tbuckley/cabot-search huggingface dataset:
Abstract 5517: Polymeric nanogel-based treatment regimen for enhanced efficacy and sequential administration of synergistic drug combination in pancreatic cancer
Authors: Kruti S. Soni, Michael A. Hollingsworth, Prakash Radhakrishnan, Tatiana K. Bronich
Journal: Cancer Research (2015)

Abstract Pancreatic cancer (PC) is one of the most lethal malignancies, due to aggressive tumorigenicity, early metastasis and development of drug resistance to standard care chemotherapy. Since its approval in 1997, Gemcitabine has been the first-line treatment for advanced disease. However, there is no standard second-line therapy after Gemcitabine failure. The combination of Gemcitabine with Cisplatin (CDDP) has been explored in clinical trials for metastatic disease and our preliminary in vitro studies with the free drugs on T3M4 Simple Cells (COSMC deleted cells) showed that synergy of the combination is schedule-dependent, and Gemcitabine administration followed by CDDP showed the most potent cytotoxic activity. However, this combination proved to be only marginally effective in actual practice due to combined increased toxicity of both the agents. We have shown that encapsulation of CDDP in polymeric nanogels with cross-linked ionic cores enhanced its tumor accumulation and improved its safety profile. Additionally, sustained release profile of CDDP from nanogels allows for the administration of free Gemcitabine and CDDP loaded nanogels in a single injection while still retaining schedule-dependent synergy of the combination. Pancreatic ductal adenocarcinoma cells are known to express truncated O-glycans (Tn and STn antigens) and it is anticipated that decorating the nanogels with an antibody directed against this antigen will further enhance their uptake by tumor cells while reducing off-target accumulation. Citation Format: Kruti S. Soni, Michael A. Hollingsworth, Prakash Radhakrishnan, Tatiana K. Bronich. Polymeric nanogel-based treatment regimen for enhanced efficacy and sequential administration of synergistic drug combination in pancreatic cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 5517. doi:10.1158/1538-7445.AM2015-5517
Inflammatory Cytokines, Hyperferritinemia and IgE Are Prognostic in Patients with KSHV-Associated Lymphomas Treated with Curative Intent Therapy
Authors: Thomas S. Uldrick, Manisha Bhutani, Mark N. Polizzotto, Karen O. Aleman, Kathleen M. Wyvill, Priscila H. Goncalves, Stefania Pittaluga, Armando Filie, Vickie Marshall, Adam W Rupert, Giovanna Tosato, Denise Whitby, Richard F Little, Seth M. Steinberg, Robert Yarchoan
Journal: Blood (2014)
Enhanced Killing of Chronic Myelogenous Leukemia Cells by Rapamycin and Imatinib Is Associated with Differential Inhibition of 4E-BP1 and eIF4E Phosphorylation and Decreased Protein Expression by Non-Overlapping Mechanisms.
Authors: James C. Moore, Chi Ly, Halbur Luke, S. Tiong Ong
Journal: Blood (2004)
Abstract 3218: Transcriptome characterization by RNA sequencing identifies molecular and clinical subgroups in high risk neuroblastoma
Authors: Shile Zhang, Jun S. Wei, Rajesh Patidar, Young K. Song, Sivasish Sindiri, Xinyu Wen, Shahab Asgharzadeh, Robert C. Seeger, John M. Maris, Jamie M. Guidry Auvil, Daniela S. Gerhard, Javed Khan
Journal: Cancer Research (2015)

Abstract Background/objectives: Neuroblastoma (NBL) is characterized with its heterogeneous clinical and biological behavior. Despite improvement of survival rate with multimodal chemo- and immunotherapy, high mortality and morbidity is still substantial for patients with metastatic disease. Previous DNA sequencing studies characterized the genetic basis of the disease and revealed a very low somatic mutation burden and surprisingly few recurrently somatic mutated genes comparing to adult solid tumors. In order to identify the novel molecular therapeutic target and understand the biology of the high-risk neuroblastoma, we investigated gene expression profiles of tumors from a cohort of high-risk neuroblastoma patient using RNA sequencing as an integral part of the Therapeutically Applicable Research to Generate Effective Treatments (TARGET) project. Methods: We performed RNA sequencing in a cohort of 150 high risk patients (97 survival and 53 death) using polyA selected mRNA. Gene and transcript isoform expression was used to correlate to the clinical parameters for this clinically well-annotated patient cohort. Whole exome sequencing (WES) data was available for 106 of the 150 patients cohort for combined analysis of DNA and RNA sequencing to identify expressed mutation. Results: On average, we found 12.5% of the human genome, which include 63.7% of exon, 18.0% of intron, and 4.6% of intergenic regions covered by RNA-seq reads in NB samples. Preliminary gene expression analysis showed four molecular subgroups of NB tumors with distinct outcomes (log-ranked p = 0.002). Sixty-two percent of somatic mutations identified by WES was present (&amp;gt;10% VAF) in the RNA transcriptome when the locus was expressed (10X). We found that some of the important pathogenic somatic mutations such as TP53 p.R243W can be only detectable by integrated analysis of the sequencing data of RNA and DNA, possibly due to low tumor purity. Future directions: We will assess the expressed mutations, fusion genes, mRNA expression, and splicing profiles to provide clinically relevant classification and offer insight into the tumor biology especially for those without detectable oncogenic driver mutation by DNA sequencing. Citation Format: Shile Zhang, Jun S. Wei, Rajesh Patidar, Young K. Song, Sivasish Sindiri, Xinyu Wen, Shahab Asgharzadeh, Robert C. Seeger, John M. Maris, Jamie M. Guidry Auvil, Daniela S. Gerhard, Javed Khan. Transcriptome characterization by RNA sequencing identifies molecular and clinical subgroups in high risk neuroblastoma. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3218. doi:10.1158/1538-7445.AM2015-3218
Chemoimmunotherapy with fludarabine (F), cyclophosphamide (C), and rituximab (R) improves complete response (CR), remission duration and survival as initial therapy of chronic lymphocytic leukemia (CLL)
Authors: M. J. Keating, S. O'Brien, S. Lerner, W. Wierda, H. Kantarjian
Journal: Journal of Clinical Oncology (2004)

6565 Background: Fludarabine Monophosphate (F) is the most active chemotherapy agent in CLL. Combination of F with C produced superior results to F in a German randomized trial (Blood: 102, 243a, 2003). In CLL, CR pts. have a superior survival to partial responders (PR). Addition of R to FC is reported to result in a high rate of complete clinical, flow cytomety, and molecular remissions. (Proc ASCO: 22, 2289a, 2003) Methods: We conducted multivariate analyses to evaluate the effect of FCR on CR rate, remission duration (RD), and overall survival (OS) in 552 pts. who received fludarabine based regimens as initial Rx for progressive or advanced CLL. 193 pts. were treated with F ± Prednisone (P), 135 with FC or F + mitoxantrone (M), and 224 with FCR. NCI-WG criteria for initiating Rx and evaluating response were used. Results: The results for CR, remission duration, and survival as shown in the table below: After covariate adjustment for clinically significant pretreatment variables. Response to Rx and protocol were evaluated for statistical significance. Response and FCR were associated with all three outcome parameters. Conclusions: This analysis suggests that FCR has significantly improved the prognosis for CLL when used as initial therapy. No significant financial relationships to disclose.
Abstract 1152: The regulatory effect of fructose-bisphosphate aldolase C in oral squamous cell carcinoma progression
Authors: Yueju Li, Tse-Hung Huang, Been-Ren Lin, Cheng-Chi Chang
Journal: Cancer Research (2015)

Abstract In previous studies, glycolysis machinery has been identified as a regulating pathway in cancer cell. However, the role of glycolysis in oral squamous cell carcinoma (OSCC) progression is still largely unknown. Fructose-bisphosphate aldolase C (ALDOC), one of the key enzymes in glycolysis, expresses in OSCC patients and cell lines and detects by real-time quantitative RT-PCR. The functions of ALDOC were determined by gain and loss function approaches and the orthotopic animal model was performed. ALDOC mRNA and protein expression was significantly decreased in advanced migratory cell and negatively correlated with lymph node metastasis and advanced tumor TNM stage in OSCC patients. In conclusion, ALDOC plays as an OSCC prognosis marker clinically, and functions to suppress OSCC cell migration and invasion. ALDOC could be a potential therapeutic target to block OSCC progression. Citation Format: Yueju Li, Tse-Hung Huang, Been-Ren Lin, Cheng-Chi Chang. The regulatory effect of fructose-bisphosphate aldolase C in oral squamous cell carcinoma progression. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1152. doi:10.1158/1538-7445.AM2015-1152
Serum tryptase evaluation in HCC patients who underwent transarterial chemoembolization.
Authors: G. Ranieri, V. Goffredo, A. Laterza, A. Picone, G. Gadaleta-Caldarola, G. Vinciarelli, V. Fazio, C. Oakley, M. Coviello, A. Vacca, C. D. Gadaleta
Journal: Journal of Clinical Oncology (2011)

e13543 Background: Tryptase is a serin protease stored in mast cell granules that plays a role in tumour angiogenesis. Data from experimental tumour models suggest that mast cells accumulate near tumour cells before the onset of angiogenesis and that they are required for the macroscopic expansion and metastatic spread of primary tumour cells. Hepatocellular cancer (HCC) is a well-established hypervascular tumour. This preliminary study aims to assess tryptase serum levels in 30 HCC patients before and after hepatic trans-arterial chemoambolization (TACE). Methods: In this study patients with intermediate stage (B) HCC (according to BCLC staging system) and adequate liver functional reserve (A or B status according Child-Pugh classification) were enrolled. Samples of blood were taken from HCC patients between 7 and 9 a.m.1 day before and 1 day after TACE. Venous blood was dispensed into a tube for serum (Becton Dickinson Hemogard Vacutainer Systems, Plymouth, UK). Serum blood samples were centrifuged at 1,500g for 10 minutes and then aliquoted and frozen at -80 °C. Tryptase levels were measured using the UniCAP Tryptase Fluoroenzymeimmunoassay (Pharmacia,Uppsala, Sweden). TACE was performed using doxorubicin loaded on microspheres (Dc-Bead; Biocompatibles, Farnham [GB]). Results: Mean ± s.d. tryptase level pre-TACE was 7.74 ± 3.62 μg/L, and mean ± s.d. tryptase level post TACE was 4.67 ± 2.79 μg/L. A statistically significant difference between pre-TACE and post-TACE tryptase level concentrations was found: p=0.000 by t-test. No correlation among tryptase levels and other important clinical-pathological features of patients were found. Conclusions: This is the first preliminary report that analyzes the possible significance of serum tryptase levels in HCC patients. Tryptase is one of the most powerful angiogenic mediators released by mast cells and it may be angiogenic via several mechanisms. On the other hand HCC is an hypervascular tumour. Our results demonstrated higher serum tryptase levels in HCC patients suggesting the release of tryptase from HCC tissue. As expected, after TACE, serum tryptase levels had decreased. We suggest that tryptase may play a role as a biomarker of response to TACE treatment in HCC patients.
Neoadjuvant stereotactic body radiation therapy (SBRT) for borderline resectable pancreas cancer: Moffitt Cancer Center initial experience.
Authors: M. D. Chuong, R. Shridhar, M. Patel, J. Klapman, J. S. Barthel, S. Vignesh, P. J. Hodul, G. M. Springett, M. P. Malafa, S. E. Hoffe
Journal: Journal of Clinical Oncology (2011)

302 Background: Our institution has reported a strategy of using neoadjuvant GTX (gemcitabine, docetaxel, and capecitabine) chemotherapy followed by 5FU-based intensity-modulated radiation therapy (IMRT) for borderline resectable pancreas cancer. We now report our early experience with induction chemotherapy followed by stereotactic body radiation therapy (SBRT). Methods: This retrospective review evaluates our initial 5 fraction SBRT experience in 15 patients following induction chemotherapy for borderline resectable pancreatic cancer. Staging included pancreatic protocol CT, endoscopic ultrasound, and PET/CT scan. Induction regimens consisted of GTX for 3 cycles in 12 patients and gemcitabine alone in 3. Daily SBRT was delivered to the pancreas at least 1 week after completing systemic chemotherapy. Endoscopically implanted fiducial markers and daily cone beam CT were used for image guidance. Treatment was delivered on a Varian Trilogy unit using 6-15 MV photons. Doses were selected based on dose painting the portion of tumor adjacent to the vasculature to a higher dose while meeting normal tissue constraints. The entire gross tumor received a dose of 5-6 Gy per fraction while the portion of the tumor adjacent to the vasculature resulting in the borderline designation received up to 8 Gy per fraction. Patients were re-imaged 3-4 weeks after SBRT for consideration of surgery. Results: There were no acute or late grade 3 toxicities. At the time of this analysis, not all treated patients have reached the restaging time point, but 9 of 15 (60%) were candidates for resection. Six patients have gone to resection with negative margins and without any increased complications. Two patients were found to have disease surrounding the vasculature preventing resection. One patient had cardiac issues at surgery and resection was aborted. One patient was explored and found to have liver metastases. Conclusions: Integration of SBRT in conjunction with systemic therapy is well-tolerated and appears to facilitate margin-negative resection in borderline resectable pancreatic cancer. No significant financial relationships to disclose.
Abstract 3331: Gene expression profiling after radiation in human breast cancer specimens and breast cancer cell lines
Authors: Sharareh Siamakpour-Reihani, Wei Chen, Chen-Ting Lee, Yingchun Zhou, Kouros Owzar, Jen-Tsan Chi, Janet K. Horton
Journal: Cancer Research (2015)

Abstract Background: Breast radiotherapy is currently “one size fits all” regardless of breast cancer subtype (eg. luminal, basal). Emerging clinical data suggests that these distinct subtypes of breast cancer have unique patterns of response to radiation. There is a clinical need to identify radiation response biomarkers in order to provide individualized and optimal radiotherapy. Here we report on gene expression profiles associated with radiation response from: i) a rare clinico-genomic data in women treated with preoperative breast radiation and, ii) data from a pilot study of 16 biologically diverse breast tumor cell lines. Methods: Microarray analysis was done using the Affymetrix GeneChip® Human Transcriptome Array 2.0 (HTA 2.0) and the Affymetrix HU133A2.0 arrays. RNA was harvested from paired pre- and post-radiation formalin-fixed paraffin-embedded breast cancer tissue in 26 patients treated with radiation prior to surgical resection. In addition, RNA was obtained from 16 biologically diverse breast cancer cell lines exposed to radiation treatment (5Gy and 0Gy). The genes with the highest coefficient of variation were selected and a paired sample t-test was used to evaluate the significance of these changes. We compared the top 100 significantly induced human genes with genes identified as differentially expressed in the 16 breast cancer cell lines. Findings of interest were validated using qPCR, IHC and wWestern blotting assays. Results: Fourteen genes had significant adjusted p-values for differential expression in the human data and were differentially expressed among the radiation responsive versus non-responsive cell lines. Differential expression of genes involved in: apoptosis, cell cycle and MAPK signaling pathways were observed in both the luminal human tumors and the largely luminal radiation responsive cell lines. Differential expression of FAS, a critical modulator of programmed cell death, was highly significant. Conclusion: The known function of FAS suggests a biologically plausible role in breast subtype specific radiation response. Induction of FAS is seen in human tissue, and preferentially in luminal breast cancer cell lines. Citation Format: Sharareh Siamakpour-Reihani, Wei Chen, Chen-Ting Lee, Yingchun Zhou, Kouros Owzar, Jen-Tsan Chi, Janet K. Horton. Gene expression profiling after radiation in human breast cancer specimens and breast cancer cell lines. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3331. doi:10.1158/1538-7445.AM2015-3331
Isolation and Characterization of Renal Erythropoietin-Producing Cells: Contribution of HIF3α In Vivo.
Authors: Xiaoqing Pan, Norio Suzuki, Ikuo Hirano, Shun Yamazaki, Toshiharu Yamashita, Osamu Ohneda, Naoko Minegishi, Masayuki Yamamoto
Journal: Blood (2010)
New Frontiers of Medical Illustration
Authors: Karen Bucher
Journal: JAMA (2016)

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Abstract 1548: Baseline serum levels of osteopontin and thrombospondin-1 predict shorter overall survival in primary resected non-small cell lung cancer
Authors: Mathieu Rouanne, Julien Adam, Aïcha Goubar, Angélique Robin, Caroline Ohana, Emilie Louvet, Jiemin Cormier, Olaf Mercier, Peter Dorfmüller, Soly Fattal, Vincent Thomas de Montpreville, Elie Fadel, Benjamin Besse, Ken André Olaussen, Christian Auclair, Jean-Charles Soria
Journal: Cancer Research (2015)

Abstract Background: Osteopontin and thrombospondin-1 are extracellular matrix proteins secreted by both stromal and tumor cells. These proteins may play a key role in the tumor microenvironment for cancer development and metastasis. This study focused on the prognostic value of circulating osteopontin and thrombospondin-1 in primary resected NSCLC patients. Methods: Between January and December of 2012, serums were collected from 171 patients prior to primary surgery and from age-matched cancer-free individuals (n = 20). At baseline, circulating osteopontin and thrombospondin-1 levels were measured by ELISA. Tissue protein expression in primary tumor samples was determined by immunohistochemical analysis. Results: High levels of serum osteopontin and thrombospondin-1 levels were found in the cohort study. The difference between patients and healthy individuals was statistically significant (p&amp;lt;0.0001). Serum levels of osteopontin and thrombospondin-1 were independent prognostic factors of overall survival in multivariate analysis (HR 1.71, 95% CI 1.04-2.82, p = 0.04 for an increase in osteopontin of 50 ng/mL; HR 0.18, 95% CI 0.04-0.87, p = 0.03 for an increase in thrombospondin-1 of 10 ng/mL) similarly to their combination (HR is 1.31, 95% CI 1.03-1.67, p = 0.03 for an increase in osteopontin/thrombospondin-1 ratio of 6 ng/mL). Osteopontin and thrombospondin-1 levels were inversely correlated to survival rates. Conclusions: Baseline osteopontin and thrombospondin-1 serum levels, and even more importantly their combination, can serve as strong independent prognostic factors to predict overall survival in primary resected NSCLC patients, and therefore reflect the aggressiveness of the tumor. Citation Format: Mathieu Rouanne, Julien Adam, Aïcha Goubar, Angélique Robin, Caroline Ohana, Emilie Louvet, Jiemin Cormier, Olaf Mercier, Peter Dorfmüller, Soly Fattal, Vincent Thomas de Montpreville, Elie Fadel, Benjamin Besse, Ken André Olaussen, Christian Auclair, Jean-Charles Soria. Baseline serum levels of osteopontin and thrombospondin-1 predict shorter overall survival in primary resected non-small cell lung cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1548. doi:10.1158/1538-7445.AM2015-1548