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670s Tumor Biology 10557 General Poster Session (Board #44F), Mon, 1:15 PM-5:15 PM Exosomal-miRNA profiles as diagnostic biomarkers in cervical cancer. Presenting Author: Hirotaka Nishi, Department of Obstetrics and Gynecology, Tokyo Medical University, Tokyo, Japan Background: MicroRNA (miRNA) expression is altered in cancer cells and associated with the development and progression of various types of cancer. miRNA could serve as diagnostic or prognostic biomarker for cancer patients. Our study was designed to analyze circulating exosomalmiRNA in patients with cervical cancer. Methods: Total RNA was extracted from serum in healthy women and patients with cervical intraepithelial neoplasia (CIN) and cervical cancer. We first explored miRNA expression profiles using miRCURY LNA microRNA Array (Exiqon) in each six malignant and healthy serum samples. miRNAs with significant differences in expression were validated in larger sample sets by a quantitative real-time RT-PCR using TaqMan gene expression assays (Applied Biosystems). Results: Six of 1223 miRNAs compared in serum samples from cervical cancer and normal control were found to have a �3.0-fold change with a P value �0.01 using miRCURY LNA microRNA Array. In a validation set (n�101), expression of 3 of the 6 miRNAs, miR-483-5p, miR-1246 and miR-1275, was significantly different between the cervical cancer (n�40) and control (n�20) samples. We also found that the median levels of these miRNAs were significantly higher in patients with cervical cancer (n�40) than those in CIN (n�41). Circulating miRNAs were not correlated with clinical-pathological parameters except for miR-1246. Compared to patients with squamous cell carcinoma, the miR-1246 level was significantly higher in those with adenocarcinoma. Whereas, receiver-operator characteristic (ROC) curve analyses suggest that these serum miRNAs may be useful markers for discriminating patients with cervical cancer from healthy controls. Conclusions: Expression of circulating miR-483-5p, miR-1246 and miR-1275 is significantly higher in the blood of cervical cancer patients compared to controls and may potentially serve as a useful biomarker for cervical cancer diagnosis. Especially, miR-1246 may be a candidate for early detection of cervical adenocarcinoma. Larger-scaled studies are warranted to fully explore the role of circulating exosomalmiRNAs in cervical cancer. 10559 General Poster Session (Board #44H), Mon, 1:15 PM-5:15 PM Use of next-generation sequencing (NGS) to detect high frequency of targetable alterations in primary and metastatic breast cancer (MBC). Presenting Author: Lajos Pusztai, University of Texas M. D. Anderson Cancer Center, Houston, TX Background: The aim of this study was to assess the frequency of genomic alterations in breast cancer potentially treatable with approved targeted agents or investigational drugs in clinical trials. NGS was performed in a CLIA setting (Foundation Medicine). Methods: DNA was extracted from needle biopsies of 33 pre-therapy primary and 17 MBCs (mean age 52 yrs; 58% ER�, 20% HER2�, 30% triple negative) obtained prospectively for biomarker discovery and preserved in RNAlater. Patients with MBC received an average of 7 drugs (range 5-17) including adjuvant therapy before biopsy for this research; 13 biopsies were from soft tissues, 3 from liver and 1 from bone. Sequencing was targeted to 3230 exons in 182 cancer-related genes and 37 introns in 14 genes often rearranged in cancer. Average median depth was �1200x. Results: All biopsies yielded sufficient DNA. NGS revealed a total of 117 known driver mutations across 36 genes (per-tumor average�2.5, range 1-6), including 37 base substitutions (32%), 28 indels (24%), 42 amplifications (36%) and 10 homozygous deletions (9%). NGS identified HER2 gene amplification in 6/7 cases scored HER2� by FISH. The average number of functionally important alterations was surprisingly similar, 2.3 in primaries vs 2.8 in heavily treated MBCs (p�0.32). Remarkably, 25/33 (76%) of primary and 14/17 (82%) of MBCs had at least 1 genomic alteration targetable with an FDA approved drug or novel agent in clinical trials. These included: ERBB2 alterations (n�9), PIK3CA mutations (n�8), NF1 mutations (n�4, candidate for PI3K/MEK inhibitors), AKT1-3 mutations (n�5, PI3K inhibitors), BRCA1/2, (n�6, PARP inhibitors), and CCND2 (n�3)/CDKN2A (n�3) mutations (CDK inhibitors). Numerous other alterations with less apparent therapeutic implications were also observed. Conclusions: Comprehensive NGS profiling in breast cancer needle biopsies showed high frequency of genomic alterations linked to a clinical treatment option or clinical trials of targeted therapies. These results demonstrate it is feasible to use NGS to guide targeted therapy. Prospective testing of the diagnostic/predictive value of this patient selection approach is currently under way. 10558 General Poster Session (Board #44G), Mon, 1:15 PM-5:15 PM Evaluation of gene expression by RNA-seq after single dose of trastuzumab (T) reveals predictors of pathologic complete response (pCR) in HER2positive early breast cancer. Presenting Author: Natalie Galanina, Yale University School of Medicine, Yale Comprehensive Cancer Center, New Haven, CT Background: The use of a ‘brief exposure’ to single agent T allows the measurement of dynamic changes in the transcriptome that may predict response to T-based combinations. We have shown that most gene expression changes in HER2� tumors treated with T occur in tumors that ultimately achieve a pCR. Our further analysis suggests several patterns of transcriptional change in pCR tumors suggesting different mechanisms of action of T. RNA-seq analysis provides more in-depth annotation of these mechanisms. Methods: Fresh tumor core biopsies were taken at a 2 week time point after a single dose of T (8mg/m2) from 80 HER2� early breast cancer patients enrolled on a clinical trial of T�T�C. Nucleic acids were extracted using Qiagen AllPrep and were analyzed with Illumina HT12v3 Beadchip and Illumina 610 QUAD V1 SNP arrays. RNA was also processed for sequencing using the Ovation RNA-Seq System and paired-end sequenced using an Illumina Genome Analyzer IIxRNA-seq data was analyzed with Tophat/Cufflinks. Network analysis was performed with Metacore. Results: Among pCR tumors, distinct patterns of differential expression pre/post T were observed, in both microarray and RNA-seq data. ERBB2 down-regulation was characteristic of pCR in one subgroup by microarray. In this group, differentially expressed genes belonged to interaction networks involved in apoptosis and cell cycle regulation. In contrast, tumors with no change in ErbB2 showed differentially expressed genes that belonged to networks related to chromatin assembly and regulation of immune pathways. NOLC1, RPL41, ZCHHC17, and B2M had altered alternative splicing product distributions in both groups. In the ERBB2 down-regulated group, genes with changed expression were enriched for targets of STAT3 and YY1. Conclusions: RNA-seq and microarray reveal distinct responses in tumors that achieve pCR to T-containing regimens. These methods provide predictive markers for validation in subsequent clinical trials. 10560 General Poster Session (Board #45A), Mon, 1:15 PM-5:15 PM EGFR exon 20 insertion mutations: Incidence and clinicopathologic characteristics in U.S. patients with lung adenocarcinoma. Presenting Author: Maria E. Arcila, Memorial Sloan-Kettering Cancer Center, New York, NY Background: Activating insertion mutations in exon 20 of EGFR are reported in a small subset of lung adenocarcinomas (ADC). In contrast to the classic EGFR mutations, they appear to confer primary resistance to currently approved EGFR tyrosine kinase inhibitors. Their incidence and clinicopathologic features are not well established. Methods: Lung ADCs (n�1500) were screened for major activating mutations in EGFR (exons 19 and 21) and KRAS (exon 2). Negative cases were tested for EGFR exon 20 insertions by a PCR-based sizing assay. Extended testing for additional recurrent point mutations in EGFR, KRAS, BRAF, NRAS, PIK3CA, MEK1 and AKT was performed in all cases by Sequenom mass spectrometry. A subset of cases was also tested for ALK rearrangements by FISH. Results: We identified 32cases withEGFRexon 20 insertions, accounting for 11% of all EGFR mutations. EGFRexon 20 insertions were mutually exclusive with the other genetic alterations tested except for PIK3CA mutations. The incidence was higher among never-smokers (p�0.0001) but there was no association with sex, ethnic origin or stage at diagnosis. Insertions were 3, 6, 9 or 12bp; 9bp insertions were most common (50%, 16/32). Morphologically, 90% of tumors were moderate to poorly differentiated with a predominant mixed ADC phenotype. Conclusions: EGFR exon 20 testing may identify a unique subset of EGFR mutant lung ADCs which is significantly larger than previously reported, making this the third most common type of EGFR mutation after exon 19 deletions and L858R. This population could potentially benefit from alternate targeted therapies, many of which are currently in clinical development. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
10561 General Poster Session (Board #45B), Mon, 1:15 PM-5:15 PM Independent validation of prognostic value of 22 micrornas (miRs) in stage I-II squamous cell lung cancer (SqCLC). Presenting Author: Marcin Tomasz Skrzypski, Medical University of Gdansk, Gdansk, Poland Background: About 50% of NSCLC patients (pts) will develop distant metastases following pulmonary resection. Currently, apart from clinical stage at diagnosis, there are no reliable factors to select high risk pts for adjuvant chemotherapy. We previously demonstrated prognostic value of 22 miRs in frozen tissue samples of early stage SqCLC, and the feasibility of their expression assessment in formalin fixed paraffin embedded (FFPE) samples (Skrzypski et. al. J Clin Oncol 2010;28;15s). In this study, we validated the prognostic value of these miRs in an independent cohort of early SqCLC pts. Methods: FFPE tumor samples were obtained from 132 stage I-II SqCLC pts who underwent radical pulmonary resection, 42% of whom developed distant metastases. Median follow-up of pts who did not develop metastases was 5.6 years (range, 4.1-10.0 years). miRs were isolated from tumor tissue with RecoverAll kit (Ambion). Expression of 22 miRs previously found to be related to the risk of metastases was analyzed by RT-PCR assay (Appliedbiosystems). Raw data were normalized vs. the expression of U6. Individual miRs and the risk score comprising 5 most predictive miRs were correlated with distant metastases-free survival (MFS). Results: Eight miRs were significantly relatedtoMFS. MiR-192 was significantly correlated with MFS (p�0,0007; p�0,02 after correction for multiple comparisons). The 5-miR risk score was an independent prognostic factor (p�1.70E-06) in a multivariate analysis comprising stage (p�1,10E-03) and histological grade (p�0,46). Using the median of the risk score as a cut-off value, the median MFS was 1.73 years in the high risk group, and not reached in the low risk group (HR�2.11). The sensitivity and specificity of the risk score to predict the occurrence of distant metastases were 66% and 64%, respectively. Conclusions: Risk score based on expression of 5 miRs is a strong and independent predictor of distant relapse in operable early SqCLC. 10563 General Poster Session (Board #45D), Mon, 1:15 PM-5:15 PM Effect of the loss of the type III TGF� receptor during tumor progression on tumor microenvironment: Preclinical development of TGF� inhibition and TGF�-related biomarkers to enhance immunotherapy efficacy. Presenting Author: Brent Allen Hanks, Duke University Medical Center, Durham, NC Background: Overall, the clinical efficacy of tumor immunotherapy has been limited. Our incomplete understanding of the complex interplay between tumors and the immune microenvironment has contributed to these modest outcomes. Our work has revealed that several tumors downregulate the expression of the type III TGF� receptor (T�RIII) with progression. T�RIII is shed from the cell surface to generate soluble T�RIII (sT�RIII) which is capable of sequestering TGF�. Methods and Results: Using both breast cancer and melanoma tumor models we have demonstrated that the loss of T�RIII expression is associated with diminished tumor infiltrating CD8� T cells and increased regulatory T cells (Tregs) within the tumor microenvironment. Our data implies that these alterations correlate with suppressed tumor antigen-specific T cell responses and more rapid disease progression. We show that these changes are due to enhanced TGF� signaling within the immune compartment of the tumor microenvironment resulting in enhanced expression of the indoleamine 2,3-dioxygenase immunoregulatory enzyme by local plasmacytoid dendritic cells (DCs) as well as increased expression of the Treg-recruiting CCL22 chemokine by local myeloid DCs. Microarray analysis indicates that these same gene expression associations also exist in human breast cancers. Consistent with these studies, we have demonstrated that TGF-� inhibition synergistically enhances the efficacy of a Her2/neu vaccine in a breast cancer model and that plasma levels of sT�RIII correlate with clinical response and overall survival in stage III melanoma patients. Conclusions: We have elucidated a novel mechanism that tumors utilize to suppress the generation of anti-tumor immunity by establishing a link between the loss of an endogenous suppressor of tumor metastasis, T�RIII, and the generation of an immunotolerant tumor microenvironment. We are pursuing a phase I clinical trial to investigate the efficacy of combining a TGF-� inhibitor with a tumor vaccine while also determining if sT�RIII may function as a predictive biomarker for this approach. Tumor Biology 671s 10562 General Poster Session (Board #45C), Mon, 1:15 PM-5:15 PM Lymphopenia combined with low TCR diversity to predict overall survival in metastatic breast cancer patients. Presenting Author: Manuarii Manuel, Centre de Recherche en Cancérologie de Lyon, Inserm U1052 CNRS 5286, Centre Léon Bérard, Lyon, France Background: Lymphopenia (�1 Giga/L) before initiation of chemotherapy is a predictive factor for toxicity and death in metastatic phase for cancer patients. Combinatorial diversity of T Cell Receptor beta chain (TCR-ß), as a measure of T cell repertoire diversity, was investigated and tested either alone or in combination with lymphopenia as a prognostic factor for overall survival (OS) in first line treatment of metastatic breast cancer (MBC) patients. Methods: Using semi quantitative multiplex PCR, the V-D-J combinatorial diversity of the TCR was measured on cryo-preserved blood samples from 2 cohorts of MBC patients before the initiation of the first line chemotherapy: in an experimental cohort (cohort A, n�66) and in a validation series (cohort B, n�67). A prognostic score, defined NDL (Number & Diversity of Lymphocytes) combining lymphocyte count and TCR diversity was delineated. Univariate and multivariate analysis of prognostic factors for OS were performed in both cohorts. Results: Lymphopenia (�1 Giga/L) was associated with shorter OS for cohort B while TCR diversity �33% (called divpenia) was associated with a reduced OS in cohort A. The combination of lymphopenia with low TCR diversity (called lympho-divpenia) was associated with poor OS compared to patients with either lymphocyte count �1 Giga/L or diversity �33% or both, in cohort A (median OS: 7.6 vs 24.5 months, p.value �0.0006) and cohort B (median OS 10.6 vs 22.9 months, p.value �0.0035). In a multivariate analysis, including all significant clinical factors from the univariate analysis (PS, liver metastasis, hemoglobin) lympho-divpenia was found to be an independent prognostic factor in the pooled cohort (A�B) (p�0.005) along with triple negative tumors (p�0.011) and hemoglobin level (11.5 g/dL) (p�0.009). Conclusions: NDL score combining lymphopenia and reduced TCR diversity seems to be a strong prognostic factor for OS and could be use to improve care quality of MBC patients. 10565 General Poster Session (Board #45F), Mon, 1:15 PM-5:15 PM Involvement of NK cell molecular signatures in favorable prognosis of breast cancer patients. Presenting Author: Maria Libera Ascierto, National Institutes of Health, Bethesda, MD Background: Tumor cell recognition by NK cells is mediated by the interaction of activating and inhibitory NK cell receptors with their ligands expressed on tumor cells. In addition, NK cells express adhesion molecules that facilitate formation of the immunological synapse with the tumor targets. Here, we investigated whether the coordinate expression of NK activating receptors and adhesion molecules could provide a signature to segregate breast cancer patients into relapse and relapse-free outcomes. Methods: Gene expression profiling, RT-PCR screening and survival analysis were performed on RNA extracted from primary breast cancers. Tumors were obtained from patients experiencing either 5-8 years relapse-free survival or tumor relapse within 1-3 years following initial treatment. Results: Tumors from patients with a favorable prognosis were characterized by increased expression of genes involved in NK cell interaction with tumor cells and its activation signaling. In particular, up-regulation of Natural Cytotoxicity Receptors (NCRs), leukocyte function-associated antigen 1 (LFA-1), CD226 (DNAM-1) and CD96 was observed in relapse-free patients. Thus, the expression of the NK activating receptors and relevant adhesion molecules involved in NK cell:target interactions can predict relapse free survival in breast cancer patients. Conclusions: Results from the present study, highlighted the effector cooperation between the innate and adaptive immune components within the tumor microenvironment. The NK cells parameters identified in this study, together with the prognostic B and T cell signatures previously reported by us, represent a powerful tool for predicting breast cancer outcome which might be easily introduced in clinical practice. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
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Volume 30, Issue 15S, Part I of II
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Editor: Michael A. Carducci, MD Man
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Volume 30, Issue 15S Supplement to
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El Sherbeiny, Esam e15129 El-Deiry,
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Fayad, Luis 6501, 8067 Fayette, Jer
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Gang, Wu 7091, e14511 Gangaram, Anj
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Granowetter, Linda 9537 Grant, Barb
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Hainsworth, John D. 618, 1018, 1086
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Hong, Seung-Mo 3568 Hong, Sook Hee
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Im, Young-Hyuck 598^, 644, TPS649,
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Rose, Steven C. 3590 Rosell, Rafael
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Sha, Dan 3564 Sha, Huifang e13528 S
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Silva, Jose D. 5567 Silva, Milton J
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Sousa, Carlos Eduardo Pires 643 Sou
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Su, Xinying 4124 Su, Yu-Chieh e1600
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Tan, Chee Seng 1064, e19523 Tan, Ch
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Tillmanns, Todd D. 5014, e15514 Til
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Uchiyama, Tomotaka e21108 Udovitsa,
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Videtic, Gregory M.M. e14611, e1466
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Wang, Yuan e15124 Wang, Yunfei 547
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Wischnewsky, Manfred 1078 Wischnik,
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Zhang, Xinmin e16022 Zhang, Xu Dong
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Annual Meeting Proceedings Part 1 - American Society of Clinical ...

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