tbuckley/cabot-search huggingface dataset:
PO10AN INVESTIGATION INTO THE POTENTIAL OF THE KETOGENIC DIET IN THE CELLULAR METABOLISM OF PAEDIATRIC BRAIN TUMOURS
Authors: Lisa C.D. Storer, Lucy V. Elliman, Richard G. Grundy
Journal: Neuro-Oncology (2015)

INTRODUCTION: Paediatric high grade gliomas (pHGGs) are aggressive malignant tumours with very poor prognosis. Advances in treatment have been limited and so novel therapies are needed. The Ketogenic Diet (KD) is a high fat diet which forces the body to burn fat instead of carbohydrate, thus starving the glycolytic dependent tumour cells whilst providing ketone bodies as an energy source for normal neurons and glial cells. The KD has also been shown to increase sensitivity to radiotherapy and chemotherapy in HGG animal models and to have anti-angiogenic effects. We aimed to discover how many pHGG patients may benefit from this adjuvant therapy. METHOD: Expression of the ketolytic enzymes (potential markers for KD response) 3-oxoacid CoA-transferase (OXCT1) and D-beta-hydroxybutyrate dehydrogenase (BDH1) were evaluated by immunohistochemistry using formalin-fixed paraffin embedded material of 69 pHGG cases. Expression was assessed as either low ( 20%). RESULTS: IHC showed that 75% of samples were low expressors of OXCT1 and 77% of samples were low expressors of BDH1. Patients with low expression of the ketolytic enzymes, OXCT1 and/or BDH1 are more likely to benefit from participating in a KD trial. Whilst the patients in this cohort did not undertake the KD, the mean overall survival and event free survival was higher in those patients who had low expression of these enzymes. CONCLUSION: Our results suggest that IHC in a routine histopathology laboratory could be used to indicate those patients who may respond to the KD. In our cohort at least 75% of pHGG patients were low expressors of OXCT1 and BDH1 suggesting that the majority of pHGG patients may benefit from a KD.
IκBNS enhances follicular helper T-cell differentiation and function downstream of ASCl2
Authors: Junichi Hosokawa, Kotaro Suzuki, Kazuyuki Meguro, Shigeru Tanaka, Yuko Maezawa, Akira Suto, Lisa Fujimura, Akemi Sakamoto, Hans Clevers, Osamu Ohara, Hiroshi Nakajima
Journal: Journal of Allergy and Clinical Immunology (2016)
Abstract 1608: CTC categorization: Subpopulations of CTCs and their potential clinical significance
Authors: Chengsen Xue, Thomas W. Mc Closkey
Journal: Cancer Research (2015)

Abstract Circulating tumor cells (CTCs) were previously rare events difficult to identify. In clinical practice, CTC enumeration has now been recognized for its prognostic value. Furthermore, as CTC technology has rapidly improved, CTCs are now readily available for further investigation. The tumor cells isolated from CTC instruments may be analyzed for molecular profiles and mutation screening. Here we propose three new subsets of CTCs: elongated CTC (EL-CTC), miniature CTC (Mini-CTC) and cluster CTC (CL-CTC). Elongated CTC have an elongated shape and some of these cells have an enlarged tail composed of the nucleus. The enlarged tail is formed during intravasation because of the less flexible nuclear membrane and these cells represent highly motile tumor cells. The mini-CTCs are much smaller than regular tumor cells and may be dormant and gain the advantage of escaping immune surveillance. The CTC clusters are formed by a group of tumor cells and lymphocytes as well as macrophages. There is strong evidence that these clusters are highly malignant. These three subsets are recognized morphologically and their unique features may directly relate to their functionality and clinical significance. Additional investigation in the area of CTC research, specifically enhanced understanding of CTC subpopulations, may lead to novel therapeutic approaches in oncology. Citation Format: Chengsen Xue, Thomas W. Mc Closkey. CTC categorization: Subpopulations of CTCs and their potential clinical significance. [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 1608. doi:10.1158/1538-7445.AM2015-1608
Outcome of Allogeneic Hematopoietic Stem Cell Transplantation in Patients with Prior Invasive Aspergillosis
Authors: Marina O Popova, Alisa G Volkova, Soulaiman Elias Soulaiman, Olga N Pinegina, Svetlana M Ignatyeva, Tatyana S Bogomolova, Anna G Smirnova, Maria D Vladovskaya, Sergey N Bondarenko, Ludmila S Zubarovskaya, Nikolay N Klimko, Boris V Afanasyev
Journal: Blood (2015)
Decreasing Early Deaths in Acute Promyelocytic Leukemia (APL) By Using a Simplified Treatment Algorithm and Establishing a Network with Academic and Community Centers in USA
Authors: Anand Jillella, Martha Arellano, Asad Bashey, Sarah I. Vidito, Robert K. Stuart, Caleb Leung, Kaitlin Sitchenko, Manila Gaddh, Leonard T Heffner, Ravindra B. Kolhe, Jacques Galipeau, Amelia Langston, Vamsi K Kota
Journal: Blood (2015)
Multilineage Dysplasia Is Associated with Worse Clinical Outcome Independent of the Diagnosis of Acute Myeloid Leukemia or Myelodysplastic Syndrome.
Authors: Hesham M. Amin, Sherry A. Pierce, Elihu H. Estey, Hagop M. Kantarjian, Susan M. O’Brien, Francis J. Giles, Maher Albitar
Journal: Blood (2004)
Abstract 3996: Integrated analysis of miRNA profiling and bioinformatics reveals the potential key miRNAs in gastric cancer
Authors: Xiaojing Zhang, Xianling Feng, Yin Peng, Mengting Yang, Yong Huang, Xinmin Fan, Stephen J. Meltzer, Zhe Jin
Journal: Cancer Research (2015)

Abstract Supported by: National Natural Science Foundation of China, No.81172282; National Natural Youth Science Foundation of China, No.81302151; Shenzhen Peacock Plan, No.KQCX20130621101141669; Planned Science and Technology Project of Shenzhen, No.GJHS20120621142654087; the Key Laboratory Project of Shenzhen, No.ZDSY20130329101130496; Technological innovation group of SZU grants, No.T201202; NIH grants DK087454, CA146799, CA173390; an American Cancer Society Clinical Research Professorship. Gastric cancer (GC) remains a major health threat worldwide, and is one of the leading causes of cancer-related deaths in China. The discovery of microRNAs (miRNAs) has provided a new and powerful tool for studying diagnostic biomarkers and effective therapeutic targets in GC. By using microarray analyses of benign and malignant gastric epithelial cell lines (HFE145, NCI-N87, MKN28, RF1, KATO III and RF48), we discovered dysregulated 16 miRNAs, of which 11 were validated by real-time qRT-PCR. Based on miRWalk online database scans, 2532 potential mRNA targets of these 16 miRNAs were identified. Bioinformatic analyses suggested that these predicted targets were principally involved in tumor pathogenesis, MAPK signaling, and apoptosis. Finally, miRNA-gene network analyses identified miRNA- 125b as being potentially vitally important in GC. Citation Format: Xiaojing Zhang, Xianling Feng, Yin Peng, Mengting Yang, Yong Huang, Xinmin Fan, Stephen J. Meltzer, Zhe Jin. Integrated analysis of miRNA profiling and bioinformatics reveals the potential key miRNAs in gastric 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 3996. doi:10.1158/1538-7445.AM2015-3996
A phase III multicenter trial comparing two different sequences of second/third line therapy (irinotecan/cetuximab followed by FOLFOX-4 vs. FOLFOX-4 followed by irinotecan/cetuximab in K-RAS wt metastatic colorectal cancer (mCC) patients refractory to FOLFIRI/Bevacizumab
Authors: G. Rosati, G. Nasti, S. Lonardi, A. Zaniboni, A. Romiti, M. Aglietta, D. Bilancia, V. Iaffaioli, V. Marsico, M. Giordano, D. Corsi, F. Ferraù, R. Labianca, R. Berardi, F. Galli, L. Frontini, S. Cascinu
Journal: Annals of Oncology (2015)
Clinical Efficacy of Lenalidomide {Revlimid®} in Patients with Relapsed or Refractory Chronic Lymphocytic Leukemia (CLL): Updated Results of a Phase II Clinical Trial.
Authors: Asher Alban Chanan-Khan, Kena C. Miller, Laurie Musial, Swaminatha Padmanabhan, David Lawrence, Zale P. Bernstein, Kenichi Takeshita, David Spaner, Catriona Byrne, Cynthia Chrystal, Myron S. Czuczman
Journal: Blood (2006)
Proteomic Profiling of 128 Proteins In 194 Acute Lymphocytic Leukemia (ALL) Patients Using Reverse Phase Proteins Arrays (RPPA) Reveals Recurrent Proteins Expression Signatures with Prognostic Implications
Authors: Steven M. Kornblau, Yi Hua Qiu, Nianxiang Zhang, Kevin R Coombes, Susan O'Brien, Hagop M. Kantarjian, Deborah A Thomas
Journal: Blood (2010)
Correlation of kinase genotypes and activity of sunitinib in imatinib failure gastrointestinal stromal tumor.
Authors: J. Li, L. Shen, J. Gao, L. J. Hong
Journal: Journal of Clinical Oncology (2011)

e20521 Background: Sunitinib, which targets KIT, PDGFR, VEGFR, has demonstrated efficacy in patients with GIST after they experience imatinib failure. A study from JCO reported GIST patients with exon 9 gene mutation or wild type had more benefit receiving sunitinib treatment. We analysed the impact of primary and secondary gene mutation on sunitinib treatment in Chinese GIST patients. Methods: We assessed the tumor response according to RECIST criterion in 31 patients with imatinib-resistant/intolerant GIST, and examined the Kit/PDGFRA mutation status by using tumor specimens obtained before or after prior imatinib therapy. Progression-free survival (PFS) was evaluated with Kaplan-Meier methods and log-rank tests. Results: Primary gene mutations examination were performed in all the patients and secondary gene mutations in nine patients. Primary gene mutations were identified in 77.4% GIST. 61.3% had exon 11 mutation, 12.9% had exon 9 mutation, 3.2% obtained exon 17 mutation, no PDGFR gene mutation was found. 77.8% patients had secondary gene mutation of the nine patients and the more commonly secondary mutation were located in exon 13 and exon 17. Disease control rate with sunitinib were observed for primary genotype: KIT exon 9 (75%),wild-type Kit/PDGFRA(57%) and Kit exon11(53%). The patients with exon 9 mutation had more longer PFS (60 weeks, vs. wild type 21 weeks, p=0.022; vs. exon 11 mutation 29 weeks, p=0.070). Two patient with secondary Kit exon 13 mutation and one patient without secondary mutation had PR or SD, but those patients with primary or secondary Kit exon 17 muations showed no clinical benefit. Conclusions: GIST patients with KIT exon 9 mutation response well to sunitinib treatment; GIST with KIT exon 17 mutation is sunitinib-resistant.
Randomized Clinical Trials to Evaluate Mental Health Interventions in Resource-Poor Societies
Authors: Richard Neugebauer
Journal: JAMA (2016)

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Abstract 13434: Cardioprotection of Rosuvastatin Against Cardiac Dysfunction After Coronary Microembolization via Alleviating Inflammatory Induced Microinfarctions
Authors: Zhangwei Chen, Yuanyuan Cao, Juying Qian, Jianying Ma, Yunzeng Zou, Junbo Ge
Journal: Circulation (2015)

Backgrounds: It has been demonstrated that statins plays a critical role on prevention the risk of myocardial infarction. However, it is unclear about the effect of statins on coronary microembolization (CME), which is one of common complication after coronary intervention. Objectives: This experimental study was designed to evaluate the protective role of rosuvastatin on cardiac dysfunction caused by CME. Methods: Mice CME models were developed by injecting a total of 500,000 polyethylene micro-particles (average 9-12 diameters) into the left ventricle when transiently obstructed the ascending aorta for 15 seconds. There were three groups: sham-operation group (n=6), CME group (n=8) and rosuvastatin therapy group (n=7, oral received 20mg/kg per day one week before CME). Cardiac function was evaluated by echocardiography at baseline, 3 days and 10 days after procedure. HE staining was performed to detect the area of microinfarctions, while serum and myocardial expression of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were detected by ELISA and immunohistochemistry. Results: Compared with sham-operation group, left ventricular ejection fraction (LVEF) was significantly decreased in CME group (3 days later: 53.2±6.0% vs. 62.8±6.8%, P=0.002; 10 days later: 54.4±8.1% vs. 64.3±5.7%, P=0.014). Pre-treatment with oral rosuvastatin one week before CME improved cardiac dysfunction (3 days later: 59.8±5.4% vs. 53.2±6.0%, P=0.013; 10 days later: 61.2±5.2% vs. 54.4±8.1%, P=0.037). We also found that rosuvastatin therapy not only decreased the average area of microinfarctions (7.4±3.7% vs. 3.2±3.2%, P=0.012), but also inhibited myocardial expression of inflammatory factors, including TNF-α and IL-6. Conclusions: Inflammation mediated microinfarctions could be involved in cardiac dysfunction after coronary microembolization. Rosuvastatin could improve heart function by alleviating local myocardial inflammatory responses.
Combination Therapy with Rituximab and Fludarabine in Waldenstrom’s Macroglobulinemia.
Authors: Steven P. Treon, Andrew Branagan, Parveen Wasi, Christos A. Emmanouilides, Stanley R. Frankel, Andrew Lister, Pierre Morel, Jeffrey Matous, Sari Heitner Enschede, Eva Kimby
Journal: Blood (2004)
Results From the Phase III Randomized Trial of Onartuzumab Plus Erlotinib Versus Erlotinib in Previously Treated Stage IIIB or IV Non–Small-Cell Lung Cancer: METLung
Authors: David R. Spigel, Martin J. Edelman, Kenneth O’Byrne, Luis Paz-Ares, Simonetta Mocci, See Phan, David S. Shames, Dustin Smith, Wei Yu, Virginia E. Paton, Tony Mok
Journal: Journal of Clinical Oncology (2017)

Purpose The phase III OAM4971g study (METLung) examined the efficacy and safety of onartuzumab plus erlotinib in patients with locally advanced or metastatic non–small-cell lung cancer selected by MET immunohistochemistry whose disease had progressed after treatment with a platinum-based chemotherapy regimen. Patients and Methods Patients were randomly assigned at a one-to-one ratio to receive onartuzumab (15 mg/kg intravenously on day 1 of each 21-day cycle) plus daily oral erlotinib 150 mg or intravenous placebo plus daily oral erlotinib 150 mg. The primary end point was overall survival (OS) in the intent-to-treat population. Secondary end points included median progression-free survival, overall response rate, biomarker analysis, and safety. Results A total of 499 patients were enrolled (onartuzumab, n = 250; placebo, n = 249). Median OS was 6.8 versus 9.1 months for onartuzumab versus placebo (stratified hazard ratio [HR], 1.27; 95% CI, 0.98 to 1.65; P = .067), with a greater number of deaths in the onartuzumab arm (130 [52%] v 114 [46%]). Median progression-free survival was 2.7 versus 2.6 months (stratified HR, 0.99; 95% CI, 0.81 to 1.20; P = .92), and overall response rate was 8.4% and 9.6% for onartuzumab versus placebo, respectively. Exploratory analyses using MET fluorescence in situ hybridization status and gene expression showed no benefit for onartuzumab; patients with EGFR mutations showed a trend toward shorter OS with onartuzumab treatment (HR, 4.68; 95% CI, 0.97 to 22.63). Grade 3 to 5 adverse events were reported by 56.0% and 51.2% of patients, with serious AEs in 33.9% and 30.7%, for experimental versus control arms, respectively. Conclusion Onartuzumab plus erlotinib did not improve clinical outcomes, with shorter OS in the onartuzumab arm, compared with erlotinib in patients with MET-positive non–small-cell lung cancer.
Abstract 693: A yeast synthetic lethal screen identifies a conserved interaction between PLK1 and CKS1b affecting cancer cell viability
Authors: Robert J. Reid, Xing Du, Ivana Sunjevaric, Vinayak Rayannavar, John Dittmar, Matthew Maurer, Rodney Rothstein
Journal: Cancer Research (2015)

Abstract The CKS1b gene is located on chromosome 1q21 and is frequently amplified in breast, lung and liver cancers. CKS1b codes for a conserved regulatory subunit of cyclin-CDK complexes that functions at multiple stages of cell cycle progression. We used a high throughput screening protocol to mimic cancer-related over-expression in Saccharomyces cerevisiae mutants to identify genes whose functions become essential only when CKS1 is over- expressed, a genetic interaction termed synthetic dosage lethality (SDL). Mutations in genes affecting the mitotic entry checkpoint and genes affecting mitotic exit are evident among the SDL interactions identified. The mitotic entry checkpoint controls the stability of the mitotic inhibitor Swe1 (Human WEE1), resulting in delayed mitosis when cell polarity is disrupted. Swe1 is a tyrosine kinase that inhibits the cyclin-dependent kinase (CDK) complex by phosphorylation of a conserved tyrosine-19 on Cdc28 (Human CDK1). We find that the SDL interaction between Cks1 and the mitotic entry checkpoint requires both Swe1 and the Cdc28 tyrosine-19 residue. The mitotic exit network is a signaling cascade that controls post-anaphase inhibition of CDK activity necessary for progression into G1. Since the polo-like kinase Cdc5 (Human PLK1) functions in both the mitotic entry and mitotic exit pathways, we investigated the effect of targeting PLK1 in breast cancers with varying expression of CKS1b. We analyzed published datasets and found that growth inhibition resulting from PLK1 knockdown was strongly correlated with increased CKS1b expression levels in breast cancer cell lines [Marcotte, R., Brown, K., Suarez, F., &amp; Sayad, A. (2012). Cancer Discovery, 2:172]. We independently confirmed sensitivity to PLK1 knockdown in 8 breast cancer cell lines in which 3 of 4 sensitive lines had high CKS1b expression and 3 of 4 insensitive lines had low CKS1b expression. We modified CKS1b expression in hMEC cells and showed that increased expression enhanced apoptosis upon PLK1 knockdown while decreased CKS1b expression abrogated sensitivity. Thus identification of a yeast synthetic dosage lethal (SDL) interactions identifies a conserved interactions that may be targeted to kill cancer cells. Citation Format: Robert J. Reid, Xing Du, Ivana Sunjevaric, Vinayak Rayannavar, John Dittmar, Matthew Maurer, Rodney Rothstein. A yeast synthetic lethal screen identifies a conserved interaction between PLK1 and CKS1b affecting cancer cell viability. [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 693. doi:10.1158/1538-7445.AM2015-693
A Phase I/II Study of Pomalidomide-Cyclophosphamide-Prednisone (PCP) in Patients with Multiple Myeloma Relapsed/Refractory to Lenalidomide
Authors: Antonio Palumbo, Alessandra Larocca, Angelo Michele Carella, Davide Rossi, Vittorio Montefusco, Samantha Ferrari, Alberto Santagostino, Tommasina Guglielmelli, Monica Galli, Antonio Capaldi, Nicola Giuliani, Giacinto La Verde, Paola Omedè, Ileana Baldi, Mario Boccadoro, Paolo Corradini
Journal: Blood (2011)
Abstract 5351: Oral delivery of doxorubicin using bile enhancer for metronomic maintenance chemotherapy
Authors: Seho Kweon, Foyez K.A. Mahmud, Hyo Won Chang, Have Yoon Nam, Mi Ra Kim, Jung Je Park, Youngro Byun, Sang Yoon Kim
Journal: Cancer Research (2015)

Abstract Conventional chemotherapy requires therapy holiday due to their toxic adverse effects. However, the therapy holiday has been allowing cancer cell to relapse and caused secondary metastasis to occur in other tissue. On the contrast, metronomic maintenance chemotherapy (MMC) treats anticancer drugs frequently to reduce the adverse effects from normal tissues by maintaining low concentration in the blood. In this context, an oral route is more suitable for MMC than a parenteral route. Our oral delivery system that uses electrochemical property of bile acid derivatives increases bioavailability of doxorubicin (DOX) from below 5% to 26% by eluding p-gp. The antitumor studies showed that 5mg/kg/day oral DOX complex inhibited 70% of tumor volume in C3H mice model bearing SCC7 tumor. The H&amp;E staining of intestines and liver and the blood analysis proved that there were no histological and hematological toxicities. In addition, low dose of the DOX complex affects cell cycle regulation to arrest cancer cells. The concentration of 10nM, 30nM of DOX restricted the cell cycle at checkpoints in G1 phase of MCF-7 cells which are p-53 wild type and checkpoints in G2-M phase of MDA-MB 231 cells which are p-53 disruptive type. When MK8776, a inhibitor of cell cycle checkpoints, is treated with the low concentration of DOX, the cancer cells went through apoptosis or senescence depending on a type of cancer. In conclusion, our oral delivery of doxorubicin can offer safe and effective chemotherapy. Note: This abstract was not presented at the meeting. Citation Format: Seho Kweon, Foyez K.A. Mahmud, Hyo Won Chang, Have Yoon Nam, Mi Ra Kim, Jung Je Park, Youngro Byun, Sang Yoon Kim. Oral delivery of doxorubicin using bile enhancer for metronomic maintenance chemotherapy. [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 5351. doi:10.1158/1538-7445.AM2015-5351