment is a key contributor to cancer development and progression. Here, we present a bioengineered breast tumour angiogenesis model comprised of mammary derived epithelial, endothelial and fibroblast cells, to dissect the mechanisms of cancer-associated fibroblasts (CAFs) on microvascular-like network formation and epithelial spheroid morphology. Primary patient-derived mammary endothelial cells, normal breast fibroblasts (NBF, patient matched) and CAFs were cultured within three-dimensional (3D) semi-synthetic hydrogels where CAFs promoted an increase in the density and morphology of the microvascular-like network. The mammary microenvironment also increased the number of MCF-10a epithelial spheroids when compared with a non-mammary microenvironment, and a malignant mammary microenvironment resulted in further morphological differences in the epithelial spheroids. The morphological changes observed following interactions between breast CAFs and endothelial cells, highlight the plasticity of the malignant stroma in tumour vascularisation. Our in vitro bioengineered breast cancer microenvironment provides a robust model to study cell-cell and cell-matrix interactions. Statement of Significance In recent years there has been an increase in the sophistication of 3D culture models, however less attention has been paid to the cell source utilised. In this study, we describe the influence of a normal and malignant stromal microenvironment on vessel-like behaviour in a 3D model. Using a semi-synthetic hydrogel, we studied the effects of mammary-derived cancer-associated fibroblasts and normal fibroblasts on human umbilical vein endothelial cells or human mammary microvascular endothelial cells. An increase in vessel-like network and epithelial cell density was seen in a mammary versus non-mammary microenvironment. This study highlights the importance of using tissue-specific endothelial cells in cancer research and demonstrates the microenvironmental impact of fibroblasts on endothelial and epithelial growth and morphology.

Breast cancer is a heterogeneous disease displaying different histopathological characteristics, molecular profiling and clinical behavior. This study describes the expression patterns of senescence markers P53, DEC1 and DCR2 and assesses their significance on patient survival as a single or combined marker with P16 or P14 using breast cancer progression series. One thousand and eighty (1080) patients with primary invasive ductal carcinoma, no special type, were recruited through an 11-year retrospective study period. We constructed tissue microarrays of normal, benign hyperplasia, ductal carcinoma in situ and invasive ductal carcinoma from each patient and performed immunohistochemical staining to study the protein expression. Statistical analysis includes Pearson chi-square, Kaplan-Meier log ran test and Cox proportional hazard regression were undertaken to determine the associations and predict the survival outcomes. P53, DEC1 and DCR2 expression correlated significantly with normal, benign, premalignant and malignant tissues with (p<0.05). The expression profile of these genes increases from normal to benign to premalignant and plateaued from premalignant to malignant phenotype. There is a significant association between P53 protein expression and age, grade, staging, lymphovascular invasion, estrogen receptor, progesterone receptor and HER2 whereas DCR2 protein expression significantly correlated with tumour grade, hormone receptors status and HER2 (p<0.05 respectively). P53 overexpression correlated with increased risk of relapse (p = 0.002) specifically in patients who did not receive hormone therapy (p = 0.005) or chemotherapy (p<0.0001). The combination of P53+/P16+ is significantly correlated with poor overall and disease-free survival, whereas a combination of P53+/P14+ is associated with worse outcome in disease-free survival (p<0.05 respectively). P53 overexpression appears to be a univariate predictor of poor disease-free survival. The expression profiles of DEC1 and DCR2 do not appear to correlate with patient survival outcomes. The combination of P53 with P16, rather P53 expression alone, appears to provide more useful clinical information on patient survival outcomes in breast cancer.

Calcium (Ca2+) influx pathways are remodelled in a variety of disease states, and alterations in the expression of specific Ca2+ permeable ion channels are a feature of some breast cancer subtypes. However, no studies have yet assessed possible alterations in Ca2+ influx pathways in the context of cancer-associated fibroblasts (CAFs), which are important in the tumor microenvironment and disease progression. The aim of this study was to identify possible changes in the nature of Ca2+ influx in CAFs and to define the role of Ca2+ signaling in the induction of breast CAFs. Levels of mRNA for voltage-gated and store-operated Ca2+ entry (SOCE) components were assessed in paired normal and CAF patient samples using qRT-PCR. The immortalised human mammary fibroblast cell line HMF3S, was treated with transforming growth factor beta (TGFβ) to induce a CAF phenotype (HMF3S-CAF) as confirmed by the expression of alpha smooth muscle actin (αSMA). HMF3S-CAF and HMF3S were also compared for expression of Ca2+ channels using qRT-PCR and functional store operated Ca2+ entry (SOCE) using a Fluorescence Imaging Plate Reader (FLIPR) Ca2+ assay. Specific Ca2+ channel subtypes were pharmacologically inhibited during TGFβ treatment to assess their role in CAF induction. Ca2+channel levels were altered in CAF patient samples compared to their paired controls and also in TGFβ-treated HMF3S cells. Voltage-gated Ca2+channel inhibitors significantly decreased TGFβ-mediated CAF activation. These data suggest that Ca2+ signaling is remodeled in CAFs and that the Ca2+ signal is important in breast CAF induction.Citation Format: Greg Monteith, Francisco Sadras, Teneale Stewart, Melanie Robitaille, Priyakshi Kalita-de Croft, Patsy Soon, Jodi Saunus, Sunil Lakhani, Sarah Roberts-Thomson. Remodeling of calcium influx pathways in models of cancer associated fibroblasts in breast cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 99.

Objective: Little is known about the experience of women of culturally and linguistically diverse (CALD) backgrounds in relation to breast reconstruction following mastectomy as treatment for their breast cancer. The aim of this study was to explore the factors that influenced Vietnamese- and English-speaking women's decisions about breast reconstruction post-mastectomy for their breast cancer, in Australia.Design: The participants in this study comprised of Vietnamese-speaking women of Vietnamese heritage, and English-speaking women from mixed ethnicities (Vietnamese included). In this qualitative study, Vietnamese-speaking and English-speaking women who had breast cancer treated by mastectomy with or without breast reconstruction participated in in-depth interviews. Interviews were undertaken in the woman's chosen language (Vietnamese or English), audio-recorded, transcribed/translated and analysed using thematic analysis.Results: Fourteen Vietnamese-speaking and 13 English-speaking patients were recruited. Participants identified age, lack of information, concerns regarding surgical procedure, fears about complications and cancer recurrence as barriers to breast reconstruction. Many more Vietnamese-speaking participants identified lack of information about breast reconstruction as a barrier compared to English-speaking participants. Both groups described the ability to wear clothing of their choice, partner influence, and the need to feel 'normal' as facilitators to having breast reconstruction. Vietnamese-speaking participants in particular identified doctor recommendation of breast reconstruction as a major facilitator.Conclusion: Lack of information about reconstruction was a persistent theme, though it was identified by more Vietnamese women as a barrier to having breast reconstruction. The results reinforce the importance of doctors' recommendations in helping particularly the Vietnamese women make an informed decision about reconstruction following mastectomy as treatment for their breast cancer.

Background & purpose: In breast conservation surgery (BCS) correct interpretation of margin status is imperative to avoid unnecessary re-excisions. Evolution of practice to the SSO-ASTRO guidelines1 of no ink on tumour margin for invasive disease and 2mm for insitu disease should decrease re-excision rates. The aim of this paper is to assess current re-excision rates and pathological factors that correlate with a higher incidence of residual cancer in re-excisions.

Objectives. The most widely used approach for the clinical management of women with high-grade serous ovarian cancer (HGSOC) is surgery, followed by platinum and taxane based chemotherapy. The degree of macroscopic disease remaining at the conclusion of surgery is a key prognostic factor determining progression free and overall survival. We sought to develop a non-invasive test to assist surgeons to determine the likelihood of achieving complete surgical resection. This knowledge could be used to plan surgical approaches for optimal clinical management. Methods. We profiled 170 serum microRNAs (miRNAs) using the Serum/Plasma Focus miRNA PCR panel containing locked nucleic acid (LNA) primers (Exiqon) in women with HGSOC (N = 56) and age-matched healthy volunteers (N = 30). Additionally, we measured serum CA-125 levels in the same samples. The HGSOC cohort was further classified based on the degree of macroscopic disease at the conclusion of surgery. Stepwise logistic regression was used to identify predictive markers. Results. We identified a combination of miR-375 and CA-125 as the strongest discriminator of healthy versus HGSOC serum, with an area under the curve (AUC) of 0.956. The inclusion of miR-210 increased the AUC to 0.984; however, miR-210 was affected by hemolysis. The combination of miR-34a-5p and CA-125 was the strongest predictor of completeness of surgical resection with an AUC of 0.818. Conclusion. A molecular test incorporating circulating miRNA to predict completeness of surgical resection for women with HGSOC has the potential to contribute to planning for optimal patient management, ultimately improving patient outcome. (C) 2017 Elsevier Inc. All rights reserved.

Ductal carcinoma in situ (DCIS), invasive breast cancer (IBC) and lympho-vascular invasion (LVI) represent distinct stages in breast cancer progression with different clinical implications. Altered microRNA (miRNA) expression may play a role in mediating the progression of DCIS to IBC and LVI. The aim of this pilot study was to investigate whether differential miRNA expression could play a role in breast cancer progression. Cancer cells from DCIS, IBC and LVI were microdissected from formalin fixed paraffin embedded (FFPE) tissue of five breast cancer samples. MiRNA profiling of extracted RNA was performed using the TaqMan® Array Human MicroRNA Cards A and B v3.0. Candidate miRNAs and gene targets were validated by qPCR. 3D culture of MCF10A, MCF10DCIS.com and T47D cells were used as models for normal, DCIS and IBC. Immunohistochemistry of candidate genes was performed on FFPE 3D cell cultures as well as on tissue microarray which included cores of DCIS and IBC samples. MiR-150, miR-126 and miR-155 were found to be more highly expressed in IBC and LVI compared to DCIS. Gene targets of these miRNAs, RhoA, PEG10 and MYB, were found to be more highly expressed in DCIS compared to IBC by qPCR and in MCF10A and MCF10DCIS.com cells compared to T47D cells by immunohistochemistry. There was no difference in intensity of staining of RhoA by immunohistochemistry in DCIS versus IBC samples on tissue microarray. In this pilot study, we found evidence to support a potential role for variation in miRNA levels in the transition from DCIS to IBC.

microRNAs have emerged as powerful regulators of many biological processes, and their expression in many cancer tissues has been shown to correlate with clinical parameters such as cancer type and prognosis. Present in a variety of biological fluids, microRNAs have been described as a ‘gold mine’ of potential noninvasive biomarkers. Release of microRNA content of blood cells upon hemolysis dramatically alters the microRNA profile in blood, potentially affecting levels of a significant number of proposed biomarker microRNAs and, consequently, accuracy of serum or plasma-based tests. Several methods to detect low levels of hemolysis have been proposed; however, a direct comparison assessing their sensitivities is currently lacking. In this study, we evaluated the sensitivities of four methods to detect hemolysis in serum (listed in the order of sensitivity): measurement of hemoglobin using a Coulter® AcT diff™ Analyzer, visual inspection, the absorbance of hemoglobin measured by spectrophotometry at 414 nm and the ratio of red blood cell-enriched miR-451a to the reference microRNA miR-23a-3p. The miR ratio detected hemolysis down to approximately 0.001%, whereas the Coulter® AcT diff™ Analyzer was unable to detect hemolysis lower than 1%. The spectrophotometric method could detect down to 0.004% hemolysis, and correlated with the miR ratio. Analysis of hemolysis in a cohort of 86 serum samples from cancer patients and healthy controls showed that 31 of 86 (36%) were predicted by the miR ratio to be hemolyzed, whereas only 8 of these samples (9%) showed visible pink discoloration. Using receiver operator characteristic (ROC) analyses, we identified absorbance cutoffs of 0.072 and 0.3 that could identify samples with low and high levels of hemolysis, respectively. Overall, this study will assist researchers in the selection of appropriate methodologies to test for hemolysis in serum samples prior to quantifying expression of microRNAs.

Introduction: Seroma formation in breast cancer patients who have undergone axillary lymph node dissection (ALND) is a source of significant discomfort and morbidity. We aimed to ascertain seroma incidence after ALND, when Harmonic Focus (HF) scalpel is used for dissection instead of conventional diathermy (CD).Methods(and patients): This retrospective study was carried out in a single hospital over 6 years. Patients were allocated into HF group (HFG) or CD group (CDG). Seroma volume, hospital stay, and complications were evaluated.Results: Of 94 patients, 42 were in the HFG and 52 in the CDG. Two day median seroma volume was 205 ml (IQR 95-265) for HF, and 227.5 ml (IQR 149-385) for CD. The total median seroma output was 270 ml (IQR 160-478) for HF, and 385 ml (IQR 220-558) for CD. No statistically significant differences between HFG and CDG were identified in these data, as well as patient demographics, operative time, and complication rates. Duration of surgery >2.5 h increased seroma formation (p < 0.001). Mastectomy and ALND increased seroma formation compared to wide local excision (WLE) and ALND (p < 0.05). Nodal involvement, number of lymph nodes resected, and extra nodal spread did not influence seroma formation.Discussion(and conclusion): In our hands, HF use was not superior to CD in limiting seroma formation in ALND for breast cancer. Increased seroma formation in surgeries >2.5 h in duration is commensurate with surgeries involving mastectomy and ALND (>2.5 h in our study), which entails greater and sustained tissue and lymphovascular trauma. (c) 2016 IJS Publishing Group Ltd. Published by Elsevier Ltd. All rights reserved.

Abstract Fibroblasts represent one of the predominant stromal cell populations present in the breast tumor microenvironment. Cancer-associated fibroblasts found growing in close proximity to the tumor site are thought to influence tumor behavior. While a number of protein and mRNA markers showing differential expression between cancer-associated and non-cancer associated fibroblasts have been proposed, current understanding of the phenotypic differences between these two cell populations remains incomplete. Calcium signaling plays an important role in each of the cancer hallmarks and is altered in a variety of disease states including cardiovascular disease. The aim of this study was to investigate the potential remodeling of the calcium signal and calcium channel and pump expression as a consequence of the transition from a normal to cancer-associated phenotype in human breast fibroblasts. To investigate expressional changes, RNA was isolated from primary cultures of matched normal and cancer-associated fibroblasts established from human breast cancer tissue specimens. Real time RT-PCR was used to assess mRNA levels of a total of 36 proteins involved in the movement of Ca2+ into and out of the cytoplasmic space, and included different classes of plasma membrane localized Ca2+ channels, as well as Ca2+ pumps of intracellular organelles. To further study potential differences in Ca2+ signaling between normal and cancer-associated fibroblast phenotypes, the immortalized human breast fibroblast line HMF3S was treated with transforming growth factor beta 1 (TGFβ1) (0, 0.01, 0.1, 1 and 10 ng/mL, 48 h), a growth factor implicated in the tumor microenvironment and myofibroblast differentiation. Successful TGFβ1-mediated activation of fibroblasts to a cancer-associated phenotype was confirmed by induction of smooth muscle alpha actin (SMαA) protein via immunoblotting. Real time RT-PCR was used to assess mRNA levels of classes of Ca2+ channels and pumps showing altered expression in patient matched normal and cancer-associated fibroblast pairs. In addition to assessing expression changes, potential functional differences in intracellular Ca2+ signaling profiles of HMF3S cells treated with TGFβ1 were assessed using a fluorometric imaging plate reader (FLIPRTETRA) and cells loaded with the Ca2+ sensitive indicator Fluo-4. Using both clinical samples, and an in vitro model of cancer-associated fibroblasts, our findings reveal a differential remodeling of plasma membrane calcium channels and organellar pumps of different classes in cells representative of cancer-associated relative to non-cancer associated fibroblasts. In addition to expression changes, there also appears to be a functional remodeling of the calcium signal in HMF3S fibroblasts induced to transition from a normal to cancer-associated phenotype by TGFβ1. This is the first study to assess changes in calcium pumps, channels and channel regulators, as well as remodeling of the calcium signal, in breast cancer-associated fibroblasts. This work may suggest that the breast cancer-associated fibroblast phenotype is associated with altered Ca2+ signaling. Citation Format: Teneale A. Stewart, Patsy S. Soon, Sarah J. Roberts-Thomson, Gregory R. Monteith. Assessment of gene expression of calcium pumps, channels, and channel regulators in human breast cancer-associated fibroblasts. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Breast Cancer Research; Oct 17-20, 2015; Bellevue, WA. Philadelphia (PA): AACR; Mol Cancer Res 2016;14(2_Suppl):Abstract nr B57.