tbuckley/cabot-search huggingface dataset:
Early Pharmacodynamic Changes in T-Cell Activation, Proliferation, and Cytokine Production Confirm the Mode of Action of BFCR4350A, a FcRH5/CD3 T-Cell-Engaging Bispecific Antibody, in Patients with Relapsed/Refractory Multiple Myeloma
Authors: Rin Nakamura, Sean Lear, Deanna Wilson, Hartmut Koeppen, Anjali Vaze, Suzanne Trudel, Andrew Spencer, Simon J Harrison, Adam D. Cohen, Bernard M Fine, Mengsong Li, James Cooper, Teiko Sumiyoshi
Journal: Blood (2020)
BCL10 Gain-of-Function Mutations Aberrantly Induce Canonical and Non-Canonical NF-Kb Activation and Resistance to Ibrutinib in ABC-DLBCL
Authors: Min Xia, Liron David, Matthew Teater, Ozlem Onder, Kojo S. J. Elenitoba-Johnson, Lorena Fontan, Hao Wu, Ari Melnick
Journal: Blood (2020)
Optimal Duration of Imatinib Treatment / Deep Molecular Response for Treatment-Free Remission after Imatinib Discontinuation from a Canadian Tyrosine Kinase Inhibitor Discontinuation Trial
Authors: Dennis Dong Hwan Kim, Igor Nicolas Novitzky-Basso, Taehyung Kim, Eshetu G Atenafu, Lynn Savoie, Isabelle Bence-Bruckler, Donna L. Forrest, Lambert Busque, Robert Delage, Anargyros Xenocostas, Mary-Margaret Keating, Elena Liew, Kristjan Paulson, Tracy L. Stockley, Pierre Laneuville, Jeffrey H. Lipton, Suzanne Kamel-Reid, Brian Leber
Journal: Blood (2020)
Contribution of Red Blood Cell Derived Extracellular Vesicles to Sickle Red Blood Cell Adhesion Discerned Using an Endothelialized Microfluidic Assay
Authors: Ran An, Yuncheng Man, Erdem Kucukal, Kevin Cheng, William Wulftange, Jane A. Little, Umut A. Gurkan
Journal: Blood (2020)
REGN5458, a BCMA x CD3 Bispecific Monoclonal Antibody, Induces Deep and Durable Responses in Patients with Relapsed/Refractory Multiple Myeloma (RRMM)
Authors: Deepu Madduri, Ashley Rosko, Jason Brayer, Jeffrey Zonder, William I. Bensinger, Jingjin Li, Linzhi Xu, Lieve Adriaens, Dhruti Chokshi, Weijiang Zhang, Anita Boyapati, Manish Sharma, Frank Seebach, L. Andres Sirulnik, David M. Weinreich, George D. Yancopoulos, Madhav V. Dhodapkar, Suzanne Lentzsch, Dennis Cooper, Sundar Jagannath
Journal: Blood (2020)
Efficacy and Safety of Venetoclax Combinations in t(11;14) Multiple Myeloma: Real World Data Collected from 7 Hungarian Centers
Authors: Virág Réka Szita, Gábor Mikala, János Fábián, Péter Rajnics, László Rejtő, Tamás Szendrei, Hussain Alizadeh, Laszlo Varoczy, Árpád Illés, Tamas Masszi, Gergely Varga
Journal: Blood (2020)
m<b>6</b>A Regulates Liver Metabolic Disorders and Hepatogenous Diabetes
Authors: Yuhuan Li, Qingyang Zhang, Guanshen Cui, Fang Zhao, Xin Tian, Bao-Fa Sun, Ying Yang, Wei Li
Journal: Genomics Proteomics & Bioinformatics (2020)

Abstract N 6-methyladenosine (m6A) is one of the most abundant modifications on mRNAs and plays important roles in various biological processes. The formation of m6A is catalyzed by a methyltransferase complex (MTC) containing a key factor methyltransferase-like 3 (Mettl3). However, the functions of Mettl3 and m6A modification in hepatic lipid and glucose metabolism remain unclear. Here, we showed that both Mettl3 expression and m6A level increased in the livers of mice with high fat diet (HFD)-induced metabolic disorders. Overexpression of Mettl3 aggravated HFD-induced liver metabolic disorders and insulin resistance. In contrast, hepatocyte-specific knockout of Mettl3 significantly alleviated HFD-induced metabolic disorders by slowing weight gain, reducing lipid accumulation, and improving insulin sensitivity. Mechanistically, Mettl3 depletion-mediated m6A loss caused extended RNA half-lives of metabolism-related genes, which consequently protected mice against HFD-induced metabolic syndrome. Our findings reveal a critical role of Mettl3-mediated m6A in HFD-induced metabolic disorders and hepatogenous diabetes.
Base Editing Eliminates the Sickle Cell Mutation and Pathology in Hematopoietic Stem Cells Derived Erythroid Cells
Authors: Jonathan S Yen, Gregory A. Newby, Thiyagaraj Mayuranathan, Shaina N. Porter, Yu Yao, Kaitly J. Woodard, Kalin Mayberry, Kelcee Everette, Jingjing Zhang, Jordana M Henderson, Anton P Mccaffrey, Jonathan Yen, John F. Tisdale, Shengdar Q. Tsai, David R. Liu, Mitchell J. Weiss
Journal: Blood (2020)
Education and Outreach in Physical Sciences in Oncology
Authors: Sierra A. Walker, Anthony Pham, Sara Nizzero, Mingee Kim, Bob Riter, Julie Bletz, Sheila Judge, Benette Phillips, Dorottya Noble, Diana Murray, Erin Wetzel, Susan Samson, Mariah McMahon, Carl Flink, Jennifer Couch, Claire Tomlin, Kristin Swanson, Alexander R.A. Anderson, David Odde, Haifa Shen, Shannon Hughes, Nastaran Zahir, Heiko Enderling, Joy Wolfram
Journal: Trends in cancer (2020)
A Revised International Prognostic Scoring System of 3.5 Points Stratifies Patients with Myelodysplastic Syndromes into 2 Risk Categories
Authors: Maria Julia Montoro, Margarita Ortega, Guillermo Villacampa, Teresa Bernal, Helena Pomares, Elvira Mora Casterá, Antonieta Molero, Laura Vilorio, Mar Tormo, Marina Diaz-Beyá, Merchan Brayan, Andres Jerez, Eugenia Rivero, Maria Jose Lys, Paula Cárcel, Joan Bargay, Fernando Ramos, Blanca Xicoy, Maria Diez-Campelo, David Valcarcel
Journal: Blood (2020)
Evaluating Gvhd Outcomes Using Post-Transplant Cyclophosphamide/Tacrolimus/Mycophenolate Mofetil As Gvhd Prophylaxis Compared with Methotrexate/Tacrolimus in Matched-Related and Matched-Unrelated Hematopoietic Stem Cell Transplant in Relation to the Haplo-Identical Setting: A Single Center Experience
Authors: Mindy Hsiao, Preet M. Chaudhary, George Yaghmour
Journal: Blood (2020)
Complement Regulates the Procoagulant Effects of HIT Immune Complexes
Authors: Sanjay Khandelwal, Lubica Rauova, Ayiesha Barnes, Ann Rux, Serge Yarovoi, Sooho S Myoung, Alexandra Johnson, Grace M Lee, Madelaine Duarte, Mortimer Poncz, Gowthami M. Arepally, Douglas B. Cines
Journal: Blood (2020)
Abstract MP131: The CDK2-FOXO1 Axis Mediates Doxorubicin-induced Cardiomyocyte Apoptosis and Atrophy
Authors: Peng Xia, Jingrui Chen, Yuening Liu, Maya Fletcher, Brian C Jensen, Zhaokang Cheng
Journal: Circulation Research (2020)

Recent clinical investigations indicate that anthracycline-based chemotherapy induces early declines in heart mass in cancer patients. A decline in heart mass can be caused by a decrease in cardiac cell number due to exaggerated cell death, and/or a reduction in cell size via atrophy. Our previous study reveals that the anthracycline doxorubicin (DOX) induces apoptotic death of cardiomyocytes through activation of cyclin-dependent kinase 2 (CDK2). However, the signaling pathway downstream of CDK2 remains to be characterized. In addition, it is unclear whether the same pathway also mediates cardiac atrophy. Here we demonstrated that DOX exposure induced CDK2-dependent phosphorylation of forkhead box O1 (FOXO1) at S249, leading to transcription of its pro-apoptotic target gene Bim. In cultured cardiomyocytes, treatment with the small molecule FOXO1 inhibitor AS1842856, or transfection with FOXO1-specific siRNAs protected against DOX-induced apoptosis and mitochondrial damage. Oral administration of AS1842856 in mice hindered apoptosis and prevented DOX-induced decline in left ventricular systolic function. Intriguingly, pharmacologic inhibition of FOXO1 also attenuated DOX-induced cardiac atrophy, likely due to repression of MuRF1, a pro-atrophic FOXO1 target gene. In conclusion, DOX exposure induces CDK2-dependent FOXO1 activation, resulting in cardiomyocyte apoptosis and atrophy. Our results identify FOXO1 as a promising drug target for DOX-induced cardiotoxicity. FOXO1 inhibitors may represent a novel class of therapeutics for cardioprotection during chemotherapy.
Oxidized CaMKII and O-GlcNAcylation cause increased atrial fibrillation in diabetic mice by distinct mechanisms
Authors: Olurotimi O. Mesubi, Adam G. Rokita, Neha Abrol, Yuejin Wu, Biyi Chen, Qinchuan Wang, Jonathan M. Granger, Anthony Tucker-Bartley, Elizabeth D. Luczak, Kevin R. Murphy, Priya Umapathi, Partha S. Banerjee, Tatiana N. Boronina, Robert N. Cole, Lars S. Maier, Xander H. Wehrens, Joel L. Pomerantz, Long-Sheng Song, Rexford S. Ahima, Gerald W. Hart, Natasha E. Zachara, Mark E. Anderson
Journal: Journal of Clinical Investigation (2020)

Diabetes mellitus (DM) and atrial fibrillation (AF) are major unsolved public health problems, and diabetes is an independent risk factor for AF. However, the mechanism(s) underlying this clinical association is unknown. ROS and protein O-GlcNAcylation (OGN) are increased in diabetic hearts, and calmodulin kinase II (CaMKII) is a proarrhythmic signal that may be activated by ROS (oxidized CaMKII, ox-CaMKII) and OGN (OGN-CaMKII). We induced type 1 (T1D) and type 2 DM (T2D) in a portfolio of genetic mouse models capable of dissecting the role of ROS and OGN at CaMKII and global OGN in diabetic AF. Here, we showed that T1D and T2D significantly increased AF, and this increase required CaMKII and OGN. T1D and T2D both required ox-CaMKII to increase AF; however, we did not detect OGN-CaMKII or a role for OGN-CaMKII in diabetic AF. Collectively, our data affirm CaMKII as a critical proarrhythmic signal in diabetic AF and suggest ROS primarily promotes AF by ox-CaMKII, while OGN promotes AF by a CaMKII-independent mechanism(s). These results provide insights into the mechanisms for increased AF in DM and suggest potential benefits for future CaMKII and OGN targeted therapies.
Influenza, Varicella, and Mumps Outbreaks in US Migrant Detention Centers
Authors: Nathan C. Lo, Sindiso Nyathi, Lloyd A. C. Chapman, Isabel Rodriguez-Barraquer, Margot Kushel, Kirsten Bibbins-Domingo, Joseph A. Lewnard
Journal: JAMA (2020)

This study uses US Immigration and Customs Enforcement (ICE) Health Service Corps data to describe incident cases and outbreaks of influenza, varicella, and mumps in 22 US ICE detention centers between 2017 and March 2020.
GTB-3550 TriKE™ for the Treatment of High-Risk Myelodysplastic Syndromes (MDS) and Refractory/Relapsed Acute Myeloid Leukemia (AML) Safely Drives Natural Killer (NK) Cell Proliferation At Initial Dose Cohorts
Authors: Erica D. Warlick, Daniel J. Weisdorf, Daniel A. Vallera, Rose Wangen, Dixie Lewis, JoAnn Knox, Martin Schroeder, Martin Felices, Jeffrey S. Miller
Journal: Blood (2020)
Acute interstitial nephritis, a potential predictor of response to immune checkpoint inhibitors in renal cell carcinoma
Authors: Viral Patel, Roy Elias, Joseph Formella, William Schwartzman, Alana Christie, Qi Cai, Venkat Malladi, Payal Kapur, Miguel Vazquez, Renee McKay, Ivan Pedrosa, Raquibul Hannan, Hans Hammers, James Brugarolas
Journal: Journal for ImmunoTherapy of Cancer (2020)

Immune checkpoint inhibitors (ICIs) such as nivolumab and ipilimumab have improved outcomes in metastatic renal cell carcinoma (mRCC) patients, but they are also associated with immune-related adverse events (irAEs). As observed in melanoma, we hypothesized that patients experiencing an autoimmune reaction directed against the tissue of origin may be more likely to benefit from ICI. Specifically, we asked whether patients with immune-related acute interstitial nephritis (irAIN) exhibited improved outcomes. Using Kidney Cancer Explorer (KCE), a data portal and i2b2-based central database for clinical, pathological and experimental genetic data, we systematically identified all patients with mRCC at UT Southwestern Medical Center (UTSW) from 2014–2018 who received at least one dose of ICI. More recent cases were identified through a provider query. We extracted creatinine (Cr) values at baseline and over the entirety of each patient ICI treatment course using KCE. Patients with ≥ 1.5-fold Cr increase over baseline were investigated. The likelihood of irAIN was determined based on the work-up (biopsy, if available), or by clinical criteria (timing of kidney injury, exclusion of other etiologies, treatment with immunosuppressants and response). We identified 177 mRCC patients who received at least one dose of ICI, 36 of whom had ≥ 1.5-fold increase in Cr over baseline while on treatment. Of those, two had biopsy-proven irAIN and one was clinically diagnosed, resulting in an incidence of 1.7%. One additional biopsy-proven case past 2018 was identified through a provider query, for a total of four patients. Two received combination nivolumab and ipilimumab in the first line, whereas the remaining received nivolumab after first line therapy. irAIN onset ranged from 1.5 to 12 months. All four patients stopped ICI with recovery of renal function, at least partially, three after receiving systemic steroids. Notably, all four patients had a deep response. In conclusion, irAIN is a rare event, but it may portend a higher likelihood of response. One possible explanation is antigenic overlap between normal renal tubular cells and tumor cells.
Hepatic stellate and endothelial cells maintain hematopoietic stem cells in the developing liver
Authors: Yeojin Lee, Juliana Leslie, Ying Yang, Lei Ding
Journal: The Journal of Experimental Medicine (2020)

The liver maintains hematopoietic stem cells (HSCs) during development. However, it is not clear what cells are the components of the developing liver niche in vivo. Here, we genetically dissected the developing liver niche by systematically determining the cellular source of a key HSC niche factor, stem cell factor (SCF). Most HSCs were closely associated with sinusoidal vasculature. Using Scfgfp knockin mice, we found that Scf was primarily expressed by endothelial and perisinusoidal hepatic stellate cells. Conditional deletion of Scf from hepatocytes, hematopoietic cells, Ng2+ cells, or endothelial cells did not affect HSC number or function. Deletion of Scf from hepatic stellate cells depleted HSCs. Nearly all HSCs were lost when Scf was deleted from both endothelial and hepatic stellate cells. The expression of several niche factors was down-regulated in stellate cells around birth, when HSCs egress the developing liver. Thus, hepatic stellate and endothelial cells create perisinusoidal vascular HSC niche in the developing liver by producing SCF.
Synergizing sunitinib and radiofrequency ablation to treat hepatocellular cancer by triggering the antitumor immune response
Authors: Xiaoqiang Qi, Ming Yang, Lixin Ma, Madeline Sauer, Diego Avella, Jussuf T Kaifi, Jeffrey Bryan, Kun Cheng, Kevin F Staveley-O’Carroll, Eric T Kimchi, Guangfu Li
Journal: Journal for ImmunoTherapy of Cancer (2020)

Background Minimally invasive radiofrequency ablation (RFA) is used as a first-line treatment option for hepatocellular cancer (HCC) with the weaknesses of incomplete ablation, tumor recurrence, and inferior outcomes. To overcome this limitation, we proposed to develop sunitinib-RFA integrated therapy with a potential of activating anti-HCC immune response. Methods Using our unique murine model, we developed a novel RFA platform with a modified human cardiac RF generator. Therapeutic efficacy of sunitinib–RFA combined treatment in HCC was tested in this platform. Tumor progression was monitored by MRI; tumor necrosis and apoptosis were detected by H&amp;E and terminal deoxynucleotidyl transferase dUTP nick end labeling; immune reaction was defined by flow cytometry; and signaling molecules were examined with real-time PCR (qPCR), western blot, and immunohistochemical staining. Results A significantly reduced tumor growth and extended lift span were observed in the mice receiving combined treatment with RFA and sunitinib. This combined treatment significantly increased the frequency of CD8 + T cell, memory CD8 + T cell, and dendritic cells (DCs); decreased the frequency of regulatory T cells; and activated tumor-specific antigen (TSA) immune response in tumor microenvironment. We found that RFA caused PD-1 upregulation in tumor-infiltrated T cells by boosting hepatocyte growth factor (HGF) expression, which was suppressed by sunitinib treatment. We have also demonstrated that sunitinib suppressed VEGF’s effect in enhancing PD-L1 expression in DCs and attenuated heat-sink effect. The results indicate that RFA induced tumor destruction and release of in situ TSAs which can activate a tumoricidal immune response in sunitinib-treated mice, significantly improving anti-HCC therapeutic efficacy. Conclusions Sunitinib enables RFA-released in situ TSA to ignite an effective anti-tumor immune response by suppressing HGF and VEGF signaling pathways. Sunitinib–RFA as a synergistic therapeutic approach significantly suppresses HCC growth.
Incident Type 2 Diabetes and Risk of Fracture: A Comparative Cohort Analysis Using U.K. Primary Care Records
Authors: Gabrielle S. Davie, Kingshuk Pal, Elizabeth Orton, Edward G. Tyrrell, Irene Petersen
Journal: Diabetes Care (2020)

OBJECTIVE To estimate risk of fracture in men and women with recent diagnosis of type 2 diabetes compared with individuals without diabetes. RESEARCH DESIGN AND METHODS In this cohort study, we used routinely collected U.K. primary care data from The Health Improvement Network. In adults (&amp;gt;35 years) diagnosed with type 2 diabetes between 2004 and 2013, fractures sustained until 2019 were identified and compared with fractures sustained in individuals without diabetes. Multivariable models estimated time to first fracture following diagnosis of diabetes. Annual prevalence rates included at least one fracture in a given year. RESULTS Among 174,244 individuals with incident type 2 diabetes and 747,290 without diabetes, there was no increased risk of fracture among males with diabetes (adjusted hazard ratio [aHR] 0.97 [95% CI 0.94, 1.00]) and a small reduced risk among females (aHR 0.94 [95% CI 0.92, 0.96]). In those aged ≥85 years, those in the diabetes cohort were at significantly lower risk of incident fracture (males: aHR 0.85 [95% CI 0.71, 1.00]; females: aHR 0.85 [95% CI 0.78, 0.94]). For those in the most deprived areas, aHRs were 0.90 (95% CI 0.83, 0.98) for males and 0.91 (95% CI 0.85, 0.97) for females. Annual fracture prevalence rates, by sex, were similar for those with and without type 2 diabetes. CONCLUSIONS We found no evidence to suggest a higher risk of fracture following diagnosis of type 2 diabetes. After a diagnosis of type 2 diabetes, individuals should be encouraged to make positive lifestyle changes, including undertaking weight-bearing physical activities that improve bone health.
Impact of Minimal Residual Disease (MRD) By Multiparameter Flow Cytometry (MFC) and Next-Generation Sequencing (NGS) on Outcome: Results of Newly Diagnosed Transplant-Eligible Multiple Myeloma (MM) Patients Enrolled in the Forte Trial
Authors: Stefania Oliva, Elisa Genuardi, Maria Teresa Petrucci, Mattia D'Agostino, Daniel Auclair, Antonio Spadano, Allison P. Jacob, Michele Cea, Luca De Rosa, Alessandro Gozzetti, Marina Ruggeri, Andrea Capra, Milena Gilestro, Norbert Pescosta, Angelo D. Palmas, Agostina Siniscalchi, Ilan R. Kirsch, Paolo Corradini, Pellegrino Musto, Mario Boccadoro, Elena Zamagni, Francesca Gay
Journal: Blood (2020)
Inhibition of P-Selectin Rescues the Phenotype of a Novel Genetic Animal Model for Idiopathic Pulmonary Fibrosis
Authors: Francesca Gobbo, Paola Verachi, Barbara Bacci, Maria Zingariello, Angelo Peli, Carolyn Mead-Harvey, Amylou C. Dueck, Giuseppe Sarli, Anna Rita Migliaccio
Journal: Blood (2020)
Preliminary Results from a Phase 1 Study of APVO436, a Novel Anti-CD123 x Anti-CD3 Bispecific Molecule, in Relapsed/Refractory Acute Myeloid Leukemia and Myelodysplastic Syndrome
Authors: Justin M. Watts, Tara Lin, Eunice S. Wang, Alice S. Mims, Elizabeth H. Cull, Prapti A. Patel, Paul J. Shami, Roland B. Walter, Christopher R. Cogle, Ruth A. Chenault, Bret Macpherson, Allison Given Chunyk, Catherine J. McMahan, Jane A. Gross, Scott Stromatt
Journal: Blood (2020)
Abstract 362: Role of Dysregulated Exosomal MiRNAs in Functional Impairment of Cardiac Endothelial Cells
Authors: Prabhat Ranjan, Rajesh Kumari, Harish Pal, Prasanna Krishnamurthy, Gangjian Qin, Raj Kishore, Suresh K Verma
Journal: Circulation Research (2020)

Objective: Endothelial cells (ECs) play critical role to maintain the normal heart function. It is shown that fibroblast-derived exosomes have the ability to enhance cardiac myocytes hypertrophy in pressure-overloaded myocardium. However, their effect on endothelial cell function has not been studied. Others and we have previously shown that stress-induced chronic inflammation induces cardiac fibroblasts and mediates endothelial cells dysfunction. Here we hypothesized that activated cardiac fibroblasts-derived exosomes (FB-Exo) mediates cardiac ECs dysfunction and leads for cardiac pathology and restoring the altered FB-Exo contents will improve endothelial cells function and biology. Methods: We cultured mouse primary endothelial cells in EC growth media. Cells were treated with fibroblasts-derived-Exo. Exosomes were isolated from fibroblast condition media by ultracentrifugation and characterized by nanosight &amp; electron microscopy. Results: Fibroblasts were significantly activated by TGFβ treatment as shown by qPCR and western blot (smad2/3, p-Smad2/3, p38, p-p38) data. Endothelial cells dysfunction as shown by Matrigel assay, real-time Q-PCR and western data (eNOS and Hif1α) data was observed in TGFβ-FB-Exo treatment endothelial cell. MTT, TUNEL and migration assay also followed the same trend as TGFβ-FB-Exo treatment significantly induced endothelial cell death and inhibits its proliferation and migration. Furthermore, microRNA array and PCR analysis revealed dysregulation of miR-132-3p, miR-2001-3p and miR-125b-5p in TGFβ-FB-Exo treated endothelial cells. Conclusions: Taken together, this study demonstrates that TGFβ treated fibroblasts-derived exosomes are enriched in pro-fibrotic factors and can lead to endothelial dysfunction and promotes cardiac fibrosis in PO myocardium. In future study, we will modulate the target miRs in fibroblasts to see whether it rescue reparative function of endothelial cell and inhibits cardiac fibrosis in failing heart.
Impact of Imaging FDG-PET/CT Minimal Residual Disease Assessment on Outcomes and Matching with Bone Marrow Techniques in Newly Diagnosed Transplant Eligible Multiple Myeloma (MM) Patients: Results of the Phase II Randomized Forte Trial
Authors: Elena Zamagni, Cristina Nanni, Francesca Gay, Luca Dozza, Delia Rota Scalabrini, Mattia D'Agostino, Rossella Ribolla, Monica Galli, Manuela Racca, Renato Zambello, Elena Rivolti, Domenico Albano, Annibale Versari, Mariella Grasso, Rossella Troia, Antonio Spadano, Francesca Patriarca, Marina Ruggeri, Marco Rensi, Anna Pascarella, Pietro Zucchetta, Paola Tacchetti, Stefano Fanti, Mario Boccadoro, Michele Cavo, Pellegrino Musto, Stefania Oliva
Journal: Blood (2020)
FLT3 and LSD1 Inhibitor Combinations Synergistically Repress Growth of FLT3-Mutant Acute Myeloid Leukemia Via Blockage of MYC Function
Authors: Daniel J. Coleman, Brittany M. Smith, Cody Coblentz, Rowan L. Callahan, Jake VanCampen, Garth L. Kong, Brian J. Druker, Julia E. Maxson, Theodore P. Braun
Journal: Blood (2020)
Government’s plan to digitise NHS risks wasting billions, MPs warn
Authors: Gareth Iacobucci
Journal: BMJ (2020)

The UK government is at risk of wasting vast sums of taxpayers’ money by repeating the mistakes of previous NHS IT failures, MPs have warned.

The Commons Public Accounts Committee’s review into digital transformation in the NHS concluded that current proposals to transform digital services lacked effective governance, realistic and detailed plans, sufficient investment nationally and locally, and clear accountability.1

The MPs warned that lessons may not have been learnt from the failed national programme for IT from 2002 to 2011, which cost the government £10bn (€11.1bn; $13.1bn).2

The committee’s report noted that the Department of Health and Social Care had still not achieved its headline 2014 target …