tbuckley/cabot-search huggingface dataset:
Abstract 626: Application of patient-derived xenograft model in nasopharyngeal carcinoma research
Authors: Cheng-Lung Hsu, Yung-Chia Kuo, Yenlin Huang, Yin-Cheng Huang, Kar-Wai Lui, Kai-Ping Chang, Tung-Liang Lin, Hsien-Chi Fan, An-Chi Lin, Chia-Hsun Hsieh, Li-Yu Lee, Hung-Ming Wang, Hsin-Pai Li, Angel Chao, Yu-Sun Chang
Journal: Cancer Research (2016)

Abstract Nasopharyngeal carcinoma (NPC) was an Epstein Barr virus (EBV)-related malignancy and tumor microenvironment had a pivotal role in tumor progression. Paucity of good NPC animal models hindered the research in this field. Recently, patient-derived xenograft (PDX) had been shown to be a good preclinical model for drug screening and cancer related research. We had developed two PDX mice lines from engrafting NPC metastatic tumors. Positive EBV-encoded small RNAs staining confirmed these tumors harboring EBV. Further gene expression profile analysis showed higher similarity of PDX to primary parent tumor than NPC cell line xenograft. In vivo drug screening in the PDX system demonstrated gemcitabine had the best antitumor effect among the tested drugs. In this PDX corresponding patient also showed excellent response to gemcitabine treatment. Combination of gemcitabine and valproic acid had synergistic antitumor effect. Further adding ganciclovir in this two combined regimen enhancing cytolytic viral activation had the best antitumor response among the tested regimens. This three combined regimen treated group had lower plasma EBV-DNA load and tumor viral concentration and less viable tumor cells than gemcitabine + valproic acid group. These promising results would open a new era for EBV-targeting therapy in NPC treatment. Citation Format: Cheng-Lung Hsu, Yung-Chia Kuo, Yenlin Huang, Yin-Cheng Huang, Kar-Wai Lui, Kai-Ping Chang, Tung-Liang Lin, Hsien-Chi Fan, An-Chi Lin, Chia-Hsun Hsieh, Li-Yu Lee, Hung-Ming Wang, Hsin-Pai Li, Angel Chao, Yu-Sun Chang. Application of patient-derived xenograft model in nasopharyngeal carcinoma research. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 626.
DNA methylation signature to define cell ontogeny of renal cell carcinomas.
Authors: Gabriel G. Malouf, Xiaoping Su, Jianping Zhang, Thai Huu Ho, Yue Lu, Noel J-M Raynal, Jose A Karam, Pheroze Tamboli, Frederick Allanick, Roger Mouawad, David Khayat, Christopher G. Wood, Jaroslav Jelinek, Nizar M. Tannir
Journal: Journal of Clinical Oncology (2016)

536 Background: DNA methylation is a heritable covalent modification that is developmentally regulated and is critical in tissue-type definition. Although genotype-phenotype correlations have been described for different subtypes of renal cell carcinoma (RCC), it is unknown if DNA methylation profiles correlate with morphological or ontology based phenotypes. Here we test the hypothesis that DNA methylation signatures can discriminate between putative precursor cells in the nephron. Methods: We performed deep profiling of DNA methylation in diverse histopathological RCC subtypes and validated DNA methylation and transcriptome signatures in The Cancer Genome Atlas Clear Cell and Chromophobe Renal Cell Carcinoma Datasets. Results: Our data provide the first mapping of methylome epi-signature and indicates that RCC subtypes can be grouped into two major epi-clusters: C1 which encompasses clear cell RCC, papillary RCC, mucinous and spindle cell carcinomas and translocation RCC; C2 which comprises oncocytoma and chromophobe RCC. Interestingly, C1 epi-cluster displayed three fold more hypermethylation as compared to C2 epi-cluster. Of note, differentially methylated regions between C1 and C2 epi-clusters occur in gene bodies and intergenic regions, instead of gene promoters. Transcriptome analysis of C1 epi-cluster suggests a functional convergence on Polycomb targets, whereas C2 epi-cluster displays DNA methylation defects. Furthermore, we find that our epigenetic ontogeny signature is associated with worse outcomes of patients with clear-cell RCC. Conclusions: Taken together, our data defines the epi-clusters that can discriminate between distinct RCC subtypes and for the first time, to our knowledge, define the epigenetic basis for proximal versus distal tubule derived kidney tumors.
Association of Regional Intensity of Ductal Carcinoma In Situ Treatment With Likelihood of Breast Preservation
Authors: Rinaa S. Punglia, Angel M. Cronin, Hajime Uno, Natasha K. Stout, Elissa M. Ozanne, Caprice C. Greenberg, Elizabeth S. Frank, Deborah Schrag
Journal: JAMA Oncology (2016)

<h3>Importance</h3> Large regional variation exists in the use of radiotherapy after breast-conserving surgery (BCS) for ductal carcinoma in situ (DCIS). Although patients who do not receive initial radiotherapy for DCIS are candidates for subsequent BCS if they experience a second breast event, many undergo mastectomy instead. <h3>Objective</h3> To examine whether regional practice patterns of radiotherapy for DCIS affect the use of mastectomy in these patients. <h3>Design, Setting, and Participants</h3> A retrospective analysis of population-based databases (Surveillance, Epidemiology, and End Results [SEER] and SEER-Medicare). Data were obtained for 2679 women in SEER with a diagnosis of DCIS between 1990 and 2011 and for 757 women in SEER-Medicare with a DCIS diagnosis between 1991 and 2009 who had not undergone radiotherapy for DCIS and experienced a subsequent breast cancer or DCIS diagnosis. <h3>Exposures</h3> Treatment intensity for primary DCIS (high, medium, low), as defined by separating health service areas (HSAs) into 3 clusters based on radiotherapy use. <h3>Main Outcomes and Measures</h3> Mastectomy vs BCS at a second breast event defined as DCIS recurrence or new invasive cancer. <h3>Results</h3> The median (SD) ages of the participants was 64 (13) years for the 2679 SEER population and 79 (6) years for the SEER-Medicare cohort. Residence in an HSA characterized by greater radiotherapy use for DCIS increased the likelihood of receiving mastectomy vs BCS at a subsequent breast event, even among women who had not previously received radiotherapy for DCIS. Adjusted odds ratios for receiving mastectomy were 1.43 (95% CI, 1.10-1.85) and 1.90 (95% CI, 1.27-2.84) in SEER and SEER-Medicare databases, respectively, among women residing in an HSA with the greatest radiotherapy use vs the least, corresponding to an adjusted increase from 40.8% to 49.6%, and from 38.6% to 54.5%. <h3>Conclusions and Relevance</h3> Areas with more radiotherapy use for DCIS had increased use of mastectomy at the time of a second breast event even among patients eligible for breast conservation. This association suggests that physician-related factors are affecting the likelihood of breast preservation.
Allogeneic Stem Cell Transplantation in a Pediatric Patient with Whim Syndrome
Authors: Saleh Bhar, Khaled Yassine, Caridad Martinez, Ghadir S. Sasa, Swati Naik, Donald Mahoney, Carl Allen, Nabil Ahmed, Meenakshi G. Hegde, Helen E. Heslop, Stephen Gottschalk, Robert A. Krance, Kathryn S. Leung
Journal: Blood (2015)
EFFICACY AND TOLERANCE OF TENOFOVIR DISOPROXIL FUMARATE PLUS EMTRICITABINE COMBINATION IN PATIENTS WITH CHRONIC HEPATITIS B - A EUROPEAN MULTICENTER STUDY
Authors: Si-nafaa Si-ahmed, Pierre Pradat, Maria Buti, Roeland Zoutendijk, Vincent Mallet, Claire Cruiziat, Katja Deterding, Jérôme Dumortier, Harry L. Janssen, Heiner Wedemeyer, Fabien Zoulim
Journal: Hepatology (2010)
Concurrent PI3K and NF-κB activation drives B-cell lymphomagenesis
Authors: H Y Jin, M Lai, J Shephard, C Xiao
Journal: Leukemia (2016)

Aberrant activation of the PI3K and NF-κB pathways occurs frequently in human B-cell lymphomas.1, 2 Recent studies suggested reciprocal molecular interactions between these two pathways in lymphomagenesis. For example, PI3K inhibition suppresses NF-κB activity in human Burkitt's lymphoma and diffuse large B-cell lymphoma,3, 4 while blockade of NF-κB causes suppression of PI3K activity in primary effusion lymphoma cell lines.5 Despite frequent alterations and molecular interactions of these two pathways in human lymphomas, genetic activation of anyone of these two pathways was not sufficient to initiate lymphoma development in mice.6, 7, 8
Abstract 2946: Increased ALDH7A1 expression enhances the resistance to the anticancer drugs and colony formation in lung cancer cell lines
Authors: Yuichi Sakamori, Hiroaki Ozasa, Eiji Kunii, Yoshitaka Yagi, Takahiro Tsuji, Takeshi Nomizo, Hiroki Nagai, Young Hak Kim, Ken Maeno, Tetsuya Oguri, Michiaki Mishima
Journal: Cancer Research (2016)

Abstract Background: Aldehyde dehydrogenase (ALDH) forms a superfamily of enzymes that catalyze conversion of aldehydes into carboxylic acids, and they are categorized into 19 families in human. Increased ALDH activity was reported to be a potential marker of cancer stem cell (CSC) in various solid tumors including lung cancer. Furthermore, High ALDH expression has been shown to be involved in drug resistance to conventional cytotoxic drugs. Recent studies revealed that ALDH7A1 is highly expressed in prostate cancer and associated with recurrence in patients with surgically resected non-small-cell lung cancer. However, there is not a fundamental link between ALDH7A1 expression and malignant phenotype, including drug resistance and colony formation. Material and methods: Anticancer drug resistant cell lines were established from lung cancer cell lines (PC-6, DMS53, PC-14, PC-9, NCI-H23 and NCI-H2228 cells) by exposure to various anticancer drug, including 7-ethyl-10-hydroxycamptothesin (SN-38), gemcitabine (GEM), cisplatin (CDDP), etoposide, paclitaxel (TXL), pemetrexed, amrubicin, erlotinib and crizotinib. Protein expression was determined by western blotting and gene expression was examined by RT-PCR. ALDH enzyme activity was measured by ALDEFLOUR TM assay. Proliferation was measured using MTS assay. ALDH7A1encoding plasmid was stably transfected into PC-14 cell. These transfected cells displayed sphere formation on ultralow binding plates and survived for more than 3 weeks. Results: We found that the levels of ALDH7A1 expression were higher in various anticancer drug-resistant lung cancer cell lines compared with the parental cells. ALDH enzyme activity was about 4-9 fold higher in SN-38, TXL, CDDP and GEM resistant cell lines (PC6/SN38, PC6/TXL, PC14/CDDP and PC14/GEM) than the parents cells. Up-regulation of ALDH7A1 expression by using a forced expression vector in PC14 cell altered cytotoxicity to SN-38 and TXL. Furthermore, overexpression of ALDH7A1in PC-14 cells enhanced sphere formation relative to the cells transfected with control vector. Conclusion: These results suggested that increased ALDH7A1 expression in lung cancer cell lines might be one of the mechanisms of acquired resistance to anticancer agents and enhance colony formation. Citation Format: Yuichi Sakamori, Hiroaki Ozasa, Eiji Kunii, Yoshitaka Yagi, Takahiro Tsuji, Takeshi Nomizo, Hiroki Nagai, Young Hak Kim, Ken Maeno, Tetsuya Oguri, Michiaki Mishima. Increased ALDH7A1 expression enhances the resistance to the anticancer drugs and colony formation in lung cancer cell lines. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2946.
Reconstructing the Human Hematopoietic Niche: Opportunities for Studying Normal and Malignant Hematopoiesis,
Authors: Richard W Groen, Willy A Noort, Reinier Raymakers, Henk-Jan Prins, Linda Aalders, Frans M Hofhuis, Berris van Kessel, Petra Moerer, Henk Rozemuller, Jan J. Schuringa, Joost de Bruijn, Michel de Weers, Paul W.H.I. Parren, Henk M. Lokhorst, Tuna Mutis, Anton CM Martens
Journal: Blood (2011)
"Salvage" therapy?
Authors: R Levin
Journal: Journal of Clinical Oncology (1994)

Article Tools Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.1994.12.9.1997 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 8083725 "Salvage" therapy? R LevinxR LevinSearch for articles by this author https://doi.org/10.1200/JCO.1994.12.9.1997 PDF ""Salvage" therapy?." Journal of Clinical Oncology, 12(9), pp. 1997–1998© 1994 by American Society of Clinical Oncology
Système de surveillance de laboratoire des infections à Chlamydia trachomatis et à Neisseria gonorrhoeae au Danemark
Authors: Steen Hoffmann
Journal: Eurosurveillance (2001)

Cet article presente les resultats de surveillance des infections C. trachomatis et N. gonorrhoeae au Danemark. En 1999 et 2000, on compte respectivement 291 et 309 cas de gonorrhee chez les hommes et 43 cas pour les femmes pour ces deux annees. Le taux de resistance a la penicilline est stable, avec une prevalence de 40 % des cas en 1999, alors que le taux de resistance aux fluoroquinolones a augmente de 0% des cas en 1990 a 27% en 1999. 
Le nombre de cas de chlamydiase s'est maintenu a environ 13 000 cas annuels. Les plus touches sont les hommes de 20-29 ans et les femmes de 15-24 ans.
T-Cell Depleted Allogeneic Hematopoietic Stem Cell Transplantation For Patients With Relapsed Multiple Myeloma and High-Risk Cytogenetics Permits Long-Lasting Remissions In The Absence Of Graft-Versus-Host Disease
Authors: Guenther Koehne, Sean M. Devlin, Heather Landau, Hani Hassoun, Alex Lesokhin, Nikoletta Lendvai, David J Chung, Christina Bravo, Sergio Giralt
Journal: Blood (2013)
Changes in Clinical Context for Kaposi's Sarcoma and Non-Hodgkin Lymphoma Among People With HIV Infection in the United States
Authors: Elizabeth L. Yanik, Chad J. Achenbach, Satish Gopal, Anna E. Coghill, Stephen R. Cole, Joseph J. Eron, Richard D. Moore, W. Christopher Mathews, Daniel R. Drozd, Ayad Hamdan, Mary E. Ballestas, Eric A. Engels
Journal: Journal of Clinical Oncology (2016)

Purpose The biology of HIV-associated cancers may differ depending on immunologic and virologic context during development. Therefore, an understanding of the burden of Kaposi's sarcoma (KS) and non-Hodgkin lymphoma (NHL) relative to antiretroviral therapy (ART), virologic suppression, and CD4 count is important. Patients and Methods KS and NHL diagnoses during 1996 to 2011 were identified among patients with HIV infection in eight clinical cohorts in the United States. Among patients in routine HIV clinical care, the proportion of cases in categories of ART use, HIV RNA, and CD4 count at diagnosis were described across calendar time. Person-time and incidence rates were calculated for each category. Results We identified 466 patients with KS and 258 with NHL. In recent years, KS was more frequently diagnosed after ART initiation (55% in 1996 to 2001 v 76% in 2007 to 2011; P-trend = .02). The proportion of patients with NHL who received ART was higher but stable over time (83% overall; P-trend = .81). An increasing proportion of KS and NHL occurred at higher CD4 counts (P &lt; .05 for KS and NHL) and with undetectable HIV RNA (P &lt; .05 for KS and NHL). In recent years, more person-time was contributed by patients who received ART, had high CD4 counts and had undetectable HIV RNA, whereas incidence rates in these same categories remained stable or declined. Conclusion Over time, KS and NHL occurred at higher CD4 counts and lower HIV RNA values, and KS occurred more frequently after ART initiation. These changes were driven by an increasing proportion of patients with HIV who received effective ART, had higher CD4 counts, and had suppressed HIV RNA and not by increases in cancer risk within these subgroups. An improved understanding of HIV-associated cancer pathogenesis and outcomes in the context of successful ART is therefore important.
Incidence of Acute Respiratory Distress Syndrome
Authors: Kamran Zafar
Journal: JAMA (2016)

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Role and therapeutic targeting of miR-21 in bladder cancer.
Authors: Alexandra Drakaki, Christos Polytarchou, Neil A. O'Brien, Dimitrios Iliopoulos, Dennis J. Slamon
Journal: Journal of Clinical Oncology (2015)

e15542 Background: MicroRNAs are small non-coding RNAs implicated in the pathogenesis of multiple types of cancer, including bladder cancer. MicroRNA-21 (miR-21) has been identified to have oncogenic function in most human cancers, by regulating essential signaling pathways. However, its role in bladder cancer oncogenesis has not been well studied. Thus, our aim was to evaluate miR-21 expression levels in different stages of human bladder cancer initiation and progression and examine the effectiveness of a novel miR-21 chemical inhibitor to suppress bladder cancer growth. Methods: MiR-21 expression was examined by real-time PCR in RNAs derived from 5 normal and 12 bladder cancer tissues and in a large panel of 28 bladder cancer cell lines. Suppression of miR-21 expression by a locked nucleic acid miR-21 (LNA-miR-21) was assessed by real-time PCR. The activity of the LNA-miR-21 chemical inhibitor in T24 bladder cancer cells was assessed by both cell growth and colony formation assays. Results: MiR-21 was found to be 5-fold up-regulated in bladder cancer relative to normal tissues. Furthermore, we identified that miR-21 expression was increased (3-fold) in advanced relative to early stage bladder tumors, suggesting its potential involvement in bladder cancer progression. MiR-21 was detected in all 28 bladder cell lines, with highest levels ( > 10-fold increase) in six (T24, 1A6, 5367, EJ28, SCABER, SW13) bladder cancer cell lines. Treatment with the LNA-miR-21 in T24 bladder cancer cells suppressed > 90% miR-21 expression levels, 72h post treatment. LNA-miR-21 suppressed ( > 60%) the growth of T24 cells in two-dimensional culture, 72h post treatment. Treatment with LNA-miR-21 reduced ( > 75%) the ability of T24 cells to form colonies in three-dimensional culture (soft agar). Conclusions: Our data revealed that miR-21 expression is up-regulated during human bladder cancer initiation and progression. Furthermore, we found that a novel miR-21 chemical inhibitor is highly effective in suppressing miR-21 expression and blocking the tumorigenicity of bladder cancer cells. Therefore, our studies identify that the novel microRNA-chemical compound could have therapeutic potential in bladder cancer and warrants further investigation in vivo models of this disease.
SNP Analysis Of The VWF GENE Identifies Multiple Common Variants THAT Affect VWF Levels and OCCUR At Different Frequencies In Patients With TYPE 1 VWD
Authors: Jesse Hinckley, Trudy Burns, Kai Wang, Ayse Bilge Ozel, Meadow Heiman, Amy Shapiro, Robert R. Montgomery, Lawrence Brody, Karl C. Desch, Jorge Di Paola
Journal: Blood (2013)
Neuro-ectodermal tumours
Authors: C. A. Hoefnagel
Journal: Clinical Nuclear Medicine (1998)

Since its first reported use in humans in 1981 [1], 131I-meta-iodobenzylguanidine (MIBG) has been used with success for the scintigraphic diagnosis of a variety of neuroendocrine tumours [2]. Derived from the neural crest, many of these tumours maintain the characteristic features of these cells, such as an active uptake-1 mechanism at the cell membrane and neurosecretory storage granules in the cytoplasm, which are responsible for the specific uptake and retention of MIBG.
Less Toxic Gemcitabine-Oxaliplatin Based Induction Regimen (R-GIDIOX) Prior to Autologous SCT Produces Outcomes Similar to High-Dose Cytarabine Containing Intensive Induction Regimen in Mantle Cell Lymphoma – a Follow up Report of the Multicenter Study
Authors: Vladimir I. Vorobyev, Sergei K. Kravchenko, Eduard G. Gemdzhian, Jana K. Mangasarova, Elena Baryakh, Alla M. Kovrigina, Tatiana N. Obukhova, Kamil Kaplanov, Egor I. Dubrovin, Ivan A Vorobjev, Natalya G. Turina, Valeri G. Savchenko
Journal: Blood (2014)
Comparison of drug approval between health Canada (HC) and the U.S. Food and Drug Administration (FDA).
Authors: Doreen Anuli Ezeife, Patricia Tang, Daniel Yick Chin Heng, Stephen Welch
Journal: Journal of Clinical Oncology (2012)

6082 Background: Differences in drug approval processes between countries can impact patient access to new therapies. In Canada, patients can freely access a new treatment after regulatory approval by Health Canada (HC) followed by funding approval from the provincial government. The aims of this study were to delineate the Canadian drug approval timeline and to compare the time to drug approval between HC and the US FDA. Methods: Cancer drugs approved by the FDA from 1989 to 2011 were reviewed. For each drug, the following endpoints were determined: publication date of phase I and pivotal phase III trial, date of FDA and HC approval, HC submission date, and funding approval in Alberta (AB). Time intervals between the aforementioned endpoints were calculated. Results: Of 55 FDA-approved drugs, 51 drugs are approved by HC with 40 of these drugs funded in AB. HC approval occurs an average of 14.4 months post FDA approval (95% CI -36.9 to 66.1, sign rank test p&lt;0.0001). However, there was no significant difference between the mean time from Phase I to FDA approval (48.5 months; 95% CI 21.2 to 75.8) and Phase I to HC approval (61.5 months; 95% CI 32.4 to 90.5). Most drugs (74%) were approved by the FDA prior to publication of the phase III trial. There was a trend towards faster drug approval from Phase III to FDA approval compared to HC (-14.97 versus 0.1 months, p = 0.05). HC submission occurs before FDA drug approval 77% of the time (mean 3.0 months prior; 95%CI: -59.1 to 43.4, p = 0.0206). HC approval occurs on average 17 months post HC submission. AB funding approval occurs on average 22 months after HC approval. The time interval from Phase I to AB funding approval was significantly shorter for targeted compared to cytotoxic agents (mean time 58 vs. 120 months; p = 0.039). Conclusions: HC drug approval lags behind FDA approval by about 14 months. Time from Phase III to drug approval tends to be shorter for the FDA compared to HC. This is the first documentation, to our knowledge, of the time required to bring a drug from phase I trial to provincial funding approval.