tbuckley/cabot-search huggingface dataset:
Phase III multicenter web-based study demonstrating survival equivalents of nonplatinum-based chemotherapy for advanced non-small cell lung cancer (NSCLC): Subgroup analysis from D0112
Authors: J. R. Rigas, M. Carey, K. H. Dragnev, S. A. Simeone, R. D. Page, M. S. Rubin, H. Ghazal
Journal: Journal of Clinical Oncology (2008)

8100 Background: Based on limited data, NSCLC guidelines from ASCO includes non-platinum (non-P) therapy. D0112 provided the highest evidence supporting this guideline. Survival for this non-P and a carboplatin combination were equivalent. Recently, treatment choices and duration are based on subgroups of NSCLC. This report addresses the outcomes for subgroups from this trial. Methods: Eligibility patients (pts) with IIIB/IV NSCLC, performance status (PS) 0–2, and no prior chemotherapy. Randomized pts were stratified by stage (IIIB vs IV) and PS (0–1 vs 2) to arm A: carboplatin + docetaxel or arm B: gemcitabine + docetaxel. Therapy duration following 6 cycles was at the discretion of the investigator. Gender, histology, stage, PS, prior radiation, and central nervous system (CNS) metastasis were identified as independent variables. Multivariable analysis was performed using a proportional hazards regression. Wald test was performed. Treatment effect for each subgroups was evaluated. Results: Median follow-up time for 930 pts was 25.3 mos with 754 deaths. Median survival time (MST) for both treatment groups was 7.9 mos. Non-P arm was non-inferior to the platinum arm, unadjusted hazard ratio of 1.03 (95% confidence interval: 0.89 to 1.18) p = 0.017. By Wald tests, female (p = 0.002), IIIB (p = 0.025), adenocarcinoma (p = 0.002), and PS 0 (p < 0.001) had longer MST. Relative risk for each subgroups was not different for either treatment arm. Pts with non- squamous, no CNS disease and PS 0–1 had a MST of 9.5 mos. 314 pts (34%) received 6 cycles of therapy. Beyond 6 cycles, 163 pts received additional therapy and 151 pts had chemotherapy discontinued without disease progression. MSTs were 15.2 mos (1-yr 66%) and 13.1 mos (1-yr 55%) (p = 0.13), respectively. SAEs were more common for pts with more than 6 cycles (24% of pts) compared to treatment discontinued (16% of pts). Conclusions: For the palliative care of advanced NSCLC, non-P-based chemotherapy provides equivalent survival to carboplatin-based therapy. Females, intrathoracic disease, adenocarcinoma, and good PS do better with either therapy. This trial like others raises questions about the appropriate duration of therapy for incurable NSCLC. No significant financial relationships to disclose.
MPTH-38. TRANSFORMING GROWTH FACTOR-BETA GENE EXPRESSION AS A NEW PROGNOSTIC BIOMARKER FOR GLIOBLASTOMA
Authors: Laurent-Olivier Roy, Marie-Belle Poirier, Marie Blanchette, David Fortin
Journal: Neuro-Oncology (2016)

Glioblastoma (GBM) is the most common and aggressive malignant primary brain tumour in adults. Response to standard therapy is transitory, recurrence is inevitable and patients median overall survival is inferior to 15 months. The GBM phenotype is characterized by anarchic proliferation and invasiveness together with radio-/chemoresistance abilities. These features are strongly upregulated by transforming growth factor-beta (TGF-b). Therefore, we hypothesized that TGF-b gene expression could correlate with GBM patients overall survival (OS) and be utilized as a prognostic biomarker. Using targeted qPCR, we investigated the expression of TGF-b1 and -b2 in 159 GBM specimens harvested during surgery and 18 non-tumoral brain tissue. We found that both isoforms were significantly upregulated in GBM tumours (33- and 11-fold respectively). While TGF-b1 was the dominant isoform in newly diagnosed tumours (2-fold), no significant difference was observed in recurrent GBMs. Furthermore, TGF-b1 expression levels significantly correlated with OS and progression-free survival (PFS) in newly diagnosed patients. Indeed, multivariate analysis (Cox model) using expression levels as well as numerous clinical surrogates, revealed that high and moderate TGF-β1 expressing patients had a much poorer prognosis than the low TGF-β1 expressing tumours (hazard ratio [95% CI] was 1.998 [1.103 - 3.620]; p=0.022). Interestingly, at recurrence, neither isoforms had meaningful influence on clinical surrogates. In this study we show that TGF-b1 is the prevailing isoform in newly diagnosed GBM rather than the previously recognized TGF-b2. To our knowledge, this study is the first to reveal a significant correlation between TGF-b1 gene expression and OS or PFS in newly diagnosed GBM. Therefore, we believe that TGF-b1 could be used as a prognostic biomarker and/or target which could influence treatment planning and clinical followup of GBM patients.
KRAS mutations(m) in lung adenocarcinoma (AC) patients(p) receiving standard chemotherapy (ch) and immune checkpoint inhibitors (i-CI): Impact of KRAS clonality and coexisting TP53m
Authors: N. Pardo Aranda, F. Ruiz, A. Martinez Marti, S. Cedres, A. Navarro Mendivil, Idela fuente, A. Martinez de Castro, A. Vivancos, R. Dienstmann, E. Felip
Journal: Annals of Oncology (2016)
Predictors for in-Hospital Mortality in Patients with Autoimmune Thrombotic Thrombocytopenia Purpura (TTP): A Single Center Experience
Authors: Huy P. Pham, Wenjing Cao, Lance A. Williams, Alexander Z. Feldman, Rance C. Siniard, Robin G. Lorenz, Dheeraj Raju, Marisa B. Marques, X. Long Zheng
Journal: Blood (2016)
IMST-41. PARALLEL PROFILING OF MUTATIONAL LANDSCAPE, GENE EXPRESSION, AND T-CELL RECEPTOR REPERTOIRES IN SUBEPENDYMOMA REVEALS IMMUNOPHENOTYPIC HETEROGENEITY
Authors: Jennifer Sims, Xiaoyun Sun, Jun Wei, Jorge Samanamud, Justin Neira, Raymond Sawaya, Gregory Fuller, Amy Heimberger, Yufeng Shen, Peter Canoll, Jeffrey Bruce
Journal: Neuro-Oncology (2016)

Subependymomas, classified as WHO grade I gliomas, proliferate slowly, are largely benign, and are considered relatively homogenous by pathology. Radiographically they are indistinguishable from ependymomas and mixed subependymoma/ependymoma tumors. Little is known about the subependymoma microenvironment and how this sculpts immunological responses. Recent studies for malignant tumors have suggested a relationship between mutational load and immunotherapeutic efficacy; however immune reactivity in benign CNS tumors has not yet been directly characterized. In parallel with whole-genome/whole-exome sequencing and RNAseq profiling of surgical biopsies (n=16), we used high-throughput T cell receptor (TCR) sequencing to profile tissue-infiltrating lymphocytes (TILs) of seven subependymoma patients, one with mixed subependymoma/ependymoma. Despite the overall low mutation rate (median 29 somatic mutations/case), subependymomas were distinctly clustered by expression of cytokines and immune marker pathways; whereas the mixed tumor case expressed DNA damage and growth factor pathways, suggesting a more aggressive clinical phenotype. Using entropy-based statistics on the antigen-binding portion of the TCR, we found that divergence of the TIL repertoires from peripheral blood varied greatly across this cohort, indicating tumor-associated expansion of T cell clonotypes in certain subependymomas and the mixed tumor – similar to our prior findings in WHO grade II and IV gliomas (Sims et al. PNAS, 2016). As in that cohort, distinct “signature” TCR sequences, detectable in peripheral blood, inversely correlated with high divergence of the infiltrating, tumor-associated TCRs; whereas high abundance of this signature corresponded with low TIL divergence, as observed in non-neoplastic brain tissue and other subependymomas. Thus, the strong relationship between signature TCR usage and TIL divergence from blood (rho=-0.87, p=0.001), first identified in higher-grade tumors, was recapitulated in this cohort. Subependymomas, with low rates of mutation, nonetheless harbor microenvironmental and immunological heterogeneity. TCR repertoire-based, non-invasive predictors of these intratumoral immunophenotypes may be applicable to diagnosis and monitoring of subependymomas.
Dysregulation of metabolic pathways in a mouse model of allergic asthma
Authors: K. D. Quinn, M. Schedel, Y. Nkrumah‐Elie, A. Joetham, M. Armstrong, C. Cruickshank‐Quinn, R. Reisdorph, E. W. Gelfand, N. Reisdorph
Journal: Allergy (2017)

Abstract Background Asthma is a complex lung disease resulting from the interplay of genetic and environmental factors. To understand the molecular changes that occur during the development of allergic asthma without genetic and environmental confounders, an experimental model of allergic asthma in mice was used. Our goals were to (1) identify changes at the small molecule level due to allergen exposure, (2) determine perturbed pathways due to disease, and (3) determine whether small molecule changes correlate with lung function. Methods In this experimental model of allergic asthma, matched bronchoalveolar lavage ( BAL ) fluid and plasma were collected from three groups of C57 BL 6 mice (control vs sensitized and/or challenged with ovalbumin, n=3‐5/group) 6 hour, 24 hour, and 48 hour after the last challenge. Samples were analyzed using liquid chromatography‐mass spectrometry‐based metabolomics. Airway hyper‐responsiveness ( AHR ) measurements and differential cell counts were performed. Results In total, 398 and 368 dysregulated metabolites in the BAL fluid and plasma of sensitized and challenged mice were identified, respectively. These belonged to four, interconnected pathways relevant to asthma pathogenesis: sphingolipid metabolism ( P =6.6×10 −5 ), arginine and proline metabolism ( P =1.12×10 −7 ), glycerophospholipid metabolism ( P =1.3×10 −10 ), and the neurotrophin signaling pathway ( P =7.0×10 −6 ). Furthermore, within the arginine and proline metabolism pathway, a positive correlation between urea‐1‐carboxylate and AHR was observed in plasma metabolites, while ornithine revealed a reciprocal effect. In addition, agmatine positively correlated with lung eosinophilia. Conclusion These findings point to potential targets and pathways that may be central to asthma pathogenesis and can serve as novel therapeutic targets.
Activity of intravesical CG0070 in Rb-inactive superficial bladder cancer after BCG failure: Updated results of a phase I/II trial.
Authors: Terence W. Friedlander, Vivian K. Weinberg, Alex Yeung, James Burke, Donald L. Lamm, James M. McKiernan, John J. Nemunaitis, Joe Stephenson, Eric Jay Small, Lawrence Fong, Maxwell V. Meng
Journal: Journal of Clinical Oncology (2012)

4593 Background: Loss of retinoblastoma (Rb) tumor suppressor activity occurs commonly in bladder cancer and leads to upregulation of the E2F-1 transcription factor. CG0070 is a replication-competent oncolytic adenovirus genetically modified to express GMCSF under control of the human E2F-1 promoter. Updated results from a phase I study of CG0070 in patients with recurrent superficial bladder cancer (T1, Ta, Tcis) after BCG treatment are presented here. Methods: The V-0046 phase I/II study previously reported the safety and evidence of efficacy of single and multiple doses of intravesical CG0070. Efficacy was determined using quarterly cystoscopy, biopsy, and/or urine cytology. Tumor Rb status was assessed immunohistochemically in 18 tumors. Results: 35 patients were treated with either a single dose (n=13) of CG0070 ranging from 1x10 12 to 3x10 13 viral particles (vp) or with weekly x 6 (n=9) or every 4 week x 3-6 doses (n=13) ranging from 1x10 12 to 1x10 13 vp per dose. The most common adverse events regardless of schedule were flu-like illness, dysuria, hematuria, bladder spasm, and nocturia. No maximum tolerated dose was reached. Urine GMCSF and CG0070 levels were detectable in almost all patients suggesting in-vivo viral replication. The CR rate in the single dose cohort was 23% (3/13), and 64% (14/22) in the multi-dose cohorts. The CR rate for patients with either CIS or Ta tumors was 65% (15/23). Of all responders, 11 recurred with a remission duration ranging from 3.0 - 33.4 months and 6 patients, all in the multiple dose cohorts, remain in remission as of last follow-up with a remission duration ranging from 3.3 – 38.2 months. Phosphorylated (inactive) Rb was detected in 13 of the 18 (72%) patients evaluated. Nine of these 13 patients (70%) had a complete response. All patients (5/5, 100%) with known phosphorylated Rb treated in the weekly cohort experienced a CR. Conclusions: CG0070 was well tolerated with minimal toxicities. Complete responses were more frequently observed in the multiple-dose cohorts, including durable CRs in patients with inactive Rb and in patients with CIS. Further study in Rb-inactive superficial tumors is warranted.
The Novel FLT3-N676K Mutant Induces Acute Leukemia Independently of the Inv(16) Chimeric Gene CBFB-MYH11
Authors: Kezhi Huang, Min Yang, Zengkai Pan, Florian H. Heidel, Michaela Scherr, Matthias Eder, Thomas Fischer, Guntram Buesche, Nils von Neuhoff, Arnold Ganser, Zhixiong Li
Journal: Blood (2015)
STMC-03. REPOSITIONING CHLORPROMAZINE AGAINST CHEMORESISTANT GLIOMA THROUGH THE INHIBITION OF CYTOCHROME C OXIDASE
Authors: Corinne E. Griguer, Claudia Oliva
Journal: Neuro-Oncology (2016)

Chlorpromazine (CPZ) is an FDA-approved phenothiazine widely used as psychotropic in clinical practice. The pharmacological mechanism is through blockage of dopamine receptor. Recent reports have demonstrated some anti-proliferative activity against colon and brain tumors. However, the effect of CPZ in chemoresistant glioma has not yet been reported. Chemoresistant patient derived glioma stem cells and glioma cell lines were used to investigate the inhibitory mechanism of CPZ. CPZ effectively inhibited tumor growth and induced cell cycle arrest through the inhibition of cytochrome c oxidase subunit 4 isoform 1. Inhibition of cell growth by CPZ is reactive oxygen species- dependent through p38 MAP-kinase activation and down-regulation of the oncoprotein BMI, resulting in stem cell depletion. Moreover, in orthotopic mouse brain tumor models, CPZ treatment is associated with significant increase in the median overall survival. These data suggest that CPZ can be repositioned for treating chemoresistant glioma tumors.
Introduction of a Quick Assay for ADAMTS13 Activity Improved a Survival of Acquired TTP Patients Who Received Platelet Transfusions
Authors: Yumi Yoshii, Masanori Matsumoto, Kurumatani Norio, Ayami Isonishi, Masahito Uemura, Yuji Hori, Masaki Hayakawa, Hideo Yagi, Charles L Bennett, Yoshihiro Fujimura
Journal: Blood (2014)
Symptom response in non-small cell lung cancer (NSCLC) patients (pts) treated with erlotinib: Quality of life analysis of the NCIC CTG BR.21 trial
Authors: A. Bezjak, F. Shepherd, D. Tu, G. Clark, P. Santabarbara, J. Pater, L. Seymour
Journal: Journal of Clinical Oncology (2005)

7018 Background: Erlotinib (Tarceva) prolongs survival in previously treated NSCLC pts (ASCO 2004). In the palliative setting, assessing symptoms and quality of life (QOL) is also important. Methods: BR.21 was a double blind placebo controlled phase III trial which randomized 731 pts with stage IIIB or IV NSCLC, who had failed 1st or 2nd line chemotherapy, to erlotinib 150 mg/day PO or placebo, in a 2:1 ratio. Primary endpoint was survival; QOL was a secondary endpoint, as assessed by EORTC QLQ-C30 and the lung cancer module at baseline and q 4 weeks until progression. Primary endpoint for QOL analysis was time to deterioration of cough, dyspnea and pain. In addition, mean changes from baseline in QOL domains and symptoms were compared between the arms, as well as proportions of patients improving/deteriorating. Results: Compliance to QOL completion was high (87% at baseline, >70% in follow up for >12 cycles). Both arms had comparable baseline QOL, with pts showing greatest impairments in global QOL (mean score 53–55), role (59–60) and physical functioning (64–65), and greatest symptom burden for fatigue (42–45), cough (43–39), dyspnea (35–36) and pain (34–38). 451 pts were included in primary symptom analysis for cough, 522 for dyspnea, and 527 for pain. Pts on erlotinib had clinically and statistically significantly longer time to deterioration of tumor-related symptoms: 4.9 vs 3.68 mo for cough (p=0.04), 4.7 vs 2.89 mo for dyspnea (p=0.01), and 2.79 vs 1.91 mo for pain (p=0.02). These findings were confirmed by analysis of proportion of pts with >10 point improvement in these symptoms (44%, 34% and 30% respectively, all significantly different from placebo). Differences in QOL domains were seen in the physical function (31% improved on erlotinib vs 19% on placebo, p 0.01), and in global QOL (35% vs 26%, p<0.01). Analysis of change over time revealed that there was a general trend towards improvement in most symptoms and QOL domains in erlotinib arm (with the exception of diarhea), but deterioration in the placebo arm. Conclusions: Erlotinib improves survival in previously treated pts with NSCLC, as well as tumor-related symptoms and some aspects of QOL. Author Disclosure Employment or Leadership Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration OSI OSI
Cell Cycle Entry Potentiates Elimination of Chemotherapy-Resistant Human AML Stem Cells.
Authors: Yoriko Saito, Naoyuki Uchida, Satoshi Tanaka, Mariko Tomizawa-Murasawa, Nahoko Suzuki, Shinsuke Takagi, Yuho Najima, Yuki Aoki, Akiko Sone, Atsushi Wake, Shuichi Taniguchi, Leonard D. Shultz, Fumihiko Ishikawa
Journal: Blood (2009)
First Report of the Prophylactic Administration of Ex Vivo Co-Stimulated Donor Lymphocyte Infusion (DLI) from Related and Unrelated Donors after Reduced Intensity Conditioning for High Risk Hematologic Malignancies
Authors: Steven C Goldstein, Bruce Levine, Jacqueline Smith, Joanne Hinkle, Selina Luger, Alexander Perl, Alison Loren, Noelle Frey, Edward Stadtmauer, Daniel Schullery, Jean Boyer, Dennis L. Confer, David Porter, Carl H. June
Journal: Blood (2008)
Discovery of a New Molecular Marker, Prohibitin, and Development of Candidates for New Chemotherapeutic Agents Targeting Prohibitin in Primary AML Cells.
Authors: Hye-Ran Kim, Myung-Geun Shin, Sun-Woo Lee, Hee-Nam Kim, Il-Kwon Lee, Hyeoung-Joon Kim, Hoon Kook, Jong- Hee Shin, Soon-Pal Suh, Dong-Wook Ryang
Journal: Blood (2008)
Ammonia lowering reverses sarcopenia of cirrhosis by restoring skeletal muscle proteostasis
Authors: Avinash Kumar, Gangarao Davuluri, Rafaella Nascimento e Silva, Marielle P.K.J. Engelen, Gabrie A.M. Ten Have, Richard Prayson, Nicolaas E.P. Deutz, Srinivasan Dasarathy
Journal: Hepatology (2017)

Sarcopenia or skeletal muscle loss is a frequent, potentially reversible complication in cirrhosis that adversely affects clinical outcomes. Hyperammonemia is a consistent abnormality in cirrhosis that results in impaired skeletal muscle protein synthesis and breakdown (proteostasis). Despite the availability of effective ammonia-lowering therapies, whether lowering ammonia restores proteostasis and increases muscle mass is unknown. Myotube diameter, protein synthesis, and molecular responses in C2C12 murine myotubes to withdrawal of ammonium acetate following 24-hour exposure to 10 mM ammonium acetate were complemented by in vivo studies in the hyperammonemic portacaval anastomosis rat and sham-operated, pair-fed Sprague-Dawley rats treated with ammonia-lowering therapy by l-ornithine l-aspartate and rifaximin orally for 4 weeks. We observed reduced myotube diameter, impaired protein synthesis, and increased autophagy flux in response to hyperammonemia, which were partially reversed following 24-hour and 48-hour withdrawal of ammonium acetate. Consistently, 4 weeks of ammonia-lowering therapy resulted in significant lowering of blood and skeletal muscle ammonia, increase in lean body mass, improved grip strength, higher skeletal muscle mass and diameter, and an increase in type 2 fibers in treated compared to untreated portacaval anastomosis rats. The increased skeletal muscle myostatin expression, reduced mammalian target of rapamycin complex 1 function, and hyperammonemic stress response including autophagy markers normally found in portacaval anastomosis rats were reversed by treatment with ammonia-lowering therapy. Despite significant improvement, molecular and functional readouts were not completely reversed by ammonia-lowering measures.Ammonia-lowering therapy results in improvement in skeletal muscle phenotype and function and molecular perturbations of hyperammonemia; these preclinical studies complement previous studies on ammonia-induced skeletal muscle loss and lay the foundation for prolonged ammonia-lowering therapy to reverse sarcopenia of cirrhosis. (Hepatology 2017;65:2045-2058).
Molecular profile in primary and metastatic breast cancer treated with Exemestane and Everolimus
Authors: M.E. Filieri, S.R. Bettelli, A. Maiorana, C. Caprera, S. Manfredini, F. Caggia, E. Iattoni, S. Cascinu, C. Omarini, F. Piacentini
Journal: Annals of Oncology (2016)
Rituximab Plus Bendamustin (R-B) Treatment In Patients with Aggressive Large B-Cell Lymphoma (LBCL): Response and Tolerability - a Single Institution Experience
Authors: Julia Horn, Martina Kleber, Ulrike Kohlweyer, Stefanie Hieke, Regina Herzog, Annette Schmitt-Gräff, Monika Engelhardt
Journal: Blood (2010)
Intermediate Dose Ara-C Followed by G-CSF: An Effective and Predictable Mobilization Regimen in Hematological Malignancies.
Authors: Francesca Ricci, Marco Montillo, Alessandra Tedeschi, Sara Miqueleiz, Erika Ravelli, Liliana Intropido, Barbara Scarapati, Enrica Morra
Journal: Blood (2007)
Liquid biopsy testing in routine clinical management of advanced non-small cell lung cancer: clinical validation in a single biopathology laboratory
Authors: A.T. Falk, M. Ilié, E. Long, V. Tanga, V. Lespinet, O. Bordone, M. Allegra, C. Ribeyre, J. Otto, M. Poudenx, C.-H. Marquette, V. Hofman, P. Hofman
Journal: Annals of Oncology (2016)
Therapeutic Plasma Exchange (TPE, plasmapheresis) for Treatment of Refractory Autoimmune Hemolytic Anemia (AIHA)
Authors: Vijay Sandilya, Lingyi Chen, Rachna Anand, Eugene Choi, Akhil Chopra, Michael Styler, Pamela Crilley, David Topolsky, Kristine Ward
Journal: Blood (2008)
Characteristics, Outcomes and Treatment of Patients with T-Cell Prolymphocytic Leukemia (T-PLL) - Single-Center Experience
Authors: Etsuko Aoki, Preetesh Jain, Alessandra Ferrajoli, Zeev Estrov, Michael Keating, Susan M. O'Brien, William G. Wierda, Nitin Jain, Philip A Thompson, Elias Jabbour, Sherry Pierce, Chitra Hosing, Hagop M. Kantarjian, Farhad Ravandi, Tapan M. Kadia
Journal: Blood (2016)
Spindle Cell Sarcoma of the Iliac Vein on 18 F-FDG PET/CT
Authors: Chung-Shin Bek, Hae Won Kim, Kyoung Sook Won, Bong-Il Song
Journal: Clinical Nuclear Medicine (2017)

A 44-year-old woman with a protruding mass of the right thigh underwent an 18F-FDG PET/CT and gadolinium-enhanced MRI. The 18F-FDG PET/CT scan revealed mildly increased 18F-FDG uptake in a large mass involving the right common and external iliac veins. The gadolinium-enhanced MRI revealed a well-enhancing soft tissue mass inside the right common and external iliac veins. The mass was diagnosed as high-grade spindle cell sarcoma with fibroblastic differentiation.
T-Cell Depleted Haematopoietic Stem Cells (HSC) Transplantation with Add Back of CD45RA Negative DLI: About 2 Cases
Authors: Liliane Liliane Dal-Cortivo, Rita Creidy, Aurélie Gabrion, Sébastien Héritier, Guilhem Cros, Anne Brignier, Jean-Marc Luby, Capucine Picard, Christophe Cambouris, Salima Hacein-Bey, Alain Fischer, Marina Cavazzana-Calvo
Journal: Blood (2012)
A Phase 1b Study of Midostaurin (PKC412) in Combination with Daunorubicin and Cytarabine Induction and High-Dose Cytarabine Consolidation in Patients Under Age 61 with Newly Diagnosed De Novo Acute Myeloid Leukemia: Overall Survival of Patients Whose Blasts Have FLT3 Mutations Is Similar to Those with Wild-Type FLT3.
Authors: Richard M Stone, Thomas Fischer, Ronald Paquette, Gary Schiller, Charles A. Schiffer, Gerhard Ehninger, Jorge Cortes, Hagop M. Kantarjian, Daniel J. DeAngelo, Alice Huntsman-Labed, Catherine Dutreix, Sumita Rai, Frank Giles
Journal: Blood (2009)