tbuckley/cabot-search huggingface dataset:
Abstract 543: Clinical Development of Cardiac Reprogramming Gene Therapy
Authors: Huanyu Zhou, Laura M Lombardi, Christopher A Reid, Jin Yang, Chetan Srinath, Aliya Zeng, Elena C Leon, Tawny N Qureshi, Emily R Nettesheim, Emma Xu, Zoe Duclos, Jun Liu, Samantha Jones, Charles Feathers, Tae Won Chung, Frank Jing, William Prince, JianMin Lin, Timothy Hoey, Kathryn Ivey
Journal: Circulation Research (2020)

Heart failure affects an estimated 38 million people worldwide and is typically caused by cardiomyocyte (CM) loss or dysfunction. Although CMs have limited ability to regenerate, a large pool of non-myocytes, including cardiac fibroblasts (CFs), exist in the postnatal heart. In vivo reprogramming of non-myocytes into functional CMs is emerging as a potential new approach to treat heart failure and substantial proof-of-concept has been achieved in this new field. However, challenges remain in terms of clinical application. First, reported human reprogramming cocktails often consist of five to seven factors that require multiple AAV vectors for delivery. Thus, a less complex cocktail that is able to fit into one AAV vector is needed for this technology to impact human health. Second, the lack of specificity in AAV tropism further complicates the safety and regulatory landscape. A means to limit the expression of reprogramming factors to target cells is critical for maximizing long-term safety. Lastly, although promising studies in small animals have already been reported, safety and efficacy results in large animal MI models are critical to justify cardiac reprogramming in human clinical trials. We have developed a novel human cardiac reprogramming cocktail that consists of only two transcription factors and one miRNA. This new cocktail has been engineered into a single AAV cassette to efficiently reprogram human CFs into cardiomyocytes. We also substantially improved transduction of hCFs through AAV capsid engineering and eliminated CMs expression through a microRNA de-targeting method. Moreover, our novel cardiac reprogramming gene therapy improved cardiac function in both rat and swine MI models upon delivery at various time-points after MI without inducing arrhythmias. Given these promising safety and efficacy results in larger animals, we endeavor to translate direct cardiac reprogramming for clinical application.
IDH Mutations Identify a Subgroup of <i>NPM1</i> Patients with a More Favorable Prognosis. a Retrospective Multicenter Study of the Filo Group
Authors: Sylvain Garciaz, Marie Anne Hospital, Colombe Saillard, Yosr Hicheri, Evelyne D'Incan, Jerome Rey, Catherine Lacombe, Arnaud Pigneux, Marie-Christine Béné, Christian Recher, Marie-Joelle Mozziconacci, Norbert Vey
Journal: Blood (2020)
Impact of MYC and BCL2 structural variants in tumors of DLBCL morphology and mechanisms of false-negative MYC IHC
Authors: Brett J Collinge, Susana Ben-Neriah, Lauren C. Chong, Merrill Boyle, Aixiang Jiang, Tomoko Miyata-Takata, Pedro Farinha, Jeffrey W Craig, Graham W. Slack, Daisuke Ennishi, Anja Mottok, Barbara Meissner, Elizabeth A. Chavez, Alina S. Gerrie, Diego Villa, Ciara L. Freeman, Kerry J. Savage, Laurie H. Sehn, Ryan D. Morin, Andrew J Mungall, Randy D. Gascoyne, Marco A. Marra, Joseph M Connors, Christian Steidl, David W. Scott
Journal: Blood (2020)
AB0020 INTERACTION MTHFR 677C/T AND PON1 -108C/T POLYMORPHISMS IS ASSOCIATED TO ATHEROGENIC RISK IN RHEUMATOID ARTHRITIS PATIENTS FROM SOUTHERN MEXICO
Authors: Iris Paola Guzmán-Guzmán, Oscar Zaragoza-García, José Eduardo Navarro-Zarza, MA. Elena Moreno-Godínez, Isela Parra-Rojas
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background:</h3> The risk of cardiovascular disease in rheumatoid arthritis (RA) patients is 1.5 times higher compared to the general population. Some factors relationships to cardiovascular disease in RA are high clinic activity of the disease, the autoantibodies-positive, the disease duration and pharmacological treatment<sup>1</sup>, as well as single nucleotide polymorphisms. Methylenetetrahydrofolate reductase (MTHFR) is a key enzyme in folate metabolism and is considered a drug-metabolizing enzyme; MTHFR 677C/T polymorphism was described leading to reduced enzyme activity, increasing serum concentration of homocysteine, an intermediate product of methotrexate metabolism. Paraoxonase 1 (PON1) is a multifunctional enzyme that can detoxify through its homocysteine thiolactonase activity, the polymorphism identified in the position PON1 -108C/T exerts effects on serum activity and expression levels. <h3>Objectives:</h3> We evaluate the association between the interaction MTHFR 677C/T and PON1 -108C/T polymorphisms and cardiovascular risk (CVR) in RA patients. <h3>Methods:</h3> A cross-sectional study was performed including 250 RA patients diagnosed according to ACR/EULAR 2010 criteria, attended in a public hospital from southern Mexico. MTHFR 677C/T and PON1 -108C/T genotypes were determined by PCR-RFLP method. The clinic and metabolic parameters were evaluated. CVR was defined using different diagnostic tools. Logistic regression models were used to evaluate the association between interaction polymorphisms and CVR. <h3>Results:</h3> We show high CVR in a variable prevalence according to diagnostics tools: TGs/HDL-c (64.8%), Castelli (50%) and Kannel (43%). Alleles frequency of 667C/T were 33% for C and 67% for T allele; PON1-108C/T 52% for C and 43% for T allele. In a multiple regression model adjusting by duration of disease, pharmacological therapy and DAS28-hsCRP score, carriers of the 667TT and -108CC genotypes had higher CVR according to TGs/HDL-c (&gt;3%) (OR=4.68, p=0.019), Castelli (&gt;3%) (OR=2.99, p=0.03) and Kannel index (&gt;4.5% in woman and &gt;5% in men) (OR=2.03, p=0.13). <h3>Conclusion:</h3> Our results demonstrate an interaction between MTHFR 677C/T and PON1 -108C/T polymorphisms on the CVR, associated to atherogenic indexes in RA patients from southern Mexico. <h3>References</h3> [1] Mackey RH, Kuller LH, Moreland LW. Cardiovascular disease risk in patients with rheumatic diseases. Clin Geriatr Med. 2017;33(1):105-117. doi: 10.1016/j.cger.2016.08.008. <h3>Disclosure of Interests:</h3> None declared
The Two-Step Approach to Haploidentical Hematopoietic Stem Cell Transplantation (HI HSCT): 15 Years of Transplants in Patients 19-78 Years Old
Authors: Dolores Grosso, Matthew Carabasi, Joanne Filicko-O'Hara, John L. Wagner, William O'Hara, Shaik Rashid, Usama Gergis, Neal Flomenberg
Journal: Blood (2020)
Targeting of glioma stem-like cells with a parthenolide derivative ACT001 through inhibition of AEBP1/PI3K/AKT signaling
Authors: Yanli Hou, Bowen Sun, Wenxue Liu, Bo Yu, Qiqi Shi, Fei Luo, Yongrui Bai, Haizhong Feng
Journal: Theranostics (2020)

Glioblastoma (GBM) is the most lethal primary brain tumor in adults with a median survival of around 15 months.A potential treatment strategy involves targeting glioma stem-like cells (GSCs) that are able to initiate, maintain, and repopulate the tumor mass.Here, we identify ACT001, a parthenolide derivative, targeting GSCs through regulation of adipocyte enhancer binding protein 1 (AEBP1) signaling.Methods: The effects of ACT001 on cell survival of normal human astrocytes (NHA) and patient-derived glioma stem-like cells (GSCs) were evaluated.RNA-Seq were performed to detect differentially expressed genes.ACT001 efficacy as a single agent or in combination with SHP-2 inhibitor SHP099 was assessed using a GSC orthotopic xenograft model.Results: GSCs exhibit high response to ACT001 in compared with normal human astrocytes.AEBP1 is a putative target of ACT001 by RNA-Seq analysis, which expression associates with prognosis of GBM patients.Knockdown of AEBP1 inhibits GSC proliferation and glioma sphere formation.Treatment with ACT001 or PI3K inhibitor or AEBP1 depletion would impair AKT phosphorylation and GSC proliferation, whereas constitutive AKT activation rescues ACT001 treatment or AEBP1 depletion-inhibited cell proliferation.Moreover, ACT001 blocks TGF-β-activated AEBP1/AKT signaling in GSCs.ACT001 exhibits antitumor activity either as a single agent or in combination with SHP099, which provides significant survival benefits for GSC tumor xenograft-bearing animals.Conclusions: Our data demonstrate AEBP1 as a new druggable target in GBM and ACT001 as a potential therapeutic option for improving the clinical treatment of GBM in combination with SHP099.
Abstract 9995: Beta3-Adrenergic-Receptor-Deficient Mice Protected From Diabetes-Induced Cardiomyopathy: Pivotal Role of the Prevention of Cardiac CaMKII Upregulation
Authors: Heng-Jie Cheng, Zhe Chen, Yixi Liu, Xiaowei Zhang, Donald A McClain, Dalane Kitzman, Che Ping Cheng
Journal: Circulation (2019)

Background: Diabetic cardiomyopathy (DCM) is a serious complication of diabetes mellitus (DM). As yet, no effective approaches to preventing its development in the clinic. Recently, we found that d...
C3 Inhibition with Pegcetacoplan in Patients with Paroxysmal Nocturnal Hemoglobinuria: Results from the Paddock and Palomino Trials
Authors: Raymond S Wong, Kalina Ignatova, Humphrey Pullon, Jameela Sathar, Pimjai Niparuck, Tontanai Numbenjapon, Eric Tse, Surapol Issaragrisil, Eloy Roman, Ismail Amine, Lisa Tan, Carl Di Casoli, Pascal Deschatelets, Cedric Francois, Federico Grossi, Andrija Bogdanovic
Journal: Blood (2020)
Evaluation of Secondhand Smoke Exposure in New York City Public Housing After Implementation of the 2018 Federal Smoke-Free Housing Policy
Authors: Lorna E. Thorpe, Elle Anastasiou, Katarzyna Wyka, Albert Tovar, Emily Gill, Ana Rule, Brian Elbel, Sue A. Kaplan, Nan Jiang, Terry Gordon, Donna Shelley
Journal: JAMA Network Open (2020)

<h3>Importance</h3> Secondhand smoke (SHS) exposure is associated with many health conditions in children and adults. Millions of individuals in the US are currently exposed to SHS in their homes. <h3>Objective</h3> To investigate whether a federal ban on smoking in public housing settings was associated with a decrease in indoor SHS levels in New York City public housing developments 12 months after the policy's implementation. <h3>Design, Setting, and Participants</h3> This cohort study tracked indoor air quality longitudinally from April 2018 to September 2019 and used difference-in-differences analysis to examine SHS exposure before vs after implementation of the 2018 federal smoke-free housing (SFH) policy in 10 New York City Housing Authority (NYCHA) buildings vs 11 matched low-income buildings not subject to the SFH policy (ie, Section 8 buildings). <h3>Exposures</h3> Federal SFH policy implementation, beginning July 30, 2018. <h3>Main Outcomes and Measures</h3> Comparison of nicotine concentration levels from passive, bisulfate-coated filters before vs 12 months after implementation of the federal SFH policy. Secondary outcomes included changes in particulate matter less than 2.5 μm in diameter, measured with low-cost particle monitors, and counts of cigarette butts in common areas. <h3>Results</h3> Air quality was measured repeatedly in a total of 153 NYCHA and 110 Section 8 nonsmoking households as well as in 91 stairwells and hallways. Before the SFH policy implementation, air nicotine was detectable in 19 of 20 stairwells (95.0%) in NYCHA buildings and 15 of 19 stairwells (78.9%) in Section 8 buildings (<i>P</i> = .19) and in 17 of 19 hallways (89.5%) in NYCHA buildings and 14 of 23 hallways (60.9%) in Section 8 buildings (<i>P</i> = .004). Nicotine was detected less frequently inside nonsmoking apartments overall (26 of 263 [9.9%]) but more frequently in NYCHA apartments (20 of 153 [13.1%]) than in Section 8 apartments (6 of 110 [5.5%]) (<i>P</i> = .04). One year after policy implementation, there was no differential change over time in nicotine concentrations measured in stairwells (DID, 0.03 μg/m<sup>3</sup>; 95% CI, –0.99 to 1.06 μg/m<sup>3</sup>) or inside nonsmoking households (DID, –0.04 μg/m<sup>3</sup>; 95% CI, –0.24 to 0.15 μg/m<sup>3</sup>). Larger decreases in nicotine concentration were found in NYCHA hallways than in Section 8 hallways (DID, –0.43 μg/m<sup>3</sup>; 95% CI, –1.26 to 0.40 μg/m<sup>3</sup>). <h3>Conclusions and Relevance</h3> The findings suggest that there was no differential change in SHS in NYCHA buildings 12 months after SFH policy implementation. Additional support may be needed to ensure adherence to SFH policies.
Receptor-mediated targeted drug delivery systems for treatment of inflammatory bowel disease: Opportunities and emerging strategies
Authors: Peng Liu, Caifang Gao, Hongguo Chen, Chi Teng Vong, Xu Wu, Xudong Tang, Shengpeng Wang, Yitao Wang
Journal: Acta Pharmaceutica Sinica B (2020)

Inflammatory bowel disease (IBD) is a chronic intestinal disease with painful clinical manifestations and high risks of cancerization. With no curative therapy for IBD at present, the development of effective therapeutics is highly advocated. Drug delivery systems have been extensively studied to transmit therapeutics to inflamed colon sites through the enhanced permeability and retention (EPR) effect caused by the inflammation. However, the drug still could not achieve effective concentration value that merely utilized on EPR effect and display better therapeutic efficacy in the inflamed region because of nontargeted drug release. Substantial researches have shown that some specific receptors and cell adhesion molecules highly expresses on the surface of colonic endothelial and/or immune cells when IBD occurs, ligand-modified drug delivery systems targeting such receptors and cell adhesion molecules can specifically deliver drug into inflamed sites and obtain great curative effects. This review introduces the overexpressed receptors and cell adhesion molecules in inflamed colon sites and retrospects the drug delivery systems functionalized by related ligands. Finally, challenges and future directions in this field are presented to advance the development of the receptor-mediated targeted drug delivery systems for the therapy of IBD.
A Phase Ib, Open-Label, Randomized Study to Assess Safety and Preliminary Efficacy of Tafasitamab (MOR208) or Tafasitamab + Lenalidomide in Addition to R-CHOP in Patients with Newly Diagnosed Diffuse Large B-Cell Lymphoma: Analysis of the Safety Run-in Phase
Authors: David Belada, Grzegorz S. Nowakowski, Juan Miguel Bergua Burgues, Marc André, Katerina Kopeckova, Don A. Stevens, Marek Trněný, Ernesto Pérez Persona, Petra Pichler, Pia Klöpfer, Bettina Brackertz, Emanuel Lohrmann, Anirban Lahiry, Neha Shah, Günter Fingerle-Rowson, Wolfram Brugger, John M. Burke
Journal: Blood (2020)
Abstract 527: Role of IGFBP3 in Neonatal Heart Regeneration
Authors: Shah R Ali, Waleed El-Helaly, Ivan Menendez-Montes, Ngoc Uyen Nhi Nguyen, Suwannee Thet, Hesham A Sadek
Journal: Circulation Research (2020)

Background: The adult mammalian heart is unable to regenerate after an injury. However, newborn mice are able to fully regenerate the heart after myocardial infarction (MI). The neonatal MI model therefore is a potential blueprint for regenerating the adult heart that could offer novel therapies for patients suffering from heart disease. To investigate the mechanism by which neonatal heart regeneration occurs, we screened for secreted proteins that are upregulated after neonatal MI but not after adult MI. We hypothesized that such a protein could be a cardiomyocyte mitogen that underlies the cardiomyocyte proliferation that occurs after neonatal MI. Methods: We performed microarrays on neonatal and adult MI (and sham) heart tissue samples: we identified IGFBP3 (Insulin Growth Factor Binding Protein 3), which canonically transports IGF ligands in circulation, as a secreted protein that is uniquely upregulated after neonatal MI. We used in situ hybridization, reporter mice, and immunostaining to validate the findings from the microarray. Single cell RNA-seq data revealed that IGFBP3 is expressed in vascular cells. Results: We first tested whether IGFBP3 is necessary during neonatal heart regeneration: we performed neonatal (P1) MI in global Igfbp3 knockout mice and wild-type mice, and found that knockout mice have more fibrosis and worse ejection fraction (EF) one month after P1 MI. To determine if IGFBP3 is sufficient to promote cardiomyocyte proliferation, we injected recombinant IGFBP3 protein into the heart of one week-old mice (P7) and saw more cycling myocytes. We generated novel transgenic vascular-Igfbp3-overexpression mice, which exhibit less fibrosis as well as improved EF after P7 MI compared to controls. Conclusions: IGFBP3 is a secreted protein that is necessary for complete regeneration after a neonatal MI. Its ectopic expression can cause cardiomyocyte proliferation and can improve systolic function, and it prolongs the window of neonatal heart regeneration. Therefore, IGFBP3 may represent a cardiomyocyte mitogen with potential therapeutic value for adult heart disease.
Response to Bridging Therapy (BT) before CAR-T Cell Infusion Predicts Outcomes for Relapsed/Refractory (R/R) Aggressive B-Cell Non-Hodgkin Lymphoma (NHL)
Authors: Arushi Khurana, Abdullah S. Al Saleh, Sangeetha Gandhi, Tuan A Truong, Nabila Bennani, Jonas Paludo, Jose C Villasboas, Patrick B. Johnston, Stephen M. Ansell, Yi Lin
Journal: Blood (2020)
Pharmacologic Targeting MCL1 with AZD5991 Induces Apoptosis and Mitochondrial Dysfunction in Non-Hodgkin Lymphoma (NHL) Cells
Authors: Tingting Liu, Fei Xu, Elana Thieme, Vi Lam, Guang Fan, Liana Nikolaenko, Stephen E Kurtz, Jeffrey W. Tyner, Olga Danilova, Alexey Danilov
Journal: Blood (2020)
Vincristine Sulfate Liposome Injection (VSLI) with Bendamustine and Rituximab As First-Line Therapy for Indolent B-Cell Lymphomas: A Phase 1 Study
Authors: Thomas A Ollila, James Butera, Pamela C Egan, John L Reagan, Anthony G Thomas, Inna Yakirevich, Kelsey MacKinnon, Jeannine Margolis, Valerie Rosati, Jessica McMahon, Jordan Robison, Adam J Olszewski
Journal: Blood (2020)
Induction of Fetal Hemoglobin By FTX6058, a Novel Small Molecule Development Candidate
Authors: Peter Rahl, Ivan Efremov, Billy Stuart, Keqiang Xie, Mark Roth, Richard Barnes, Kingsley Appiah, David Peters, Qingyi Li, Steven Kazmirski, Paul Bruno, Kim Stickland, Lucienne Ronco, Diego Cadavid, Lorin Thompson, Owen Wallace, Christopher Moxham
Journal: Blood (2020)
Atezolizumab Versus Docetaxel in Pretreated Patients With NSCLC: Final Results From the Randomized Phase 2 POPLAR and Phase 3 OAK Clinical Trials
Authors: Julien Mazieres, Achim Rittmeyer, Shirish Gadgeel, Toyoaki Hida, David R. Gandara, Diego L. Cortinovis, Fabrice Barlesi, Wei Yu, Christina Matheny, Marcus Ballinger, Keunchil Park
Journal: Journal of Thoracic Oncology (2020)

The phase 2 POPLAR and phase 3 OAK studies of the anti-programmed death-ligand 1 (PD-L1) immunotherapy atezolizumab in patients with previously treated advanced NSCLC revealed significant improvements in survival versus docetaxel (p = 0.04 and 0.0003, respectively). Longer follow-up permits evaluation of continued benefit of atezolizumab. This study reports the final overall survival (OS) and safety findings from both trials.POPLAR randomized 287 patients (atezolizumab, 144; docetaxel, 143) and OAK randomized 1225 patients (atezolizumab, 613; docetaxel, 612). The patients received atezolizumab (1200 mg fixed dose) or docetaxel (75 mg/m2) every 3 weeks. Efficacy and safety outcomes were evaluated.A longer OS was observed in patients receiving atezolizumab versus docetaxel in POPLAR (median OS = 12.6 mo versus 9.7 mo; hazard ratio = 0.76, 95% confidence interval [CI]: 0.58-1.00) and OAK (median OS = 13.3 versus 9.8 mo; hazard ratio = 0.78, 95% CI: 0.68-0.89). The 4-year OS rates in POPLAR were 14.8% (8.7-20.8) and 8.1% (3.2-13.0) and those in OAK were 15.5% (12.4-18.7) and 8.7% (6.2-11.3) for atezolizumab and docetaxel, respectively. Atezolizumab had improved OS benefit compared with docetaxel across all PD-L1 expression and histology groups. Most 4-year survivors in the docetaxel arms received subsequent immunotherapy (POPLAR, 50%; OAK, 65%). Of the 4-year survivors, most had Eastern Cooperative Oncology Group performance status of 0 and nonsquamous histological classification and approximately half were responders (POPLAR: atezolizumab, seven of 15; docetaxel, three of four; OAK: atezolizumab, 24 of 43; docetaxel, 11 of 26). Treatment-related grade 3/4 adverse events occurred in 27% and 16% of atezolizumab 4-year survivors in POPLAR and OAK, respectively.Long-term follow-up suggests a consistent survival benefit with atezolizumab versus docetaxel in patients with previously treated NSCLC regardless of PD-L1 expression, histology, or subsequent immunotherapy. Atezolizumab had no new safety signals, and the safety profile was similar to that in previous studies.
Short Daratumumab Consolidation in Patients with AL Amyloidosis or Lcdd Improves Complete Response Rates and Modifies Bone Marrow Microenvironment
Authors: Efstathios Kastritis, Pantelis Roussakis, Ioannis V Kostopoulos, Foteini Theodorakakou, Despina Fotiou, Nikolaos Kanellias, Ioanna Dialoupi, Magdalini Migkou, Maria Roussou, Evangelos Eleutherakis-Papaiakovou, Asimina Papanikolaou, Anastasia Gatou, Ourania E. Tsitsilonis, Maria Gavriatopoulou, Evangelos Terpos, Meletios A Dimopoulos
Journal: Blood (2020)
Epigallocatechin gallate (EGCG) causes antiproliferation and induction of apoptosis of Ewing sarcoma tumor cells through the inhibition of IGF-1R
Authors: Hyung-Gyoo Kang, Jasmine Jenabi, Timothy Triche, Poul Sorensen
Journal: Cancer Research (2007)

1814  The IGF/IGF-1R pathway including the IGF, IGF-1R, and IGFBPs proteins, plays an important role in the growth and survival of Ewing family tumors. In general, activation of IGF-1R results in intramolecular receptor autophosphorylation and phosphorylation of critical downstream targets. This leads to activation of several signaling pathways, including the PI3K/Akt pathway and the Ras/MAPK pathway, which results in activation of specific genes for cell survival and proliferation. Therefore, development of the therapeutic way for the effective inhibition of IGF-1R signal pathway may provide a promising strategy for the prevention and treatment of Ewing sarcoma tumors. It has been reported that in several tumors EGCG, the major biologically active component of green tea, inhibits activation of the RTKs such as EGFR, HER2, HER3, and IGF-1R. Cascadely it is associated with inhibition of multiple downstream signaling pathways for cell survival and proliferation. In this study, we determined the growth inhibitory and pro-apoptotic properties of EGCG on Ewing sarcoma tumors. Our data demonstrated that a treatment of EGCG resulted in a significant inhibition of the growth and viability of the Ewing tumor cell lines. EGCG treatment resulted in a significant inhibition of the activation of IGF-1R. As evident from BrdU incorporation experiments, EGCG treatment to the cells was found to result in significant inhibition of cell proliferation and dramatic increase of apoptosis. In addition, EGCG treatment caused the deactivation of Akt and MEK. In contrast, when we treated EGCG on HBMEC (Human Brain Microvascular Endothelial Cells) we could not see any effects on cell antiproliferation and proapoptosis. So we think the effects of EGCG are very specific to tumor cells. Based on this study, we suggest that EGCG could be developed as a chemopreventive agent or as a treatment therapy for the management of Ewing sarcoma. However, detailed mechanistic in vitro and in vivo studies are needed to further evaluate the anti-tumor efficacy of EGCG in appropriate culture and animal models.
Transcend CLL 004: Phase 1 Cohort of Lisocabtagene Maraleucel (liso-cel) in Combination with Ibrutinib for Patients with Relapsed/Refractory (R/R) Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma (CLL/SLL)
Authors: William G. Wierda, Kathleen A. Dorritie, Javier Munoz, Deborah M. Stephens, Scott R. Solomon, Heidi H. Gillenwater, Lucy Gong, Lin Yang, Ken Ogasawara, Jerill Thorpe, Tanya Siddiqi
Journal: Blood (2020)
Patient Reported Outcomes Among Systemic Mastocytosis (SM) Patients in Routine Clinical Practice: Results from the TouchStone Survey
Authors: Ruben A. Mesa, Erin M. Sullivan, David Dubinsky, Brittany Carroll, Valerie M. Slee, Susan Jennings, Celeste Finnerty, Linda Bohannon, Susan Mathias, Mariana Castells
Journal: Blood (2020)