bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 1157: MicroRNA-625-3p is associated with response to first-line oxaliplatin-based treatment of metastatic colorectal cancer.
Authors: Rasmussen Mads H. , Jensen Niels F. , Tarpgaard Line S. , Qvortrup Camilla , Rømer Maria U. , Stenvang Jan , Hansen Tine P. , Christensen Lise-Lotte , Lindebjerg Jan , Hansen Flemming , Jensen Benny V. , Hansen Torben F. , Jakobsen Anders M. , Pfeiffer Per , Brünner Nils , Ørntoft Torben F. , Andersen Claus L. 
Published: August 2014

Abstract
The backbone of current oncologic treatment of metastatic colorectal cancer (mCRC) consists of fluoropyrimidine together with either oxaliplatin (XELOX/FOLFOX) or irinotecan (XELIRI/FOLFIRI). With an overall objective response rate of approximately 50% for either treatment combination, a major unsolved problem is that no predictors of response to these treatments currently are available. To address this issue, we profiled 742 microRNAs in laser-capture microdissected cancer cells from responding and non-responding patients receiving XELOX/FOLFOX as first-line treatment for mCRC, and identified, among others, high expression of miR-625-3p, miR-181b and miR-27b to be associated with poor clinical response. In a validation cohort of 98 mCRC patients treated first-line with XELOX, high expression of miR-625-3p was confirmed to be associated with poor response (OR 6.25, 95%CIOR [1.8; 21.0]). Independent analyses showed that miR-625-3p was not dysregulated between normal and cancer samples, nor was its expression associated with recurrence of stage II or III disease, indicating that miR-625-3p solely is a response marker. Finally, we also found that these miRNAs are up-regulated in oxaliplatin resistant HCT116/oxPt (miR-625-3p, miR-181b and miR-27b) and LoVo/oxPt (miR-181b) CRC cell lines as compared with their isogenic parental cells. Altogether, our results suggest an association between miR-625-3p and response to first-line oxaliplatin based chemotherapy of mCRC.
Citation Format: Mads H. Rasmussen, Niels F. Jensen, Line S. Tarpgaard, Camilla Qvortrup, Maria U. Rømer, Jan Stenvang, Tine P. Hansen, Lise-Lotte Christensen, Jan Lindebjerg, Flemming Hansen, Benny V. Jensen, Torben F. Hansen, Anders M. Jakobsen, Per Pfeiffer, Nils Brünner, Torben F. Ørntoft, Claus L. Andersen. MicroRNA-625-3p is associated with response to first-line oxaliplatin-based treatment of metastatic colorectal cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1157. doi:10.1158/1538-7445.AM2013-1157
Abstract 1162: Caspase recruitment domains: New potential markers for diagnosis of hepatocellular carcinoma in Egyptian patients.
Authors: Zekri Abdel-Rahman N. , Bahnassy Abeer 
Published: August 2014

Abstract
Background: Chronic HCV is a major leading cause of HCC development. Caspase Recruitment Domains (CARD) is protein modules that regulate apoptosis. Besides; numerous CARD proteins play an important role in various carcinogenesis processes. Aim: To assess the possible role of CARD9, CARD10 and Caspase only protein (COP) in progression of liver fibrosis and pathogenesis of HCC in chronic HCV G4 Egyptian patients.
Methods: One hundred and thirty patients were recruited and classified into 4 groups; group I: Chronic HCV, group II: Chronic active hepatitis, group III: Liver cirrhosis, group IV: HCV related HCC. Biochemical, virological studies, abdominal ultrasonography and liver biopsy were performed. Quantitative estimation of mRNA of CARD9, CARD10 and COP were performed by reverse transcription PCR in liver biopsy from all collected patients.
Results: In HCC patients; age, AFP and liver profile were significantly higher, HB and platelets were significantly lower, (p value &lt;0.01). The expression levels of mRNA of CARD9, CARD10 and COP in liver biopsies of HCC group (IV) were significantly higher than other groups (p value&lt;0.01). On differentiation between HCC and non HCC patients each CARD was assessed separately then in combination with others as follow; CARD 9, CARD 10, COP and AFP separately showed best cutoff at (87, 89.5, 20.3, 10.35) with sensitivity (80%, 90%, 90%, 87%) and specificity (80%, 63%, 81%, 68%) with positive predictive value (61%, 51.4%, 69.2%, 54%) and negative predictive value (85.7%, 93.3%, 94.8%, 91%) respectively. On combing AFP with CARD9 then CARD 10 then COP, they showed (93%, 100%, 100% sensitivity), (57%, 46%, 57% specificity), with positive predictive value (49%, 45%, 51%) and negative predictive value (94%, 100%, 100%) respectively. On combing the 3 CARDs (CARD 9, CARD 10, COP), the sensitivity was 100%, specificity was 48%, with positive predictive value 47% and negative predictive value 100% as shown in figure 1.
Conclusions: CARD9, CARD10 and COP had no role in liver fibrosis but may be involved in hepatic carcinogenesis processes and they could be used as markers for HCC diagnosis
Citation Format: Abdel-Rahman N. Zekri, Abeer Bahnassy. Caspase recruitment domains: New potential markers for diagnosis of hepatocellular carcinoma in Egyptian patients. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1162. doi:10.1158/1538-7445.AM2013-1162
Abstract 1181: Association between DNA methylation profile and neo-adjuvant treatment response in breast cancer patients.
Authors: Choi Ji-Yeob , Kim Taehyun 
Published: August 2014

Abstract
Epigenetic alterations are common in breast cancer, yet how these modifications contribute to chemotherapy response is poorly understood. This study aimed to define a DNA methylation profile associated with response to neo-adjuvant treatment in breast cancer and to identify possible candidate genes associated with resistance as predictors.
Eleven pre-treatment and 12 post-treatment serum samples with 6 pairs of FFPE tissues were collected in neo-adjuvant chemotherapy with operable and locally advanced breast cancer. Illumina HumanMethylation450K BeadChip technology for serum DNA and Roche Nimblegen Human DNA Methylation 3x720K CpG Island Plus RefSeq Promoter Arrays, MeDIP-chip technology for FFPE DNA were used for simultaneous analysis of 450,000 CpG sites for serum DNA and 27,728 for FFPE DNA, respectively.
Genes generated from pre-treatment samples were compared with those genes obtained from post-treatment samples, which showed differential modulation following neo-adjuvant chemotherapy. Association on 11 pre-treatment serum DNA highlighted 102 genes significantly related to Ki67 level change as the treatment response (p =0.2) after excluding genes changed by neo-adjuvant chemotherapy. Among them, 16 genes showed consistent methylation levels between serum and tissue (hypermethylation including ITIH3, p-value=0.0015, 8.9 fold-change; hypomethylation including ARID3A, p-value=0.0037, 1.4 fold-change). Hypomethylation of DBH, PRDM16, SLC12A7 and VSX2 in pre-treatment serum and tissue DNA were also predicted to another response surrogate measured by the changes of tumor size (p =0.2).
Our study suggests that testing for methylation levels of genes identified in this study may be beneficial in predicting individual patient response to neo-adjuvant therapies.
Citation Format: Ji-Yeob Choi, Taehyun Kim. Association between DNA methylation profile and neo-adjuvant treatment response in breast cancer patients. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1181. doi:10.1158/1538-7445.AM2013-1181
Abstract 120: Detection of acrolein-derived cyclic DNA adducts in human cells by monoclonal antibodies.
Authors: Pan Jishen , Awoyemi Bisola , Xuan Zhuoli , Vohra Priya , Wang Hsiang-Tsui , Dyba Marcin , Greenspan Emily , Fu Ying , Creswell Karen , Zhang Lihua , Berry Deborah , Tang Moon-Shong , Chung Fung-Lung 
Published: August 2014

Abstract
Acrolein (Acr) is a ubiquitous environmental pollutant found in cigarette smoke and automobile exhaust. It can also be produced endogenously by oxidation of polyunsaturated fatty acids. The Acr-derived 1,N2-propanodeoxyguanosine (Acr-dG) adducts in DNA are mutagenic lesions that are potentially involved in human cancers. In this study, monoclonal antibodies were raised against Acr-dG adducts and characterized using ELISA. They showed strong reactivity and specificity towards Acr-dG, weaker reactivity towards crotonaldehyde- and trans-4-hydroxy-2-nonenal-derived 1,N2-propanodeoxyguanosines, and weak or no reactivity towards 1,N6-ethenodeoxyadenosine, 8-oxo-deoxyguanosine, and benzo(a)pyrene- and malondialdehdye-derived adducts. Using these novel antibodies, we developed assays to detect Acr-dG in vivo: First, a simple and quick FACS-based assay for detecting these adducts directly in cells; Second, a highly sensitive direct ELISA assay for measuring Acr-dG in cells and tissues using only one μg DNA; And third, a competitive ELISA for better quantitative measurement of Acr-dG levels in DNA. The assays were validated using Acr-treated HT29 cell DNA samples or calf thymus DNA and the results were confirmed by LC-MS/MS-MRM. An immunohistochemical assay was also developed to detect and visualize Acr-dG in HT29 cells as well as in human oral cells. These antibody-based methods provide useful tools for the studies of Acr-dG as a cancer biomarker and of the molecular mechanisms by which cells respond to Acr-dG as a ubiquitous DNA lesion. (This work was supported by NCI grant CA134892)
Citation Format: Jishen Pan, Bisola Awoyemi, Zhuoli Xuan, Priya Vohra, Hsiang-Tsui Wang, Marcin Dyba, Emily Greenspan, Ying Fu, Karen Creswell, Lihua Zhang, Deborah Berry, Moon-Shong Tang, Fung-Lung Chung. Detection of acrolein-derived cyclic DNA adducts in human cells by monoclonal antibodies. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 120. doi:10.1158/1538-7445.AM2013-120
Abstract 121: Markers of cell proliferation and growth as potential preneoplastic biomarkers of risk for colorectal neoplasms.
Authors: Tu Huakang , Woodard Jill , Daniel Carrie , Gonzalez-Feliciano Amparo , Ahearn Thomas , Bostick Roberd M. 
Published: August 2014

Abstract
Background: Increased colorectal epithelial cell proliferation and growth are early, common events in sporadic colorectal cancer. To assess the potential of cell proliferation and growth markers as pre-neoplastic biomarkers of risk for colorectal neoplasms, we conducted a pilot, colonoscopy-based case-control study (n = 51 cases and 154 controls) of incident, sporadic colorectal adenoma.
Methods: We evaluated transforming growth factor alpha (TGFα), TGFβ1, and telomerase reverse transcriptase (hTERT) expression in normal-appearing mucosa from the rectum and ascending and sigmoid colon using automated immunohistochemistry and quantitative image analysis in a subset of cases and controls (n = 40 and 46, respectively). Mean differences in staining batch-standardized biomarker labeling optical density between cases and controls were assessed using analysis of covariance, and associations of the biomarkers with adenomas were assessed using unconditional logistic regression.
Results: In the normal rectal mucosa, hTERT expression was 13% (P = 0.06) higher in cases than in controls, and higher hTERT expression (above the median in controls) was associated with a three-fold increased risk of colorectal adenoma (OR = 3.28, 95% confidence interval [CI], 1.04 – 10.35). TGFα expression was 31% (P = 0.25) higher in cases than in controls, and higher TGFα expression was associated with a 44% increased risk of colorectal adenoma (OR = 1.44, 95% CI 0.50 – 4.16). TGFβ1 expression alone and the ratio of TGFα to TGFβ1 expression were 3% (P = 0.86, OR = 0.91, 95% CI 0.39 – 2.11) and 61% (P = 0.30, OR = 1.23, 95% CI 0.45 – 3.36), respectively, higher in cases than in controls.
Conclusions: These preliminary data suggest that hTERT and TGFα expression and, perhaps especially, the balance of TGFα and TGFβ1 expression in the normal rectal mucosa may be directly associated with risk for incident, sporadic colorectal neoplasms, providing support for further investigation of these markers as potential biomarkers of risk for colorectal neoplasms.
Citation Format: Huakang Tu, Jill Woodard, Carrie Daniel, Amparo Gonzalez-Feliciano, Thomas Ahearn, Roberd M. Bostick. Markers of cell proliferation and growth as potential preneoplastic biomarkers of risk for colorectal neoplasms. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 121. doi:10.1158/1538-7445.AM2013-121
Abstract 1214: RET fusion gene: translation to the therapy of lung adenocarcinoma.
Authors: Kohno Takashi , Ichikawa Hitoshi , Tsuta Koji , Mizukami Tatsuji , Shimada Yoko , Kato Mamoru , Sakamoto Hiromi , Tsuchihara Katsuya , Watanabe Shun-ichi , Nokihara Hiroshi , Goto Koichi , Yokota Jun , Yoshida Teruhiko , Shibata Tatsuhiro 
Published: August 2014

Abstract
A considerable proportion of lung adenocarcinomas, the most common histological type of lung cancer that comprises 40% of the total cases, develops through activation of oncogenes, for example, somatic mutations in EGFR or KRAS or fusion of ALK, in a mutually exclusive manner. Tyrosine kinase inhibitors targeting the EGFR and ALK proteins are effective in the treatment of lung adenocarcinomas that carry EGFR mutations and ALK fusions, respectively. We performed whole-transcriptome sequencing (RNA sequencing) of 30 lung adenocarcinoma specimens from Japanese individuals to identify new chimeric fusion transcripts that could be targets for therapy. Then, we identified KIF5B (kinesin family 5B)-RET fusion gene, as another druggable oncogene that is present in 2% (6/319) of lung adenocarcinomas (Kohno et al., Nat Med, 2012). The KIF5B-RET fusion leads to aberrant activation of RET kinase and is considered to be a new driver mutation segregating from mutations or fusions in EGFR, KRAS, HER2 and ALK. The RET fusion has preferentially been detected in well or moderately differentiated tumors of never smokers. The RET fusion in lung adenocarcinoma was also identified by three other groups: Dr. Ju et al of Seoul National University, Dr. Takeuchi et al of Japanese Foundation for Cancer Research, and Dr. Lipson et al of Foundation Medicine, USA. A clinical trial to address the therapeutic efficacy of a RET tyrosine kinase inhibitor, vandetanib, will be started in 2013 by Dr. Koichi Gotoh (kgoto@east.ncc.go.jp) of National Cancer Center Hospital East, Japan.
Citation Format: Takashi Kohno, Hitoshi Ichikawa, Koji Tsuta, Tatsuji Mizukami, Yoko Shimada, Mamoru Kato, Hiromi Sakamoto, Katsuya Tsuchihara, Shun-ichi Watanabe, Hiroshi Nokihara, Koichi Goto, Jun Yokota, Teruhiko Yoshida, Tatsuhiro Shibata. RET fusion gene: translation to the therapy of lung adenocarcinoma. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1214. doi:10.1158/1538-7445.AM2013-1214
Abstract 1221: Targeting interferon-λ1 with a stabilized dimer of anti-tumor Fab .
Authors: Liu Donglin , Rossi Edmund A. , Cardillo Thomas M. , Goldenberg David M. , Chang Chien-Hsing 
Published: August 2014

Abstract
Background: The type-III interferons (IFNs), comprising IFN-λ1, IFN-λ2, and IFN-λ3, are functionally similar to the type-I IFN-α in eliciting anti-viral, anti-tumor, and immune-modulating activities. Due to its more restricted cellular targets, IFN-λ is being considered as a potential alternative to existing therapeutic regimens based on IFN-α, whose adverse effects in patients limit its use. The development of antibody-targeted IFN-λ may further improve its safety, potency and pharmacokinetics. Methods: We generated three DOC-AND-LOCKTM (DNLTM) complexes, designated (E1)-λ1, (15)-λ1, and (C2)-λ1, by conjugating IFN-λ1 site-specifically to a stabilized dimer of humanized Fab derived from hRS7 (anti-Trop-2), hMN-15 (anti-CEACAM6), and hL243 (anti-HLA-DR), respectively, which were affinity-purified and evaluated in human malignant cell lines of cervix (ME-180), colon (HT-29), esophagus (TE-11, T.Tn), lung (SK-MES-1, A549), liver (HepG2, Huh-7), and skin (A375). Results: As determined by flow cytometry, Trop-2 was highly expressed on the surface of ME-180, TE-11, and T.Tn; moderately on SK-MES-1 and HT-29; and negligibly on HepG2, Huh-7, A549, and A375. In comparison, CEACAM6 was undetectable on SK-MES-1 and A375, but positive on the remaining 7 cell lines, yet at a considerably lower level than Trop-2. Targeting of these immunocytokines to antigen-expressing cells markedly increased the amount of IFN-λ1 localized at the cell surface, as demonstrated by (E1)-λ1 on ME-180 (Trop-2+), (15)-λ1 on HepG2 (CEACAM6+), and (C2)-λ1 on A375 (HLA-DR+), respectively. In MTS assays, (E1)-λ1 inhibited the in vitro proliferation of ME-180, SK-MES-1, and TE-11, with EC50 &lt;1 pM, which was 1,000-fold more potent than commercial IFN-λ1. Likewise, the anti-proliferation activity of (15)-λ1 was enhanced ∼100-fold in ME-180 and TE-11, but not in CEACAM6-negative SK-MES-1. The observed potency was further substantiated by enhanced cell signaling, including STAT phosphorylation and MHC-I up-regulation induced by (15)-λ1 in HepG2 cells. In the Pk study, (E1)-λ1 showed a mean residence time of 12 h with a T1/2 of 8.6 h, and clearance of 2.2 ml/h in mouse serum, which is comparable to PEG-IFN-λ1. Conclusions: These promising results, attributable to increased localization and stronger binding to antibody-targeted cells, warrant further exploration of these novel immunocytokines as potential cancer therapeutics.
Citation Format: Donglin Liu, Edmund A. Rossi, Thomas M. Cardillo, David M. Goldenberg, Chien-Hsing Chang. Targeting interferon-λ1 with a stabilized dimer of anti-tumor Fab . [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1221. doi:10.1158/1538-7445.AM2013-1221
Abstract 1225: Serum cytokine profiling in metastatic colorectal cancer patients: IL-8, MCP-1, and MCP-3 are theranostic targets.
Authors: Chen Zhi-Yuan , He Wen-Zhuo , Peng Li-Xia , Guo Rong-Ping , Xia Liang-Ping , Qian Chao-Nan 
Published: August 2014

Abstract
Background: The prognostic value of many circulating cytokines in metastatic colorectal cancer (CRC) patients is undetermined. By using high through-put approach, this study was to evaluate the prognostic values of circulating cytokines in patients with metastatic CRC and identify potential therapeutic targets.
Methods: Thirty-nine cytokines were simultaneously analyzed in serum samples from 99 patients with metastatic CRC by using multiplex bead-based Luminex technology. Three CRC cell lines, together with three more aggressive lines derived from them, were used to validate three potential therapeutic targets by applying neutralizing antibodies.
Results: Elevated levels of 17 cytokines were found to be significant risk factors for the overall survival (OS) of patients. Only macrophage-derived chemokine (MDC) positively correlated with better prognosis. Interleukin-8 (IL-8), monocyte chemotactic protein-1 (MCP-1), MCP-3 and MDC were significant independent predictor of OS in multivariate analyses. The risk scoring system developed by combining IL-8, MCP-1, MCP-3, and MDC, was more effective than each individual factor to predictor the OS. IL-8 was secreted by three CRC cell lines, with higher expression observed in more-aggressive cells. Blocking of IL-8 with a neutralizing antibody inhibited the invasiveness of CRC cells. MCP-1 and MCP-3 were secreted by SW480 cell line, with higher expression in more-aggressive cell. Neutralizing antibodies against MCP-1 or MCP-3 significantly inhibited the cellular invasion.
Conclusions: The serum levels of 18 cytokines correlated with the prognosis of metastatic CRC patinets. Among them, IL-8, MCP-1, MCP-3 and MDC were independent prognostic factors for OS. IL-8, MCP-1, and MCP-3 are potential therapeutic targets in CRC.
Citation Format: Zhi-Yuan Chen, Wen-Zhuo He, Li-Xia Peng, Rong-Ping Guo, Liang-Ping Xia, Chao-Nan Qian. Serum cytokine profiling in metastatic colorectal cancer patients: IL-8, MCP-1, and MCP-3 are theranostic targets. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1225. doi:10.1158/1538-7445.AM2013-1225
Abstract 1226: Interleukin-6 (IL-6) as a therapeutic target in prostate cancer.
Authors: Kura Yurie , De Velasco Marco A. , Kobayashi Yasuyuki , Ando Naomi , Fukushima Emiko , Yamamoto Yutaka , Hatanaka Yuji , Shimizu Nobutaka , Yoshimura Kazuhiro , Nozawa Masahiro , Yoshikawa Kazuhiro , Nishio Kazuto , Uemura Hirotsugu 
Published: August 2014

Abstract
Interleukin-6 or IL-6 is a pleiotropic cytokine which is implicated in the regulation of immune response, but is also involved in regulating the growth of various malignant tumors. Mounting evidence suggests that IL-6 contributes to prostate cancer progression. Activated IL-6 has been shown to be elevated in the sera from patients with metastatic prostate cancer and it appears that the prostate tissue itself is a source of IL-6 and its receptor. Experimental data suggests that the IL-6/IL-6R signaling axis is an autocrine and paracrine growth factor in androgen independent prostate cancer cell lines and can activate a variety of signal transduction cascades, some of which may activate androgen receptor activity. In the present study we examined the role of IL6-induced Stat3 activation in the development and progression of prostate cancer and its possible role as a target for the treatment of prostate cancer using the prostate-specific conditional targeting PTEN knockout mouse model. In PTEN-mutant mice, elevated levels of IL6/IL-6R correlated with increased cellular proliferation in non-castrate and castrate prostate cancer (CRPC). Similar to human prostate cancer, mice with CPRC showed elevated levels of IL-6 and IL6-R in both serum and prostate tissue. To establish a therapeutic role for IL6/IL6R inhibition, we conducted a series of pharmacodynamic studies using an anti-mouse IL-6R antibody (MR-16) in tumor bearing homozygous PTEN-mutant mice. Our data shows that STAT3 activation was inhibited in a dose dependent manner during acute IL6-R blockade. Inhibition of STAT3 activity after chronic IL-6R blockade was transient. However, at day 45 of treatment, tumor cell proliferation was inhibited and apoptosis was induced. These findings show that this mouse model is relevant for the study of Stat3 signaling and tumor progression and inhibition of Stat3 transcriptional activation by upstream signal blockade may be a promising approach for molecularly targeted therapeutic strategies in human prostate cancer. Thus this study will serve as the foundation for future drug intervention studies designed to assess the efficacy of targeting the JAK/STAT signal pathway using targeted monotherapy and combination drug therapy models.
Citation Format: Yurie Kura, Marco A. De Velasco, Yasuyuki Kobayashi, Naomi Ando, Emiko Fukushima, Yutaka Yamamoto, Yuji Hatanaka, Nobutaka Shimizu, Kazuhiro Yoshimura, Masahiro Nozawa, Kazuhiro Yoshikawa, Kazuto Nishio, Hirotsugu Uemura. Interleukin-6 (IL-6) as a therapeutic target in prostate cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1226. doi:10.1158/1538-7445.AM2013-1226