tbuckley/cabot-search huggingface dataset:
Utility of novel dynamic clinical indices in patients (pts) enrolled in a phase I (Ph I) oncology trial as markers of prognosis and treatment benefit.
Authors: J. E. Ang, D. Olmos, V. Moreno Garcia, A. Brunetto, D. Papadatos-Pastos, H. Arkenau, M. Blanco, R. D. Baird, P. A. Cassier, D. S. W. Tan, R. S. Kristeleit, S. Dolly, K. J. Shah, B. Amin, B. G. Anghan, L. R. Molife, U. Banerji, J. S. De Bono, S. B. Kaye
Journal: Journal of Clinical Oncology (2011)

2555 Background: Stable disease (SD) over a defined time interval is used in early clinical trials of novel anticancer agents as an indicator of clinical efficacy. However, this assessment is likely to be confounded by the presence of slowly progressive disease pre-treatment. In this context, dynamic clinical indices that capture the evolution of malignancies are lacking. Hence, we derived the clinical tumor growth rate (CTGR) and the non-progression index (NPI). We hypothesized that the application of CTGR and NPI can help identify Ph I pts with SD who derive survival benefit from therapy. Methods: We retrospectively collected data from 973 pts consecutively treated in Ph I trials between 2004 and 2009 at the Royal Marsden Hospital. In addition to baseline pt and clinico-pathologic variables and trial outcomes, we derived 2 new variables, namely: CTGR, a log ratio of time between diagnosis of advanced cancer and Ph I entry over number of treatment lines, and NPI, a ratio of progression free survival (PFS) on Ph I trial over CTGR. We randomly divided our series into derivation (n=635) and validation (n=338) models for Cox regression analysis. Results: Median age of pts was 59 years (range 18-86) with a F/M ratio of 1.2. The commonest diagnoses were gynecologic (15%), colorectal (13%) and prostate cancer (13%). Median PFS and overall survival (OS) from Ph I entry were 10 and 39 weeks, respectively. Median CTGR was 26 weeks/treatment line (95%CI 24-28) and median NPI was 0.35 (95%CI 0.28-0.38). CTGR was an independent prognostic factor (for OS) in both models: derivation (p=0.012) and validation (p=0.036). RECIST-objective response (OR) and SD at 3 and 6-months were associated with improved OS, whereas prolonged SD was associated with slower growing tumors (p<0.001). The use of NPI identified 2 strata of pts with SD at 3 months: that with NPI>1.3 had OS approximating pts with OR while that with NPI<1.3 had OS approximating pts with frank progressive disease (p=0.012). Conclusions: The novel dynamic clinical index, CTGR, is independently prognostic for OS in our series, while the NPI provides an additional tool to help identify pts with SD at 3 months who are likely to derive survival benefit from Ph I therapy.
EBV-Negative Post-Transplant Lymphoproliferative Disorder (PTLD): A Retrospective Case-Control Study of Clinical and Pathological Characteristics, Response to Treatment and Survival
Authors: Ran Reshef, Alicia K. Morgans, Nicklas R. Pfanzelter, Roy D. Bloom, Susan C. Brozena, Vivek N. Ahya, Kim M. Olthoff, Donald E. Tsai
Journal: Blood (2008)
Dose Escalation of Caspofungin for Invasive Aspergillosis - A Phase II Trial
Authors: O. A Cornely, J. J Vehreschild, M. J Rüping, S. Schwartz, C. Heussel, Gerda Silling, J. Franklin, F. Farowski, T. Lehrnbecher, A. J Ullmann, A. Groll, Meinolf Karthaus
Journal: Blood (2010)
A Novel Function of MLL in the S Phase Checkpoint: MLL Is Phosphorylated by ATR Upon DNA Damage, Which Blocks Its Degradation by the SCFskp2 Proteasome, Leading to Its Accumulation That Directly Inhibits DNA Replication.
Authors: Han Liu, Shugaku Takeda, Rakesh Kumar, Todd Westergard, Tej Pandita, Emily Cheng, James J.-D. Hsieh
Journal: Blood (2009)
TRAXAR study: a randomized phase 2 trial of axitinib and TRC105 versus axitinib alone in patients with advanced or metastatic renal cell carcinoma (mRCC)
Authors: T. Choueiri, N. Agarwal, T. Ho, S.K. Pal, B. Seon, M. Jivani, B. Adams, R. Shazer, C. Theuer
Journal: Annals of Oncology (2016)
Phase I study of DKN-01 (D), an anti-DKK1 monoclonal antibody, in combination with gemcitabine (G) and cisplatin (C) in patients (pts) with advanced biliary cancer (ABC)
Authors: J. Eads, S. Stein, A. El-Khoueiry, G. Manji, T. Abrams, A.A. Khorana, R. Miksad, D. Mahalingam, C. Sirard, A.X. Zhu, L. Goyal
Journal: Annals of Oncology (2016)
Serum Uric Acid Levels Can Serve As a Sensitive Biomarker for Immunologic Activity in Patients Undergoing Hematopoietic Cell Transplantation
Authors: Sebastian P. Haen, Vicky Eyb, Nora Roth, Christoph Faul, Hans-Georg Rammensee, Lothar Kanz, Wolfgang A. Bethge
Journal: Blood (2011)
RARE-34. DIAGNOSIS AND MOLECULAR CHARACTERIZATION OF CSF-CTCs IN LEPTOMENINGEAL DISEASE (LMDz) FROM UVEAL MELANOMA (UM)
Authors: Inna Fedorenko, Brittany Evernden, Rajappa Kenchappa, Solmaz Sahebjam, Elena Ryzhova, John Puskas, Anthony Magliocco, Arnold B. Etame, Nam D. Tran, William Harbour, Keiran Smalley, Peter Forsyth
Journal: Neuro-Oncology (2016)

Uveal melanoma (UM) is uncommon and accounts for only ~5% of all melanomas. In spite of the physical proximity of UM to the brain, brain metastases and leptomeningeal disease (LMDz) are rare. Instead UM preferentially metastasize to the liver. We report a rare patient with LMDz from UM. Conventional methods (cytologies and LM biopsy) failed to diagnose LMDz or its tumor of origin. This is a case report where the clinical, laboratory and imaging data were reviewed. A diagnosis was made by isolating and genomically analyzing melanoma circulating tumor cells (CTCs) in the cerebrospinal fluid (CSF) we adapted using the CellSearch® platform and cell pellet. This is a 48 yo female with a history of UM 2 years ago, new neurologic radicular symptoms in her legs and an MRI showing classical LMDz. Systemic staging (e.g. Body PET/CT, mammograms etc.), cytology and a meningeal biopsy was non diagnostic. However, 138 CTCs/ml of CSF were enumerated (CD34-, CD45-, MEL-PE+), allowing for DNA isolation and further sequencing. This sequencing revealed a Q209P mutation in GNAQ, a mutation commonly found in UM confirming the CTCs’ origin as uveal. Other genes analyzed, without mutations detected, included AKT1, ALK, APC, BRAF, CDH1, CTNNB1, EGFR, ERBB2, FBXW7, FGFR2, FOXL2, GNAS, KIT, KRAS, MAP2K1, MET, MSH6, NRAS, PDGRFA, PIK3CA, PTEN, SMAD4, SRC, STK11 and TP53. Treatment consisted of IT chemo., a MEKi and a CTLA-4 AB. CSF CTCs decrease in number while she progressed. It is possible to make a diagnosis and molecular characterization of LMDz when conventional methods fail using CSF-CTCs. A focused mutational analysis for potential therapeutically relevant targets can be used to guide treatment. The relationship of this selected CSF-CTC marker to the population of CSF-CTCs and therapeutic decisions are being clarified.
Prospective study of EGFR intron 1 CA tandem repeats to predict factor benefit from cetuximab and irinotecan.
Authors: Carlotta Antoniotti, Fotios Loupakis, Chiara Cremolini, Wu Zhang, Dongyun Yang, Takeru Wakatsuki, Marta Schirripa, Lisa Salvatore, Vincenzo Ricci, Francesco Graziano, Gianluca Masi, Annamaria Ruzzo, Melissa Janae Labonte, Yan Ning, Rita El-Khoueiry, Alfredo Falcone, Heinz-Josef Lenz
Journal: Journal of Clinical Oncology (2012)

3540 Background: Retrospective experiences have investigated the potential influence of EGFR intron 1 CA repeats on the efficacy of cetuximab-containing treatments. Different series, adopting different criteria to define short (S) and long (L) variants, have provided contrasting results. Methods: We designed a prospective confirmatory study, to detect a HR for PFS of 1.75 for L- compared to SS genotypes in a population of KRAS and BRAF wild-type irinotecan-resistant mCRC pts treated with cetuximab and irinotecan. Estimating a prevalence of 60% of the SS variant and setting a two-sided alfa=0.05 with a power of 80%, 104 events were required. We defined S and L allelic variants those presenting &lt; and ≥20 CA repeats, respectively. EGFR (CA) n repeat polymorphism was assessed following a 5’-end [γ-33P] ATP-labeled PCR protocol. Results: One-hundred-fifteen pts were included. At a median follow up of 21.9 months, PFS and OS were 5.2 and 13.4 months, respectively. Thirty-three (29%) out of 114 evaluable pts achieved response. EGFR (CA) n repeat genotype was L- and SS in 45 (40%) and 68 (60%) out of 113 evaluable cases. No differences in PFS or OS were observed between L- and SS genotypes (median PFS: 4.4 vs. 5.3 months, HR: 1.00 [95%CI: 0.67-1.51], p=0.991; median OS: 11.3 vs. 14.2 months, HR: 1.30 [95%CI: 0.80-2.22], p=0.261). Ten (22%) out of 45 L- pts achieved response compared to 22 (33%) out of 67 SS pts (Fisher’s Exact test: p=0.617). Other exploratory analyses adopting different cut-off values reported in literature led to similar results. Conclusions: This prospective study, including a clinically homogenous and molecularly selected population, does not confirm any predictive or prognostic effect for EGFR (CA) n repeat allelic variants with respect to the efficacy of cetuximab and irinotecan in advanced lines of treatment. The present experience strengthens the need of prospectively challenging retrospective findings, as an essential step on biomarkers’ way toward clinical practice.
gastrointestinal tumours, non-colorectal Olaparib in combination with paclitaxel in patients with advanced gastric cancer who have progressed following first-line therapy: Phase III GOLD study
Authors: Y.-J. Bang, N. Boku, K. Chin, K.-W. Lee, S.H. Park, S. Qin, S.Y. Rha, L. Shen, N. Xu, S.-A. Im, G. Locker, P. Rowe, X. Shi, D. Hodgson, Y.-Z. Liu, R. Xu
Journal: Annals of Oncology (2016)
The optimal tumor response assessment in patients with HCC after treatment of TACE.
Authors: E. Jung, J. Kim, E. Yoon, H. Lee, Y. Lee, J. Yeon, K. Byun
Journal: Journal of Clinical Oncology (2011)

215 Background: WHO or RECIST has been considered as suboptimal methods for tumor response assessment in HCC, especially receiving locoregional therapies. Recently, new modified methods having concept of viable tumor has been proposed. Herein we compared the efficacy to assess response and to predict prognosis between WHO, RECIST, EASL, mRECIST in HCC patients receiving TACE. Methods: We retrospectively reviewed 141 HCC patients who were newly diagnosed and received TACE between August 2005 and November 2006. Among them, 98 patients who were available for assessing treatment response were analyzed at 1 month after 2nd TACE. We evaluated intermethod aggreement between methods and assessed the efficacy predicting time to progression (TTP) and overall survival (OS). Results: The results of tumor responses (number of CR/ PR/ SD/ PD) by WHO/ RECIST/ EASL/ mRECIST were 1/ 14/ 74/ 9, 1/ 12/ 77/ 8, 34/ 34/ 25/ 5, 34/ 28/ 31/ 5, respectively. The κvalue of intermethod agreement for EASL vs WHO, EASL vs RECIST, mRECIST vs WHO, and mRECIST vs RECIST was 0.102, 0.088, 0.112 and 0.122, respectively. The κvalue for WHO vs RECIST and EASL vs mRECIST was 0.759 and 0.883 (p=0.00). Hazard ratios for TTP in responders compared with nonresponders were 0.313 (95% CI; 0.19-0.52, p=0.00) for EASL and 0.335 (95% CI; 0.21-0.54, p=0.00) for mRECIST. Hazard ratios for survival in responders compared with nonresponders were 0.208 (95% CI; 0.12-0.37, p=0.00) for EASL and 0.269 (95% CI; 0.15-0.48, p=0.00) for mRECIST. In the univariate analysis, tumor size, infiltrative type, PVT, EASL responder, and mRECIST responder were significant risk factors for survival. Multivariate analysis showed EASL responder (HR 0.165, 95% CI 0.056-0.486, p=0.001) and infiltrative type (HR 4.504, 95% CI 1.579-12.848, p=0.005) were independent predictable factors for survival. Conclusions: The recent proposed methods showed different characteristics from preexisting methods in assessing treatment response and furthermore, responder by EASL method was independent predictor for survival in HCC patients receiving TACE. EASL method should be applied as response assessment method for HCC patients receiving TACE. No significant financial relationships to disclose.
CSIG-16. DEPLETION OF CLK2 SENSITIZES GLIOMA CELLS TO PI3K/mTOR AND FGFR INHIBITION
Authors: Soon Young Park, Jianwen Dong, Emmanuel Martinez-Ledesma, Yuji Piao, Roel G.W. Verhaak, John F. de Groot
Journal: Neuro-Oncology (2016)

The Cdc2-like kinase 2 (CLK2) has previously been reported to regulate various physiological processes. Inhibiting CLK2 blocked glioma cell growth in vivo via regulation of the cell cycle through the Akt/FOXO3a/p27 pathway. Clearly, effective therapies for glioblastoma will require targeting multiple pathways to overcome heterogeneity and redundancy in these signaling pathways. The present study was designed to determine therapies that are synergistic when combined with CLK2 knockdown. In GSC7-2, GSC272 and GSC20 cells, treatment with mTOR inhibitors in CLK2 knockdown lines led to modest reduction in cell viability compared to drug treatment alone. Depletion of CLK2 cells led to a synergistic combination effect at the higher concentration of FGFR inhibitor in GSC7-2, GSC272 and GSC20. GSK2126458, PI3K/mTOR, had the lowest IC50 values in all of the GSCs with an IC50 below 0.5 μM. Response to FGFR inhibition was shown to be cell line specific. GSC11, GSC7-2, GSC231, GSC295 and GSC300 being the most responsive with an IC50 of < 3 μM but GSC272, GSC8-11, GSC6-27, GSC20, GSC17 and GSC28 being the most resistant with an IC50 of > 3 μM. FGFR1 was more highly expressed than FGFR2 or FGFR3. The more sensitive cell lines had higher FGFR1 total expression levels and phosphorylation of FGFR1 (Tyr766) compared to resistant cell lines. Phosphorylation of FGFR1 and STAT3 also decreased in a dose dependent fashion upon treatment with FGFR inhibitor. Phosphorylation of mTOR, Akt, S6 kinase, and 4EBP1 decreased in a dose dependent manner following treatment with GSK2126458. PI3K/mTOR and FGFR inhibitors induced apoptosis in a dose dependent. Treatment with PI3K/mTOR and FGFR inhibitors in CLK2 knockdown lines led to synergistic apoptosis induction compared to drug treatment alone. Our findings suggest that the combination of CLK2 knockdown in combination with PI3K/mTOR or FGFR inhibitors may provide an effective therapeutic approach for glioblastoma.
Sequential Analysis of the α- and β-Globin Gene Expressions during Erythropoietic Differentiation from Primate ES Cells.
Authors: Umeda Katsutsugu, Toshio Heike, Gen Shinoda, Masato Arai, Feng Ma, Hirofumi Suemori, Hong Yuan Luo, Devid H.K. Chui, Ryuzo Torii, Masabumi Shibuya, Norio Nakatsuji, Tatsutoshi Nakahata
Journal: Blood (2005)
Impact of Lenalidomide Maintenance Therapy on Immune Polarization and Activation in Multiple Myeloma
Authors: Manisha Bhutani, David Foureau, Tammy Cogdill, Kyle Madden, Qing Zhang, Sarah A Baxter, Lawrence J Druhan, Nilanjan Ghosh, Belinda R Avalos, Edward A. Copelan, Saad Z Usmani
Journal: Blood (2015)
In Vivo Depletion of Cynomolgus Monkey B Cells Targeted by a Novel Monoclonal Antibody (Xi-20H5) Specific for a Shared Portion of the Human Immunoglobulin Variable Light Chain Lambda 1.
Authors: Thierry Sornasse, Keri Tate, Kimberly Milner, Thomas Theriault, Dan W. Denney
Journal: Blood (2007)
Excessive Respiratory Modulation of Blood Pressure Triggers Hypertension
Authors: Clément Menuet, Sheng Le, Bowen Dempsey, Angela A. Connelly, Jessica L. Kamar, Nikola Jancovski, Jaspreet K. Bassi, Keryn Walters, Annabel E. Simms, Andrew Hammond, Angelina Y. Fong, Ann K. Goodchild, Simon McMullan, Andrew M. Allen
Journal: Cell Metabolism (2017)
Child vs Adult Onset of Attention-Deficit/Hyperactivity Disorder—Reply
Authors: Arthur Caye, Ana M. B. Menezes, Luis Augusto Rohde
Journal: JAMA Psychiatry (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Psychiatry HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Psychiatry journal
TMOD-04. NATURALLY OCCURRING CANINE GLIOMA AS A MODEL FOR NOVEL THERAPEUTICS
Authors: Molly Hubbard, Susan Arnold, Abdullah Bin Zahid, Matthew McPheeters, Elizabeth Pluhar, Matthew Hunt
Journal: Neuro-Oncology (2016)

Human gliomas are among the most difficult tumors to treat. Current animal models are limited to small animal models that may or may not be fully relevant to aspects of human disease. We provide data for naturally occurring canine gliomas, which are a more similar model to human disease allowing for evaluation of combined medical and surgical therapies. We reviewed our case series of dogs with any type of glioma that underwent surgery as part of the Canine Brain Tumor Clinical Trials Program at the University of Minnesota. Breed, date of surgery, median progression-free (PFS) and overall survival (OS) times and cause of death were recorded for multivariate analysis. A total of 95 dogs (39 female, 56 male; mean age = 8.3 years) were included in the analysis. Gross total resection was reported in 81 cases based on postoperative MRI imaging. 70 were found to have high grade tumors (grade III or grade IV), 8 were excluded as final pathology was not tumor. Seizure was the most common presenting symptom, being present in 83 dogs. The average survival after surgery was >200 days. Grade II tumors had longer OS when compared high-grade tumors (474 days, 95% CI 249-698 for grade II; 191 days, 95% CI 119-264 for grade IV; p=0.032), but age (cox regression, p-value=0.14) and sex (Kaplan-Meier test, p-value 0.22) did not. This abstract offers descriptive data for a naturally occurring canine glioma model, which can be used to test different therapies prior to human trials. The classification of tumor grading did correlate with median survival after surgery. The survival did not correlate with age, sex, or breed. Further work will focus on the effects of different therapies, including chemotherapy, radiation therapy immunotherapy, or other targeted therapies.
Neuromedin U to increase IL-6 levels and to expand cancer stem cells in HER2-positive breast cancer cells.
Authors: Vanesa Gabriela Martinez, Sweta Rani, Claire Corcoran, John Crown, Lorraine O'Driscoll
Journal: Journal of Clinical Oncology (2015)

614 Background: Neuromedin U (NmU) is a neuropeptide belonging to the neuromedin family. Recently, a significant association between NmU signaling and cancer has been described, particularly correlated with increased aggressiveness and resistance to chemotherapy, although the mechanism through which it exerts this effect remains unexplained. Methods: HER2-positive breast cancer cells were stably transfected with NmU and IL-6 levels were measured by ELISA. Migration was evaluated in the presence of anti-NMUR antibodies by wound healing assays, while drug toxicity was assessed by the acid phosphatase assay. Results: Over-expression of NmU increases secreted levels of IL-6 (0 vs 0.303 ± 0.12 ng/µg, p = 0.04), a cytokine involved in promoting migration, expansion of the cancer stem cell population and drug resistance in breast cancer cells. NmU-transfected cells also show an increased proportion of cancer stem cells (CD44+/CD24-) (52.78 ± 5.765 vs 67.42 ± 5.172 in NmU-overexpressing cells, p = 0.07; fold change, 1 vs 1.31 ± 0.14, p = 0.00015) and increased expression of the lymphocyte activation inhibitor PD-L1, as detected by flow cytometry (49.50 ± 4.213 vs 60.06 ± 1.628, p = 0.0327); Furthermore, NmU over-expressing cells were shown to display enhanced resistance to antibody-dependent cell cytotoxicity mediated by Trastuzumab (47.13 ± 3.31% lysis of mock-transfected cells vs 36.46 ± 4.33% lysis in NmU-overexpressing cells, p = 0.05). Treatment with antibodies that block NmU receptors NMUR1 and NMUR2 reduces cell migration and enhances toxicity of HER2-targeted drugs in NmU over-expressing cells, suggesting that interaction of NmU with NMUR1 and NMUR2 are necessary for its effects. Conclusions: Altogether, our results show a new mechanism of action of NmU in HER2-positive breast cancer cells that enhances resistance to HER2-targeted drugs and the anti-tumor immune response, and is at least partially mediated by IL-6. Acknowledgements: Science Foundation Ireland's funding of MTCI 08/SRC/B1410; HRB’s Health Research Award [HRA-POR-2014-658]; Irish Cancer Society’s Breast-Predict [CCRC13GAL]; and HEA’s PRTLI Cycle 5 support of TBSI.
Estrogen-Induced Kidney Tumors in the Golden Hamster. I. Biochemical Composition During Tumorigenesis&lt;xref ref-type="fn" rid="FN1"&gt;2&lt;/xref&gt;
Authors: Robert F. McGregor, Joseph D. Putch, Darrell N. Ward
Journal: JNCI Journal of the National Cancer Institute (1960)

Male golden hamsters were treated with diethylstilbestrol to produce renal tumors. Analyses of total fat, protein, carbohydrate, and nucleic acid levels in both kidney and liver were made during the early stages of carcinogenesis (3 months), as tumors became detectable microscopically (8 months), and at a time when the tumors were well established (10 months). Appropriate controls were also examined. Appreciable changes in concentration of the foregoing constituents were not observed until the tumors were well established. Increased kidney weight appeared to be one of the earliest manifestations of tumorigenesis. Regression of the kidney tumors after 10 months of treatment with diethylstilbestrol followed by 1 month without estrogen was studied. Regression was complete in only 60 percent of the animals. For about one half of the animals, some factor other than removal of the excess estrogen appeared to be involved in the regression. Kidney function, as measured by urea clearance, was not affected after 8 months of treatment with diethylstilbestrol.
Reversal Multidrug Resistance and Biodistribution of Targeted Nanoparticles Tf-Peg-PLL-PLGA Combined with Daunorubicin and Tetrandrine in Tumor-Bearing Nude Mice
Authors: Liting Guo, Ping Liu, Fei Wang, Guohua Xia, Yonglu Wang, Wei Chen, Haixiang Yin, Baoan Chen
Journal: Blood (2014)
The Combination of ISS 3, High LDH and t(4;14) and/or Del(17p) Identify a Simple Prognostic Index for Overall Survival in Patients Treated with Novel Agents-Based Induction Therapy and Front-Line Autologous Stem Cell Transplantation, and Allow the Definition of a Subgroup of Patients At High-Risk of Early Death From Progressive Disease
Authors: Philippe Moreau, Lucie Planche, Michel Attal, Cyrille Hulin, Thierry Facon, Denis Caillot, Gerald Marit, Lotfi Benboubker, Anne-Marie Stoppa, Mauricette Michallet, Laurent Garderet, Philippe Casassus, Brigitte Pegourie, Brigitte Kolb, Laurent Voillat, Bruno Lioure, Murielle Roussel, Cyrille Touzeau, Xavier Leleu, Jean-Luc Harousseau, Herve Avet-Loiseau, Jean-Yves Mary
Journal: Blood (2012)
Prognostic Value of CD34 Expression in Patients with Acute Myeloid Leukemia Treated by Conventional Chemothearpy.
Authors: Jooseop Chung, Ho-Jin Shin, Young-Jin Choi, Goon-Jae Cho, Young-Don Joo, Won-Sik Lee, Eun-Yup Lee, Yun-Sik Yang
Journal: Blood (2005)
Consolidation Chemotherapy Is Not Beneficial for Adult Acute Lymphoblastic Leukemia Patients with Available Donor Undergoing Myeloablative Allogeneic Hematopoietic Cell Transplantation in First Complete Remission: A CIBMTR Study
Authors: Nelli Bejanyan, Aleksandr Lazaryan, Mei-Jie Zhang, Hai-Lin Wang, Marcos de Lima, Brenda M. Sandmaier, Mary M. Horowitz, H. Jean Khoury, Daniel J. Weisdorf
Journal: Blood (2016)