bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 3743: Magnetic resonance imaging shrinkage patterns after neoadjuvant chemotherapy for breast carcinomas: Correlation with molecular subtypes
Authors: Mori Tsuyoshi , Tomida Kaori , Kitamura Mina , Sakai Sachiko , Kawai Yuki , Shimizu Tomoharu , Umeda Tomoko , Ueki Tomoyuki , Kaida Sachiko , Miyake Toru , Iida Hiroya , Akabori Hiroya , Kitamura Naomi , Yamaguchi Tsuyoshi , Sonoda Hiromichi , Naka Shigeyuki , Tani Masaji 
Published: July 2017

Abstract
Background: Neoadjuvant chemotherapy (NAC) is widely performed for patients with locally advanced breast carcinomas. It is important to obtain precise information using imaging modalities about the distribution of residual carcinomas after NAC to predict the success of breast conserving surgery. However, the relationship between magnetic resonance imaging (MRI) shrinkage patterns and molecular subtypes of breast carcinomas has not yet been investigated.
Methods: We analyzed the MRI shrinkage and pathological patterns of residual carcinomas after NAC in 54 consecutive breast carcinomas. The shrinkage patterns were classified into five categories: Type I and II (concentric shrinkage with or without any surrounding lesion), type III (shrinkage with residual multinodular lesions), type IV (diffuse contrast enhancement in the entire quadrant), and non-visualization.
Results: The most common MRI shrinkage pattern was type I (39%) followed by non-visualization (26%). The most common pathological shrinkage pattern was type III (33%), followed by type II (28%) and non-visualization (22%). The concordance rates of the MRI patterns of non-visualization and type I were significantly lower than those of the MRI patterns of type II, III, and IV (p = 0.018). Moreover, in the luminal subtypes, the concordance rates of the MRI patterns of non-visualization and type I were significantly lower than those of the MRI patterns of type II, III, and IV (p = 0.026); however, in the non-luminal subtypes, this correlation was not significant. Conclusions: The results of the present study suggest that the cases with MRI shrinkage patterns of non-visualization and type I require caution regarding the surgical margins compared with the other types, especially the luminal subtypes.
Citation Format: Tsuyoshi Mori, Kaori Tomida, Mina Kitamura, Sachiko Sakai, Yuki Kawai, Tomoharu Shimizu, Tomoko Umeda, Tomoyuki Ueki, Sachiko Kaida, Toru Miyake, Hiroya Iida, Hiroya Akabori, Naomi Kitamura, Tsuyoshi Yamaguchi, Hiromichi Sonoda, Shigeyuki Naka, Masaji Tani. Magnetic resonance imaging shrinkage patterns after neoadjuvant chemotherapy for breast carcinomas: Correlation with molecular subtypes [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 3743. doi:10.1158/1538-7445.AM2017-3743
Abstract 376: Biospecimen and data resources for cancer research from NCI’s BPV program
Authors: Guan Ping , Moore Helen M. 
Published: July 2017

Abstract
The Biospecimen Preanalytical Variables (BPV) Program was initiated by the National Cancer Institute’s Biorepositories and Biospecimen Research Branch to evaluate the impact of preanalytical factors on the molecular integrity of biospecimens. Selected preanalytical factors including cold ischemic time (delay to formalin fixation (DTF)), time in formalin (TIF), freezing methods, and storage temperatures and durations were examined for their potential effects on molecular profiles from surgical resection tissues and matched blood from four cancer types (kidney, ovary, colon and lung). The BPV program has collected tumor specimens from 364 cancer patients. Each specimen was annotated with 300+ data elements that cover steps in the collection, handling, and processing procedures, pathology review, and clinical information. NCI conducted multiple studies using these specimens to evaluate the preanalytical impacts on different analytical platforms including gene expression profiling, copy number variation, proteomics and metabolomics profiling. The program invites interested organizations to work with NCI through collaboration to further evaluate preanalytical effects on molecular analyses (https://techtransfer.cancer.gov/availabletechnologies/e-000-2013). The remaining specimens are available to support relevant research focusing on biospecimen science and/or clinical biomarker assay development (https://specimens.cancer.gov/search/). The IT infrastructure that was developed to support BPV biospecimen collection and management has been further developed into open source products (https://github.com/NCIP/CDR and https://github.com/NCIP/CDR-Lite). The controlled vocabulary that records the terms and definitions used in describing the overall biospecimen collection efforts has been refined and published at publicly accessible CDE repositories: NCI’s caDSR (https://cdebrowser.nci.nih.gov/CDEBrowser/ ) and NIH’s CDE portal (https://cde.nlm.nih.gov/cde/search ). An ongoing collaboration with an academic ontology consortium will map the CDEs to existing biobanking ontology frameworks and make them publicly available. The BPV program has generated a wide range of ~omics data. We are preparing a BPV data compendium to be submitted to dbGaP at NCBI. These data will be used as the experimental evidence to develop evidence-based best practices for fit-for-purpose collection, processing, and storage of biospecimens for cancer research.
Citation Format: Ping Guan, Helen M. Moore. Biospecimen and data resources for cancer research from NCI’s BPV program [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 376. doi:10.1158/1538-7445.AM2017-376
Abstract 3790: Circulating tumor cells at disease recurrence in patients with head and neck cancer after curative therapy
Authors: Hsieh Jason Chia-Hsun , Yeh Ting-Hsiuan , Wang Hung-Ming , Lin Yung-Chang , Lin Nina Ming-Jung , Ye Siou-Ru , Lee Jane Ying-Chieh , Wu Min-Hsien 
Published: July 2017

Abstract
Background: Circulating tumor cell (CTC) has been prognostic and predictive in numerous types of cancer; however, its role in early diagnosis of relapse remains unclear.
Methods: Eighty-six patients were prospectively enrolled between March 2015 and June 2016. Among these patients, 51 head and neck squamous cell carcinoma (HNSCC) patients had suspicious recurrent lesion(s), whilst 35 HNSCC patients were newly diagnosed. CTC test was performed by negative selection strategy and CD45-negative and EpCAM-positive cells were identified as CTCs. Biopsy on suspicious lesion(s) and CTC analysis were performed simultaneously. We analyzed the differences of CTC numbers among HNSCC patients with true recurrence, biopsy-negative and newly-diagnosed.
Results: Mean±standard deviation(SD) of CTC numbers in baseline at diagnosis (n=35), true recurrence (n=40) and biopsy-negative (n=11) groups were 41.98±32.02, 81.75±64.91 and 16.55±6.82 cells/mL, respectively. The difference of CTC numbers among three groups was significant (P &lt;0.001). CTCs (mean±SD) among different failure types were 110.89±84.69, 105.67±50.77, 73.31±37.82 and 59.11±54.09 in lung metastasis, second primary tumor, extrapulmonary metastasis and locoregional recurrence respectively and significantly different (P = 0.049). Also, CTC numbers between first cancer (baseline at diagnosis) and second primary tumor were different (P = 0.004).
Conclusion: CTCs numbers are significantly higher in true recurrence than the biopsy-negative group when a patient had a lesion suspected to be a recurrence. CTC test may be useful to help distinguish true recurrence in HNSCC patients after curative therapy.
Citation Format: Jason Chia-Hsun Hsieh, Ting-Hsiuan Yeh, Hung-Ming Wang, Yung-Chang Lin, Nina Ming-Jung Lin, Siou-Ru Ye, Jane Ying-Chieh Lee, Min-Hsien Wu. Circulating tumor cells at disease recurrence in patients with head and neck cancer after curative therapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 3790. doi:10.1158/1538-7445.AM2017-3790
Abstract 3805: Pre-diagnostic statin use among breast cancer patients - the relation to HMG-CoA reductase expression and disease-free survival
Authors: Tryggvadottir Helga , Gustbée Emma , Markkula Andrea , Simonsson Maria , Nodin Björn , Jirström Karin , Rose Carsten , Ingvar Christian , Borgquist Signe , Jernström Helena 
Published: July 2017

Abstract
Background: The purpose of this study was to investigate whether pre-diagnostic statin use was associated with tumor expression of HMG-CoA reductase (HMGCR) and disease-free survival (DFS) in breast cancer. Previous studies have shown anti-carcinogenic properties of statins and a significantly longer survival among breast cancer patients using statins. We recently showed, that the target of statins, HMGCR, was up-regulated in breast cancer among patients preoperatively treated with statins in a window-of-opportunity trial.
Methods: A population-based cohort of primary breast cancer patients in Lund, Sweden was assembled between October 2002 and June 2012. Patients completed a questionnaire including information on medication use. Statin use in relation to DFS was analyzed in 985 patients. Tumor tissue microarrays were constructed and stained with a polyclonal HMGCR antibody to assess HMGCR expression (n=848).
Results: Patients were followed for up to 11 years (median follow-up time 5.0 years). In the present study, pre-diagnostic statin use was neither associated with HMGCR expression (P=0.53) nor with DFS (P=0.92), overall or separately in any of the HMGCR expression groups (negative, weak, moderate/strong). Moreover, statin use was not associated with clinical tumor characteristics (tumor size, axillary lymph node involvement, histological grade, hormone receptor status or HER-2 amplification).
Conclusion: In contrast to previous studies, the present study did not show any significant association between pre-diagnostic statin use and DFS. It is possible that patients who already used statins have developed tumors that are less dependent on cholesterol metabolism and consequently less influenced by statin treatment. The timing of statin use in relation to breast cancer diagnosis and prognosis should be evaluated in another cohort with preferably longer follow-up time.
Citation Format: Helga Tryggvadottir, Emma Gustbée, Andrea Markkula, Maria Simonsson, Björn Nodin, Karin Jirström, Carsten Rose, Christian Ingvar, Signe Borgquist, Helena Jernström. Pre-diagnostic statin use among breast cancer patients - the relation to HMG-CoA reductase expression and disease-free survival [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 3805. doi:10.1158/1538-7445.AM2017-3805
Abstract 3821: Biochemical parameters of breast cancer patients in Nigeria
Authors: Udegbe Sandra A. , Oyinbo Atinuke G. , Akaiso Andiyenema N. , Nwaonumah Kingsley E. , Iweala Emeka Eze 
Published: July 2017

Abstract
Studies have revealed the importance of differential biochemical parameters of cancer patients in the development of critical biomarkers for accurate diagnosis and treatment. There is a dearth of information on the biochemical characteristics of breast cancer patients in Nigeria which may vary from other climes. The discovery of new biomarkers will provide a deeper understanding of the disease and wider scope of diagnosis and hence improvement in management of breast cancer. In this line of investigation, we examined some biochemical parameters including Alanine transaminase (ALT), Alkaline phosphatase (ALP), Low density lipoprotein (LDL), High density lipoprotein (HDL) and triglycerides (TRIG) in the plasma of 53 breast cancer patients and 14 controls. The data obtained indicates that there were no significant differences in the ALP, LDL and TRIG while ALT and HDL were significantly difference. This indicates the possible implication of ALT and HDL in breast cancer disease in Nigeria and their potential to be further developed into biomarkers for diagnosis.
Citation Format: Sandra A. Udegbe, Atinuke G. Oyinbo, Andiyenema N. Akaiso, Kingsley E. Nwaonumah, Emeka Eze Iweala. Biochemical parameters of breast cancer patients in Nigeria [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 3821. doi:10.1158/1538-7445.AM2017-3821
Abstract 3826: Clinical validation of a serum protein panel (FLNA, FLNB and KRT19) for diagnosis and prognosis of prostate cancer
Authors: Ravipaty Shobha , Wu Wenfang , Dalvi Aditee , Tanna Nikunj , Andreazi Joe , Friss Tracey , Klotz Allison , Liao Chenchen , Garren Jeonifer , Schofield Sally , Diamandis Eleftherios P. , Klein Eric A. , Dobi Albert , Srivastava Shiv , Tekumalla Poornima , Kiebish Michael A. , Vishnudas Vivek K. , Sarangarajan Rangaprasad , Narain Niven R. , Akmaev Viatcheslav 
Published: July 2017

Abstract
Background: Prostate cancer (PrCa) is a leading cause of cancer deaths in males in the US. Current tests of prostate-specific antigen (PSA) screening and the diagnostic prostate biopsy are often inconclusive. Many patients with a PSA positive blood test often undergo invasive repeat biopsy procedures. Additionally, there is a need for diagnostic tests that differentiate between low and high-risk cancers. This study reports on the development of a novel serum protein panel of three PrCa biomarkers, Filamin A, Filamin B and Keratin-19 (FLNA, FLNB and KRT19) using multivariate models for disease screening and prognosis.
Methods: ELISA and IPMRM (LC-MS/MS) based assays were developed and analytically validated by quantitative measurements of the biomarkers in serum. Retrospectively collected and clinically annotated serum samples with PSA values and Gleason scores (GS) were analyzed from 503 subjects who underwent prostate biopsy, and showed no evidence of cancer with or without indication of prostatic hyperplasia, or had a definitive pathology diagnosis of prostatic adenocarcinoma. Probit linear regression models were used to combine the analytes into score functions to address the following clinical questions: does the biomarker test augment PSA for population screening? Can aggressive disease be differentiated from lower risk disease, and can the panel discriminate between benign prostate hyperplasia (BPH) and PrCa? Results: Table 1: Berg PrCa Panel AUC summary for the four clinical indications.
Conclusion: As shown in Table 1, modelling of the data demonstrated that the new PrCa biomarkers and PSA in combination were better than PSA alone in identifying PrCa, improved the prediction of high and low risk disease, and improved prediction of BPH versus PrCa.
Citation Format: Shobha Ravipaty, Wenfang Wu, Aditee Dalvi, Nikunj Tanna, Joe Andreazi, Tracey Friss, Allison Klotz, Chenchen Liao, Jeonifer Garren, Sally Schofield, Eleftherios P. Diamandis, Eric A. Klein, Albert Dobi, Shiv Srivastava, Poornima Tekumalla, Michael A. Kiebish, Vivek K. Vishnudas, Rangaprasad Sarangarajan, Niven R. Narain, Viatcheslav Akmaev. Clinical validation of a serum protein panel (FLNA, FLNB and KRT19) for diagnosis and prognosis of prostate cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 3826. doi:10.1158/1538-7445.AM2017-3826
Abstract 3828: The role of CK2 for overcoming paclitaxel resistance in gastric cancer
Authors: Jung Minkyu 
Published: July 2017

Abstract
Despite advances in cancer treatment, gastric cancer is still one of the most fatal cancers. This is because paclitaxel, the most widely used treatment for gastric cancer, has limited clinical utility by the development of resistance. Casein kinase 2 (CK2) activation has been reported to be involved in proliferation in various tumors and resistance form chemotherapy. Therefore, we investigated the association between paclitaxel resistance and CK2 activation. CK2 expression was evaluated by immunohistochemistry (IHC) on formalin-fixed, paraffin-embedded tumors from 59 AGC patients who were treated with paclitaxel as second line therapy. Patients with high expression of CK2 (29/59, 39%) showed lower disease control rate (DCR) (47.7 % vs. 72.3 %, p=0.017) and shorter progression free survival (PFS) (2.8 months vs. 4.8 months, p=0.009) compared to those who with low expression. Cell proliferation assay were carried out by MTT assay after drug treatment with paclitaxel, CX-4945 (CK2 inhibitor) in 49 gastric cancer cell lines. CK2 protein expression was shown to be associated with paclitaxel sensitivity. Of the gastric cancer cell lines, SNU-1 was selected for paclitaxel resistance, high expression of CK2, and high sensitivity to CX-4945. Combination therapy CX-4945 and paclitaxel showed synergistic antitumor effect in SNU-1 by MTT assay and showed inhibition of down signaling of PI3K/AKT pathway on western blot. In conclusion, CK2 activation was shown to be related to paclitaxel resistance. CX-4945 in combination with paclitaxel could be treatment of choice in gastric cancer with paclitaxel resistance.
Citation Format: Minkyu Jung. The role of CK2 for overcoming paclitaxel resistance in gastric cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 3828. doi:10.1158/1538-7445.AM2017-3828
Abstract 3832: Optimization strategy for fluorescent multiplex immunohistochemistry tissue staining
Authors: zheng Yi , Coltharp Carla , Dilworth Ryan , Liu Linying , Unfricht Darryn , Hoyt Cliff , Rajopadhye Milind , Miller Peter 
Published: July 2017

Abstract
Introduction: Recent insights into the tumor microenvironment have fueled the need for additional information beyond the one or two phenotypes provided by traditional immunohistochemistry (IHC). As a response, manual and automated fluorescent multiplex immunohistochemistry (fIHC) techniques have been recently developed and accepted by the immuno-oncology space. Fluorescent multiplex immunohistochemistry (fIHC) assays are designed to simultaneously measure multiple biomarkers in tissue sections with visual context that is lost in other methods, such as flow cytometry. Here we describe a novel optimization strategy to achieve quantitative, robust, and specific multiplex fIHC staining results with both manual and automated multiple-color Opal procedures.
Methods: Formalin-fixed paraffin-embedded samples of primary tumors were immunostained using Opal™ reagents both manually and on a fully automated Leica BOND RX™ stainer. The impact of different reagent concentrations and quantities were analyzed in respect to signal specificity and robustness, stripping efficiency, signal co-localization, signal to noise, and color separation. Images were acquired on a Vectra 3.0® automated imaging system, and analyzed with inForm® software.
Results: The goals of this study were two-fold:
-to understand the impact of Opal reagent concentrations/quantities on fluorescent signal intensities acquired from cells within the context of tissue.
-to develop an Opal reagent optimization method that yields more consistent, quantitative results from separated and co-localized fluorescent signals.
We’ve applied this novel fIHC experimental approach and optimization strategy to Opal monoplex and multiplex assays and explored staining robustness, contextual specificity, staining order independence, and co-localized signal separation. Using the novel optimization strategy, we have achieved optimal staining patterns with improved confidence in the quantitative characteristics of the assay. Tissue sections stained after optimization have exhibited staining order independence and closely align with traditional IHC patterns.
Conclusion: This novel optimization strategy, developed for Opal fIHC assays, is more quantitative, improves staining results, and minimizes interference between co-localized biomarkers.
Citation Format: Yi zheng, Carla Coltharp, Ryan Dilworth, Linying Liu, Darryn Unfricht, Cliff Hoyt, Milind Rajopadhye, Peter Miller. Optimization strategy for fluorescent multiplex immunohistochemistry tissue staining [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 3832. doi:10.1158/1538-7445.AM2017-3832
Abstract 3878: Musashi-2 (MSI2) regulation of ERBB family proteins in non-small cell lung cancer (NSCLC)
Authors: Kudinov Alexander , Deneka Alexander , Nikonova Anna N. , Nicolas Emmanuelle , Korobeynikov Vladislav A. , Serebriiskii Ilya G. , Karanicolas John , Golemis Erica A. , Boumber Yanis 
Published: July 2017

Abstract
The purpose of this study is to establish whether a new signaling axis we recently described can be targeted to improve patient survival in lung cancer, one of the leading causes of death worldwide, with over 1.6 million deaths annually. Non-small cell lung cancer (NSCLC) is the most common form of lung cancer. A small number of targeted therapies have been shown to be useful in lung cancer, including inhibitors of EGFR, but these are typically only active in a subset of tumors that maintain epithelial characteristics. Musashi-2 (MSI2), an RNA-binding protein that regulates mRNA translation, has been linked to maintenance of a stem cell state in multiple hematologic and solid tumor malignancies. We recently established (Kudinov et al, PNAS 2016, PMID:27274057) that MSI2 is elevated in a subset of NSCLC tumor upon progression and drives NSCLC metastasis, in part based on activity supporting a TGF-beta/SMAD3/claudin signaling cascade that enhances epithelial-mesenchymal transition (EMT). Using reverse phase protein array (RPPA) analysis of MSI2-depleted versus control KrasLA1/+;P53R172HΔG/+ murine NSCLC cell line models identified a significant 2.7-fold upregulation of HER3 upon MSI2 depletion. Negative MSI2-dependent regulation of ERBB3 protein expression was confirmed in multiple additional murine and human KRAS-dependent NSCLC models, based on analysis of MSI2 depletion or overexpression. In contrast, MSI2 positively regulated expression of the EGFR/ERBB1 protein in the same models. In detailed analysis, we have addressed the mechanism by which MSI2 regulates expression of the ERBB group of receptor tyrosine kinases. In addition, these data suggested the hypothesis that MSI2 expression might predict response to EGFR-targeted inhibitors, and that dual targeting of MSI2 and EGFR might be therapeutically valuable. We will present data on the activity of EGFR inhibitors in the context of depleted or elevated MSI2 expression, and the effect of combining inhibition of EGFR with recently developed MSI2 inhibitors. In summary, these results for the first time indicate a role of MSI2 in supporting EGFR expression in NSCLC and suggest that MSI2 may drive NSCLC development and progression in part via EGFR, and may modulate response to EGFR-targeted agents.
Citation Format: Alexander Kudinov, Alexander Deneka, Anna N. Nikonova, Emmanuelle Nicolas, Vladislav A. Korobeynikov, Ilya G. Serebriiskii, John Karanicolas, Erica A. Golemis, Yanis Boumber. Musashi-2 (MSI2) regulation of ERBB family proteins in non-small cell lung cancer (NSCLC) [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 3878. doi:10.1158/1538-7445.AM2017-3878