bluuebunny/crossref_metadata_2025 huggingface dataset:
Abstract P6-01-20: Effects of local and radiation enhanced TGFβ on the invasive nature of inflammatory breast cancer cells
Authors: Barkataki S , van Golen K
Published: March 2017

Inflammatory Breast Cancer (IBC) is the deadliest form of epithelial breast cancer, accounting for ~10% of breast cancer deaths in the United States. A hallmark of IBC is the formation intralymphatic emboli that are known to be chemotherapy and radiation resistant and contribute to rapid metastasis. This form of breast cancer progresses very quickly, expressing aggressive behavior. IBC and melanoma share a number of similarities in disease presentation and progression. Both spread via dermal lymphatics, form intralymphatic emboli and have a propensity to form cutaneous metastases. Melanoma can also present as “inflammatory melanoma”, which resembles IBC phenotypically. Thus, new leads for studying cutaneous metastasis can be gathered from the melanoma literature. Studies demonstrate a role for transforming growth factor beta (TGFβ) in the etiology of melanoma cutaneous metastasis. TGFβ promotes tumor cell invasion and its expression can be induced in the stroma by radiation treatment. Recently, our lab has demonstrated low expression of TGFβ in IBC patients, which we believe promotes cohesive invasion of IBC cells. Stimulation of IBC cells with 2ng/ml of TGFβ causes altered tumor cell behavior such as stimulating single cell invasion. The invasion of KPL4, SUM149 and MDA-MB231 cell lines were significantly higher in TGFβ stimulated cells compared to non-stimulated cells. As in melanoma cells we hypothesize that radiation enhanced local TGFβ production in the stroma. We radiated normal human epidermal fibroblasts cells with 0gy, 0.5gy, 1.0gy, 2.5gy and 5.0gy intensity and observed that the invasion was significantly higher in 1.0gy, 2.5gy and 5.0gy. We have also looked at the levels of TGFβ-1 in different conditioned medium. ELISA results don't show significant level of increase in TGFβ-1. Since there are two more TGFβ receptors in the TGFβ pathway (TGFβ -2 TGFβ -3), next I will look at the level of TGFβ-2 and 3 on the different intensity of radiation-conditioned medium. Our prediction is that the increase in the invasion of IBC cells is because of TGFβ, which alters the cohesive nature of IBC cells, and enhance single cell invasion. Moreover, radiation increases TGFβ levels in the stroma, which is responsible for rapid metastasis of IBC cells to the skin.

Citation Format: Barkataki S, van Golen K. Effects of local and radiation enhanced TGFβ on the invasive nature of inflammatory 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 P6-01-20.
Abstract P6-02-06: Metabolomic profiling of breast cancer and adjacent tissue
Authors: Santos JR , Brentanni MM , Tortelli T , Dale I , Waitzberg A , Waitzberg D , Ravacci G
Published: March 2017

Breast cancer (BC) is the most common cause of death among women worldwide. Nowadays, research directed toward the discovery of cancer molecular characteristics has extended into various biological aspects, from early investigations of cancer genomics and proteomics to recent efforts in cancer metabolomics. We consider that breast cancer cells display significantly altered cellular processes, and thus metabolites, compared to normal cells. In this regard, the application of metabolomics towards cancer research can led to the discovery of metabolite cancer biomarkers and the identification of target therapeutics. Methods: Metabolomics signature was extracted from primary BC and adjacent tissue samples from a cohort of 182 breast cancer patients from the Institut Gustave-Roussy and Institute Curie – Paris, University of Debrecen – Hungary, and University of Tartu – Estonia. The Biocrates Life Science® company, performed the metabolomics analysis using the Absolute IDQ p180 kit. Statistical analysis was performed by MetaboAnalyst 3.0 software (p <0.05). Results: We observed 99 differential metabolites between breast tumor and adjacent tissues (p<0,05). In the tumor tissue we observed an increase of glycolysis, glutamine uptake and synthesis, glutamate production, intermediates for redox homeostasis, as well reduction in tricarboxylic acid cycle and β –oxidation impairment. Together, these pathways, favor lipogenesis with a consequent increase in saturated fatty acids and cholesterol synthesis for the formation of membranes and lipid rafts in tumors. The increase in rafts in tumors maintains proliferation signaling via membrane receptors, making them important biomarkers. Conclusion: Metabolomics analysis is useful in identifying differential metabolites between breast cancer and adjacent tissue. In this scenario, cancer cells may be dependent on some metabolites for its development, making them therapeutically valuable biomarkers.

Citation Format: Santos JR, Brentanni MM, Tortelli T, Dale I, Waitzberg A, Waitzberg D, Ravacci G. Metabolomic profiling of breast cancer and adjacent tissue [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 P6-02-06.
Abstract P6-05-03: Investigating the effects of low-dose mixtures of environmental contaminants on breast cancer initiation
Authors: Silva E , Ermler S , Widschwendter M , Maund PR
Published: March 2017

This abstract was not presented at the symposium.
Abstract P6-05-05: The expression of lysyl oxidase and fibrotic focus is related to inflammation in breast cancer
Authors: Park SH , Jeong YJ , Bong JG , Oh HK
Published: March 2017

Background: Lysyl oxidase (LOX) is an extracellular matrix enzyme that catalyzes the

cross-linking of collagens or elastin. Our hypothesis is that LOX contributes to the formation

of a fibrotic focus (FF), which is related to inflammation in breast carcinogenesis.

In this study, we analyzed the association between the expression LOXs and FF, and

investigated prognostic significance in breast cancer.

Methods: Tissue microarrarys were constructed from the specimens of 444 patients

with primary invasive breast cancer. Immunohistochemical staining for LOX, LOXlike

(LOXL)-, LOXL-2 and LOXL-3 was performed. The status of FF within the tumor

was assessed. The number of CD4+ T cells, CD8+ T cells, CD68+ macrophages was

counted, and intratumoral and peritumoral lymphocyte infiltration were evaluated.

The clinicopathologic characteristics of the patients were analyzed.

Result: The percentage of positive FF was 39.2% and positive rate of LOX expression

was 50% in primary breast cancer tissues. FF was found to be significantly associated

with intratumoral and peritumoral inflammation, lymph node metastasis, high histologic

grade, larger tumor size. LOX was associated with intratumoral and peritumoral

inflammation, CD8+ T cells and menopausal status. LOXL-3 was significantly associated

with positive expression of ER and PR, and molecular subtype.

Conclusions: FF and the expression of LOX were associated with inflammation in

breast cancer in this study. Our results suggest that LOXs may contribute to the formation

of a FF indirectly in relation with inflammation in breast cancer. Further studies

are needed to clarify the role of LOXs, FF and inflammation in tumorigenesis and

prognostic value of them in breast cancer.

Citation Format: Park SH, Jeong YJ, Bong JG, Oh HK. The expression of lysyl oxidase and fibrotic focus is related to inflammation 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 P6-05-05.
Abstract P6-07-30: Identifying novel glycosylation markers in Her2+ breast cancer using MALDI mass spectrometry
Authors: Scott DA , Angel P , Xu H , Drake R , Yeh E
Published: March 2017

Breast cancer characterized by human epidermal growth factor receptor 2 (HER2) overexpression represents approximately 25-30% of all breast cancer cases. Many patients acquire resistance to current chemotherapies, leading to a more aggressive disease state with severe clinical outcomes. Lapatinib, a first generation tyrosine kinase inhibitor of HER2 and EGFR (epidermal growth factor receptor), is commonly used to treat HER2+ breast cancer. Resistance to lapatinib is steadily increasing among HER2+ patients, highlighting the need for therapy development. Identifying markers that predict treatment response or potential drug targets could enhance treatment efficacy and patient survival. To investigate this, we have used MALDI mass spectrometry to identify N-linked glycans specific to human breast cancer cell lines with known resistance and sensitivity to lapatinib treatment, JIMT-1 (resistant) HER2+ and BT474 (sensitive) HER2+. After different lapatinib dose and time course experiments, N-linked glycans were isolated and comparatively profiled by high resolution MALDI mass spectrometry. Differences in the levels of fucosylation and sialylation of glycans from sensitive and resistant cell lines, before and after treatment, were evaluated. In addition, mouse xenograft tumor tissues derived from the same cell lines treated with and without lapatinib were processed for on-tissue imaging of N-glycans using a MALDI imaging mass spectrometry approach. Tissues from HER2+ human breast tumors were also imaged with the same MALDI imaging approach. Cumulatively, these preliminary studies have identified novel glycosylation patterns associated with lapatinib treatment sensitivity and resistance.

Citation Format: Scott DA, Angel P, Xu H, Drake R, Yeh E. Identifying novel glycosylation markers in Her2+ breast cancer using MALDI mass spectrometry [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 P6-07-30.
Abstract P6-09-38: Interaction between body mass index and hormone receptor status as a prognostic factor in node-positive breast cancer
Authors: Chung IY , Lee JW , Lee JS , Park YR , Lee Y , Lee SB , Kim HJ , Ko BS , Son BH , Ahn SH
Published: March 2017

Purpose: The aim of this study was to investigate the interaction between BMI at breast cancer diagnosis and the various factors including hormone-receptor, menopausal and nodal status, and to find a specific subgroup where BMI has an effect on breast cancer prognosis.

Methods: We retrospectively analyzed the data of 8,763 non-metastatic invasive breast cancer patients from the Asan Medical Center's research database. Overall survival (OS) and breast cancer-specific survival (BCSS) among BMI groups were compared using the Kaplan-Meier method and Cox proportional hazard model with interaction term.

Results: Only in node-positive breast cancer, there was a significant interaction between obesity (BMI ≥ 30.0 kg/m2) at diagnosis and positive hormone receptor which showed worse overall survival (OS) and breast cancer specific survival (BCSS) than normal weight patients (adjusted hazard ratio [HR] = 1.65, 95% confidence interval [CI] = 1.01 to 2.69 and HR = 1.90, 95% CI = 1.15 to 3.15, respectively). Underweight (BMI<18.50 kg/m2) which interacted with negative hormone receptor status in node-positive breast cancer was associated with decreased OS (HR = 2.01, 95% CI = 1.02 to 3.98) and BCSS (HR = 2.15, 95% CI = 1.08 to 4.26). There was no significant interaction between BMI and hormone receptor status in node-negative setting and BMI did not interact with menopausal status in any population.

Conclusions: BMI interacts with hormone receptor status in node positive setting, thereby playing a role in the breast cancer prognosis.

Citation Format: Chung IY, Lee JW, Lee JS, Park YR, Lee Y, Lee SB, Kim HJ, Ko BS, Son BH, Ahn SH. Interaction between body mass index and hormone receptor status as a prognostic factor in node-positive 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 P6-09-38.
Abstract P6-09-47: The development of personalized diagnostic tests and therapeutic strategies in breast cancer
Authors: Kutasovic JR , Rozali E , Miranda M , Lakhani SR , Al-Ejeh F
Published: March 2017

Despite some improvement in the overall survival rates of breast cancer, it remains as a leading cause of cancer-related deaths in women. Currently, we are unable to accurately predict patients' response to therapies and their long-term outcome. We developed and patented a 275-gene signature based on in silico meta-analysis of global transcriptome profiles (approximately 10,000 cases) that can predict which patients suffer from aggressive disease and succumb to their disease within 5 years of diagnosis. This test, the integrated Breast Cancer Recurrence (iBCR) score outperformed every clinicopathological indicator available in three independent, large cohorts of breast cancer. The iBCR can also predict the likelihood of response to standard treatments and which emerging targeted therapies should be added to an individual's treatment regime to improve outcomes. In addition, 21 of the genes in this signature are novel potential drug targets that have not previously been described in aggressive breast tumours. We performed a pilot study using the NanoString nCounter Dx platform to measure the expression of the top 125 genes within the signature in a cohort of 48 patients. We have validated with 100% accuracy the prognostic power of the iBCR in the Queensland Follow Up (QFU) cohort with 25 years of follow up (p<0.0001), irrespective of clinicopathological features. Our pilot study using the Nanostring platform successfully counted mRNA molecules from samples that averaged 26.8 years of age (range 24 – 29 years), with an average RNA Integrity (RIN) score of 2.4. Future work will expand this test to the full 275-gene set across 500 patients from the QFU cohort. In vitro siRNA screening of the 21 novel genes revealed that at least 10 of these genes are required for breast cancer cell survival. We have started validation of the top 4 hits and these studies confirm the requirement of these genes in breast cancer progression. These data will pave the way towards the study of these genes as new drug targets. Collectively, our test addresses the significant issue of heterogeneous responses to breast cancer treatment. The iBCR platform aims to improve both patients' clinical outcome and quality of life by directing more appropriate treatment with greater likelihood of success, and preventing overtreatment for those with a less aggressive tumor type.

Citation Format: Kutasovic JR, Rozali E, Miranda M, Lakhani SR, Al-Ejeh F. The development of personalized diagnostic tests and therapeutic strategies 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 P6-09-47.
Abstract P6-11-01: CDK2 inhibition prevents ERpS294 and restores the ability of tamoxifen to induce regression in breast tumors expressing mutant ESR1
Authors: Benz C , Scott G , Chu D , Malato J , Hann B , Park B
Published: March 2017

This abstract was withdrawn by the authors.
Abstract P6-11-07: Methylation of BRCA1 and response to the PARP inhibitor veliparib
Authors: Puhalla SL , Katz TA , Diergaarde B , Yu J , Oesterreich S
Published: March 2017

This abstract was not presented at the symposium.
Abstract P6-11-14: Src homology 2 domain containing transforming protein 1 and steroid receptor coactivator-3 as novel targets for triple-negative breast cancer
Authors: Chang Y-F , Wang Y , Greene GL
Published: March 2017

Triple-negative breast cancer (TNBC) accounts for 15-20% of breast cancer cases and is more prevalent among young women and African American women. Metastasis and chemoresistance remain significant challenges in TNBC. The development of targeted therapies for TNBC may dramatically improve the survival of patients and the quality of life. An adaptor protein, Src Homology 2 Domain Containing Transforming Protein 1 (SHC1) and steroid receptor coactivator-3 (NCOA3) are found to be overexpressed in breast cancers and important in the regulation of tumor progression and metastasis and drug resistance in ER+ breast cancer. The elevated SHC1 or NCOA3 correlates with poor prognosis in breast cancer patients. However, the biological significance of SHC1 and NCOA3 in TNBC is not well known. In this study, we performed siRNA-mediated knockdown to determine the importance of SHC1 and NCOA3 in the cell proliferation and death of TNBC. The effect of siSHC1 or siNCOA3 on the invasion and chemoresistance was also assayed in vitro. We found that although SHC1 and NCOA3 knockdown slightly inhibited the tumor growth of TNBC cells (MDA-MB-231, BT549, and HS578T), siSHC1 + paclitaxel and siNCOA3 + paclitaxel significantly decreased cell proliferation and increased caspase-3/7 activity in vitro, compared to drug alone. In vivo studies using MDA-MB-231 xenografts and a TNBC PDX model also showed that siSHC1 and siNCOA3 significantly augmented paclitaxel-induced tumor shrinkage. In invasion assays, SHC1 and NCOA3 knockdown significantly decreased the invasion of TNBC cells. These results suggest that targeting SHC1 and NCOA3 is worth investigating for the treatment of TNBC.

Citation Format: Chang Y-F, Wang Y, Greene GL. Src homology 2 domain containing transforming protein 1 and steroid receptor coactivator-3 as novel targets for triple-negative 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 P6-11-14.
Abstract P6-12-05: Targeting estrogen receptor mutations for treatment of endocrine therapy resistance in breast cancer
Authors: Alluri PG , Larios JM , Malik R , Hayes DF , Speers CW , Rae JM , Chinnaiyan AM
Published: March 2017

This abstract was withdrawn by the authors.
Abstract P6-12-07: Neutralization of BCL2/XL enhances the cytotoxicity of T-DM1 in vivo
Authors: Zoeller JJ , Dillon DA , Bronson RT , Sampath D , Leverson J , Brugge JS
Published: March 2017

This abstract was not presented at the symposium.
Abstract PD2-06: Mismatch repair deficiency induces endocrine therapy resistance in breast cancer
Authors: Haricharan S , Schmelz J , Schmidt C , Singh P , Holloway K , Anurag M , Suman V , Olson JA , Hunt K , Bainbridge MN , Ellis MJ
Published: March 2017

Estrogen receptor positive (ER+) breast cancer accounts for the majority of breast cancers diagnosed worldwide but fortunately, outcomes are markedly improved by pharmacological interventions that interrupt ER function. Unfortunately, suppression of relapse risk from early stage disease with endocrine therapy (anti-estrogens or aromatase inhibitors) is only ∼50%, and for advanced disease, pan endocrine therapy resistance is almost inevitable. While many mechanisms for intrinsic and acquired endocrine resistance have been explored, links between defects in DNA repair, the fundamental drivers of cancer pathogenesis, and endocrine therapy resistance have been understudied. Here we link mismatch repair (MMR) deficiency to poor clinical outcomes in ER+ breast cancer using whole exome DNA sequencing data and mRNA expression analysis. We subsequently demonstrate that MMR deficiency bypasses ER dependent cell cycle regulation through disruption of Chk2/p21-mediated feedback inhibition of CDK4 in breast cancer cell lines and tumor samples, as well as through correlations with human clinical data. We also show that pharmacological targeting of CDK4 significantly inhibits growth of MMR-deficient ER+ breast cancer cells in vitro and in vivo. This mechanism provides a new explanation for why endocrine therapy resistant ER+ breast cancers can respond to CDK inhibition and suggests that primary tumors exhibiting MMR deficiency are good candidates for adjuvant CDK4 inhibitor treatment.

Citation Format: Haricharan S, Schmelz J, Schmidt C, Singh P, Holloway K, Anurag M, Suman V, Olson JA, Hunt K, Bainbridge MN, Ellis MJ. Mismatch repair deficiency induces endocrine therapy resistance 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 PD2-06.
Abstract PD8-01: Race and age differences in PAM50 biomarker status in the Carolina breast cancer study
Authors: Troester MA , Sun X , Allott EH , Kit C-K , Thorne L , Mathews M , Cohen SM , Geradts J , Kirk E , Li Y , Hu Z , Robinson W , Hoadley KA , Reeder-Hayes K , Earp S , Olshan AF , Carey LA , Perou CM
Published: March 2017

Background: African American breast cancer patients have lower relative frequency of hormone receptor (HR)-positive/HER2-negative disease and higher subtype-specific mortality. However, few population-based studies have RNA-based subtyping data, and racial differences in the biology of HR-positive/HER2-negative tumors are not well understood.

Methods: Using data and biospecimens from the Carolina Breast Cancer Study (CBCS) Phase 3 (2008-2013), we classified approximately 1,000 invasive breast cancers according to PAM50 subtype and two risk of recurrence scores (ROR-P and ROR-PT). Relative frequency of Luminal A, Luminal B, Her2-enriched, and Basal-like subtypes and ROR scores (low/medium/high) were compared by race (blacks vs. whites) and age (≤50 years vs. >50 years), overall and among HR-positive/HER2-negative cases.

Results: Black women of all ages had significantly higher relative frequency of Basal-like breast cancer (36 and 31% in blacks vs. 18 and 15% in whites; younger and older, respectively) and lower frequency of Luminal A breast cancer (26 and 34% in blacks vs. 43 and 52% in whites; younger and older, respectively). Frequency of Luminal B and HER2-enriched breast cancer did not vary by race or age. Among clinically HR-positive, HER2-negative cases, Luminal A subtype comprised only half of the cases among black women, and was significantly less common than among white women (51% vs 60% in whites, p<0.05). Black women with HR-positive/HER2-negative disease also had significantly higher ROR scores (ROR-P medium or high 82% vs. 66% in whites, p=0.01; ROR-PT medium or high 85% vs. 69% in whites, p<0.01).

Conclusions: Multi-gene assays highlight disparities in frequency of aggressive, poorer prognosis tumor subtypes and implicate differences in tumor biology as an important contributor to mortality disparities among HR-positive/HER2-negative patients.

Citation Format: Troester MA, Sun X, Allott EH, Kit C-K, Thorne L, Mathews M, Cohen SM, Geradts J, Kirk E, Li Y, Hu Z, Robinson W, Hoadley KA, Reeder-Hayes K, Earp S, Olshan AF, Carey LA, Perou CM. Race and age differences in PAM50 biomarker status in the Carolina breast cancer study [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 PD8-01.
Abstract PL3: Global cost of cancer care
Authors: Bach PB
Published: March 2017

According to a 2014 IMS health report, cancer drugs represent 26% of specialty drug spending, more than $32B in the US in 2014, and specialty drug spending is growing faster than any other sector of healthcare. Unsurprisingly, cancer drugs are the largest sub-segment. These price rises are not just an economic curiosity. Because of the structure of many insurance products, the co-insurance on these expensive drugs is crippling, impacting access on a large scale. A recent study reported that more than 10% of Medicare beneficiaries with a cancer diagnosis face out of pocket expenses exceeding their incomes. In a nationally representative survey conducted in 2006, twenty-five percent of patients reported exhausting all or most of their savings. In a recent analysis of discontinuation rates among patients taking Gleevec and other highly effective drugs for Chronic Myeloid Leukemia, patients with high copayments were 42% more likely to be nonadherent.

Dr. Bach has researched this problem with a data-driven set of related projects that aim to achieve substantive change to pricing of and access to specialty drugs, beginning with cancer drugs because of established expertise, but expanding to other analogous areas rapidly.

In 2009, Dr. Bach's team began tracking the launch prices of new cancer drugs, a project which has shown a 100-fold increase in introductory cancer drug prices, after adjusting for inflation. A follow-on study found that the increase in price is not accompanied in an increase in clinical value, with the cost of a year of life increasing by $8,500 a year.

In 2012, on behalf of Memorial Sloan Kettering Cancer Center, Dr. Bach publicly rejected the pricing of the cancer drug, Zaltrap, by announcing the hospital's position in the New York Times. In response, the company lowered its price by 50%, proving that the price is not tied to any specific metric (i.e. R&D costs), but is rather determined by what the market can bear.

Dr. Bach launched a project in 2015 called the DrugAbacus (drugabacus.org), an interactive web based tool that allows users to manipulate various metrics to determine the ‘value’ of cancer drugs. DrugAbacus shifted the conversation of value-based pricing from one of theory to one more focused on implementation, and has been cited as a source of pricing for both CVS and Express Scripts. The Zaltrap stance, the DrugAbacus, and much of his work has made MSKCC a leader in using evidence to shift the discussion on drug pricing, a consistent theme of which has been that the price a manufacturer sets is a product of the marketplace, not a product of the costs of their business or something else structural.

Citation Format: Bach PB. Global cost of cancer care [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 PL3.
Abstract A06: All Nations Breath of Life: A culturally tailored smoking cessation program for heterogeneous urban American Indian communities
Authors: Gunville Jordyn , Goeckenr Ryan , Hale Jason , Smith T Edward , Nazir Niaman , Daley Sean , Choi Won , Daley Christine M.
Published: March 2017

Prevalence of cigarette smoking is highest among American Indians, yet few culturally appropriate smoking cessation programs have yet been developed and tested for multi-tribal American Indian adult populations. This study tested for effectiveness the All Nations Breath of Life culturally tailored smoking cessation program in multi-tribal urban and suburban American Indian communities in 7 locations across 5 states (N=312).

This single-arm implementation effectiveness study used community-based participatory research to conduct a 12-week intervention. Participants were followed through month 6 in person and month 12 via telephone. The primary outcome was continuous abstinence from recreational cigarette smoking at 6 months post-baseline, verified through voluntary provision of salivary cotinine levels.

At program completion, 53.3% of program completers remained abstinent; using an intent-to-treat analysis labeling those lost to follow-up as smokers resulted in a 41.4% quit rate. At 6 months post-baseline, 31.1% of retained participants quit smoking (p<0.0001 compared to the highest quit rates among multi-tribal populations reported in the literature, 7%); final quit rate was 22.1% using an intent-to-treat analysis (p=0.002). Retention rate at endpoint was 71.2%. 12-month follow-up was attempted with all participants and had a retention rate of 49.0%. Of those participants reached, 34.0% were smoke-free; using an intent-to-treat analysis, the quit rate at 12 months post-baseline was 16.7%.

All Nations Breath of Life is an effective smoking cessation program for multi-tribal urban American Indian communities. It can be successfully implemented in a variety of urban settings.

Citation Format: Jordyn Gunville, Ryan Goeckenr, Jason Hale, T Edward Smith, Niaman Nazir, Sean Daley, Won Choi, Christine M. Daley. All Nations Breath of Life: A culturally tailored smoking cessation program for heterogeneous urban American Indian communities. [abstract]. In: Proceedings of the Ninth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2016 Sep 25-28; Fort Lauderdale, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(2 Suppl):Abstract nr A06.
Abstract A37: Outcomes of a Randomized Community Trial to Increase Pap Testing among Pacific Islanders in Southern California
Authors: Tanjasiri Sora Park , Weiss Jie W. , Mouttapa Michele , Santos Lola Sablan
Published: March 2017

Background: Pap tests comprise an essential cervical cancer prevention and detection method for women in the U.S. Unfortunately, the Pap test remains significantly underutilized among many ethnic/racial groups, particularly Pacific Islanders (PIs) who have low rates of Pap testing and high rates of cervical cancer incidence and mortality.

Methods: A randomized community trial tested the efficacy of a social support-informed culturally developed intervention on increasing Pap testing among Chamorro, Samoan and Tongan women in Southern California. Using community-based participatory research (CBPR), Pacific Islander women and their husbands/partners were recruited from social organizations (churches and clans) that had been randomly assigned to receive the intervention or control education. Three waves (pretest, posttest and 6-month follow-up) of data collection included demographics, cervical cancer beliefs, social support between women and their husbands/partners, and Pap test attitudes and behaviors.

Results: CBPR recruitment resulted in a total of 81 social organizations recruited that included n=575 Pacific Islander women and n=461 husbands/partners. Significant differences between groups at baseline included acculturation and health insurance coverage. Six month follow-up found that all women from baseline significantly increased knowledge and decreased fatalistic attitudes towards Pap testing. Women who were not adherent to Pap test guidelines in the intervention group had significantly higher rates of Pap testing compared to controls at six month follow-up. No differences were found in either women's perceived social support nor men's provision of social support for Pap testing.

Conclusion: CBPR-informed behavioral interventions can increase cervical cancer screening in Pacific Islander women. Although social support did not mediate the relationship between women's knowledge and behavior, it did inform the development of a culturally tailored intervention for Chamorro, Samoan and Tongan women. Future studies can build upon these results by addressing other early detection (e.g., mammograms, colorectal exams, etc) and prevention (e.g., HPV vaccination) in these and other disparity populations.

Citation Format: Sora Park Tanjasiri, Jie W. Weiss, Michele Mouttapa, Lola Sablan Santos. Outcomes of a Randomized Community Trial to Increase Pap Testing among Pacific Islanders in Southern California. [abstract]. In: Proceedings of the Ninth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2016 Sep 25-28; Fort Lauderdale, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(2 Suppl):Abstract nr A37.
Abstract B47: Combating cancer with combination therapy in underserved populations
Authors: Homayouni Tina , Mokhtari Reza Bayat , Tyker Albina , Kazemi Parandis , Morgatskaya Zhenya , Baluch Narges , Dhalla Sara , Rekhi Shreya , Kumar Sushil , Yeger Herman
Published: March 2017

Combination therapy is an emerging treatment modality that combines two or more agents to produce a therapeutic effect. The combined use of therapeutic agents enhance efficacy compared to the monotherapy approach because it characteristically targets main key pathways with a synergistic or an additive effect. This approach potentially reduces drug-resistance, while simultaneously producing therapeutic anti-cancer benefits, such as the potential in reducing tumor growth and metastasis, arresting the cell cycle, reducing cancer stem cell populations, and inducing apoptosis. The 5-year survival rate for most cancers are still quite low, and the process of developing a new anti-cancer drug is long and extremely time consuming. Therefore, new strategies that target the survival pathways while providing efficient and effective results, as well as affordability, are being considered.

One such approach incorporates the testing of therapeutic agents initially used for the treatment of different diseases on cancer. This approach is effective primarily when the FDA approved agent targets similar pathways found in cancer. Because one of the drugs used in combination therapy is already FDA approved and requires less funding to research, overall costs of combination therapy research are reduced. This increases cost efficiency of therapy and reduces the price of treatment, benefiting the “medically underserved”. In addition, an approach that combines repurposed pharmaceutical agents with other therapeutics have shown promising results in mitigating tumor size and volume.

Note: This abstract was not presented at the conference.

Citation Format: Tina Homayouni, Reza Bayat Mokhtari, Albina Tyker, Parandis Kazemi, Zhenya Morgatskaya, Narges Baluch, Sara Dhalla, Shreya Rekhi, Sushil Kumar, Herman Yeger. Combating cancer with combination therapy in underserved populations. [abstract]. In: Proceedings of the Ninth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2016 Sep 25-28; Fort Lauderdale, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(2 Suppl):Abstract nr B47.
Abstract C02: Electronic personal health records, minorities and prevention
Authors: Raska Paola , Schneider Katherine , Zivoder Jordan , Steele Scott , Abraham Jame
Published: March 2017

Introduction:

Cancer outcome disparities are in large part attributable to impediments to access to care for minority populations and individuals of lower socio-economic status. The use of electronic personal health records (ePHR) such as myChart, which allow patients to directly interact with their health record and their healthcare providers, has been drastically increasing with cancer patients overall but disproportionately less so in the underserved. We need to better understand the factors that underlie disparities in usage of ePHR, particularly for prevention, in order to be better able to leverage on this technology to improve access to care.

Methods:

In 2012 Cleveland Clinic implemented an opt out program where every patient is given a myChart activation code at check in. This has resulted in close to a million “newly active” patients and almost half a million activated MyChart users. All patients with an email address on file were invited to participate in a survey inquiring about patient knowledge, use and preferences for myChart. We used logistic regression to test for differences across ethnicity after controlling for factors that confound factors such as age and illness.

Results:

A total of 18,599 369 myChart users responded to the survey. 633 (3%) responders self-identified as Hispanic (His) and 1265 (7%) as African American (AA). Both His and AA tended to be younger and healthier (less chronic conditions) than non-Hispanic White (WHI) responders (AA OR=1.4, p = 0.001, His OR 2.0, p = 0.001). Despite this His and AA have higher frequencies of visits to their PCP and to the ER after controlling for chronic conditions and age. Although younger WHI responders were more likely to say that they would use myChart more if they visited their PCP more, this was not the case for His and AA. Instead we find that His and AA are more likely to say that they do not discuss preventative measures with their PCP (AA OR =1.3, p=0.01, His OR = 1.5, p = 0.002)

Conclusion: Our results suggest that adding functionality to ePHR that will more actively promote discussion and planning of prevention between primary care providers and His and AA may be a way to improve the impact of this technology on how minorities engage with prevention.

Citation Format: Paola Raska, Katherine Schneider, Jordan Zivoder, Scott Steele, Jame Abraham. Electronic personal health records, minorities and prevention. [abstract]. In: Proceedings of the Ninth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2016 Sep 25-28; Fort Lauderdale, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(2 Suppl):Abstract nr C02.
Abstract C32: MicroRNA mediated megative regulation of caveolin 1 as a biological mechanism driving breast cancer disparities
Authors: Turner David P. , King Brooke , Guo Qi , Blake Bobbie , Nogueira Lourdes M. , larue amanda c. , salley judith d. , ford marvella e. , evans-knowell ashley , Findlay Victoria J.
Published: March 2017

In South Carolina, mortality differences between African American (AA) and non-Hispanic white (NHW) women breast cancer patients are amongst the highest in the country. Evidence suggests that the observed racial disparity exists independent of socioeconomic and standard of care issues, suggesting a potential biological factor may be involved. The loss of Caveolin-1 (Cav1) in the tumor stromal compartment has emerged as a novel biomarker for predicting poor clinical outcome in all of the most common subtypes of breast cancer, however the mechanism of Cav1 loss is unknown. We identified miR-510 as a novel oncomir and propose that its elevated expression in breast tumors results in stromal Cav1 loss and a subsequent worse outcome. In this study we used luciferase, western blot and quantitative PCR analysis to study Caveolin-1 as a direct target of miR-510. We used a co-culture system to assess crosstalk between epithelial and stromal compartments in vitro and a mouse model to assess this in vivo. Our research shows that Cav1 is a direct target of miR-510 and that overexpression of miR-510 leads to downregulation of Cav1 protein expression, specifically in the stromal compartment. This may be racially significant as our studies also show that miR-510 levels are elevated and Cav1 levels are reduced in AA breast cancer patients compared to their NHW counterparts. Data from our in vivo studies shows that cancer-associated fibroblasts (CAFs) isolated from miR-510 expressing epithelial derived tumors lead to more aggressive tumor growth when co-injected with breast tumor epithelial cells when compared to scrambled control CAF co-injections and breast tumor epithelial cells alone. Our results suggest that elevated miR-510 expression in breast epithelial cells leads to stromal Cav1 loss and is a mechanism driving racial disparity in breast cancer.

Citation Format: David P. Turner, Brooke King, Qi Guo, Bobbie Blake, Lourdes M. Nogueira, amanda c. larue, judith d. salley, marvella e. ford, ashley evans-knowell, Victoria J. Findlay. MicroRNA mediated megative regulation of caveolin 1 as a biological mechanism driving breast cancer disparities. [abstract]. In: Proceedings of the Ninth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2016 Sep 25-28; Fort Lauderdale, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(2 Suppl):Abstract nr C32.
Abstract C36: Gastric intestinal metaplasia: Epidemiological and demographic characterization in Puerto Rican Hispanics
Authors: Gonzalez-Pons Maria , Cruz-Cruz Jorge J. , Carla Cepero , Valle Alberto Del , Colon Giancarlo , Alicea Kimberly , Rosado Kathia , Cruz-Correa Marcia
Published: March 2017

Background: Gastric intestinal metaplasia (GIM), a key event in gastric carcinogenesis, is the replacement of gastric mucosa by an epithelium that histologically resembles intestinal mucosa. Helicobacter pylori (H. pylori), the most common chronic bacterial infection in humans, is known to be associated with gastric carcinogenesis. Classification of GIM by histological subtype and pattern sets an important goal for proper surveillance measures. Incomplete GIM confers 4- to 11-fold increased risk for gastric cancer. Despite this, there is no previous data available of GIM prevalence and characterization in Puerto Rico (PR). The aim of this study is to determine the prevalence of GIM within the cohort of patients in PR who underwent diagnostic endoscopy for the period of 2012-2014, and to characterize the demographical and clinicopathological profile of individuals with GIM.

Methods: A cross sectional study design using pathology reports of 4,707 endoscopic biopsies with confirmed diagnosis of GIM between 2012-2014 was performed. These reports were reviewed, and the demographic, geographic, and histopathological data provided were analyzed for characterization of this condition. Study characteristics were described using frequency distributions for categorical variables. SPSS version 17 was used for statistical analysis.

Results: Between 2012-2014, the prevalence of GIM was 10.7%, of which 26.9% of cases were positive for H. pylori. GIM was frequently found at incisura angularis and antrum biopsies. Approximately 99.6% and 71.2% of the reviewed pathology reports lack information about GIM histological subtype and pattern.

Conclusion: The prevalence of GIM is difficult to establish due to asymptomatic nature of the lesion, insufficient number of biopsies or inappropriate localization of biopsies. Despite this, the prevalence of GIM in PR appears to be higher than in United States. We observed that pathology reports lack the proper characterization of GIM necessary to provide adequate surveillance.

Citation Format: Maria Gonzalez-Pons, Jorge J. Cruz-Cruz, Cepero Carla, Alberto Del Valle, Giancarlo Colon, Kimberly Alicea, Kathia Rosado, Marcia Cruz-Correa. Gastric intestinal metaplasia: Epidemiological and demographic characterization in Puerto Rican Hispanics. [abstract]. In: Proceedings of the Ninth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2016 Sep 25-28; Fort Lauderdale, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(2 Suppl):Abstract nr C36.
Abstract C61: [Advocate Abstract:] PSA Testing: Black Lives Matter - screenings decreases unnecessary deaths
Authors: Coppin Randall
Published: March 2017

Introduction: The US Preventative Services Task Force (USPSTF) 2012 recommendation against prostate-specific antigen (PSA)-based screening for prostate cancer has been controversial. If theree are excess deaths among black patients, why abandon the one proven screening test? PSA and Black men: The burden of Prostate Cancer falls disproportionately on African American men; the incidence of prostate cancer is almost 60% higher and the mortality rate is two - three times greater in African American men than in Caucasian men. These disparities can be explained by differences in PSA values, socioeconomic status and transformation rate of prostate cancer in black men vs Caucasian men. Because of the greater tumor cell burden, it has been hypothesized that PSA testing at an earlier age for African American men may allow diagnosis of lower risk prostate cancer, potentially reducing disparities between African American and Caucasian men between the ages of 40 and 54. Solutions: According to various reports, community based interventions in barbershops, community centers and churches have been to shown to significantly increase intention to screen. There is also a groundswell of work done in the last 4 years suggesting that screening with PSA across all groups is actually beneficial (as originally thought) Conclusion: As a patient advocate, it is my job to educate and inform the public by attending scientific seminars and spreading the word in community based interventions about the benefits of screening. There is nothing more valuable than a person's life.

Citation Format: Randall Coppin. [Advocate Abstract:] PSA Testing: Black Lives Matter - screenings decreases unnecessary deaths. [abstract]. In: Proceedings of the Ninth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2016 Sep 25-28; Fort Lauderdale, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(2 Suppl):Abstract nr C61.
Abstract C86: Distance to free and low cost screening centers and cervical cancer screening behaviors of low income women in New Jersey
Authors: Gardner Michelle L. , Bandera Elisa V. , Jones Beth A. , Demisse Kitaw , Silvera Stephanie AN
Published: March 2017

Racial/ethnic disparities in cancer outcomes have been well documented. Access to Pap testing may account for some of the variation in the racial and socioeconomic differences in cervical cancer outcomes. The rate of Pap testing within the past three years has been shown to vary by both race/ethnicity and by access to medical care. Given this, there has been an increase in the use of GIS to explore and understand cancer screening behaviors. The goal of this analysis was to evaluate and characterize the relationship between geographic proximity to free or low-cost cancer screening facilities and screening behaviors among low-income women in New Jersey using data collected from a cross-sectional survey (N= 459). Address data from 376 participants were geocoded using an ArcGIS address locator, using TIGER road map data as the source, to conduct a distance analysis between participant location and New Jersey Cancer Education & Early Detection (NJCEED) locations, which offer free and low cost screenings based on income. A majority of participants (60.6%) lived less than five miles from the nearest NJCEED location. There was no statistically significant difference in being screened between living <2 miles versus > 8 miles from a NJCEED location (OR = 1.40, 95%CI = 0.60 - 3.26) after adjusting for age, race, transportation, BMI, insurance, and perceived risk. However, when stratified by race, African American women who lived within 2 miles of a screening location were 5.59 times more likely to report being screened compared to women living more than 8 miles away (95% CI = 1.08 - 28.90), although this trend was not statistically significant (p=.06). Distance to free and low cost screening centers were associated with screening behaviors among low income African American women in NJ, but not low income white and Hispanic women, indicating a need for tailored interventions to reach this at risk population.

Citation Format: Michelle L. Gardner, Elisa V. Bandera, Beth A. Jones, Kitaw Demisse, Stephanie AN Silvera. Distance to free and low cost screening centers and cervical cancer screening behaviors of low income women in New Jersey. [abstract]. In: Proceedings of the Ninth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2016 Sep 25-28; Fort Lauderdale, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(2 Suppl):Abstract nr C86.