tbuckley/cabot-search huggingface dataset:
HLA-Haploidentical Hematopoietic Cell Transplantation after TCR-Αβ and CD45RA+ Depletion Following Reduced Intensity Conditioning in Adults and Children with Hematological Malignancies- Two-Year Follow-up of Multicenter Study in Singapore
Authors: Li Mei Poon, Yeh Ching Linn, Poh Lin Tan, Ziyi LIM, Balamurugan Vellayappan, Rajat Bhattacharyya, Ah Moy Tan, Lip Kun Tan, Teck Guan Soh, Colin Phipps Diong, Wing H. Leung, Liang Piu Koh
Journal: Blood (2019)
A Novel Cereblon E3 Ligase Modulator Eradicates Acute Myeloid Leukemia Stem Cells through Degradation of Translation Termination Factor GSPT1
Authors: Liqing Jin, Nathan Mbong, Stanley W.K. Ng, Jean C.Y. Wang, Mark D. Minden, Jinhong Fan, Daniel W. Pierce, Michael Pourdehnad, John E. Dick
Journal: Blood (2019)
ACTR-48. CLINICAL DEVELOPMENT TARGETING AXL IN RECURRENT GLIOBLASTOMA
Authors: Ichiro Nakano
Journal: Neuro-Oncology (2019)

Abstract Glioblastoma (GBM) is a lethal disease without effective therapies. Previously we reported that the TAM receptor tyrosine kinase family member AXL is upregulated in mesenchymal GBM and its knockdown induces apoptosis of mesenchymal but not proneural glioma sphere cultures (GSCs). In this study, we report that BGB324, a novel small molecule inhibitor for AXL, prolongs the survival of immunocompromised mice bearing mesenchymal GSC-derived GBM-like intracranial tumors by inhibition of AXL activation in tumor cells. Mechanistically, we identified that protein S (PROS1), known as a ligand for other TAM receptors, is secreted by tumor-associated macrophages, thereby physically associates and activates AXL in mesenchymal GSCs. The PROS1-driven phosphorylation of AXL resulted in the NF-kB activation in mesenchymal GSCs and this activation was eliminated by BGB324 treatment. In addition, BGB324 downregulated the immune checkpoint protein PD-L1 both in vitro and in vivo. Combination of BGB324 with Nivolumab - the neutralizing antibody for PD-1 (a receptor for PD-L1) was effective to prolong the survival of immunocompetent mice bearing syngeneic GBM models. Clinically, both AXL and PROS1 expression indicated poorer prognosis of GBM patients. These data suggest that the PROS1/AXL pathway regulates intrinsic mesenchymal signaling as well as extrinsic immune microenvironment, contributing to the growth of aggressive GBM tumors. To translate the pre-clinical data to human GBM patients, we designed a surgical PK/PD clinical trial with BGB324 for recurrent GBM. As of May 2019, this trial, termed ABTC1701, is in pending approval by the Brain Malignancy Steering Committee in the National Cancer Institute.
Cachexia at Diagnosis adversely predicts outcomes in patients with Aggressive B-Cell NHL receiving standard of care treatment: A Prospective Observational Study from India
Authors: Vivek S Radhakrishnan, Reena Nair, Anwesha Patra, Saurabh Jayant Bhave, Jeevan Kumar Garg, Mohandas Mallath
Journal: Blood (2019)
GENE-35. MGMT PROMOTER METHYLATION IN NEWLY DIAGNOSED LGG AS A POTENTIAL BIOMARKER FOR TMZ-ASSOCIATED HYPERMUTATION AT RECURRENCE
Authors: Radhika Mathur, Yalan Zhang, Matthew Grimmer, Chibo Hong, Mitchel Berger, Annette Molinaro, Nancy Ann Oberheim-Bush, Susan Chang, Joseph Costello
Journal: Neuro-Oncology (2019)

Abstract Low-grade gliomas (LGGs), which include grade II astrocytoma and grade II oligodendroglioma, inevitably recur despite aggressive treatment with surgery, and sometimes, with radiation and the chemotherapeutic agent temozolomide (TMZ). The clinical benefit of TMZ in LGG is unclear, and a subset of TMZ-treated LGGs recur with hypermutation in association with malignant progression to high-grade tumors. It is currently unknown why some TMZ-treated LGGs recur with hypermutation while others do not. O6-methylguanine-DNA methyltransferase (MGMT) is a DNA repair protein that reverses mutagenic lesions induced by TMZ. The amount of MGMT protein in a cell is regulated at the epigenetic level by promoter methylation. Here, we hypothesize that epigenetic silencing of MGMT by promoter methylation facilitates TMZ-induced mutagenesis and contributes to the development of hypermutation. We demonstrate in a cohort of 37 TMZ-treated patients with an initial diagnosis of IDH-mutant LGG that methylation level of the MGMT promoter in initial untreated tumors is significantly associated with hypermutation at recurrence. We also confirm our previous finding that methylation level of the MGMT promoter in recurrent hypermutated tumors is higher than in recurrent tumors that are not hypermutated. These results provide a plausible mechanistic basis for observed differences in propensity of TMZ-treated LGG patients to develop hypermutation at recurrence. Furthermore, they establish the potential of MGMT promoter methylation level to inform treatment decisions in the clinic for patients with newly diagnosed LGG.
B-cell leukemia transdifferentiation to macrophage involves reconfiguration of DNA methylation for long-range regulation
Authors: Alberto Bueno-Costa, David Piñeyro, Marta Soler, Biola M. Javierre, Helena Raurell-Vila, Marc Subirana-Granés, Lorenzo Pasquali, Jose A. Martinez-Climent, Manel Esteller
Journal: Leukemia (2019)
Evaluation of Clinical, Hematological and Flow Cytometry Dates in Elderly Patients with Acute Myeloid Leukemia: Impact on Clinical Outcome
Authors: Alessandra Suelen Jardim Silva, Lenilton Silva DA Silva Júnior, Gustavo Henrique de Medeiros Oliveira, Antonia Eduarda Martins Oliveira Elói Silva, João Pedro Andrade Lima, Victor lima Soares, Rodrigo Villar Freitas, Frank Bahia, Taissa Moura Oliveira, Dany GKC Silva, Valéria SF Sales, Hugo Diogenes De Oliveira Paiva, Rafael Santiago Araujo, Aldair Sousa Paiva, Geraldo Barroso Cavalcanti
Journal: Blood (2019)
R-Interferon Treatment before Imatinib Reverses the Negative Impact of e13a2 Transcript Type on Treatment Free Remission Duration after Tyrosine Kinase Inhibitors Discontinuation in Chronic Myeloid Leukemia Patients
Authors: Mariella D'Adda, Mirko Farina, Angela Passi, Rosa Daffini, Doriana Gramegna, Elisa Cerqui, Samantha Ferrari, Chiara Bottelli, Chiara Pagani, Erika Borlenghi, Diego Bertoli, Silvana Archetti, Mirella Marini, Giuseppe Rossi
Journal: Blood (2019)
RUNX2 Regulates Cell Migration in T-Cell Lineage Acute Lymphoblastic Leukemia
Authors: Nitesh Devinarayan Sharma, Christian C. Nickl, Huining Kang, Wojciech Ornatowski, Stuart S. Winter, Mignon L. Loh, Stephen P. Hunger, Ksenia Matlawska-Wasowska
Journal: Blood (2019)
DDIS-26. HIGH-THROUGHPUT DRUG SCREENING OF MENINGIOMAS IDENTIFIES HDAC INHIBITORS AS PROMISING TARGETS ACROSS GRADES
Authors: Philip Tatman, Anthony Fringuello, Teddy Wroblewski, Sam Scherer, William Foreman, D Ryan Ormond, Denise Damek, Kevin Lillehei, Randy Jensen, Michael Graner
Journal: Neuro-Oncology (2019)

Abstract Meningiomas are a common central nervous system (CNS) tumor, accounting for one third of CNS neoplasms. To date, no FDA approved pharmacotherapy exists for meningiomas. In an effort to identify potential treatments for meningiomas we created a culture system that allows us to grow and screen tumors across hundreds of compounds within two weeks of resection. We screened 32 meningiomas, six of which were World Health Organization (WHO) grade II, against the National Cancer Institute’s (NCI) FDA-approved cancer compound library and Caymen Chemical’s epigenetic inhibitor library, totaling to more than 300 compounds. The NCI library was screened at 1um, and the Caymen library was screened at 5um. Each library was screened in triplicate, allowing us to calculate statistical significance. We used an MTS assay to determine cell viability after three days. The data was background subtracted and normalized to controls. Significant changes in cell viability were determined for individual drugs using a Mann-Whitney-U test compared to untreated controls. On average, regardless of grade, 5.9 compounds per hundred screened significantly reduced tumor viability. We identified four compounds in the NCI FDA-approved library that reduced cell viability, on average across all tumors screened, by at least 50%: romidepsin, panobinostat, daunorubicin, and carfilzomib. Using the same criteria, we identified the following drugs from the Caymen epigenetic library: LAQ824, panobinostat, and HC toxin. Of the six compounds implicated as possible treatments for meningiomas, four are histone deacetylase (HDAC) inhibitors. HDAC inhibitors may represent a promising target for the treatment of meningiomas. Based on this data, we have begun in vivo work using PDX mouse models to investigate the therapeutic potential of HDAC inhibitors for the treatment of meningiomas.
Outcomes in Molecular Subgroups and Resistance Patterns with Ten-Day Decitabine and Venetoclax (DEC10-VEN) in Acute Myeloid Leukemia
Authors: Abhishek Maiti, Caitlin R. Rausch, Jorge E. Cortes, Naveen Pemmaraju, Naval G. Daver, Farhad Ravandi, Guillermo Garcia-Manero, Gautam M. Borthakur, Kiran Naqvi, Maro Ohanian, Nicholas J. Short, Yesid Alvarado, Christopher B. Benton, Tapan M. Kadia, Koichi Takahashi, Musa Yilmaz, Nitin Jain, Steven M. Kornblau, Koji Sasaki, Michael Andreeff, Prithviraj Bose, Alessandra Ferrajoli, Ghayas C. Issa, Elias Jabbour, Lucia Masarova, Michael E. Rytting, Philip A. Thompson, Sa A Wang, Sergej Konoplev, Zhining Chen, Maitrayee Goswami, Rita Maduike, Julio A Guerrero, Qi Zhang, Antonio Cavazos, Helen Ma, Carol A. Bivins, Allison Wade, Shadiat L Adewale, Susan Tse, Robin Thomas, Kenneth Vaughan, Sherry A. Pierce, Jing Ning, Wei Qiao, John S. Welch, Keyur P. Patel, Hagop M. Kantarjian, Marina Y Konopleva, Courtney D. DiNardo
Journal: Blood (2019)
"Osteonecrosis of Jaw (ONJ) after Bisphosphonate Treatment in Patients with Multiple Myeloma (MM) : Monocentric Experience of Decreasing ONJ Incidence after Preventive Measures."
Authors: Gioacchino Catania, Federico Monaco, Marco Ladetto, Paola Pepe, Giulia Limberti, Manuela Alessio, Anna Baraldi, Antonella Fasciolo, Vittorio Fusco
Journal: Blood (2016)
High Pre-Transplant Free Interleukin-18 Is Associated with Poor Hematopoietic Recovery after Allogeneic Stem Cell Transplantation
Authors: Lambros Kordelas, Aleksandar Radujkovic, Hao Dai, Rashit Bogdanov, Dietrich W. Beelen, Carsten Müller-Tidow, Peter Dreger, Thomas Luft
Journal: Blood (2019)
Mononuclear phagocyte system blockade improves therapeutic exosome delivery to the myocardium
Authors: Zhuo Wan, Lianbi Zhao, Fan Lu, Xiaotong Gao, Yan Dong, Yingxin Zhao, Mengying Wei, Guodong Yang, Changyang Xing, Li Liu
Journal: Theranostics (2019)

Rationale: Exosomes are emerging as a promising drug delivery carrier.However, rapid uptake of exosomes by the mononuclear phagocyte system (MPS) remains an obstacle for drug delivery into other targeted organs, including the heart.We hypothesized that prior blocking of uptake of exosomes by the MPS would improve their delivery to the targeted organs.Methods: Exosomes were isolated from the cell culture medium.Fluorescence-labeled exosomes were tracked in vitro and in vivo by fluorescence imaging.The expression of clathrin heavy chain (Cltc), cavolin1, Pak1 and Rhoa, known genes for endocytosis, were profiled in various cell lines and organs by qPCR.The knockdown efficiency of siRNA against Cltc was analyzed by Western blotting.Exosome control and exosome blocking were constructed by encapsulating isolated exosomes with siControl or siClathrin via electroporation, while exosome therapeutic was constructed by encapsulating isolated exosomes with miR-21a.Doxorubicin-induced cardiotoxicity model was used to verify the therapeutic efficiency of the exosome-based miR-21a delivery by echocardiography.Results: Exosomes were preferentially accumulated in the liver and spleen, mainly due to the presence of abundant macrophages.Besides the well-known phagocytic effect, efficient endocytosis also contributes to the uptake of exosomes by macrophages.Cltc was found to be highly expressed in the macrophages compared with other endocytosis-associated genes.Accordingly, knockdown of Cltc significantly decreased the uptake of exosomes by macrophages in vitro and in vivo.Moreover, prior injection of exosome blocking strikingly improved the delivery efficiency of exosomes to organs other than spleen and liver.Consistently, compared with the direct injection of exosome therapeutic , prior injection of exosome blocking produced a much better therapeutic effect on cardiac function in the doxorubicin-induced cardiotoxicity mouse model.Conclusions: Prior blocking of endocytosis of exosomes by macrophages with exosome blocking successfully and efficiently improves the distribution of following exosome therapeutic in targeted organs, like the heart.The established two-step exosome delivery strategy (blocking the uptake of exosomes first followed by delivery of therapeutic exosomes) would be a promising method for gene therapy.
Preliminary results with tislelizumab, an investigational anti-PD-1 antibody, in Chinese patients with nasopharyngeal cancer (NPC).
Authors: Siyang Wang, Xiaoming Huang, Yu-Xian Bai, Ying Yuan, Jian Li, Zuobai Wang, Chenlu Wei, Xin Li, Tianshu Liu
Journal: Journal of Clinical Oncology (2019)

2556 Background: Epidemiology of NPC is characterized by a unique geographic distribution, with China having one of the highest incidence rates of NPC worldwide. Tislelizumab is an investigational monoclonal antibody with high affinity and specificity for PD-1. Tislelizumab was engineered to minimize binding to FcɤR on macrophages in order to abrogate antibody-dependent phagocytosis, a mechanism of T-cell clearance and potential resistance to anti-PD-1 therapy. Previous reports from this phase 1/2 study (CTR20160872) have shown that single-agent tislelizumab was generally well tolerated and demonstrated preliminary antitumor activity in Chinese patients (pts) with advanced solid tumors. In the dose-verification part of this study, the recommended dose was established as 200 mg IV Q3W. Here we present preliminary results from the NPC cohort of this study. Methods: Chinese pts with advanced or metastatic, histologically or cytologically confirmed WHO type II-III NPC were enrolled in the indication-expansion phase of this study. Enrolled pts received tislelizumab 200 mg IV Q3W until unacceptable toxicity, consent withdrawal, or no evidence of continued clinical benefit. Antitumor activity (per RECIST v1.1) and safety/tolerability (per NCI-CTCAE v4.03) were assessed. Results: As of 11 May 2018, 20 NPC pts (median age 49 yr [range 35–61]) were enrolled. Most pts were male (85%) and non-smokers (65%). All pts received prior radiotherapy; 19 pts (95%) received ≥1 line of systemic treatment and the median number of prior lines of systemic treatment was 2 (range 0–10). At the cut-off date, 15 pts remain on treatment and the median study follow-up was 5.5 mo (range 0.46–9.0). Of 15 response-evaluable pts, 3 achieved a confirmed partial response (PR) and 9 achieved stable disease; 1 patient had an unconfirmed PR. Seven patients experienced ≥1 treatment-related AE (TRAE); hypothyroidism (n = 3) was the only TRAE that occurred in ≥2 pts. No grade ≥3 TRAEs or serious AEs were reported. Furthermore, no AEs led to either treatment interruption or discontinuation. Conclusions: Tislelizumab was generally well tolerated and demonstrated antitumor activity in previously treated pts with advanced NPC. Clinical trial information: CTR20160872.
Preliminary Results from the Phase II Study of the IDH2-Inhibitor Enasidenib in Patients with High-Risk IDH2-Mutated Myelodysplastic Syndromes (MDS)
Authors: Guillaume Richard-Carpentier, Amy E. DeZern, Koichi Takahashi, Marina Y Konopleva, Sanam Loghavi, Lucia Masarova, Yesid Alvarado, Farhad Ravandi, Guillermo Montalban Bravo, Kiran Naqvi, Koji Sasaki, Ricardo Delumpa, Monica Kwari, Mikkael A. Sekeres, Aziz Nazha, Gail J. Roboz, Hagop M. Kantarjian, Guillermo Garcia-Manero, Courtney D. DiNardo
Journal: Blood (2019)
Diffuse Large B Cell Lymphoma (DLBCL)-Released NM23-H1 Promotes Monocyte Survival and Inflammatory Cytokine Release: A Mechanistic Link between the Dual Impacts of NM23-H1 Expression and Reduced Lymphocyte:Monocyte Ratio in DLBCL Prognosis
Authors: Sandro Trova, Maiss Al-Amere, Jayna J Mistry, Zuhal Eraslan, Bader Alhazmi, Joy Harris-Folb, Alessandro Di Maio, Mark T Drayson, Christopher M Bunce, Stuart A Rushworth, Farhat Latif Khanim
Journal: Blood (2019)
Association Between Inflammatory Diets, Circulating Markers of Inflammation, and Risk of Diverticulitis
Authors: Wenjie Ma, Manol Jovani, Long H. Nguyen, Fred K. Tabung, Mingyang Song, Po-Hong Liu, Yin Cao, Idy Tam, Kana Wu, Edward L. Giovannucci, Lisa L. Strate, Andrew T. Chan
Journal: Clinical Gastroenterology and Hepatology (2019)
CD45-ADC Plus Janus Kinase (JAK) Inhibitors As Conditioning for MHC-Mismatched Murine Hematopoietic Stem Cell Transplantation Is Associated with Minimal Toxicity and Graft Versus Host Disease
Authors: Stephen P. Persaud, Matthew L. Cooper, Julie K. Ritchey, Michael P. Rettig, John F. DiPersio
Journal: Blood (2019)
ACTR-53. MGMT PROMOTER METHYLATION ANALYSIS FOR ALLOCATING COMBINED CCNU/TMZ CHEMOTHERAPY: LESSONS LEARNED FROM THE CeTeG/NOA-09 TRIAL
Authors: Theophilos Tzaridis, Niklas Schäfer, Johannes Weller, Joachim Steinbach, Sabine Seidel, Uwe Schlegel, Michael Sabel, Peter Hau, Clemens Seidel, Dietmar Krex, Roland Goldbrunner, Joerg-Christian Tonn, Oliver Grauer, Christina Schaub, Christoph Coch, Martin Glas, Torsten Pietsch, Rolf Fimmers, Guido Reifenberger, Jörg Felsberg, Ulrich Herrlinger
Journal: Neuro-Oncology (2019)

Abstract BACKGROUND The CeTeG/NOA-09 trial recently showed a survival benefit for combination chemotherapy with CCNU/TMZ in glioblastoma patients with a methylated MGMT promoter as determined by quantitative Methylation-Specific PCR (qMSP). Identifying patient subgroups with a pronounced benefit from this novel treatment is crucial. Here, we report on the prognostic and predictive value of MGMT promoter methylation ratio determined by qMSP and investigate the concordance of pyrosequencing (PSQ) and qMSP for patients in this trial. METHODS qMSP and PSQ were used for MGMT promoter methylation analysis. The mITT population of the CeTeG/NOA-09 trial was used for multivariate analysis including the parameters MGMT promoter methylation ratio, RPA class and study center. RESULTS Patients of the mITT population of the CeTeG/NOA-09 trial (n=129) with MGMT promoter methylation ratio greater than 4 (qMSP) showed a superior overall survival compared to patients with borderline methylation ratio of 2–4 (p=0.0251). In the latter patients, treatment with CCNU/TMZ did not show a survival benefit (p=0.924). Multivariate analysis with treatment arm, RPA class and study center as covariates did not confirm a prognostic or predictive value of MGMT promoter methylation ratio (qMSP) for patients of the mITT population (n=129, HR=0.88; 95% CI: 0.72 – 1.08) or patients with a ratio greater than 4 (n=117, HR =0.86; 95% CI: 0.69 – 1.07). In a subset of 49 trial patients, qMSP and PSQ showed not only a high qualitative (45/49; 91.8%), but also a high quantitative concordance rate (Spearman correlation, r=0.83, p&lt; 0.0001). CONCLUSION Glioblastoma patients with borderline MGMT promoter methylation (qMSP ratio 2–4) do not seem to benefit from combination treatment with CCNU/TMZ. Thus, we propose a qMSP cut-off of 4 as a novel decision tool for clinicians. qMSP and PSQ show a high concordance rate indicating that a decision for combination therapy can also be based on PSQ results.
NIMG-52. UNCERTAINTY QUANTIFICATION IN RADIOMICS
Authors: Lujia Wang, Hyunsoo Yoon, Andrea Hawkins-Daarud, Kyle Singleton, Kamala Clark-Swanson, Kris Smith, Peter Nakaji, Jenny Eschbacher, Leslie Baxter, Ashlyn Gonzalez, Ashley Nespodzany, Bernard Bendok, Devi Patra, Gustavo De Leon, Richard Zimmerman, Alyx Porter, Chandan Krishna, Marcela Salomao, Joseph Hoxworth, Yuxiang Zhou, Maciej Mrugala, Nhan Tran, Teresa Wu, Kristin Swanson, Jing Li, Leland Hu
Journal: Neuro-Oncology (2019)

Abstract INTRODUCTION The quantification of intratumoral heterogeneity – through radiomics-based approaches - can help resolve the regionally distinct genetic drug targets that may co-exist within a single Glioblastoma (GBM) tumor. While this offers potential diagnostic value under the paradigm of individualized oncology, clinical decision-making must also consider the degree of uncertainty associated with each model. In this study, we evaluate the performance of a novel machine-learning (ML) algorithm, called Gaussian Process (GP) modeling, that can quantify the impact of multiple sources of uncertainty in ML model development and prediction accuracy, including variabilities in the copy number measurement, radiomics features, training sample characteristics, and training sample size. METHOD We collected 95 image-localized biopsies from 25 primary GBM patients. We coregistered stereotactic locations with preoperative multi-parametric MRI features (conventional MRI, DSC perfusion, Diffusion Tensor Imaging) to generate spatially matched pairs of MRI and copy number variants (CNV) for for each biopsy. We developed a Gaussian Process (GP) model to predict CNV for Epidermal Growth Factor Receptor (EGFR) based on MRI radiomic features in each patient. We used leave-one-patient-out cross validation to quantify prediction accuracy and model uncertainty. Spatial prediction and uncertainty (p-value) maps were overlaid to help visualize regional genetic variation of EGFR and uncertainty of the radiomic predictions. RESULT: The initial GP radiomics model for EGFR amplification (CNV &gt; 3.5) produced a sensitivity of 0.8 and specificity of 0.8. Samples/regions associated with high uncertainty (p-value &gt;0.05) correlated with either 1) extrapolation of radiomic features from the training set-defined feature space or 2) insufficient training samples in the feature space. CONCLUSION We present a ML-based model that quantifies spatial genetic heterogeneity in GBM, while also estimating model uncertainties that result from multi-source data variabilities. This approach lays the groundwork for prospective clinical integration of modeling-based diagnostic approaches in the paradigm of individualized medicine.
Machine Learning Prediction for Complete Response to Hypomethylating Agents with or without Additional Agents in Patients with Newly Diagnosed Myelodysplastic Syndrome
Authors: Koji Sasaki, Guillermo Montalban Bravo, Rashmi Kanagal-Shamanna, Elias Jabbour, Farhad Ravandi, Tapan M. Kadia, Kiran Naqvi, Naval G. Daver, Sherry A. Pierce, Koichi Takahashi, Courtney D. DiNardo, Graciela M. Nogueras González, Keyur Patel, Kelly Soltysiak, Junya Sato, Jorge E. Cortes, Hagop M. Kantarjian, Guillermo Garcia-Manero
Journal: Blood (2019)
Regional differences in the incidence and prognosis of the takotsubo syndrome
Authors: B. Björn Redfors, S. Jha, S. Thorleifsson, O. Angeras, G. Sarno, A. Ravn-Fischer, Ole Fröbert, T. Jernberg, P. Tornvall, A. Lyon, S. James, D. Erlinge, E. Omerovic
Journal: European Journal of Heart Failure (2019)
Deep DNA Sequencing Identifies Small Mutations in Patients with Acute Myelogenous Leukemia (AML) and High-Risk Myelodysplastic Syndromes (MDS): Analysis of Intratumor Genomic Heterogeneity for Prediction of Disease Relapse
Authors: Athena Kritharis, Sukhdeep Kaur, Jui Wan Loh, Mohammad Hadigol, Hossein Khiabanian, Roger Strair
Journal: Blood (2019)
Haematemesis and Melaena
Authors: N. C. Tanner
Journal: BMJ (1949)

Cases of massive gastro-duodenal bleeding treated at St. James Hospital, London, in the period of 1941-8 numbered 650.Peptic ulcer and gastritis accounted for 85% of these cases, as is shown in Table 1.TALLE I.-Finial Diagnosis Gastric ulcer . .
Atypical Protein Kinase C λ/I Oncogenic Signaling through the Chromatin Modifier Satb2 Is Required for Leukemic B-Cell Progenitor Differentiation Arrest and Leukemogenesis
Authors: Ramesh C Nayak, Mark Jordan Althoff, Ashley Wellendorf, Fatima Mohmoud, Maria Diaz-Meco, Jorge Moscat, Jose A. Cancelas
Journal: Blood (2016)