tbuckley/cabot-search huggingface dataset:
Association of Clonal Hematopoiesis in DNA Repair Genes With Prostate Cancer Plasma Cell-free DNA Testing Interference
Authors: Kendal Jensen, Eric Q. Konnick, Michael T. Schweizer, Alexandra O. Sokolova, Petros Grivas, Heather H. Cheng, Nola M. Klemfuss, Mallory Beightol, Evan Y. Yu, Peter S. Nelson, Bruce Montgomery, Colin C. Pritchard
Journal: JAMA Oncology (2020)

Cell-free DNA (cfDNA) testing is increasingly used in the treatment of patients with advanced prostate cancer. Clonal hematopoiesis of indeterminate potential (CHIP) can interfere with cfDNA testing and cause incorrect interpretation of results. There is an urgent need to better understand this problem following recent US Food and Drug Administration approval of poly(ADP) ribose polymerase inhibitors (PARPi) for metastatic prostate cancer based on variants in DNA repair genes that can be affected by CHIP.To determine the prevalence of clinically relevant CHIP interference in prostate cancer cfDNA testing.We report a case series of 69 patients with advanced prostate cancer (metastatic disease or with rising PSA following localized therapy) who had cfDNA variant testing with a large panel cancer next generation sequencing assay (UW-OncoPlexCT). To determine the source of variants in plasma, we tested paired cfDNA and whole blood control samples. The study was carried out in an academic medical center system reference laboratory.Prevalence and gene spectrum of CHIP interference in patients with prostate cancer undergoing cfDNA testing.We detected CHIP variants at 2% or more variant fraction in cfDNA from 13 of 69 men with prostate cancer (19%; 95% CI, 10%-30%). Seven men (10%; 95% CI, 4%-20%) had CHIP variants in DNA repair genes used to determine PARPi candidacy, including ATM (n = 5), BRCA2 (n = 1), and CHEK2 (n = 1). Overall, CHIP variants accounted for almost half of the somatic DNA repair gene variants detected. Participant CHIP variants were exponentially correlated with older age (R2 = 0.82). CHIP interference variants could be distinguished from prostate cancer variants using a paired whole-blood control.In this case series, approximately 10% of men with advanced prostate cancer had CHIP interference in plasma cfDNA in DNA repair genes that are used for eligibility of PARPi therapy, most frequently in ATM. Clinical cfDNA testing should include a paired whole-blood control to exclude CHIP variants and avoid misdiagnosis.
THU0119 Rheumatoid arthritis myeloid cells express an intrinsic abnormal capacity for activation
Authors: R Müller, A Skapenko, J Wendler, M Grünke, JR Kalden, H Schulze-Koops
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> Evidence suggests that monocyte precursor cells in rheumatoid arthritis (RA) might become partially activated in the bone marrow or the peripheral blood before they enter the rheumatoid synovium. However, whether this is the result of pro-inflammatory cytokines leaking from the inflamed synovium into the circulation or rather a functional abnormality of myeloid cells has not yet been conclusively delineated. <h3>Objectives</h3> To test the hypothesis that monocytes in RA might express an intrinsic abnormality for activation, we investigated the function and the phenotype of peripheral blood monocytes from patients with RA and healthy controls <i>in vitro</i>. <h3>Methods</h3> Monocytes were isolated by negative selection from patients with active, early RA and from patients with long standing RA under effective anti-inflammatory therapy with disease modifying antirheumatic drugs (DMARDs). A cell culture system was employed that permitted the differentiation of monocytes to macrophages. Expression of surface molecules indicative of activation and/or differentiation was assessed by flow cytometry. <h3>Results</h3> No differences were detected for the expression of HLA-DR, CD14, CD40, CD68, CD80 and CD86 on freshly isolated monocytes between patients and controls. During differentiation to macrophages, the expression of HLA-DR, CD14 and CD80 was increased in RA monocytes. Interestingly, patients with untreated, active early disease manifested an even higher propensity to upregulate HLA-DR during differentiation compared to patients with long standing disease under effective anti-inflammatory therapy. In contrast, the expression of CD40, CD68 and CD86 was reduced in myeloid cells from RA patients during differentiation. This feature was more pronounced in patients with long standing disease, but was not correlated with clinical activity. <h3>Conclusion</h3> The data indicate that monocytes from RA patients might have an intrinsically increased ability for activation during differentiation. This ability might contribute to clinical disease activity and emphasises the systemic nature of the disease. The data further suggest that long standing disease might alter the functional phenotype of circulating monocytes. However, the contribution of continuous treatment with DMARDs to this phenomenon remains to be elucidated.
A Novel Humanized Animal Model Reveals Clonal Architecture and Therapeutic Vulnerabilities in Myelofibrosis
Authors: Hamza Celik, Ethan Krug, Hassan Bjeije, Nancy Issa, Wentao Han, Won Kyun Koh, Ruochao CZ Zhang, Maggie J. Allen, Terrence N Wong, Daniel AC Fisher, Tiandao Li, Stephen T. Oh, Grant A. Challen
Journal: Blood (2020)
COVID-19 Testing and Cases in Immigration Detention Centers, April-August 2020
Authors: Parsa Erfani, Nishant Uppal, Caroline H. Lee, Ranit Mishori, Katherine R. Peeler
Journal: JAMA (2020)

This study describes monthly test, test positivity, and case rates for coronavirus disease 2019 (COVID-19) among individuals detained by US Immigration and Customs Enforcement (ICE) between April and August 2020.
A polygenic risk score for progressive non-alcoholic fatty liver disease risk stratification
Authors: Cristiana Bianco, Serena Pelusi, Guido Alessandro Baselli, Irene Zanoni, Alice Taliento, Paola Dongiovanni, Raffaela Rametta, Vittorio Borroni, Alessandro Federico, Umberto Vespasiani Gentilucci, Roberta D’Ambrosio, Elisabetta Bugianesi, Salvatore Petta, Luca Miele, Helen L. Reeves, Anna Ludovica Fracanzani, Giorgio Soardo, Daniele Prati, Luca Valenti
Journal: Journal of Hepatology (2020)
Single-Center Experience with Axicabtagene-Ciloleucel (Axi-cel) and Tisagenlecleucel (Tisa-cel) for Relapsed/Refractory Diffuse Large B-Cell Lymphoma: Comparable Response Rates and Manageable Toxicity
Authors: Veit Buecklein, Viktoria Blumenberg, Josephine Ackermann, Christian Schmidt, Kai Rejeski, Niklas Mueller, Anna Reischer, Louisa von Baumgarten, Florian Schoeberl, Andreas Humpe, Michael von Bergwelt, Marion Subklewe
Journal: Blood (2020)
Effect of rhG-CSF Combined With Decitabine Prophylaxis on Relapse of Patients With High-Risk MRD-Negative AML After HSCT: An Open-Label, Multicenter, Randomized Controlled Trial
Authors: Lei Gao, Yanqi Zhang, Sanbin Wang, Peiyan Kong, Yi Su, Jiong Hu, Ming Jiang, Hai Bai, Tao Lang, Jishi Wang, Li Liu, Tonghua Yang, Xiaobing Huang, Fang Liu, Shifeng Lou, Yao Liu, Cheng Zhang, Hong Liu, Li Gao, Jia Liu, Lidan Zhu, Qin Wen, Ting Chen, Ping Wang, Jun Rao, Min Mao, Cunbang Wang, Xianlin Duan, Le Luo, Xiangui Peng, Kaniel Cassady, Jiang F. Zhong, Xi Zhang
Journal: Journal of Clinical Oncology (2020)

Relapse is a major cause of treatment failure after allogeneic hematopoietic stem-cell transplantation (allo-HSCT) for high-risk acute myeloid leukemia (HR-AML). The aim of this study was to explore the effect of recombinant human granulocyte colony-stimulating factor (rhG-CSF) combined with minimal-dose decitabine (Dec) on the prevention of HR-AML relapse after allo-HSCT.We conducted a phase II, open-label, multicenter, randomized controlled trial. Two hundred four patients with HR-AML who had received allo-HSCT 60-100 days before randomization and who were minimal residual disease negative were randomly assigned 1:1 to either rhG-CSF combined with minimal-dose Dec (G-Dec group: 100 µg/m2 of rhG-CSF on days 0-5 and 5 mg/m2 of Dec on days 1-5) or no intervention (non-G-Dec group). The primary outcome was relapse after transplantation, and the secondary outcomes were chronic graft-versus-host disease (cGVHD), safety of the treatment, and survival.The estimated 2-year cumulative incidence of relapse in the G-Dec group was 15.0% (95% CI, 8.0% to 22.1%), compared with 38.3% (95% CI, 28.8% to 47.9%) in the non-G-Dec group (P < .01), with a hazard ratio (HR) of 0.32 (95% CI, 0.18 to 0.57; P < .01). There was no statistically significant difference between the G-Dec and non-G-Dec groups in the 2-year cumulative incidence of cGVHD without relapse (23.0% [95% CI, 14.7% to 31.3%] and 21.7% [95% CI, 13.6% to 29.7%], respectively; P = .82), with an HR of 1.07 (95% CI, 0.60 to 1.92; P = .81). After rhG-CSF combined with minimal-dose Dec maintenance, increasing numbers of natural killer, CD8+ T, and regulatory T cells were observed.Our findings suggest that rhG-CSF combined with minimal-dose Dec maintenance after allo-HSCT can reduce the incidence of relapse, accompanied by changes in the number of lymphocyte subtypes.
SAT0003 Intestinal colonisation with sulphate-reducing bacteria: a co-factor in the aetiopathogenesis of ankylosing spondylitis?
Authors: SM Stebbings, J Highton, G Tannock
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> Sulphate-reducing bacteria (SRB) have only recently been identified as a constituent of the normal colonic microflora humans. Such colonisation however is far from universal. Small studies in patients with ulcerative colitis (UC) have found SRB to be present in up to 92% of patients and a pathogenic role has been speculated. Approximately 65% of patients with ankylosing spondylitis (AS) have colonic inflammation, and this is now recognised as an independent risk factor for the disease. Furthermore, studies in germfree HLA-B27 transgenic rats have shown that the normal intestinal microflora is essential to the development of spondyloarthritis in these animals. <h3>Objectives</h3> We aimed to discover whether intestinal colonisation with SRB was more common in AS patients than controls, and thus whether SRB may play a role in the aetiology of AS. <h3>Methods</h3> Fifteen patients fulfilling the Modified New York criteria for AS and 15 age and gender matched controls were recruited. Each subject provided 3 faecal specimens at monthly intervals. Bacterial DNA extracts were obtained from 3 faecal samples from 14 patients and 14 controls, and one each from the remaining patient and control. PCR was performed using primers targeting a conserved region of subunit A of the adenosine-5?-phosphosulphate (APS) reductase gene a gene conserved across all SRB species. <h3>Results</h3> (See Table 1) Chi-square with Yates? correction demonstrated a highly significant association between AS and colonisation with SRB (p = 0.003). <h3>Conclusion</h3> We have discovered a much higher prevalence of faecal carriage of SRB in patients with AS compared with healthy controls. This raises the possibility that these organisms may play a role in the aetiopathogenesis of AS. An alternative possibility is that SRB reflect the presence of colonic inflammation in these individuals. <h3>References</h3> Gibson GR, Cummings JH, Macfarlane GT. Growth and activities of sulphate-reducing bacteria in gut contents of healthy subjects and patients with ulcerative colitis. FEMS Microbiol Ecol. 1991;86:103–12 Veys EM, Mielants H, De Vos M, Cuvelier C. Spondylarthropathies: from gut to target organs. Baillieres Clin Rheumatol. 1996;10(1):123–46 Taurog JD, Richardson JA, Croft JT, <i>et al</i>. The germfree state prevents development of gut and joint inflammatory disease in HLA-B27 transgenic rats. J Exp Med. 1994;180(6):2359–64
Rigosertib in Combination with Azacitidine Impacts Metabolic and Differentiation Pathways in the MDS-L Cell Line
Authors: Richa Rai, Foramben Patel, Stella Melana, Jonathan Feld, Shyamala C. Navada, Rosalie Odchimar-Reissig, Erin P. Demakos, E. Premkumar Reddy, Lewis R. Silverman
Journal: Blood (2020)
Combined Ibrutinib and Venetoclax for First-Line Treatment for Patients with Chronic Lymphocytic Leukemia (CLL): Focus on MRD Results
Authors: Nitin Jain, Michael J. Keating, Philip A. Thompson, Alessandra Ferrajoli, Jan A. Burger, Gautam Borthakur, Koichi Takahashi, Zeev E. Estrov, Koji Sasaki, Nathan H Fowler, Tapan M. Kadia, Marina Konopleva, Yesid Alvarado, Musa Yilmaz, Courtney D. DiNardo, Prithviraj Bose, Maro Ohanian, Naveen Pemmaraju, Elias Jabbour, Rashmi Kanagal-Shamanna, Keyur Patel, Wei Wang, Jeffrey L. Jorgensen, Sa A Wang, Naveen Garg, Xuemei Wang, Chongjuan Wei, Nichole Cruz, Ana Ayala, William Plunkett, Hagop M. Kantarjian, Varsha Gandhi, William G. Wierda
Journal: Blood (2020)
Abstract 14444: Application of Population Specific Streptococcal Antibody Titers to Improve Specificity of Rheumatic Fever Diagnosis in Uganda
Authors: Emmy Okello, Emma Ndagire, Rachel Sarnacki, Meghna Murali, Joselyn Rwebembera, Tom Parks, Nicholas de Klerk, Chris Longenecker, Jonathan Carapetis, Craig A Sable, Andrea Z beaton
Journal: Circulation (2019)

Introduction: Central to rheumatic fever (RF) diagnosis is evidence of streptococcal exposure, specifically antistreptolysin O (ASO) and antideoxyribonuclease B (ADB) antibodies. It is unknown if t...
Clinical &amp; Economic Implications of Hydroxyurea Intolerance in Polycythemia Vera in Routine Clinical Practice in Israel
Authors: Martin H. Ellis, Tamar Tadmor, Gabriel Chodick, Naama Yekutiel, Moti Levi, Giora Sharf, Oren Feine, Raanan Leef, Nana Ben Zvi, Oren Shavit
Journal: Blood (2020)
Co-Occurring Mutation Clusters Predict Drug Sensitivity in Acute Myeloid Leukemia
Authors: Guangrong Qin, Shmulevich Ilya, Taek-Kyun Kim, Bahar Tercan, Timothy J Martins, Jin Dai, Sylvia Chien, Andrew Carson, Bradley Patay, Elihu H. Estey, Lawrence A. Loeb, Raymond J. Monnat, Pamela S. Becker
Journal: Blood (2020)
Thrombin Generation Related to Netosis in Patients with Systemic Lupus Erythematosus
Authors: Elena Monzón Manzano, Ihosvany Fernandez-Bello, Raul Justo Sanz, Ángel Robles Marhuenda, Paula Acuña, María Teresa Alvarez Román, Elena G Arias-Salgado, Sara García Barcenilla, Miguel A Canales, Victor Jimenez-Yuste, Nora V. Butta
Journal: Blood (2020)
Abstract 438: Downregulation of Ca <sup>2+</sup> /calmodulin-dependent Protein Kinase Type II Delta in the Heart by Antisense Oligonucleotides Mitigates Development of Post-infarct Ventricular Arrhythmias
Authors: Ting-yuan T Yeh, Xin Yi Yeap, Adam E Mullick
Journal: Circulation Research (2020)

Pathological activation of Ca2+/calmodulin-dependent protein kinase type II delta (CaMK2d) has been implicated in the development of heart failure (HF) and arrhythmia. In preclinical models, inhibition or deletion of cardiac CaMK2d has shown a benefit to prevent HF progression or arrhythmia occurrence. We hypothesized that reduction of CaMK2d in the heart by antisense oligonucleotides (ASO) can mitigate the inducibility of MI-associated ventricular arrhythmias. Eight-week-old female C57BL6/N mice, which received permanent ligation of the left anterior descending coronary artery, were randomized to receive PBS, control ASO or two different mouse CaMK2d ASOs five days after the surgery. The ASOs were administered subcutaneously at 50 mg/kg weekly for four weeks. At the end of study, programmed electrical stimulation (PES) was performed to evaluate ventricular effective refractory period (VERP) and inducibility of ventricular arrhythmias (VA). PCR results showed 70% reduction of cardiac CaMK2d in the CaMK2d ASO groups and no changes of other CaMK2 isoforms. There is no significant change of VERP (VERP expressed as mean±SEM, PBS: 35.2±3.0 ms, control ASO: 36.2±3.8 ms, CaMK2d ASO1: 35.7±2.3 ms and CaMK2d ASO2: 33.8±1.4 ms) while the inducible arrhythmias by PES are declined after CaMK2d ASO treatment (VA inducibility index expressed as mean±SEM, PBS: 1.21±0.27, control ASO: 1.21±0.52, CaMK2d ASO1: 0.54±0.22, CaMK2d ASO2: 0.47±0.22). Echocardiography and invasive hemodynamic studies were unable to demonstrate significant functional improvements in the CaMK2d ASO treated groups, suggesting that the anti-arrhythmia effects of CaMK2d ASO treatment were not secondary to improved cardiac mechanics. In conclusion, ASO-mediated reduction of cardiac CaMK2d in a murine MI model ameliorates MI-associated ventricular arrhythmias, providing in vivo proof-of-concept support of the pathological role of CaMK2d activity in MI-related arrhythmia.
CARTITUDE-1: Phase 1b/2 Study of Ciltacabtagene Autoleucel, a B-Cell Maturation Antigen-Directed Chimeric Antigen Receptor T Cell Therapy, in Relapsed/Refractory Multiple Myeloma
Authors: Deepu Madduri, Jesus G. Berdeja, Saad Z. Usmani, Andrzej Jakubowiak, Mounzer Agha, Adam D. Cohen, A. Keith Stewart, Parameswaran Hari, Myo Htut, Elizabeth O'Donnell, Nikhil C. Munshi, David E. Avigan, Abhinav Deol, Alexander M. Lesokhin, Indrajeet Singh, Enrique Zudaire, Tzu-Min Yeh, Alicia J. Allred, Yunsi Olyslager, Arnob Banerjee, Jenna D. Goldberg, Jordan M. Schecter, Carolyn C. Jackson, William Deraedt, Sen Hong Zhuang, Jeffrey R. Infante, Dong Geng, Xiaoling Wu, Marlene J. Carrasco, Muhammad Akram, Farah Hossain, Syed Rizvi, Frank Fan, Sundar Jagannath, Yi Lin, Thomas Martin
Journal: Blood (2020)
Sequential Study By RNA-Seq Shows a Reduction in Inflammation and a Cell Cycle Activation in T-Lymphocytes from Myelodysplastic Syndrome with Del(5q) after Lenalidomide Treatment in Patients Included in the "Sintra-REV" Clinical Trial
Authors: Mónica Del Rey, Luis A Corchete, Teresa González, Félix López Cadenas, Eva Lumbreras, Marta Martín Izquierdo, Sandra Santos-Mínguez, Sofía M Toribio, Blanca Xicoy, Joaquín Sánchez-García, Teresa Bernal, Guillermo F Sanz, Benet Nomdedeu, Pierre Fenaux, Jesús M Hernández Rivas, Maria Diez-Campelo
Journal: Blood (2020)
Outcomes with Sequential FLT3-Inhibitor (FLT3i) Based Therapies in Patients (pts) with <i>FLT3</i>-Mutated Acute Myeloid Leukemia (AML) Exposed to Prior FLT3i Based Therapies
Authors: Musa Yilmaz, Mansour Alfayez, Tapan M. Kadia, Courtney D. DiNardo, Gautam Borthakur, Sanam Loghavi, Marina Konopleva, Rashmi Kanagal-Shamanna, Keyur Patel, Elias Jabbour, Guillermo Garcia-Manero, Naveen Pemmaraju, Sherry A. Pierce, Ghayas C. Issa, Nicholas J. Short, Guillermo Montalban Bravo, Koichi Takahashi, Rita Assi, Ahmad S Alotaibi, Michael Andreeff, Jorge E. Cortes, Hagop M. Kantarjian, Farhad Ravandi, Naval Daver
Journal: Blood (2020)
Abstract 495: A Reappraisal of Body Mass Index and Aerobic Fitness in Young Athletic Women
Authors: Alexandra Kuznetsov, Lena Trager, Garrett Loomer, Timothy Churchill, Rory B Weiner, Meagan M Wasfy, James S Guseh, Aaron L BAGGISH
Journal: Circulation Research (2020)

Background: Lower body mass is thought to enhance athletic performance. We explored the relationship between BMI and aerobic fitness in athletic younger and older men and women. Methods: We examined 2224 patients (805 women, 1419 men) ages 17 through 91, referred to the Cardiovascular Performance Program at Massachusetts General Hospital between 2011 and 2019. Cardiorespiratory fitness (CRF; Peak V0 2 ) was assessed and expressed as %- predicted peak V0 2 , using the equation of Jones to adjust for age, height, and weight. Associations were evaluated using linear regression. Results: Mean peak VO 2 was 34.3±14.1 mL/kg/min, and median %-predicted VO 2 was 105%. We observed an inverse association between BMI and CRF in adults over 30 years old ( B = -0.043, p = 3.3x10 -33 for men, B = -0.051, p = 1.6 x 10 -13 for women) (Fig 1a) and men under 30 ( B = -0.025, p = 0.005) (Fig 1b). No linear association was found in younger women ages 17 - 29 ( B = -0.0078, p = 0.38) (Fig 1b). In contrast, a quadratic model disclosed a direct relationship at lower BMI and an inverse relationship at higher BMI (Fig 1c). An examination of high fitness young adults (defined as having %-predicted VO 2 ≥ 120%) demonstrates that fit women have mean BMI’s of 23.15 ± 2.69 (Fig 1d). Conclusion: These data highlight that BMI and fitness in younger aerobically fit women do not follow a simple linear relationship but one that is parabolic in nature. High fitness in young women occurs with highest density in the upper strata of the WHO and NIH-defined range of healthy BMI. These data support a deemphasis of weight loss generally and BMI specifically to enhance aerobic performance in athletic young women.
Abstract IA26: Tumor evolution: From Darwin’s finches to breast cancer
Authors: Kornelia Polyak
Journal: Cancer Research (2020)

Abstract Tumor evolution is driven by heterogeneity for heritable traits in combination with environmental selection forces including cancer therapies. We have been investigating intratumor cellular genetic and phenotypic heterogeneity in breast tumors and described that higher heterogeneity is associated with poor clinical outcomes. We have also developed experimental models of intratumor subclonal heterogeneity and demonstrated that more heterogeneous tumors grow faster and develop heterogeneous distant metastases. By analyzing the underlying mechanisms we defined that intratumor heterogeneity is maintained by non-cell-autonomous factors and clonal cooperation drives metastases by modulating the local and systemic microenvironments. Lastly, we have identified epigenetic enzymes as regulators of cellular transcriptomic heterogeneity and showed that by modulating the activity of these enzymes, we can decrease cellular heterogeneity and therapeutic resistance. Overall, our studies demonstrate the need to study cancer patients as a whole and to apply a combination of molecular profiling, including single cell assays, and mathematical modeling to understand how tumors evolved and to develop more effective cancer therapeutic strategies based on this knowledge. Citation Format: Kornelia Polyak. Tumor evolution: From Darwin’s finches to breast cancer [abstract]. In: Proceedings of the AACR Virtual Special Conference on Tumor Heterogeneity: From Single Cells to Clinical Impact; 2020 Sep 17-18. Philadelphia (PA): AACR; Cancer Res 2020;80(21 Suppl):Abstract nr IA26.
Meta-Analysis of Genome-Wide Association Studies of Acute Myeloid Leukemia (AML) Patients Identifies Variants Associated with Risk of 11q23/<i>KMT2A</i>-Translocated and Core-Binding Factor (CBF) AML and Suggests a Role for Transcription Elongation in Leukemogenesis
Authors: Christopher J. Walker, Junke Wang, Alyssa I. Clay-Gilmour, Krzysztof Mrózek, Deedra Nicolet, Christopher C. Oakes, Jessica Kohlschmidt, Bayard L. Powell, Jonathan E. Kolitz, Andrew J Carroll, Ezgi Karaesmen, Abbas A. Rizvi, Qianqian Zhu, Li Yan, Leah Preus, Song Liu, Yiwen Wang, Daniel O. Stram, Loreall Pooler, Xin Sheng, Christopher Haiman, David Van Den Berg, Amy Webb, Guy Brock, Stephen R. Spellman, Marcelo C. Pasquini, Philip L. McCarthy, James M. Allan, Friedrich Stolzel, Kenan Onel, Richard M. Stone, Ramiro Garzon, Clara D. Bloomfield, John C. Byrd, Albert de la Chapelle, Theresa E. Hahn, Ann-Kathrin Eisfeld, Lara E. Sucheston-Campbell
Journal: Blood (2020)
Improved Markers of Cholestatic Liver Injury in Patients With Primary Biliary Cholangitis Treated With Obeticholic Acid and Bezafibrate
Authors: Lena Smets, Jef Verbeek, Hannelie Korf, Schalk van der Merwe, Frederik Nevens
Journal: Hepatology (2020)

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Efficacy and Safety Analysis of Ibrutinib-Containing Therapy for Relapsed/Refractory (R/R) Mantle Cell Lymphoma (MCL): Results from a Real-World Study in China
Authors: Qingqing Cai, Huiqiang Huang, Yuchen Zhang, Panpan Liu, Hongmei Jing, Ping Yang, Tongyu Lin, Zhongjun Xia, Zhiming Li, Wenyu Li, Liye Zhong, Xu Ye, Xueli Jin, Liling Zhang, Huilai Zhang, Xiuhua Sun, Yuyang Tian, Shuyun Ma, Ning Su, Jun Cai
Journal: Blood (2020)
CXCL12 Knock-out Enhances Leukemia Stem Cell Response to Combination Chemotherapy Plus Tyrosine Kinase Inhibition in Flt3-ITD Acute Myeloid Leukemia
Authors: Nick R Anderson, Hui Li, Mason W Harris, Shaowei Qiu, Amanda K Mullen, Andrew J Paterson, Ravi Bhatia
Journal: Blood (2020)