tbuckley/cabot-search huggingface dataset:
Hyperthermia induced by transient receptor potential vanilloid-1 (TRPV1) antagonists in human clinical trials: Insights from mathematical modeling and meta-analysis
Authors: Andras Garami, Yury P. Shimansky, Zoltan Rumbus, Robson C.L. Vizin, Nelli Farkas, Judit Hegyi, Zsolt Szakacs, Margit Solymar, Alexandra Csenkey, Dan A. Chiche, Ram Kapil, Donald J. Kyle, Wade D. Van Horn, Peter Hegyi, Andrej A. Romanovsky
Journal: Pharmacology & Therapeutics (2020)

Antagonists of the transient receptor potential vanilloid-1 (TRPV1) channel alter body temperature (Tb) in laboratory animals and humans: most cause hyperthermia; some produce hypothermia; and yet others have no effect. TRPV1 can be activated by capsaicin (CAP), protons (low pH), and heat. First-generation (polymodal) TRPV1 antagonists potently block all three TRPV1 activation modes. Second-generation (mode-selective) TRPV1 antagonists potently block channel activation by CAP, but exert different effects (e.g., potentiation, no effect, or low-potency inhibition) in the proton mode, heat mode, or both. Based on our earlier studies in rats, only one mode of TRPV1 activation – by protons – is involved in thermoregulatory responses to TRPV1 antagonists. In rats, compounds that potently block, potentiate, or have no effect on proton activation cause hyperthermia, hypothermia, or no effect on Tb, respectively. A Tb response occurs when a TRPV1 antagonist blocks (in case of hyperthermia) or potentiates (hypothermia) the tonic TRPV1 activation by protons somewhere in the trunk, perhaps in muscles, and – via the acido-antithermogenic and acido-antivasoconstrictor reflexes – modulates thermogenesis and skin vasoconstriction. In this work, we used a mathematical model to analyze Tb data from human clinical trials of TRPV1 antagonists. The analysis suggests that, in humans, the hyperthermic effect depends on the antagonist's potency to block TRPV1 activation not only by protons, but also by heat, while the CAP activation mode is uninvolved. Whereas in rats TRPV1 drives thermoeffectors by mediating pH signals from the trunk, but not Tb signals, our analysis suggests that TRPV1 mediates both pH and thermal signals driving thermoregulation in humans. Hence, in humans (but not in rats), TRPV1 is likely to serve as a thermosensor of the thermoregulation system. We also conducted a meta-analysis of Tb data from human trials and found that polymodal TRPV1 antagonists (ABT-102, AZD1386, and V116517) increase Tb, whereas the mode-selective blocker NEO6860 does not. Several strategies of harnessing the thermoregulatory effects of TRPV1 antagonists in humans are discussed.
Comprehensive analysis of BMP target gene in pancreatic cancer cell line and its functional role during cancer cell migration
Authors: Shin Hamada, Kennichi Satoh, Morihisa Hirota, Atsushi Kanno, Jun Umino, Hiromichi Itoh, Atsushi Masamune, Tooru Shimosegawa
Journal: Cancer Research (2008)

4512  Pancreatic cancer has high mortality due to its invasive nature. Clinically, at the time of diagnosis, most of the pancreatic cancer patients have distant metastasis or locally advanced unresectable tumor. The molecular mechanism of this biological process is still under investigation, and recent reports have uncovered that multiple growth factors and cytokines contribute to the cancer cell invasion and metastasis as inducers of the epithelial to mesenchymal transition (EMT), which includes the down-regulation of epithelial marker, up-regulation of mesenchymal marker and increased cell motility. We previously reported that the bone morphogenetic protein 4 (BMP4) induces EMT in pancreatic cancer cells via the induction of the homeobox gene MSX2, but its detailed molecular mechanism still remains unclear.  Hence, we performed comprehensive analysis by using cDNA microarray and elucidated possible BMP target genes in human pancreatic cancer cell line Panc-1 to clarify the molecular mechanism of BMP-induced EMT. The elucidated genes were confirmed its induction by real-time PCR. Among these up-regulated genes, the calcium-binding protein coding S100P was newly identified as a BMP target gene, and its induction was also found in normal human pancreatic duct epithelial cell line HPDE cells after BMP4 treatment. The S100P induction was further evaluated by Western blotting analysis. The siRNA-based knockdown of S100P repressed the BMP-induced cell migration in Panc-1 cells. The induction of S100P was repressed by Smad4 knockdown, indicating the involvement of canonical Smad signaling pathway. On the other hand, the cyclin-dependent kinase inhibitor p21/CIP1 was also induced by BMP4, and growth inhibitory effect was confirmed by BrdU incorporation assay and direct cell count. Cell cycle analysis revealed that BMP4 causes G1 cell cycle arrest, but not apoptosis in Panc-1 cells.  Taken together, BMP4 has dual effects on Panc-1 cells as an inducer of EMT and inhibitor of cell proliferation. These findings suggest the similarity between BMP and transforming growth factor β (TGFβ), but TGFβ did not induce S100P expression in Panc-1 cells, indicating distinct mechanism of EMT induction between BMP and TGFβ. We also reported the essential role of the homeobox gene MSX2 during BMP4-induced EMT in Panc-1 cells previously, and the relationship between MSX2 and S100P is still an open question. Further study is now under way in our group. These findings will contribute to the development of a new therapeutic strategy.
P-0124 Outcome of Gastric Lymphoma in Elderly Patients with Reduced dose Chemotherapy Followed by Involved Field Radiotherapy
Authors: Vikas Roshan, Shukla Peeyush, Faiz Ansari, Pinkey Bala, P. Jagdesan, Pavnesh Kumar, Meenal Bhandari, Parmod Julka, G.K. Rath
Journal: Annals of Oncology (2012)
The colonic macrophage transcription factor RBP-J orchestrates intestinal immunity against bacterial pathogens
Authors: Lan Kang, Xiang Zhang, Liangliang Ji, Tiantian Kou, Sinead M. Smith, Baohong Zhao, Xiaohuan Guo, Inés Pineda-Torra, Li Wu, Xiaoyu Hu
Journal: The Journal of Experimental Medicine (2020)

Macrophages play pleiotropic roles in maintaining the balance between immune tolerance and inflammatory responses in the gut. Here, we identified transcription factor RBP-J as a crucial regulator of colonic macrophage–mediated immune responses against the enteric pathogen Citrobacter rodentium. In the immune response phase, RBP-J promoted pathogen clearance by enhancing intestinal macrophage-elicited Th17 cell immune responses, which was achieved by maintenance of C/EBPβ-dependent IL-6 production by overcoming miRNA-17∼92–mediated suppressive effects. RBP-J deficiency–associated phenotypes could be genetically corrected by further deleting miRNA-17∼92 in macrophages. In the late phase, noneradicated pathogens in RBP-J KO mice recruited abundant IL-1β–expressing CD64+Ly6C+ colonic macrophages and thereby promoted persistence of ILC3-derived IL-22 to compensate for the impaired innate and adaptive immune responses, leading to ultimate clearance of pathogens. These results demonstrated that colonic macrophage–intrinsic RBP-J dynamically orchestrates intestinal immunity against pathogen infections by interfacing with key immune cells of T and innate lymphoid cell lineages.
Protective Effect of Magnesium Preloading on Nephrotoxicity Caused by Cisplatin (Over 60 MG/M2) In Patients with Thoracic Malignancy
Authors: T. Yoshida, S. Niho, M. Toda, S. Umemura, K. Yoh, K. Goto, H. Ohmatsu, K. Izumi, Y. Ohe
Journal: Annals of Oncology (2012)
Association of MCC C.*5077a &gt; G, PTCH1 G.79755c &gt; T and Ptch1 G.79456c &gt; T Polymorphisms with Inherited Risk of Cutaneous Melanoma
Authors: G.A.S. Nogueira, G.J. Lourenço, C. Oliveira, J.A. Rinck-Junior, E.F.D. Costa, A.M. Moraes, C.S.P. Lima
Journal: Annals of Oncology (2012)
Panerb Study: Which Category of Patients, Suffering from Metastatic Colorectal Cancer, Can Benefit From Panitumumab Treatment After Cetuximab-Based Regimen Failure?
Authors: J. Metges, J.F. Ramée, O. Dupuis, P. Deguiral, E. Boucher, O. Cojocarasu, M. Ferec, M. Porneuf, J. Douillard, F. Grude
Journal: Annals of Oncology (2012)
Nudix Hydrolase NUDT16 Regulates 53BP1 Protein by Reversing 53BP1 ADP-Ribosylation
Authors: Fan Zhang, Lihong Lou, Bo Peng, Xiaotian Song, Ofer Reizes, Alexandru Almasan, Zihua Gong
Journal: Cancer Research (2020)

Abstract 53BP1 controls two downstream subpathways, one mediated by PTIP and Artemis and the other by RIF1 and MAD2L2/Shieldin, to coordinate DNA repair pathway choices. However, the upstream regulator(s) of 53BP1 function in DNA repair remain unknown. We and others recently reported that TIRR associates with 53BP1 to stabilize it and prevents 53BP1 localization to DNA damage sites by blocking 53BP1 Tudor domain binding to H4K20me2 sites. Here, we report that the Nudix hydrolase NUDT16, a TIRR homolog, regulates 53BP1 stability. We identified a novel posttranslational modification of 53BP1 by ADP-ribosylation that is targeted by a PAR-binding E3 ubiquitin ligase, RNF146, leading to 53BP1 polyubiquitination and degradation. In response to DNA damage, ADP-ribosylated 53BP1 increased significantly, resulting in its ubiquitination and degradation. These data suggest that NUDT16 plays a major role in controlling 53BP1 levels under both normal growth conditions and during DNA damage. Notably, overexpression of a NUDT16 catalytically inactive mutant blocked 53BP1 localization to double-strand breaks because (i) the mutant binding to TIRR increased after IR; (ii) the mutant enhanced 53BP1 Tudor domain binding to TIRR, and (iii) the mutant impaired the interaction of 53BP1 Tudor domain with H4K20me2. Moreover, NUDT16's catalytic hydrolase activity was required for 53BP1 de–ADP-ribosylation, 53BP1 protein stability, and its function in cell survival. In summary, we demonstrate that NUDT16 regulates 53BP1 stability and 53BP1 recruitment at double-strand breaks, providing yet another mechanism of 53BP1 regulation. Significance: This study provides a novel mechanism of 53BP1 regulation by demonstrating that NUDT16 has hydrolase activities that remove ADP-ribosylation of 53BP1 to regulate 53BP1 stability and 53BP1 localization at DSBs.
Dasatinib First-Line Treatment in Gastrointestinal Stromal Tumors. a Multicenter Phase II Trial of the SAKK (SAKK 56/07)
Authors: M. Montemurro, J. Domont, P. Rutkowski, A.D. Roth, R. von Moos, R. Inauen, D. Dietrich, C. Biaggi, J. Prior, S. Leyvraz
Journal: Annals of Oncology (2012)
Dynamic Changes in Plasma Osteopontin as a Markers of Tumor Response in Metastatic Renal Cell Carcinoma (RCC) Patients Treated with Pazopanib
Authors: H.T. Tran, Y. Liu, Y. Lin, A.J. Zurita Saavedra,, K.L. Baker-Neblett, L.N. Pandite, J.V. Heymach
Journal: Annals of Oncology (2012)
Lurbinectedin (PM01183) Activity in Platinum-Resistant/Refractory Ovarian Cancer Patients. Preliminary Results of an Ongoing Two-Stage Phase II Study
Authors: D. Berton-Rigaud, J. Alexandre, M. Provansal, A. Casado, A. Gonzalez Martin, C. Fernández, C. Kahatt, S. Szyldergemajn, J.M. Del Campo, A.M. Poveda, E.M. Guerra, I. Ray-Coquard
Journal: Annals of Oncology (2012)
Anti-Programmed Death-1 (PD-1) (BMS-936558/MDX-1106/ONO-4538) in Patients (PTS) with Advanced Solid Tumors: Clinical Activity, Safety, and Molecular Markers
Authors: S.L. Topalian, J.R. Brahmer, F.S. Hodi, D.F. McDermott, D.C. Smith, S. Gettinger, J.M. Taube, A. Gupta, J.M. Wigginton, M. Sznol
Journal: Annals of Oncology (2012)
Correction to: “Hepatocellular carcinoma: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up”
Authors: A. Vogel, A. Cervantes, I. Chau, B. Daniele, J.M. Llovet, T. Meyer, J.-C. Nault, U. Neumann, J. Ricke, B. Sangro, P. Schirmacher, C. Verslype, C.J. Zech, D. Arnold, E. Martinelli
Journal: Annals of Oncology (2019)
P-0299 Effectiveness of Short-Term Preoperative Teleradiotherapy in Rectal Cancer Treatment, Based on Personal Experience
Authors: Tomasz Skóra, Katarzyna Pudełek, Jadwiga Nowak-Sadzikowska, Bogumiła Szyszka-Charewicz, Jerzy Jakubowicz
Journal: Annals of Oncology (2012)
P-0099 Two-Thirds of Pancreatic Ductal Adenocarcinomas have low Expression of Hent1 as Determined by the Sp120 Rabbit Monoclonal Antibody Immunohistochemistry Test
Authors: Mitch Raponi, Stefan Boeck, Bill Richardson, Towne Penny, Jeff Isaacson, Jim Ranger-Moore, June Clements, Steffen Ormanns, Thomas Kirchner, William Regine, Kathryn Winter, Lindsey Rolfe, Andrew Allen, Roland Andersson, Volker Heinemann, Adam Dicker, Tone Ikdahl, Elizabeth Poplin
Journal: Annals of Oncology (2012)
Injured Podocytes Are Sensitized to Angiotensin II–Induced Calcium Signaling
Authors: Julia Binz-Lotter, Christian Jüngst, Markus M. Rinschen, Sybille Koehler, Peter Zentis, Astrid Schauss, Bernhard Schermer, Thomas Benzing, Matthias J. Hackl
Journal: Journal of the American Society of Nephrology (2020)

Significance Statement Although the effects of angiotensin II (AngII) on glomerular perfusion pressure are well characterized, the relevance of AngII signaling in podocytes remains elusive. The authors’ in vivo study demonstrates that AngII elicits only a limited calcium response in podocytes in healthy mice. In contrast, in mice subjected to chemical injury or genetic deletion of the podocin-encoding gene Nphs2 , the resultant podocyte damage and proteinuria rendered podocytes responsive to pronounced AngII-induced calcium transients. These findings may explain clinical trial results in humans that demonstrated beneficial renal effects of blockade of the renin-angiotensin system in proteinuric patients, but not in patients with nonproteinuric kidney disease. This study also underscores the importance of inhibition of the renin-angiotensin system in patients with podocyte damage and proteinuria. Background Inhibition of angiotensin II (AngII) signaling, a therapeutic mainstay of glomerular kidney diseases, is thought to act primarily through regulating glomerular blood flow and reducing filtration pressure. Although extravascular actions of AngII have been suggested, a direct effect of AngII on podocytes has not been demonstrated in vivo . Methods To study the effects of AngII on podocyte calcium levels in vivo , we used intravital microscopy of the kidney in mice expressing the calcium indicator protein GCaMP3. Results In healthy animals, podocytes displayed limited responsiveness to AngII stimulation. In contrast, in animals subjected to either adriamycin-induced acute chemical injury or genetic deletion of the podocin-encoding gene Nphs2 , the consequent podocyte damage and proteinuria rendered the cells responsive to AngII and resulted in AngII-induced calcium transients in significantly more podocytes. The angiotensin type 1 receptor blocker losartan could fully inhibit this response. Also, responsiveness to AngII was at least partly mediated through the transient receptor potential channel 6, which has been implicated in podocyte calcium handling. Interestingly, loss of a single Nphs2 allele also increased podocytes’ responsiveness to AngII signaling. This direct effect of AngII on injured podocytes results in increased calcium transients, which can further aggravate the underlying kidney disease. Conclusions Our discovery that podocytes become sensitized to AngII-induced calcium signaling upon injury might explain results from large, randomized, controlled trials in which improved renal outcomes occur only in the subgroup of patients with proteinuria, indicating podocyte damage. Our findings also emphasize the need to treat every patient with a glomerular disease with either an angiotensin-converting enzyme inhibitor or an angiotensin type 1 receptor blocker.
Early Season Pediatric Influenza B/Victoria Virus Infections Associated with a Recently Emerged Virus Subclade — Louisiana, 2019
Authors: Daniel Owusu, Julie Hand, Mark W. Tenforde, Leora R. Feldstein, Juliana DaSilva, John Barnes, Grace Lee, Juliet Tran, Theresa Sokol, Alicia M. Fry, Lynnette Brammer, Melissa A. Rolfes
Journal: MMWR Morbidity and Mortality Weekly Report (2020)

Multiple genetically distinct influenza B/Victoria lineage viruses have cocirculated in the United States recently, circulating sporadically during the 2018-19 season and more frequently early during the 2019-20 season (1). The beginning of the 2019-20 influenza season in Louisiana was unusually early and intense, with infections primarily caused by influenza B/Victoria lineage viruses. One large pediatric health care facility in New Orleans (facility A) reported 1,268 laboratory-confirmed influenza B virus infections, including 23 hospitalizations from July 31 to November 21, 2019, a time when influenza activity is typically low. During this period, Louisiana also reported one pediatric death associated with influenza B virus infection. An investigation of the influenza B virus infections in Louisiana, including medical and vaccine record abstraction on 198 patients, primarily from facility A, with sporadic cases from other facilities in the state, found that none of the patients had received 2019-20 seasonal influenza vaccine, in part because influenza activity began before influenza vaccination typically occurs. Among 83 influenza B viruses sequenced from 198 patients in Louisiana, 81 (98%) belonged to the recently emerged B/Victoria V1A.3 genetic subclade. Nationally, to date, B/Victoria viruses are the most commonly reported influenza viruses among persons aged <25 years (2). Of the 198 patients in the investigation, 95% were aged <18 years. Although most illnesses were uncomplicated, the number of hospitalizations, clinical complications, and the reported pediatric death in Louisiana serve as a reminder that, even though influenza B viruses are less common than influenza A viruses in most seasons, influenza B virus infection can be severe in children. All persons aged ≥6 months should receive an annual influenza vaccination if they have not already received it (3). Antiviral treatment of influenza is recommended as soon as possible for all hospitalized patients and for outpatients at high risk for influenza complications (including children aged <2 years and persons with underlying medical conditions) (4).
Cytokine mRNA Degradation in Cardiomyocytes Restrains Sterile Inflammation in Pressure-Overloaded Hearts
Authors: Shigemiki Omiya, Yosuke Omori, Manabu Taneike, Tomokazu Murakawa, Jumpei Ito, Yohei Tanada, Kazuhiko Nishida, Osamu Yamaguchi, Takashi Satoh, Ajay M. Shah, Shizuo Akira, Kinya Otsu
Journal: Circulation (2020)

Proinflammatory cytokines play an important role in the pathogenesis of heart failure. The mechanisms responsible for maintaining sterile inflammation within failing hearts remain poorly defined. Although transcriptional control is important for proinflammatory cytokine gene expression, the stability of mRNA also contributes to the kinetics of immune responses. Regnase-1 is an RNase involved in the degradation of a set of proinflammatory cytokine mRNAs in immune cells. The role of Regnase-1 in nonimmune cells such as cardiomyocytes remains to be elucidated.
Baseline Mac-2 Binding Protein Glycosylation Isomer Level Stratifies Risks of Hepatocellular Carcinoma in Chronic Hepatitis B Patients with Oral Antiviral Therapy
Authors: Tai-Chung Tseng, Cheng-Yuan Peng, Yao-Chun Hsu, Tung-Hung Su, Chia-Chi Wang, Chun-Jen Liu, Hung-Chih Yang, Wan-Ting Yang, Chia-Hsin Lin, Ming-Lung Yu, Hsueh-Chou Lai, Yasuhito Tanaka, Mindie H. Nguyen, Chen-Hua Liu, Pei-Jer Chen, Ding-Shinn Chen, Jia-Horng Kao
Journal: Liver Cancer (2020)

Mac-2 binding protein glycosylation isomer (M2BPGi) is a novel biomarker correlating with liver fibrosis stages. However, little is known about how it predicts risks of hepatocellular carcinoma (HCC) in chronic hepatitis B (CHB) patients receiving long-term antiviral treatment.The study contained 2 parts. The first part was to explore whether M2BPGi could be an HCC predictor in 899 CHB patients receiving long-term entecavir therapy. The second part was to validate the findings in an independent cohort of 384 on-treatment CHB patients with more severe liver disease.In the discovery cohort, there were 64 patients developing HCC within an average follow-up of 7.01 years. Our data showed that M2BPGi level was positively associated with HCC development. When stratifying the patients by an M2BPGi level of 1.73 (the third quartile), the high M2BPGi group was shown to have an increased HCC risk compared to the low M2BPGi group with hazard ratio of 5.80 (95% CI 3.50-9.60). Furthermore, we found that the M2BPGi level complements PAGE-B score, a well-validated HCC prediction model, to predict HCC development. Lastly, the cutoff was validated in the independent cohort, especially those with an intermediate PAGE-B score.In CHB patients receiving long-term antiviral treatment, serum M2BPGi level not only serves as an independent HCC predictor but also complements PAGE-B in stratifying HCC risks.
Phase I and II Clinical Study of Cancer Vaccine Consisting of 5 Novel Epitope Peptides For Patients with Metastatic Colorectal Cancer (MCRC)
Authors: S. Hazama, Y. Nakamura, K. Yoshida, T. Tsunoda, H. Tanaka, K. Tahara, R. Shimizu, K. Okuno, K. Yoshimatsu, M. Oka
Journal: Annals of Oncology (2012)
Diverse <i>AR</i> Gene Rearrangements Mediate Resistance to Androgen Receptor Inhibitors in Metastatic Prostate Cancer
Authors: Yingming Li, Rendong Yang, Christine M. Henzler, Yeung Ho, Courtney Passow, Benjamin Auch, Suzanne Carreira, Daniel Nava Rodrigues, Claudia Bertan, Tae Hyun Hwang, David A. Quigley, Ha X. Dang, Colm Morrissey, Michael Fraser, Stephen R. Plymate, Christopher A. Maher, Felix Y. Feng, Johann S. de Bono, Scott M. Dehm
Journal: Clinical Cancer Research (2020)

Prostate cancer is the second leading cause of male cancer deaths. Castration-resistant prostate cancer (CRPC) is a lethal stage of the disease that emerges when endocrine therapies are no longer effective at suppressing activity of the androgen receptor (AR) transcription factor. The purpose of this study was to identify genomic mechanisms that contribute to the development and progression of CRPC.
Progesteron Receptor Status in Determining the Prognosis of Estrogen Receptor Positive / HER2-Negative Breast Carcinoma
Authors: U. Yalcintas Arslan, O. Bal, T. Ozatli, K. Helvaci, O. Esbah, B. Budakoglu, U. Uyeturk, O.U. Sonmez, I. Turker, O.B. Oksuzoglu
Journal: Annals of Oncology (2012)
P-0075 18F-FDG Uptake in Hepatocellular Carcinoma Cell Lines: Correlation with Multidrug Resistance Proteins Expression
Authors: Mónica Mendes, Ana Brito, Ana Abrantes, Fábio Veríssimo, Ana Gonçalves, Ana Sarmento-Ribeiro, José Tralhão, Maria Botelho
Journal: Annals of Oncology (2012)
Would decriminalising personal use of cannabis lead to higher rates of mental illness?
Authors: Bobby P Smyth, Mary Cannon, Andrew Molodynski, H Valerie Curran, Niamh Eastwood, Adam R Winstock
Journal: BMJ (2020)

Removing criminal penalties for possession could increase adolescent use, say <b>Bobby P Smyth</b>, <b>Mary Cannon</b>, and <b>Andrew Molodynski</b>. But <b>H Valerie Curran</b>, <b>Niamh Eastwood</b>, and <b>Adam R Winstock</b> find no evidence for this and say that liberalisation of drug laws could reduce harms
Interim Analysis of Overall Survival Per Subgroups in the Prospective, Non-Interventional Insight Study in Patients with Hepatocellular Carcinoma Treated with Sorafenib
Authors: T. Ganten, E. Schott, P. Galle, T. Göhler, P. Malfertheiner, R. Stauber, R. Buder, K. Achilles, G. Gerken
Journal: Annals of Oncology (2012)
<scp>CXCR4</scp> mutational status does not impact outcomes in patients with <scp>W</scp>aldenström macroglobulinemia treated with proteasome inhibitors
Authors: Jorge J. Castillo, Joshua N. Gustine, Kirsten Meid, Catherine A. Flynn, Maria G. Demos, Maria L. Guerrera, Cristina Jimenez, Amanda Kofides, Xia Liu, Manit Munshi, Nicholas Tsakmaklis, Christopher J. Patterson, Lian Xu, Guang Yang, Zachary R. Hunter, Steven P. Treon
Journal: American Journal of Hematology (2020)