tbuckley/cabot-search huggingface dataset:
Novel derivatives of fusarochromanone: potential therapeutic compounds
Authors: Elahe Mahdavian, Brian Salvatore, John Clifford
Journal: Cancer Research (2007)

3975  Fusarochromanone (FC-101a) is a flavinoid produced by the mold, Fusarium equiseti. FC-101a induces tibial dyschondroplasia in young chickens. This activity is the result of powerful anti-angiogenic activity, whereby mold growing on chicken feed produces FC-101a, which inhibits the growth of blood vessels in the developing bones of broiler chicks. FC-101a has an IC50 of 50 nM against human microvascular endothelial cells. Thus it could be a potent anti-angiogenic agent in man as well. It was later discovered that FC-101a also acts directly on cancer cells. The molecule9s anti-cancer potency is best demonstrated by IC50 values of less than 10 nM against both human melanoma and small cell lung cancer in vitro for the induction of apoptosis. Thus, we viewed FC-101a to be an excellent lead candidate for the discovery of new therapeutic agents. Further development of this lead compound as a drug requires that we undertake its total synthesis and a set of new FC-101a analogs that possess similar in vitro activity, but also manifest greater activity in vivo.  Our research group has synthesized a number of novel analogs of FC101a and conducted a series of preliminary assays to determine the effect of these analogs on cell viability. We have analyzed human skin squamous cell carcinoma (SCC) cells (SRB12-p9 cell line) and a clone of SRB12-p9 cells that has been stably transfected with a dominant-negative acting form of Stat3 (p9 dn5), human keratinocyte-derived cells (HaCaT cell line), and human breast carcinoma cells (MDA-MB-231 cell line). Surprisingly, most of the FC101a analogs caused an increase in cell viability for all cell lines as determined by the MTT cell viability assay, compared to untreated controls. A time course of treatment of HaCaT cells with 10_M of FC101a analogs further confirmed the positive effect on cell viability. For the seven analogs tested we observed a time dependent increase in cell number for up to 4 days, ranging from 29.8% to 66.7%.  Experiments are in progress to determine the mechanism of the enhanced cell viability effect. Fluorescence activated cell sorting (FACS) analysis and apoptosis assays are underway to determine the relative contribution of increased proliferation and/or decreased cell death to the enhanced cell numbers observed for treated cells. In addition, we are exploring the potential anti-angiogenic effect of the analogs.
THE ADDITIONAL VALUE OF NATURAL LANGUAGE PROCESSING TO IDENTIFY DISEASE PREVALENCE BASED ON ELECTRONIC MEDICAL RECORD IMAGING REPORTS
Authors: Duygu Kocyigit, Alex Milinovich, Chan M. Lee, Mazen Hanna, Andrej Gabrovesk, Jian Jin, Micheal Silverman, Maleeha Ahmad, W.H. Wilson Tang, Richard A. Grimm, Leslie Cho, Brian P. Griffin, Scott D. Flamm, Deborah Kwon
Journal: Journal of the American College of Cardiology (2020)
CONSEQUENCES OF A DELAYED LAD STEMI: CARDIOGENIC SHOCK MANAGED WITH REVASCULARIZATION, LVAD, VT ABLATION AND ASD CLOSURE
Authors: Shuktika Nandkeolyar, Tahmeed Contractor, Rahul Bhardwaj, Ravi Mandapati, Islam Abudayyeh, Anees Razzouk, Antoine Sakr, Aditya Satish Bharadwaj
Journal: Journal of the American College of Cardiology (2020)
POTENTIAL EXPLANATION FOR DISPROPORTIONATE LEFT VENTRICULAR ENLARGEMENT IN BARLOW's DISEASE: INSIGHTS FROM CARDIOVASCULAR MAGNETIC RESONANCE
Authors: Kinan Carlos El Tallawi, Danai Kitkungvan, Jiaqiong Xu, Vittorio Cristini, Eric Yota Yang, Miguel A. Quinones, Gerald M. Lawrie, William Zoghbi, Dipan J. Shah
Journal: Journal of the American College of Cardiology (2020)
Is there a benefit on survival of tyrosine-kinase inhibitors versus chemotherapy in first line in mutated EGFR patients with advanced non-small cell cancer (NSCLC)? A meta-analysis.
Authors: Gaetan Des Guetz, Bernard Uzzan, Kader Chouahnia, Patrick Nicolas, Jean F. Morere
Journal: Journal of Clinical Oncology (2012)

e18020 Background: Tyrosine-Kinase Inhibitors (TKIs) markedly improve Progression Free Survival (PFS) of advanced NSCLC patients mutated for Epidermal Growth Factor Receptor (EGFR). Results on Overall Survival (OS) are more questionable. Therefore, we performed a publication-based meta-analysis to further assess this issue. Methods: We did a PubMed query using keywords simultaneously (lung neoplasm, TKI, EGFR mutation, survival). We also searched for relevant abstracts in proceedings of ASCO, ESMO, WCLC annual meetings. We cross-checked all references from all articles. Only phase III randomized controlled trials comparing TKI and chemotherapy were included. We used EasyMA software. Results: The 6 eligible studies included 2223 patients (516 males, 1688 females, mostly Asian, median age 60 years, 2155 adenocarcinomas (97 %), 996 mutated tumors, 389 stage IIIB, 1572 Stage IV (71 %), 1989 never smokers (89.5 %). Four studies assessed gefitinib, 2 erlotinib. Chemotherapies were doublets including a platinum salt. Four studies included only mutated patients. Compared to chemotherapy, EGFR TKIs significantly improved PFS (HR=0.39, 95 % CI 0.28-0.53, random effect model). Conversely, OS was similar among patients who first received TKI or chemotherapy (HR=1.00, CI 0.83-1.22, fixed effect model). PFS was significantly worse among non mutated patients in the 2 studies including both mutated and wild-type EGFR patients, whereas OS was unchanged. Concerning side-effects, rash, diarrhoea and interstitial lung disease were significantly more frequent after TKI (RRs 5.00; 2.40 and 6.07). As expected, fatigue (RR 0.41), nausea/vomiting (0.19) and haematological disorders were all significantly more frequent after chemotherapy (RRs for neutropenia, thrombocytopenia and anaemia 0.08; 0.18 and 0.26). Conclusions: The major discrepancy between a markedly improved PFS and a similar OS after TKI compared with chemotherapy could be related to the high level of crossing-over between the 2 groups. We found no detrimental effect on OS of TKIs among wild-type patients.
British Thoracic Society Guideline for bronchiectasis in adults
Authors: Adam T Hill, Anita L Sullivan, James D Chalmers, Anthony De Soyza, J Stuart Elborn, R Andres Floto, Lizzie Grillo, Kevin Gruffydd-Jones, Alex Harvey, Charles S Haworth, Edwin Hiscocks, John R Hurst, Christopher Johnson, W Peter Kelleher, Pallavi Bedi, Karen Payne, Hashem Saleh, Nicholas J Screaton, Maeve Smith, Michael Tunney, Deborah Whitters, Robert Wilson, Michael R Loebinger
Journal: Thorax (2018)

### How should the diagnosis of bronchiectasis be determined? #### Recommendations – Imaging #### Good practice points CT imaging protocol CT features of bronchiectasis General ### In whom should the diagnosis of bronchiectasis be suspected? #### Recommendations
CORRELATION BETWEEN INTRAVASCULAR ULTRASOUND (IVUS) AND VENOGRAM WITH VENOUS DUPLEX ULTRASOUND IN THE DETECTION OF FEMORO-ILIO-CAVAL VEIN OBSTRUCTION
Authors: Robert Sogomonian, Carlos Andres Gonzalez-Lengua, Mikko A. Tesalona, Balaram Krishna Hanumanthu, Pouya Mohajer, Kevin Liu, Nima Taghipour, Ramesh Gowda, Deepika Misra
Journal: Journal of the American College of Cardiology (2020)
ASSOCIATION OF CARDIAC RESYNCHRONIZATION THERAPY WITH MORTALITY, DEFIBRILLATION, AND RIGHT VENTRICULAR FAILURE IN PATIENTS WITH LEFT VENTRICULAR ASSIST DEVICES
Authors: Douglas Darden, Enrico Ammirati, Michela Brambatti, Jonathan Chong Hsu, Oscar Braun, Palak Shah, Caroline Van De Heyning, Enrico Perna, Maja Cikes, Grunde Gjesdal, Luciano Potena, Masetti Marco, Nina Jakus, Dina De Bock, Jasper J. Brugts, Claudio Russo, Jesse Veenis, Filip Rega, Liviu Klein, Gert Pretorius, Manlio Cipriani, Maria Frigerio, Eric Adler
Journal: Journal of the American College of Cardiology (2020)
QIM20-128: Baseline Assessment of Oncology Providers’ Quality Improvement Knowledge in a Multi-Institutional Breast Cancer Quality Improvement Collaborative
Authors: Lindsey Kreutzer, Ashley Byerly, Eileen Ngo, Julie K. Johnson, Karl Y. Bilimoria, Anthony D. Yang
Journal: Journal of the National Comprehensive Cancer Network (2020)

"QIM20-128: Baseline Assessment of Oncology Providers’ Quality Improvement Knowledge in a Multi-Institutional Breast Cancer Quality Improvement Collaborative" published on 20 Mar 2020 by National Comprehensive Cancer Network.
Correlation of caveolin 1 expression with disease-free survival in skin melanoma.
Authors: Maria Magdalena Sbenghe, Agnieszka Witkiewicz, Takami Sato, Maria B Queenan, Matias Emanuel Valsecchi, Kendra J. Feeney, Michael J. Mastrangelo
Journal: Journal of Clinical Oncology (2012)

e19016 Background: As clinical and histological parameters are unable to precisely predict the behavior of skin melanoma, new criteria are required to improve risk assessment. Caveolin 1 (CAV1), a scaffolding membrane protein, has been implicated in cell proliferation, death and transformation. In melanoma cell lines, CAV1 was found to have an antimetastatic role and loss of stromal CAV1 expression in lymph nodes metastases was associated with poor survival. The objectives of this analysis were to correlate CAV1 expression in primary skin melanoma cells with tumor thickness and disease free survival (DFS). Methods: CAV1 immunostaining was performed on the primary skin melanomas of 40 patients. CAV1 expression was scored semi-quantitatively using a 3-point scale: 0 (no staining), 1 (diffuse weak staining or strong staining in less then 30% of the cells) and 2 (strong staining of 30% or more of the cells). For analysis purposes, CAV1 was dichotomized as present (score 1 or 2) or absent (score 0). Primary melanoma was classified based on 2009 AJCC T-stage. DFS was measured from removal of primary skin melanoma to development of loco-regional or systemic recurrence. Pearson Chi-Square, Kaplan Meier, and Cox-Proportional Hazard Ratio were used for data analyses. Results: T-stage distribution was: Cis 12.5%, T1 32.5%, T2 22.5%, T3 17.5%, T4 15.0%. There was a clear inverse relationship between T stage and Cav 1 expression in tumor cells, with higher CAV1 expression in less invasive melanomas (P= 0.01). Fifteen patients experienced either locoregional or distant recurrence (median time to recurrence 14 months; range &lt;1 month -105 months). Twenty-five patients remained disease free for minimum of 3 years (median 77 months; range 36 – 111 months). Presence of CAV1 in primary melanoma tumor cells was correlated with increased DFS (P = 0.05) but this association was not significant when adjusting for T stage (P=0.59). Conclusions: CAV1 expression in melanoma tumor cells correlates with clinical behavior of skin melanoma as its loss is associated with invasiveness and distant recurrence. Whether the loss of CAV1 in primary melanoma tumor cells is just an epiphenomenon or a causal event is to be decided by further work on a larger population sample.
AB0103 Acute pancreatitis as initial manifestation of anti-phospholipid syndrome
Authors: J Qu, K Kankwenda, P Ooghe, C Gregoir
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> A 17 years old Belgian man was admitted with acute non-necrotic pancreatitis. Laboratory data showed high levels of amylase and lipase, leucocytosis, erythrocyte sedimentation rate (ESR) 24 mm/h and CRP 8.7 mg/100 ml, IgM against Epstein-Barr Virus (EBV) and lupus anticoagulant (detected according to the guidelines of International Society on Thrombosis and Haemostasis) were present. The evolution was spontaneously favourable and the diagnosis of acute pancreatitis on EBV infection was retained. <h3>Objectives</h3> Four months later, recurrent abdominal pain appeared and the only positive clinical finding was a livedo reticularis. Laboratory test showed a high ESR (63 mm/h) but a normal CRP (0.2 mg/100 ml), haemolytic anaemia, leucopenia, hypocomplementemia, presence of lupus anticoagulant, antinuclear antibody at 1/640 with anti dsDNA 517, EBV IgM antibody title has not changed. Neither cutaneous nor renal involvement nor serositis was observed. Mesenteric angioCT was normal. The patient recovered under a treatment of steroids, anticoagulation and hydroxychloroquine. <h3>Methods</h3> <h3>Results</h3> Pancreatitis is a rare manifestation in the anti-phospholipid syndrome (APS) or systemic lupus erythematosus (SLE) and is often associated with severe multi-systemic complication and of poor prognosis. Although the aetiology is not known, vasculitis lesion and thrombosis, adverse effect of steroid and azathioprine were thought to be the cause. <h3>Conclusion</h3> We describe a case of pancreatitis as initial manifestation of APS, since ACR criteria for SLE are not fulfilled. No further complication was observed at 2 months? follow-up. The presence of EBV IgM antibody is probably due to polyclonal activation. <h3>References</h3> Saab S, <i>et al</i>. Corticosteroids and systemic lupus erythematosus pancreatitis: a case series. J Rhumatol. 1998;25(4):801–6 Rojas-Serrano J, <i>et al</i>. Lupus patients in an emergency unit. Causes of consultation, hospitalization and outcome. A cohort study. Lupus 2000;9(8):601–6
Nonhospice Palliative Care Within the Treatment of End‐Stage Liver Disease
Authors: Manisha Verma, Elliot B. Tapper, Amit G. Singal, Victor Navarro
Journal: Hepatology (2020)

Palliative care (PC) that has evolved from a focus on end‐of‐life care to an expanded form of holistic care at an early stage for patients with serious illnesses and their families is commonly referred to as nonhospice PC (or early PC). Patients with end‐stage liver disease (ESLD) suffer from a high symptom burden and a deteriorated quality of life (QOL), with uncertain prognosis and limited treatment options. Caregivers of these patients also bear an emotional and physical burden similar to that of caregivers for patients with cancer. Despite the proven benefits of nonhospice PC for other serious illnesses and cancer, there are no evidence‐based structures and processes to support its integration within the routine care of patients with ESLD and their caregivers. In this article, we review the current state of PC for ESLD and propose key structures and processes to integrate nonhospice PC within routine hepatology practice. Results found that PC is highly underutilized within ESLD care, and limited prospective studies are available to demonstrate methods to integrate PC within routine hepatology practices. Hepatology providers report lack of training to deliver PC along with no clear prognostic criteria on when to initiate PC. A well‐informed model with key structures and processes for nonhospice PC integration would allow hepatology providers to improve clinical outcomes and QOL for patients with ESLD and reduce health care costs. Educating hepatology providers about PC principles and developing clear prognostic criteria for when and how to integrate PC on the basis of individual patient needs are the initial steps to inform the integration. The fields of nonhospice PC and hepatology have ample opportunities to partner clinically and academically.
IN-HOSPITAL OUTCOMES OF ST ELEVATION MYOCARDIAL INFARCTION (STEMI) IN ADULTS WITH COMPLEX CONGENITAL HEART DISEASE: A NATIONWIDE STUDY
Authors: Sagar Ranka, Prakash Acharya, Farhad A. Sami, Tarun Dalia, Zubair Shah, Kamal Gupta
Journal: Journal of the American College of Cardiology (2020)
THE IMPACT OF COMPLETE SURGICAL REVASCULARIZATION ON OUTCOMES OF PATIENTS UNDERGOING CORONARY ARTERY BYPASS GRAFTING SURGERY: INSIGHTS FROM THE REGROUP TRIAL
Authors: Ronnie Ramadan, Scott Kinlay, Eileen M. Stock, Annette Phillips, Ellen J. Dematt, Deepak Bhatt, Marco Zenati
Journal: Journal of the American College of Cardiology (2020)
Rifampicin and clarithromycin (extended release) versus rifampicin and streptomycin for limited Buruli ulcer lesions: a randomised, open-label, non-inferiority phase 3 trial
Authors: Richard O Phillips, Jérôme Robert, Kabiru Mohamed Abass, William Thompson, Fred Stephen Sarfo, Tuah Wilson, Godfred Sarpong, Thierry Gateau, Annick Chauty, Raymond Omollo, Michael Ochieng Otieno, Thaddaeus W Egondi, Edwin O Ampadu, Didier Agossadou, Estelle Marion, Line Ganlonon, Mark Wansbrough-Jones, Jacques Grosset, John M Macdonald, Terry Treadwell, Paul Saunderson, Albert Paintsil, Linda Lehman, Michael Frimpong, Nanaa Francisca Sarpong, Raoul Saizonou, Alexandre Tiendrebeogo, Sally-Ann Ohene, Ymkje Stienstra, Kingsley B Asiedu, Tjip S van der Werf, Samuel Osei Mireku, Justice Abotsi, Joseph Ken Adu Poku, Richard Asamoah-Frimpong, Bright Osei-Wusu, Edward Sarpong, Beatrice Konadu, Ernest Opoku, Mark Forson, Mathias Ndogyele, Elizabeth Ofori, Felicity Aboagye, Thomas Berko, George Amofa, Anastasia Nsiah, Joyce Mensah-Bonsu, Joseph Ofori Nyarko, Yaw Ampem Amoako, Elliot Koranteng Tannor, Justice Boakye-Appiah, Aloysius Dzibordzi Loglo, Mabel Sarpong-Duah, Bernadette Agbavor, Marie Françoise Ardent, Arnaud Yamadjako, Naomi Adanmado Gersande, Ambroise Adeye, Martial Kindjinou, None Akpolan, Maxime Kiki, Espoir Sodjinou, Clémence Guegnard, Sandor-Adrian Klis, Kristien Velding, Till Omansen, David Ofori-Adjei, Sarah Eyangoh, Alan Knell, William Faber
Journal: The Lancet (2020)

Buruli ulcer is a neglected tropical disease caused by Mycobacterium ulcerans infection that damages the skin and subcutis. It is most prevalent in western and central Africa and Australia. Standard antimicrobial treatment with oral rifampicin 10 mg/kg plus intramuscular streptomycin 15 mg/kg once daily for 8 weeks (RS8) is highly effective, but streptomycin injections are painful and potentially harmful. We aimed to compare the efficacy and tolerability of fully oral rifampicin 10 mg/kg plus clarithromycin 15 mg/kg extended release once daily for 8 weeks (RC8) with that of RS8 for treatment of early Buruli ulcer lesions.
#Time2Act: Harassment and abuse in elite youth sport culture
Authors: Margo Mountjoy
Journal: British Journal of Sports Medicine (2020)

“After months of dieting and frustration, Cain found herself choosing between training with the best team in the world, or potentially developing osteoporosis or even infertility. She lost her period for 3 years and broke five bones. She went from being a once-in-a-generation Olympic hopeful to having suicidal thoughts.” 1 (Lindsay Crouse on Mary Cain) “And so trying to shame somebody into losing weight is just such, I mean, an emotionally, psychologically and mentally traumatising way to coach somebody.” (Mary Cain)

At the age of 17, Mary Cain was a running phenomenon in the USA when she joined Nike’s Oregon Project. In November 2019 Mary Cain went public in the New York Times with allegations of psychological and physical abuse by her coach, Alberto Salazar,1 who has subsequently apologized.2 As a result of the public weighing practices, being told she needed to become “thinner, thinner and thinner” to improve her performance and public body shaming, Cain developed the syndrome of Relative Energy Deficiency in Sport (RED-S). Cain’s disturbing disclosure caused a flurry of media attention exposing the dark underbelly of elite youth sport culture.

Mary Cain’s story is a ‘call to action’ for sport. Do youth sport programmes meet the International Olympic Committee (IOC)’s standards of a ‘safe sport’ culture?3 In the recent publication on Safeguarding at the Youth Olympic Games (YOG2018), 1254 athletes were asked to define their understanding of the term ‘safe sport’. The results were sobering. …
Dipeptide repeat proteins inhibit homology-directed DNA double strand break repair in C9ORF72 ALS/FTD
Authors: Nadja S. Andrade, Melina Ramic, Rustam Esanov, Wenjun Liu, Mathew J. Rybin, Gabriel Gaidosh, Abbas Abdallah, Samuel Del’Olio, Tyler C. Huff, Nancy T. Chee, Sadhana Anatha, Tania F. Gendron, Claes Wahlestedt, Yanbin Zhang, Michael Benatar, Christian Mueller, Zane Zeier
Journal: Molecular Neurodegeneration (2020)

The C9ORF72 hexanucleotide repeat expansion is the most common known genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), two fatal age-related neurodegenerative diseases. The C9ORF72 expansion encodes five dipeptide repeat proteins (DPRs) that are produced through a non-canonical translation mechanism. Among the DPRs, proline-arginine (PR), glycine-arginine (GR), and glycine-alanine (GA) are the most neurotoxic and increase the frequency of DNA double strand breaks (DSBs). While the accumulation of these genotoxic lesions is increasingly recognized as a feature of disease, the mechanism(s) of DPR-mediated DNA damage are ill-defined and the effect of DPRs on the efficiency of each DNA DSB repair pathways has not been previously evaluated.
GENDER DISPARITIES IN PATIENTS WITH OUT-OF-HOSPITAL CARDIAC ARREST IN THE ABSENCE OF ST-SEGMENT ELEVATION: A SUBSTUDY OF THE COACT TRIAL
Authors: Eva Marie Spoormans, Jorrit S. Lemkes, Gladys N. Janssens, Nina W. van der Hoeven, Lucia S.D. Jewbali, Eric A. Dubois, Peter M. van de Ven, Yolande E.A. Appelman, Niels van Royen
Journal: Journal of the American College of Cardiology (2020)
Effect of loss of a chromosome 7 containing multiple copies of EGFR gene on acquired resistance to EGFR-TKIs in EGFR mutated NSCLC.
Authors: Koh Furugaki, Toshiki Iwai, Yoichiro Moriya, Kaori Fujimoto-Ouchi
Journal: Journal of Clinical Oncology (2012)

e18091 Background: The epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) show notable effects for non-small cell lung cancers (NSCLC) harboring EGFR activating mutations. However, almost all patients eventually acquire resistance to EGFR-TKIs within several years. The major mechanisms of acquired resistance are acquisition of a secondary EGFR mutation T790M and amplification of MET. However, the mechanisms of other resistance remain unclear. In this study, we established novel erlotinib-resistant NSCLC cells and examined their resistant mechanism. Methods: Resistant cells were established by continuously exposing EGFR mutated NSCLC cells HCC827 to 0.1, 1 or 10 μM of erlotinib in 96 well plates for three months. The resistant mechanisms were determined by direct sequence analysis and EGFR FISH analysis. Results: Resistant cells were emerged from 14/96 and 3/96 wells by 0.1 μM and 1 μM of erlotinib exposure, respectively. No resistant cells appeared in the wells of 10 μM of erlotinib. The IC 50 values of these resistant cells were more than 100-fold higher than that of parental cells. No secondary mutation of T790M was detected in any of the resistant cells. Instead, we found that 13/17 resistant cells were dominated by EGFR not amplified cells and one of resistant cells B10 consisted of more than 99.9% of them, while the parental cells consisted of 2.5% of EGFR not amplified cells. Then, we isolated EGFR not amplified clone 4D8 from parental cells and found that this clone also had a resistance to erlotinib comparable to the resistant cells B10. Metaphase FISH analysis showed that EGFR amplified cells in parental cells had a chromosome 7 containing multiple copies of EGFR, while EGFR not amplified cells in B10 did not have it. Furthermore, we found that EGFR not amplified cells were constantly emerged from EGFR amplified clone isolated from parental cells under normal cell culture condition. Conclusions: Loss of a chromosome 7 containing multiple copies of EGFR causes acquired resistance in HCC827 cells when exposed to relatively low concentration of erlotinib, while high concentration of erlotinib deprives HCC827 cells of the chance of emergence of resistant cells.
Repurposing Leflunomide for Relapsed/Refractory Multiple Myeloma: A Phase 1 Trial
Authors: Michael Rosenzweig, Joycelynne M. Palmer, Ni-Chun Tsai, Ralf Buettner, Lupe Duarte, Myo Htut, Chatchada Karanes, Nitya Nathwani, Flavia Pichiorri, Firoozeh Sahebi, George Somlo, Tim Synold, Xiwei Wu, Amrita Krishnan, Stephen J. Forman, Steven T. Rosen
Journal: Blood (2017)