tbuckley/cabot-search huggingface dataset:
Numbers and phenotype of non-classical CD14dimCD16+ monocytes are predictors of adverse clinical outcome in patients with coronary artery disease and severe SARS-CoV-2 infection
Authors: Karin Anne Lydia Mueller, Carolin Langnau, Manina Günter, Simone Pöschel, Sarah Gekeler, Álvaro Petersen-Uribe, Klaus-Peter Kreisselmeier, Karin Klingel, Hans Bösmüller, Bo Li, Philippa Jaeger, Tatsiana Castor, Dominik Rath, Meinrad Paul Gawaz, Stella E Autenrieth
Journal: Cardiovascular Research (2020)

To elucidate the prognostic role of monocytes in the immune response of patients with coronary artery disease (CAD) at risk for life-threatening heart and lung injury as major complications of SARS-CoV-2 infection.From February to April 2020, we prospectively studied a cohort of 96 participants comprising 47 consecutive patients with CAD and acute SARS-CoV-2 infection (CAD + SARS-CoV-2), 19 CAD patients without infections, and 30 healthy controls. Clinical assessment included blood sampling, echocardiography, and electrocardiography within 12 h of admission. Respiratory failure was stratified by the Horovitz Index (HI) as moderately/severely impaired when HI ≤200 mmHg. The clinical endpoint (EP) was defined as HI ≤200 mmHg with subsequent mechanical ventilation within a follow-up of 30 days. The numbers of CD14dimCD16+ non-classical monocytes in peripheral blood were remarkably low in CAD + SARS-CoV-2 compared with CAD patients without infection and healthy controls (P < 0.0001). Moreover, these CD14dimCD16 monocytes showed decreased expression of established markers of adhesion, migration, and T-cell activation (CD54, CD62L, CX3CR1, CD80, and HLA-DR). Decreased numbers of CD14dimCD16+ monocytes were associated with the occurrence of EP. Kaplan-Meier curves illustrate that CAD + SARS-CoV-2 patients with numbers below the median of CD14dimCD16+ monocytes (median 1443 cells/mL) reached EP significantly more often compared to patients with numbers above the median (log-rank 5.03, P = 0.025).Decreased numbers of CD14dimCD16+ monocytes are associated with rapidly progressive respiratory failure in CAD + SARS-CoV-2 patients. Intensified risk assessments comprising monocyte sub- and phenotypes may help to identify patients at risk for respiratory failure.
Development of a Machine Learning Algorithm for Rapid, Point-of-Care Prediction of Serum Monoclonal Proteins in Multiple Myeloma
Authors: Ehsan Malek, Jeries Kort, Gi-Ming Wang, Paolo F Caimi, Kirsten M Boughan, Stanton L. Gerson, Brenda W. Cooper, Molly M Gallogly, Benjamin K. Tomlinson, Marcos de Lima, Curtis Tatsuoka, James Driscoll
Journal: Blood (2020)
Urinary Tetrahydrocannabinol After 4 Weeks of a Full-Spectrum, High-Cannabidiol Treatment in an Open-label Clinical Trial
Authors: M. Kathryn Dahlgren, Kelly A. Sagar, Ashley M. Lambros, Rosemary T. Smith, Staci A. Gruber
Journal: JAMA Psychiatry (2020)

Urinary Tetrahydrocannabinol After 4 Weeks of aFull-Spectrum, High-Cannabidiol Treatment in an Open-label Clinical Trial Despite the growing popularity of cannabidiol (CBD) products, specifically those derived from legal industrial hemp sources, 1 few studies have directly assessed whether the use of high-CBD products could yield positive results on urinary drug tests assessing cannabis use through the detection of Δ9-tetrahydrocannabinol (Δ9-THC) metabolites.A recent short-term administration study found that a single exposure to vaporized CBDdominant cannabis flower (CBD, 10.5%; Δ9-THC, 0.39%), which the authors noted was similar to hemp, resulted in positive drug test results (>15 ng/mL) for 2 of 6 participants within 4 to 8 hours of administration. 2However, to our knowledge, no studies have examined drug test results in those consistently using full-spectrum (ie, Δ9-THC-containing) CBD products.Accordingly, as part of an open-label clinical trial (NCT02548559) examining the use of a full-spectrum high-CBD product for anxiety (with unpublished results as yet), we monitored THC urinary drug status.
Beyond Mortality: Health-Related Quality of Life in Adolescent and Young Adult Patients with Lymphoma: A Longitudinal Study
Authors: Carla Casulo, Tanzy Love, Xiang Lu, Melissa C. Larson, Kathleen J. Yost, Allison C. Rosenthal, Thomas M. Habermann, Brian K. Link, Andrew L. Feldman, Susan L. Slager, Jonathon B. Cohen, Christopher Flowers, James R. Cerhan, Carrie A. Thompson
Journal: Blood (2020)
Final Analysis of the Ro-CHOP Phase III Study (Conducted by LYSA): Romidepsin Plus CHOP in Patients with Peripheral T-Cell Lymphoma
Authors: Emmanuel Bachy, Vincent Camus, Catherine Thieblemont, Rene-Olivier Casasnovas, Loic Ysebaert, Gandhi Laurent Damaj, Stephanie Guidez, Gian-Matteo Pica, Won Seog Kim, Soon Thye Lim, Marc André, Alejandro Martin Garcia-Sancho, Maria Jesus Penarrubia Ponce, Philipp B. Staber, Judith Trotman, Andreas Hüttmann, Vittorio Stefoni, Alessandro Re, Philippe Gaulard, Marie-Helene Delfau-Larue, Laurence De Leval, Michel Meignan, Ju Li, Franck Morschhauser, Richard Delarue
Journal: Blood (2020)
Guidance to Reduce the Cardiovascular Burden of Ambient Air Pollutants: A Policy Statement From the American Heart Association
Authors: Joel D. Kaufman, Mitchell S.V. Elkind, Aruni Bhatnagar, Kirsten Koehler, John R. Balmes, Stephen Sidney, Melissa S. Burroughs Peña, Douglas W. Dockery, Lifang Hou, Robert D. Brook, Francine Laden, Sanjay Rajagopalan, Katherine Bishop Kendrick, Jay R. Turner
Journal: Circulation (2020)

In 2010, the American Heart Association published a statement concluding that the existing scientific evidence was consistent with a causal relationship between exposure to fine particulate matter and cardiovascular morbidity and mortality, and that fine particulate matter exposure is a modifiable cardiovascular risk factor. Since the publication of that statement, evidence linking air pollution exposure to cardiovascular health has continued to accumulate and the biological processes underlying these effects have become better understood. This increasingly persuasive evidence necessitates policies to reduce harmful exposures and the need to act even as the scientific evidence base continues to evolve. Policy options to mitigate the adverse health impacts of air pollutants must include the reduction of emissions through action on air quality, vehicle emissions, and renewable portfolio standards, taking into account racial, ethnic, and economic inequality in air pollutant exposure. Policy interventions to improve air quality can also be in alignment with policies that benefit community and transportation infrastructure, sustainable food systems, reduction in climate forcing agents, and reduction in wildfires. The health care sector has a leadership role in adopting policies to contribute to improved environmental air quality as well. There is also potentially significant private sector leadership and industry innovation occurring in the absence of and in addition to public policy action, demonstrating the important role of public-private partnerships. In addition to supporting education and research in this area, the American Heart Association has an important leadership role to encourage and support public policies, private sector innovation, and public-private partnerships to reduce the adverse impact of air pollution on current and future cardiovascular health in the United States.
Acalabrutinib in Combination with Rituximab, Cyclophosphamide, Doxorubicin, Vincristine and Prednisolone (R-CHOP) As First Line Therapy for Patients with Diffuse Large B-Cell Lymphoma (DLBCL): The Accept Phase Ib/II Single Arm Study
Authors: Andrew Davies, Josh Caddy, Katy Mercer, Geoff N Saunders, Louise Stanton, Graham P. Collins, Thomas E C Cummin, Anna Schuh, Kirit M. Ardeshna, Andrew McMillan, John A. Radford, David John Lewis, Adam Coleman, Gareth Griffiths, Cathy Burton, Sharon Barrans, Peter Johnson
Journal: Blood (2020)
Abstract MP166: <i>PRKAR1A</i> Deficiency Abrogates Cardiac Hypertrophy Through Inhibition of Mitochondrial Fission
Authors: Yuening Liu, Peng Xia, Jingrui Chen, Patricia W Bandettini, Lawrence S Kirschner, Constantine A Stratakis, Zhaokang Cheng
Journal: Circulation Research (2020)

Protein kinase A (PKA) is pivotal for cardiac function of human heart, and its dysregulation is involved with various cardiac pathologies. PKA regulatory subunit 1α (R1α, encoded by PRKAR1A gene) controls PKA kinase activity by sequestering the PKA catalytic subunits. Patients with PRKAR1A mutations are often diagnosed with Carney complex (CNC) and may die prematurely from cardiac complications such as heart failure. However, it remains unknown whether PRKAR1A deficiency interferes with normal heart growth during postnatal development. Here, we show that left ventricular mass is reduced in young CNC patients with PRKAR1A mutations or deletions. To investigate the impact of PRKAR1A deficiency on heart growth, we generated cardiac-specific PRKAR1A heterozygous knockout mice. Ablation of the PRKAR1A gene in mice increased cardiac PKA activity, reduced heart weight to body weight ratio and cardiomyocyte size without altering contractile function. Cardiomyocyte hypertrophy in response to activation of the α1-adrenergic receptor, was completely abolished by silencing of PRKAR1A . Mechanistically, depletion of PRKAR1A provoked PKA-dependent phosphorylation of the mitochondrial fission protein Drp1 at S637, resulting in impaired mitochondrial fission and diminished cardiomyocyte hypertrophy. In conclusion, PRKAR1A deficiency abrogates cardiac hypertrophy during postnatal development, likely through inhibiting Drp1-mediated mitochondrial fission. Our study provides novel mechanistic insights regarding the cardiac mortality associated with CNC.
Combination of Bortezomib and Venetoclax Induces Synergistic Killing of Epstein-Barr Virus-Driven Lymphoproliferative Diseases By Targeting the Pro-Survival Function of Latent Membrane Protein-1 and Epstein-Barr Nuclear Antigen-3C
Authors: Alan Kwok Shing Chiang, Kam Pui Tam, Rex Kwok Him Au-Yeung
Journal: Blood (2020)
Mohawk is a transcription factor that promotes meniscus cell phenotype and tissue repair and reduces osteoarthritis severity
Authors: Kwang Il Lee, Ramya Gamini, Merissa Olmer, Yasunari Ikuta, Joe Hasei, Jihye Baek, Oscar Alvarez-Garcia, Shawn P. Grogan, Darryl D. D’Lima, Hiroshi Asahara, Andrew I. Su, Martin K. Lotz
Journal: Science Translational Medicine (2020)

Mohawk is enriched in meniscal tissue and promotes meniscus cell phenotype, enhances repair, and protects against cartilage destruction in mice.
Outpatient Transplantation during the COVID19 Pandemic: Stretching the Limits for Continuing Care
Authors: Perla R. Colunga Pedraza, Julia Esther Colunga Pedraza, Andres Gomez-De Leon, Mónica Bustillos Muñoz, Karen Lorena Osorno-Rodriguez, Jose Angel Hawing, Oscar Gonzalez Llano, Yajaira Valentine Jimenez-Antolinez, Olga Graciela Cantu Rodriguez, Cesar Homero Gutierrez-Aguirre, David Gomez-Almaguer
Journal: Blood (2020)
Abstract 517: Substrate Dependence of Mitochondrial Supercomplex Abundance in Murine Heart
Authors: Tariq R Altamimi, Timothy N Audam, Yuting Zheng, Andrew Gibb, Siqi Liu, Steven P Jones, Bradford G Hill
Journal: Circulation Research (2020)

Mitochondrial supercomplexes are prominent in mammalian tissues that have high energy demand. Nevertheless, the mechanisms that regulate supercomplex formation and abundance remain unclear. In this study, we examined how myocardial fuel preference regulated by constitutive changes in phosphofructokinase (PFK) activity in vivo or by differential substrate provision to isolated mitochondria affect mitochondrial supercomplexes. Protein complexes from digitonin-solubilized cardiac mitochondria were resolved by blue-native polyacrylamide gel electrophoresis and were identified by mass spectrometry and immunoblotting to contain Complexes I, III, and IV as well as accessory proteins. Mitochondria from hearts with low PFK activity (Glyco Lo hearts) had higher mitochondrial supercomplex abundance and activity compared with mitochondria from wild-type (WT) or Glyco Hi hearts. Incubation of WT mitochondria with fatty acyl carnitine promoted higher supercomplex formation than did incubation with pyruvate, suggesting that substrate utilization is sufficient to regulate mitochondrial supercomplex abundance. These data are consistent with the hypothesis that mitochondrial supercomplex abundance is regulated in a substrate-dependent manner and suggest that metabolic scenarios favoring fat oxidation may promote supercomplex abundance.
Allogeneic Hematopoietic Cell Transplantation Is Critical to Maintain Remissions after CD19-CAR T-Cell Therapy for Pediatric ALL: A Single Center Experience
Authors: Aimee C Talleur, Renee M. Madden, Amr Qudeimat, Ewelina Mamcarz, Akshay Sharma, Ashok Srinivasan, Ali Y Suliman, Mireya Paulina Velasquez, Timothy Lockey, Alisha Gaboriault, Seth E. Karol, Hiroto Inaba, Ying Li, Pam Young, Guolian Kang, Cheng Cheng, Wenting Zheng, Sheng Zhou, Salem M. Akel, Terrence L Geiger, Michael M Meagher, Ching-Hon Pui, Brandon M Triplett, Stephen Gottschalk
Journal: Blood (2020)
Characterizing Coagulation FVII from iPSC-Hepatocytes-like Cells: Setting the Basis for Cell Therapy Development
Authors: Maria Eugenia Chollet, Elisabeth Andersen, Maria Eugenia de la Morena-Barrio, Carlos Bravo-Perez, Marie-Christine Mowinckel, Christiane Filion Myklebust, Ellen Skarpen, Bernd Thiede, Benedicte Stavik, Javier Corral, Gareth J Sullivan, Per Morten Sandset
Journal: Blood (2020)
Intralymphatic drug delivery for treatment of breast cancer: Synthesis, characterization, pharmacokinetics and anti-cancer activity in rodents
Authors: Shuang Cai, Yumei Xie, Mark Cohen, Marcus Forrest
Journal: Cancer Research (2008)

2285  Breast cancers spread initially to regional lymph nodes prior to systemic spread, adequate evaluation and treatment of the axillary lymph nodes is paramount to treatment of early stage disease. An intralymphatically-targeted chemotherapy treating metastatic breast cancer was developed, which may significantly reduce side effects and increase the effectivity of doxorubicin (DOX) and cisplatin based chemotherapy. Doxorubicin and cisplatin were covalently conjugated to hyaluronan(HA) which is a highly biocompatible and nonimmunogenic polymer with a conjugation degree of 5-10% and 20-30%, respectively. Doxorubicin-HA and cisplatin-HA conjugates demonstrate antiproliferative efficacy similar to standard doxorubicin and cisplatin formulations in breast cancer models in vitro. IC50 values of DOX-HA and cisplatin-HA were determined to be 0.1 µg/mL, 0.5 µg/mL, 1 µg/mL and 3 µg/mL, 7 µg/mL, 7 µg/mL, respectively, using cell lines of MDA-MB-468LN, MDA-MB-231 and MCF-7. Drug-release characteristics of DOX-HA and cisplatin-HA were determined using gel permeation chromatography coupled with fluorescent or atomic absorption spectrometry, respectively; demonstrating sustained release of DOX (t1/2 of 172 hours at pH 7.4, 45 hours at pH 5.0) and cisplatin (t1/2 of 10 hours at pH 7.4) from the HA carriers. Pharmacokinetics of DOX and cisplatin were studied using female Sprague-Dawley rats. Distribution of DOX in liver, spleen, kidney, heart, lung, brain, muscle, bladder, lymph nodes, plasma and urine was determined by spectrofluorophotometry. Distribution of cisplatin was determined by graphite furnace atomic absorption spectrometry. Localization of conjugates in lymph nodes was determined by magnetic resonance imaging using gadolinium-diethylenetriaminepentaacetic acid (Gd-DTPA) tagged HA carrier, demonstrating concentration in draining nodes after 12 hours with no liver enhancement. A lymphatic metastasis model was established by orthotopic implantation of MDA-MB-468LN, a human breast cancer cell line with extensive lymph node metastasis in female athymic nude mice. On-going studies are determining tumor response to lymphatic chemotherapy compared to conventional intravenous treatment.
Inhibition of Fibroblast Growth Factor-23 (FGF-23) As a Novel Strategy to Target Bone and Hematopoietic Stem Cell Niche Defects in Beta-Thalassemia
Authors: Annamaria Aprile, Laura Raggi, Mariangela Storto, Isabella Villa, Sarah Marktel, Irene Motta, Maria Domenica Cappellini, Alessandro Rubinacci, Giuliana Ferrari
Journal: Blood (2020)
Daratumumab, Bortezomib, Dexamethasone (D-Vd) Versus Bortezomib and Dexamethasone (Vd) in Relapsed or Refractory (RR) Multiple Myeloma (MM): Pooled Subgroup Analysis of Lepus and Castor
Authors: Jin Lu, Weijun Fu, Wei Li, Jianda Hu, Gang An, Yafei Wang, Chengcheng Fu, Lijuan Chen, Jie Jin, Xinan Cen, Zheng Ge, Zhen Cai, Ting Niu, Andrew Spencer, Katja Weisel, María-Victoria Mateos, Ajay Nooka, Ming Qi, Steven Sun, Xue Gai, Weiping Liu, Xue Yang, Xiaojun Huang
Journal: Blood (2020)
Factors Predicting Long-Term Survival Following CD19 CAR T-Cell Therapy in Relapsed/Refractory B-Cell Acute Lymphoblastic Leukemia
Authors: Xian Zhang, Junfang Yang, Wenqian Li, Gailing Zhang, Yunchao Su, Yanze Shi, Dan Song, Min Zhang, Jiujiang He, Li Xu, Jingjing Li, Xinan Lu, Jianqiang Li, Xiangqun Li, Zhongwei Xu, Ziyu Li, Peihua Lu
Journal: Blood (2020)
Nonmyeloablative Allogeneic Stem Cell Transplantation with or without Inotuzumab Ozogamicin for Lymphoid Malignancies
Authors: Issa F. Khouri, Stephen K. Gruschkus, Alison Gulbis, Celina Ledesma, Nitin Jain, Tapan M. Kadia, Naveen Pemmaraju, Paolo Anderlini, Qaiser Bashir, May Daher, Partow Kebriaei, David Marin, Rohtesh Mehta, Uday R. Popat, Neeraj Saini, Samer A. Srour, Jin S. Im, Luis Fayad, Ranjit Nair, Swaminathan P Iyer, Paolo Strati, Felipe Samaniego, Loretta J. Nastoupil, Christopher Flowers, Gabriela Rondon, Hagop M. Kantarjian, Richard E. Champlin, Elias Jabbour
Journal: Blood (2020)
Cost-Effectiveness of Polatuzumab Vedotin Plus Bendamustine-Rituximab for Transplant-Ineligible Relapsed/Refractory Diffuse Large B-Cell Lymphoma in the United States
Authors: Keith A Betts, Federico Felizzi, Ibou Dieye, Jia Li, Mathias Schulz, Samuel J Hong, Anthony S Masaquel
Journal: Blood (2020)
A Phase 1 Study of LY3410738, a First-in-Class Covalent Inhibitor of Mutant IDH in Advanced Myeloid Malignancies (Trial in Progress)
Authors: Eytan M. Stein, Marina Konopleva, Raymond Gilmour, Anna M Szpurka, Elizabeth Hill, Renee Ward, Hagop M. Kantarjian, Courtney D. Dinardo
Journal: Blood (2020)
Abstract 475: Beta-adrenoceptor Stimulation Uniquely Regulates Exosome Micro-rna Content Secreted From Cardiomyocytes <i>in vitro</i> and Those Found <i>in vivo</i> Circulating in Blood
Authors: Jin Sook Kwon, Erhe Gao, Rajika Roy, jessica Ibetti, J Kurt Chuprun, Walter J Koch
Journal: Circulation Research (2020)

Background and Purpose: The influence of β-adrenoceptor (βAR) signaling on the regulation of exosomes secreted from cardiomyocytes is unknown and since catecholamines are increased in heart failure (HF), there is interest in uncovering whether βARs can induce specific changes in the content of circulating blood exosomes in HF. In this study, we have evaluated whether βAR stimulation by isoproterenol (ISO) on neonatal rat ventricle myocytes (NRVMs) and in vivo in mice can alter the number, size and microRNA (miR) content of secreted exosomes. Methods and Results: ISO treatment of NRVMs did not change exosome number and size of compared than vehicle (PBS). After purifying total RNA from treated myocytes and secreted exosomes, we evaluated the expression level of 37 candidate miR’s, which were selected from previous microarray data. We found that ISO treatment decreased 14 miR’s (miR-222, -106a, -292a, -181b, -210, -489, -214, -1947, -195, -17, -7b, -93, -532 and -19a) in exosomes and in the myocytes themselves, mir-292a and -1947 were up regulated and mir-7b, down regulated. Further, ISO was then used to treat C57 mice via osmotic pump chronically. The number and size of exosomes purified from circulating blood was not changed after 2 and 8 weeks. We evaluated expression of the 14 miRs down-regulated in myocytes as well miR-1 and -21 (important cardiac miRs) both in the blood and hearts of ISO-treated mice. MiR-1 did not change in both blood exosomes and heart tissue and miR-21 was up-regulated in heart tissue but not in blood both at 2 and 8 weeks after ISO treatment. In addition, miRNA-489 and -7b was down-regulated in hearts with miR-214 and -292a up regulated. In blood exosomes, we found only down-regulation of miR-489 and -7b but not miR-214 and 292a. Conclusions: We found that the βAR agonist ISO altered exosomal miR contents but not exosome size and number from myocytes. Importantly, this was found in myocytes in culture and in vivo blood and myocardium that were treated with ISO but several differences were found and changes in blood and myocytes were not homogeneous. However, two miRs, mir-7b and -miR-489, both changes similarly from their origin (NRVMs or mouse hearts) and also in circulating blood exosomes. Therefore, these miRs may represent biomarkers for sympathetic nervous system abnormalities in HF and their therapeutic potential should be evaluated.
Identification of Rab25 interacting molecules by a novel proteomic approach.
Authors: Kwai Cheng, Zhiyong Ding, Gordon Mills
Journal: Cancer Research (2008)

3521  We have recently demonstrated that RAB25 gene is overexpressed in the breast cancer and increased RAB25 gene expression correlated with a poor prognosis in breast cancer patients. In addition, enforced expression of Rab25 protein in breast cancer cells increases proliferation and decreases apoptosis. Together, these data suggest a pathological role of Rab25 proteins in the development and progression of breast tumors. Nevertheless, the relationship between Rab25 protein and breast cancer development and progression remain unknown. As the function of Rab GTPase can be controlled through recruiting specific interacting protein and activating downstream signaling molecules, it is of interest to identify associated partners mediating Rab25 function in breast cancer. We proposed to identify Rab25 interacting proteins in breast cancer cells utilizing a novel proteomic approach, retrovirus-based molecular two hybrid screen (ReMTH). ReMTH utilizes the technical advantages of two emerging technologies, the enhanced retroviral mutagen exon trap (ERM) and protein-fragment complementation assays (PCAs). ERM efficiently traps and tags endogenous genes by integration into the host genome occur upstream or inside of a host gene. This provides a facile approach to trap host proteins without the need to develop cDNA libraries providing a more readily applicable, sensitive, and unbiased screening for protein-protein interactions. In PCA, a green fluorescent protein homolog, improved fluorescent protein (IFP), was split into 2 halves N-terminal half of IFP (IFPN) and C-terminal half of IFP (IFPC). The two separated halves will not reconstitute or fluoresce spontaneously. When each half of GFP is fused to one of a pair of interacting protein partners, the subsequent protein interaction can bring the halves into proximity creating a stable complex and restoring fluorescence. In an attempt to isolate Rab25 interacting molecular in breast cancer cells, a MCF-7 Tet-off IFPN-Rab25 cell was established, infected with ReMTH-IFPC1 virus and selected with puromycin. Multiple fluorescence cells were selected through Fluorescence-Activated Cell Sorting flow cytometry core facility of the MD Anderson Cancer Center. The identity of the target genes interact with IFPN-Rab25 was determined using PCR followed by directly sequencing. Up to date, we have identified 5 putative Rab25-interacting molecules from the screening. This study was supported by Department of Defense Breast Cancer Idea Award W81XWH-06-1-0488.
Detection of Emerging Resistant Clones in Philadelphia-Positive Leukemia Patients Exposed to Tyrosine Kinase Inhibitors. Correlation of cDNA and Gdna Approaches
Authors: Ricardo Sanchez, Juan Manuel de la Rosa, Yanira Heredia, Jaime Carrillo, Laura Rufian, Esther Onecha, Gonzalo Carreño Gomez-Tarragona, Chongwu Wang, María Linares, Jose Sanchez-Pina, Inmaculada Rapado, Josep-Maria Ribera, Rosa Ayala, Joaquin Martinez-López, Santiago Barrio
Journal: Blood (2020)