tbuckley/cabot-search huggingface dataset:
Abstract 4809: Validation of molecular subtypes of urothelial carcinoma of bladder in multi-institutional and public cohorts
Authors: Vipulkumar Dadhania, Charles G. Guo, Tadeusz Majewski, Li Zhang, Jolanta Bondaruk, Shizhen Zhang, Woonyoung Choi, David McConkey, Colin Dinney, Keith Baggerly, Bogdan A. Czerniak
Journal: Cancer Research (2015)

Abstract BACKGROUND: Recently we have proposed a molecular sub-classification of conventional urothelial carcinoma which could be divided into two major categories designated as basal and luminal similar to the ones defined for breast cancer. In addition, luminal cancers contain a group of cases characterized by upregulation of p53 regulatory genes and is referred to as p53-like. The purpose of this project is to verify whether such subtypes can be identified in several large independent cohorts of bladder cancers. DESIGN: Gene expression profiles and molecular subtyping were performed by using previously described analytical algorithms on the following bladder cancer patient cohorts: (1) The Cancer Genome Atlas (TCGA) cohort containing tumor tissues from muscle invasive high grade urothelial carcinomas of 129 patients; (2) the MD Anderson Cancer Center (MDA) cohort of fresh frozen tumor tissues which included 65 superficial papillary carcinomas and 77 invasive carcinomas; (3) the Swedish cohort containing fresh frozen tumor samples of 116 superficial papillary tumors and 192 invasive tumors. RESULTS: The three distinct molecular subtypes defined as luminal, p53-like and basal were identified in all three cohorts. The distribution of molecular subtypes in individual cohorts was as follows: the TCGA cohort contained 50 (39%) luminal, 30 (23%) p53-like and 49 (38%) basal tumors; the MDA cohort contained 54 (38%) luminal, 61 (43%) p53-like and 27 (19%) basal; the Swedish cohort contained 102 (33%) luminal, 129 (42%) p-53 like and 77 (25%) basal tumors. Interestingly, in the MDA and Swedish cohorts virtually all superficial tumors, of either low or high grade, were of luminal type. CONCLUSION: The conventional bladder cancer can be separated into three distinct molecular subtypes with luminal phenotype defining the vast majority of superficial bladder cancers while muscle invasive tumors can be separated into luminal and basal forms. A subset of luminal cancers is characterized by upregulation of p53 regulatory genes. The identification of subtypes may help to stratify the patients for targeted therapies. Citation Format: Vipulkumar Dadhania, Charles G. Guo, Tadeusz Majewski, Li Zhang, Jolanta Bondaruk, Shizhen Zhang, Woonyoung Choi, David McConkey, Colin Dinney, Keith Baggerly, Bogdan A. Czerniak. Validation of molecular subtypes of urothelial carcinoma of bladder in multi-institutional and public cohorts. [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 4809. doi:10.1158/1538-7445.AM2015-4809
Donor Type, Chronic Gvhd Subtype , and the Severity of Chronic Gvhd at the Time of Initiation of Chronic Gvhd Treatment Affect Failure-Free Survival in the Patients with Chronic Gvhd
Authors: Jieun Uhm, Elizabeth Shin, Marc Poch Martell, Fotios V. Michelis, Auro Viswabandya, Jeffrey H. Lipton, Hans A. Messner, Dennis Dong Hwan Kim
Journal: Blood (2015)
Efficacy of Nilotinib Versus High-Dose Imatinib in Early Chronic Phase CML Patients Who Have Suboptimal Molecular Responses to Standard-Dose Imatinib (RE-NICE Multicenter Study)
Authors: Hyun-Gyung Goh, Saengsuree Jootar, Hyeoung-Joon Kim, Sang Kyun Sohn, Joon Seong Park, Sung Hyun Kim, Dae Young Zang, Suk-Joong Oh, Soo-Young Choi, Ju-Hee Bang, Soo-Hyun Kim, Eun-Jung Jang, Sung-Eun Lee, Dongho Kim, Ji-Young Byeun, Richard C. Woodman, Tomasz Szczudlo, Hee Jung Kim, Dong-Wook Kim
Journal: Blood (2011)
Anemia Associated with Increased IL-6 and IL-8 Levels Predicts for Worse Progression-Free Survival in T-Cell and NK-Cell Large Granular Lymphocyte (LGL) Leukemia but Is Improved by Treatment with Cyclophosphamide
Authors: Craig A. Portell, Valeria Visconte, Michael J. Clemente, Manuel G. Afable, Ali Tabarroki, Fabiola Traina, Yang Liu, Betty K. Hamilton, Andres Jarez, Manoj Bupathi, Leonard J. Horwitz, Alan E. Lichtin, Anjali Advani, Mikkael A. Sekeres, Jaroslaw P. Maciejewski, Ramon V. Tiu
Journal: Blood (2012)
Expression of cancer-testis genes in glioblastoma.
Authors: M. R. P. Freitas, F. T. Zamuner, S. M. F. Malheiros, A. L. Vettore
Journal: Journal of Clinical Oncology (2011)

e12518 Background: Glioblastoma (GBM) is a highly invasive and aggressive tumor which confers a dismal prognosis despite advances of current therapy. Cancer vaccines have been utilized as treatment of other tumors and might be an option for brain tumors. Cancer-testis (CT) genes represent promising targets for immunotherapeutic approaches as they are expressed in tumors and expression in normal tissues is exclusively or preferentially restricted to testis. Methods: It was performed a search on Oncomine, NextBio, SAGE and PubMed databases to select among 153 CT genes those with high expression in glioblastomas and no expression in normal brain tissues. The expression of such genes was investigated in 50 glioblastomas and 5 normal brain samples using reverse-transcription polymerase chain reaction. Results: From the 30 CT genes selected (BAGE, BRDT, CSAG2, CT45, CTAG1A, CTCFL, CXORF48, CXORF61, DDX53, FTHL17, MAGEA1, MAGEA2, MAGEB4, MAGEB6, NFX2, OIP5, PBK, ROPN1, SLCO6A1, SOX6, SPANXN1, SPANXN2, SPANXN3, SPANXN4, SPINLW1, SPO11, SSX7, XAGE1, XAGE3, ZNF165) we identified 4 genes with high expression in tumors (94%, 29%, 100% and 35%) and low or any expression in normal brain (0%, 0%, 20% and 20%), respectively. Conclusions: It was identified 4 CT genes with high expression in glioblastomas which could be useful in the development of a polyvalent glioblastoma vaccine.
Abstract 339: Different receptor tyrosine kinases mediate EMT and erlotinib-resistance in NSCLC cell lines through bypass signalling
Authors: Kristine Raaby Jakobsen, Christina Demuth, Anne Tranbjerg Madsen, Birgit Westh Mortensen, Peter Meldgaard, Anders Lade Nielsen, Boe Sandahl Soerensen
Journal: Cancer Research (2015)

Abstract Introduction: Erlotinib is a potent drug in the treatment of EGFR-driven lung cancer. Many patients initially benefit from erlotinib treatment, but nearly all acquires resistance and die of the disease. Several mechanisms related to erlotinib-resistance have been described including epithelial to mesenchymal transition (EMT). Signalling by TGFβ, Wnt or through receptor tyrosine kinases can initiate EMT, but not much is known about the trigger in relation to erlotinib-resistance. In this study, we investigate how EMT is initiated in two erlotinib-sensitive NSCLC cell lines developing erlotinib-resistance. Methods: HCC827 (EGFR mutated) and Calu-3 (HER2 amplified) were treated with erlotinib in escalating concentrations (0.01 μM - 5 μM) over approximately 3 months, and erlotinib resistant (ER) sublines were established and investigated. Results: Both HCC827ER and Calu-3ER gained EMT features including upregulation of SLUG, SNAIL and ZEB1. These changes were accompanied by increased IGF1R signalling in Calu-3ER and HCC827ER gained a MET amplification. To detect the relevance of MET and IGF1R signalling in accordance to EMT, we treated the cells with the tyrosine kinase inhibitors crizotinib (MET) and linsitinib (IGF1R). In both cases, we saw a decrease in EMT-marker transcription after the treatment. In addition, HCC827ER showed growth inhibition when treated with the MET-inhibitor crizotinib, but linsitinib did not inhibit the growth of Calu-3ER. Conclusion: Our study demonstrates how different receptor tyrosine kinase signalling pathways can induce EMT during the development of erlotinib-resistance. Furthermore, we show that EMT can accompany well-know resistance mechanisms such as MET-amplification and hereby contribute to the phenotype of the resistant cells. Citation Format: Kristine Raaby Jakobsen, Christina Demuth, Anne Tranbjerg Madsen, Birgit Westh Mortensen, Peter Meldgaard, Anders Lade Nielsen, Boe Sandahl Soerensen. Different receptor tyrosine kinases mediate EMT and erlotinib-resistance in NSCLC cell lines through bypass signalling. [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 339. doi:10.1158/1538-7445.AM2015-339
Very High Hospital Admission Rate after Outpatient Non-Myeloablative Allogeneic Stem Cell Transplant Using Fludarabine and Low Dose TBI.
Authors: Brian Bolwell, Lisa Rybicki, Matt Kalaycio, Brad Pohlman, Steven Andresen, Stacey Brown, Elizabeth Kuczkowski, Jennifer Bates, Laura Bernhard, Kelly Cherni, Janet Baker, Ronald Sobecks
Journal: Blood (2005)
381. Organotypic Multicellular Scar Model; Innovative and Novel 3-Dimensional System for Keloid Study
Authors: Hyo Min Ahn, Il-Kyu Choi, Won Jai Lee, Ju Hee Lee, Yong Oock Kim, Chae-Ok Yun
Journal: Molecular Therapy (2015)

We developed a three-dimensional organotypic multicellular spheroid scar model to mimic the microenvironment of human keloid tissues. Keloid tissues were cultured for 7 days. Changes in total cellularity and apoptotic index in the primary keloid spheroid cultures were evaluated histologically and with a TUNEL assay, respectively. The expression profiles of transforming growth factor-b (TGF-b), collagen I, collagen III, elastin, fibronectin, matrix metalloproteinase-2, and matrix metalloproteinase-9 were examined with immunohistochemistry. In addition, these expression profiles were investigated after treating primary keloid spheroids with triamcinolone acetonide. Cell viability and morphology of ex vivo cultured keloid spheroids were maintained, and the apoptotic index did not increase for up to 1 week in culture. Keloid spheroids cultivated ex vivo retained the major characteristics of keloids, such as high levels of collagen I and TGF-bexpression for up to 7 days. The biological activity of keloids responding to TGF-b was also maintained during ex vivo culture. Moreover, ex vivo triamcinolone acetonide treatment of cultivated keloidspheroidssignificantlyredu cedcollagenI, collagen III, elastin, andfibronectin expression levels, in accordance with clinical observations. The three-dimensional organotypic multicellular spheroid keloid culture will allow investigators to study keloid pathogenesis and test potential keloid therapeutic agents.
Increasing the Number of Apheresis Collections Increases Lymphocyte Collection and Affects Survival after Autologous Stem Cell Transplantation for Non-Hodgkin Lymphoma.
Authors: Luis F. Porrata, Dennis A. Gastineau, Alvaro Pineda, Jeffrey L. Winters, S. Breanndan Moore, Douglas J. Padley, Kevin L. Bundy, Mark R. Litzow, Ivana N.M. Micallef, David J. Inwards, Stephen M. Ansell, Morie A. Gertz, Martha Q. Lacy, Angela Dispenzieri, Ayalew Tefferi, Michelle Elliott, William J. Hogan, Suzanne R. Hayman, Svetomir N. Markovic
Journal: Blood (2004)
Abstract PL02-03: Early detection and prevention of liver cancer: Leveraging lessons learned from liver repair
Authors: Anna Mae E. Diehl
Journal: Cancer Research (2015)

Abstract Liver cancer is currently among the top causes of cancer mortality worldwide and is increasing in both incidence and prevalence.The fact that cirrhosis is the strongest known risk factor for primary liver cancer suggests that injured liver is carcinogenic. The presentation will summarize evidence indicating that liver injury is carcinogenic because it stimulates regenerative responses (e.g., activation of developmental morphogenic signaling pathways) that relax forces which normally constrain the inherent multi-potency of adult liver cells. There are two main take-home messages. First, cirrhosis reflects defective regulation of these normal regenerative responses and thus, sustained tissue enrichment with permissive signals for multi-potency. Second, this cirrhotic microenvironment is particularly advantageous for liver cells with epistatic genetic/epigenetic events which enable escape from counter-regulatory signals that antagonize multi-potency. Citation Format: Anna Mae E. Diehl. Early detection and prevention of liver cancer: Leveraging lessons learned from liver repair. [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 PL02-03. doi:10.1158/1538-7445.AM2015-PL02-03
Automated phone prompts can improve healthcare, concludes Cochrane review
Authors: Jacqui Wise
Journal: BMJ (2016)

Automated telephone systems may change certain health behaviours, improve health outcomes, and increase healthcare uptake, a Cochrane review of the evidence has found.1

Automated phone communication systems send voice messages and can in some cases collect health information from patients by using their telephone keypad or voice recognition software. These can be used in a range of ways including helping patients to take their medicines as prescribed, giving appointment reminders, and helping to increase the uptake of immunisation or cancer screening tests. They can also help in managing …
T-Cell Subpopulations Quantified by Flow Cytometry in Lymph Node Cell Suspensions Identify a Group of Patients with Follicular Lymphoma with Good Prognosis.
Authors: Neus Villamor, Gonzalo Gutierrez, Joaquim Carreras, Eva Gine, Gabriela Ghita, Marta Aymerich, Montserrat Torrebadell, Antonio Martinez, Luis Colomo, Emili Montserrat, Elias Campo, Armando Lopez-Guillermo
Journal: Blood (2009)
Sequential treatment strategy for metastatic colorectal cancer: A phase III study of chemotherapy (CT) with or without bevacizumab (Bev) as first-line therapy followed by two phase III studies of CT alone or CT plus bev with or without cetuximab (Cetux) as second-line therapy (ITACa Study IRST 153 01).
Authors: F. Fabbri, A. Passardi, A. Ravaioli, L. Cavanna, G. Luppi, C. Mucciarini, M. Faedi, D. Turci, E. Pasquini, B. Vertogen, C. Milandri, D. Amadori
Journal: Journal of Clinical Oncology (2011)

e14161 Background: The commercialization of two monoclonal antibodies, bevacizumab (Bev) and cetuximab (Cetux) raises important questions about their use in the first- and second-line treatment of metastatic colorectal cancer. At present, their role in clinical practice is not well defined, especially in terms of timing of administration and possible side-effects compared to chemotherapy (CT) alone. Methods: Patients eligible for first-line treatment will be randomized to either treatment arm A: CT (FOLFOX or FOLFIRI at the physician’s discretion) + Bev or arm B: CT alone. The primary objective of this part of the study is to compare progression-free survival (PFS) in treatment arms. Upon progression, patients from arm A with Kras wild-type tumors will be randomized to arm C (the other CT schedule alone) or arm D (the other CT schedule + Cetux). Arm B patients with wild-type Kras will be randomized to arm E (the other CT + Bev) or arm F (the other CT+ Bev + Cetux). The superiority hypothesis regarding the use of Bev in first-line therapy requires 310 events (progressions) in a total of 350 patients to detect an absolute increase in PFS of 3 months, corresponding to a 27% relative reduction in the progression rate, with a 2-sided 5% significance level and an 80% power. It is assumed that about 75 patients will be included in each of the second-line studies. PFS as primary objective is an amendment currently under evaluation of the Ethical Committee. The objective response rates, OS and safety are secondary endpoints. The identification and evaluation of the role of tumor markers in predicting treatment response is one of the sub studies. Results: This independent study will be funded by the Italian Ministry of Health. At the end of December 2010, 24 centers had received Ethics Committee approval, and 23 are currently recruiting patients. To date a total of 267 patients have been randomized onto the first-line study. Conclusions: We plan to close recruitment in December 2011 and perform the final analysis in September 2012.
RAD51 increased expression as a predictor of outcome in patients with breast cancer.
Authors: P. Parrella, T. P. Latiano, R. Murgo, C. D'Addetta, R. Barbano, M. Copetti, V. M. Valori, F. Pellegrini, V. M. Fazio, E. Maiello
Journal: Journal of Clinical Oncology (2011)

e21106 Background: Mutations in DNA double strand breaks (DSB) repair genes are clearly associated with the pathogenesis of hereditary breast cancer. It is still unclear whether defects in this pathway may play a role in sporadic breast tumours development and progression. The aim of our study was to evaluate whether changes in expression of DSB repair genes is associated with breast cancer clinicopathological characteristics and patient’s outcome. Methods: We used a previously published breast cancer data set (van de Vijver et al. N Engl J Med 2009) that included clinical and gene expression data for 295 breast cancer cases. Data on local recurrence free survival, distant metasases free survival and overall survival were available for all patients. Reverse transcription quantitative PCR (qPCR) for mRNA determination and immunoistochemestry for protein analysis were used to confirm the association between the relevant genes analyzed and tumour clinicopathological characteristics on two independent data sets. Results: We correlated mRNA microarray expression data for 6 DSB repair genes (BRCA1, BRCA2, G22P1/ku70, ATR, RAD51, TP53) involved in key steps of the pathway with patient’s outcome using a Cox proportional regression model which also included the known breast cancer prognostic markers (ER, PR, Ki67 and HER2). Increased expression of the RAD51 gene was associated with a higher risk of local recurrence (HR 4.82, P=0.015) and development of distant metastases (HR 6.46, P=0.009). Together with other the other prognostic markers, RAD51 high expression was also a predictor of worse overall survival (HR 7.32, P=0.013). The analysis of an independent data set of 75 breast cancers by qPCR demonstrated that increased expression of the RAD51 gene was associated with a subgroup of Luminal A tumours characterized by absence of the progesterone receptor. This latter result was confirmed at protein expression levels by performing immunohistochemical analysis of the RAD51 protein on 58 breast cancer cases represented on a tissues microarray. Conclusions: Our results indicate that increased expression of the RAD51 gene may serve as an indicator of probability of tumour recurrence (local and distant) and overall survival in breast cancer patients.
Executive Summary: 2017 ERS/ATS standards for single-breath carbon monoxide uptake in the lung
Authors: Brian L. Graham, Vito Brusasco, Felip Burgos, Brendan G. Cooper, Robert Jensen, Adrian Kendrick, Neil R. MacIntyre, Bruce R. Thompson, Jack Wanger
Journal: European Respiratory Journal (2017)

This document summarises an update to the European Respiratory Society (ERS)/American Thoracic Society (ATS) technical standards for single-breath carbon monoxide uptake in the lung that was last updated in 2005. The full standards are also available online as https://doi.org/10.1183/13993003.00016-2016 . The major changes in these technical standards relate to D LCO measurement with systems using rapidly responding gas analysers for carbon monoxide and the tracer gas, which are now the most common type of D LCO instrumentation being manufactured. Technical improvements and the increased capability afforded by these new systems permit enhanced measurement of D LCO and the opportunity to include other optional measures of lung function.
Prognostic significance of biomarkers of diffuse large B-cell lymphomas
Authors: S. Kim, S.-E. Park, J. S. Kim, S. K. Kwak, H. J. Yun, D. Jo, J. M. Kim
Journal: Journal of Clinical Oncology (2004)

9639 Background: Although Diffuse Large B-cell Lymphomas (DLBCL) is usually considered as a specific disease entity, findings suggest diversity rather than a single clinicopathological entity. Clinical prognostic systems, including the International Prognostic Index (IPI), is useful in assessing overall prognosis with some reserve. It is likely that the prognostic assessment of patients with DLBCL might be improved by using biological features. Methods: To determine the clinical significance and prognostic value of biological markers expressed in DLBCL, we retrospectively studied 26 patients diagnosed as de novo DLBCL at Chungnam National University Hospital.Immunohistochemical studies were performed with CD10, bcl-6, IRF-4, bcl-2, p16, Granzyme B, and MHC-II, Ki-67 antibodies on archival pathology specimens. Two immunophenotypic patterns were distinguished according to the pattern of differentiation: germinal center (GC; CD10±/Bcl-6+/IRF-4 −) or post–germinal center (pGC; CD10±/bcl-6±/ IRF4+)type. Results: The median age was 56 (range;37∼69). 17 patients(65.4%) were male. 5 patients(19.2%) had ‘B’ symptoms. 11 patients(42.3%) had the elevated LDH level. 5 patients (19.2%) had bulky disease. After a median follow up duration of 48 months, the median survival time was 44 months with a range of 1∼100+ months. 5-year overall survival rate was 32% by Kaplan-Meier method. The clinical factors affecting survival were serum LDH level, stage, B Symptom, bulky disease, stage at diagnosis. The only immunologic marker affecting survival was bcl-2. In patients with the same IPI scores, bcl-2 positive patients had lower survival.(p = 0.002 ) The germinal center like type had better survival than post-germinal center like type but had no statistical significance. .(p = 0.064 ) Conclusion: Immunohistochemical profiles of DLBCL maybe useful in predicting survival, especially bcl-2 expression. Germinal center type had better survival than post-Germinal center like type without statistical significance. Large scale study in more patients are warranted. No significant financial relationships to disclose.
Preliminary Results from a Phase II Study of Lenalidomide Monotherapy in Relapsed/Refractory Aggressive Non-Hodgkin’s Lymphoma.
Authors: Peter H. Wiernik, Izidore Lossos, Joseph Tuscano, Glen Justice, Julie M. Vose, Dennis Pietronigro, Kenichi Takeshita, Annette Ervin-Haynes, Jerome B. Zeldis, Thomas M. Habermann
Journal: Blood (2006)
A Phase 2 Study of Vorinostat (Suberoylanilide Hydroxamic Acid, SAHA) Plus Rituximab in Newly Diagnosed, Relapsed or Refractory Indolent Non-Hodgkin's Lymphoma
Authors: Mark Kirschbaum, Leslie Popplewell, Maria L Delioukina, Robert w Chen, Vinod Pullarkat, Paul Frankel, Joel Conrad, Joyce Hartshorn, Auayporn Nademanee, Stephen Forman
Journal: Blood (2010)