tbuckley/cabot-search huggingface dataset:
A Cost-Focused Alternative Cancer Medication Dispensing Strategy—“Pack Splitting”
Authors: R. Donald Harvey, Mark J. Ratain
Journal: JAMA Oncology (2019)

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Abstract 174: Investigating Subclinical Cardiotoxicity in Long-term Breast Cancer Survivors Following Chemotherapy With DENSE-based 3D Strain Analysis
Authors: Bryant Baldwin, Shane Johnson, Christopher Malozzi, Michael V Cohen, Maria S Figarola, Anam Chouhdry, Eduardo Rel, Angela Y Yudice, Samuel A McQuiston, Julia Kar
Journal: Circulation Research (2019)

This study investigated if left ventricular (LV) mechanical contractile parameters in addition to LV ejection fraction (LVEF) indicated cardiac remodeling and fibrosis in patients exposed to cardiotoxic chemotherapy agents (CCA). Cardiac deformation data were obtained using single-scan acquisitions with the Displacement Encoding with Stimulated Echoes (DENSE) MRI sequence. Contractile analysis consisted of automated myocardial boundary detection and unwrapping 3D DENSE phase images for intra-myocardial displacements, and followed by analyzing torsion and 3D strains with the meshfree Radial Point Interpolation Method (RPIM). Data were acquired on 13 CCA-exposed patients who were undergoing chemotherapy and/or care for cardiac complications. DENSE LVEF measurements in patients were validated against steady-state free precession (SSFP) MRI data, all contractility computations were compared to healthy subjects and Bland-Altman agreements established between strains computed by independent observers. A significant difference was not found between DENSE and SSFP LVEF computations (52 ± 11% vs 48 ± 15%, p=0.33). Significant differences were seen with enlarged LV diameters in patients versus healthy subjects (6.0 ± 1.1 cm vs 4.9 ± 0.7 cm, p&lt;0.001) and similarly for torsion and longitudinal strain but not in LVEF results (p &gt; 0.05). Bland-Altman agreements were 0.01 ± 0.06 for longitudinal strain and 0.1 ± 1.9 ° for torsion. Statistical analysis confirm changed LV size and function in patients and indicate remodeling that is otherwise not demonstrated by LVEF measurements, which may precede clinically apparent heart failure development and worsened morbidity.
Quality of care for cancer survivors: Does a model of shared care affect experience of care?
Authors: Michael T. Halpern, Julia Cohen, Lisa M Lines, Michelle Mollica, Erin E Kent
Journal: Journal of Clinical Oncology (2019)

213 Background: Cancer survivors may have unique medical care needs due to chronic/late-occurring effects of cancer or cancer treatment. “Shared care,” survivorship care delivered by both oncologists and primary care providers (PCPs), may better address these needs. Little is known about outcomes for survivors receiving shared care vs. oncologist-led or PCP-led patterns of care. We compared patient reported experiences of care for survivors receiving oncologist-led, PCP-led, shared care, or other patterns of care. Methods: Analyses of SEER-CAHPS, a data resource linking NCI's Surveillance, Epidemiology, and End Results (SEER) registry data, Medicare claims, and Medicare Consumer Assessment of Healthcare Providers and Systems (CAHPS) survey responses. Individuals age ≥ 65 in SEER-CAHPS diagnosed 2000-2011 with breast, cervical, colorectal, lung, renal, or prostate cancer or hematologic malignancies who completed a Medicare CAHPS survey ≥ 18 months after diagnosis and were continuously enrolled in Medicare A &amp; B ≥ 6 months before and 6 months after survey completion were included. CAHPS included ratings of Overall Care, Personal Doctor, Specialist Physician, Health Plan, and composite scores for Doctor Communication, Care Coordination, Getting Needed Care, Getting Care Quickly, and Getting Needed Drugs. Survivorship care patterns were identified using proportions of oncologist, PCP, and other physician encounters. Multivariable regressions examined associations between survivorship care patterns and CAHPS outcomes. Results: Among 10,132 survivors, 15% received Shared Care; 10% Oncologist-led; 33% PCP-led; and 42% Other. Compared with Shared Care, we found no significant differences in survivors' experience of care except for Getting Needed Drugs (lower for PCP-led and Other). Sensitivity analyses using different pattern of care definitions showed no associations between survivorship model and experience of care. Conclusions: Survivors’ experiences of care were similar for those in Shared Care vs. Oncologist-led, PCP-led, and Other patterns of care. Within the study’s limitations, these results do not indicate enhanced patient reported medical care experiences for survivors receiving shared care.
Abstract 853: <i>GPX4</i> Gene Expression is Dose-responsive to Doxorubicin Exposure in iPSC-Cardiomyocytes and Correlated With Mitochondrial Function
Authors: Monica E Reyes, Rashida A Callender, Jianzhong Ma, Megan L Grove, Alanna C Morrison, Michelle A Hildebrandt
Journal: Circulation Research (2019)

Impaired mitochondrial function has been implicated as a mechanism of doxorubicin-induced cardiotoxicity, however the precise genes that regulate this process in human cardiomyocytes remain to be elucidated. We hypothesized that doxorubicin significantly alters expression of genes involved in mitochondrial function in human cardiomyocytes, which in turn impairs mitochondrial respiration. Towards this, we treated human inducible pluripotent stem cell (iPSC)-cardiomyocytes with doxorubicin at 15 different time and dose conditions. Gene expression was assessed by RNAseq for each condition and 169 genes involved in mitochondrial function were analyzed for differential expression between control and treated conditions. Mitochondrial respiration (basal respiration, ATP production, maximal respiration, and spare respiratory capacity) was measured using the Seahorse Bioscience XFe96 Cell Mito Stress Test kit and correlated to gene expression levels. Of the 169 genes analyzed, 25 were significantly differentially expressed (P &lt; 0.05) including GPX4 (P = 5.70 x 10 -3 ). Expression of GPX4 remained significant in pairwise comparisons by dose for day 2 and qRT-PCR validation confirmed a dose-dependent decrease in GPX4 expression. Maximal respiration (r = -0.62; P = 0.031) and spare respiratory capacity (r = -0.67; P = 0.017) correlated with GPX4 expression in doxorubicin-treated iPSC-cardiomyocytes. GPX4 encodes a glutathione peroxidase that is responsible for protecting the cell against oxidative damage. Damage due to reactive oxygen species (ROS) is one of the established mechanisms of anthracycline-induced cardiac damage. Our findings underscore a role for mitochondrial function and ROS in the development of doxorubicin-induced cardiotoxicity and implicates GPX4 in this process. The assessment of doxorubicin-altered gene expression in iPSC-cardiomyocytes may provide insight into how impaired mitochondrial respiration leads to cardiotoxicity and heart failure in cancer survivors treated with doxorubicin and other anthracyclines.
Multidimensional Study on the Prognostic Factors of Acute Myeloid Leukemia Patients with FLT3-ITD mutations Based on the Next-Generation Sequencing Platform
Authors: Yi Zhang, Bide Zhao, Yungui Wang, Dongmei Wang, Hanzhang Pan, Chengcheng Wang, Feng Lou, Shanbo Cao, Jie Jin
Journal: Blood (2018)
Comparison of Spleen Volumes Estimated Using Planimetry and Prolate Ellipsoid Methods on MRI in Myelofibrosis Patients
Authors: Alpana Harisinghani, Manish Sharma, Michael O'Connor, Ramanaidu Darapureddi, Sayali Karve, Sanjeev Pitla, Shobitha Manikandan, Rohit Sood
Journal: Blood (2018)
Shared genetics of asthma and mental health disorders: a large-scale genome-wide cross-trait analysis
Authors: Zhaozhong Zhu, Xi Zhu, Cong-Lin Liu, Huwenbo Shi, Sipeng Shen, Yunqi Yang, Kohei Hasegawa, Carlos A. Camargo, Liming Liang
Journal: European Respiratory Journal (2019)

Epidemiological studies demonstrate an association between asthma and mental health disorders, although little is known about the shared genetics and causality of this association. Thus, we aimed to investigate shared genetics and the causal link between asthma and mental health disorders. We conducted a large-scale genome-wide cross-trait association study to investigate genetic overlap between asthma from the UK Biobank and eight mental health disorders from the Psychiatric Genomics Consortium: attention deficit hyperactivity disorder (ADHD), anxiety disorder (ANX), autism spectrum disorder, bipolar disorder, eating disorder, major depressive disorder (MDD), post-traumatic stress disorder and schizophrenia (sample size 9537–394 283). In the single-trait genome-wide association analysis, we replicated 130 previously reported loci and discovered 31 novel independent loci that are associated with asthma. We identified that ADHD, ANX and MDD have a strong genetic correlation with asthma at the genome-wide level. Cross-trait meta-analysis identified seven loci jointly associated with asthma and ADHD, one locus with asthma and ANX, and 10 loci with asthma and MDD. Functional analysis revealed that the identified variants regulated gene expression in major tissues belonging to the exocrine/endocrine, digestive, respiratory and haemic/immune systems. Mendelian randomisation analyses suggested that ADHD and MDD (including 6.7% sample overlap with asthma) might increase the risk of asthma. This large-scale genome-wide cross-trait analysis identified shared genetics and potential causal links between asthma and three mental health disorders (ADHD, ANX and MDD). Such shared genetics implicate potential new biological functions that are in common among them.
The Pan Histone Deacetylase Inhibitor Panobinostat and the Iso-Selective Inhibitor Romidepsin Reduce Glycoprotein VI Expression and Inhibit Platelet Activation in Response to Collagen Related Peptide
Authors: Mark J Bishton, Miles Prince, Ricky W Johnstone, Simon J. Harrison, Benjamin T. Kile
Journal: Blood (2011)
Loss of Plasmacytoid Dendritic Cell Differentiation Is Highly Predictive for Persistent Measurable Residual Disease and Poor Outcomes in Acute Myeloid Leukemia
Authors: Wenbin Xiao, Aaron D Goldberg, Christopher Famulare, Sean Delvin, Minal Patel, Erin McGovern, Akshar Patel, Jessica Schulman, Andrew Dunbar, Zachary D. Epstein-Peterson, Kamal Menghrajani, Bartlomiej Getta, Sheng Cai, Mark Blaine Geyer, Jacob L Glass, Justin Taylor, Aaron D Viny, Ross L. Levine, Yanming Zhang, Martin S. Tallman, Mikhail Roshal
Journal: Blood (2018)
Abstract 724: Neonatal Heart Regeneration Preserves Native Ventricular Biomechanical Properties After Myocardial Infarction
Authors: Hanjay Wang, Ross Bennett-Kennett, Michael J Paulsen, Camille E Hironaka, Akshara D Thakore, Justin M Farry, Anahita Eskandari, Haley J Lucian, Matthew A Wu, Annabel Imbrie-Moore, Amanda N Steele, Lyndsay M Stapleton, Reinhold H Dauskardt, Y. Joseph Woo
Journal: Circulation Research (2019)

Introduction: Neonatal mice exhibit natural heart regeneration after myocardial infarction (MI) until postnatal day 7 (P7). Whether this regenerated muscle is similar biomechanically to native myocardium remains unknown. We hypothesized that neonatal heart regeneration preserves native left ventricular (LV) biomechanical properties after MI. Methods: C57BL/6J mice (n=58) underwent sham surgery or left anterior descending coronary artery ligation on postnatal day 1 (P1) or P7. After 4 weeks, echocardiography was performed. The explanted anterolateral LV wall was mounted for lenticular hydrostatic deformation testing (Fig 1A-B) and pressurized to 130 mmHg with 37°C saline to impart a homogeneous stress load. Surface strain was tracked to calculate a multiaxial composite tissue modulus. Data are expressed as mean±SEM. Results: P1 MI and sham mice (n=14, each) had similar post-MI LV wall thickness (0.61±0.05 cm vs 0.66±0.03 cm, p=0.39), end-diastolic diameter (3.14±0.10 cm vs 3.05±0.12 cm, p=0.57), and ejection fraction (58.2±4.1% vs 55.2±4.4%, p=0.63). P7 MI mice (n=14) had significant LV wall thinning (0.40±0.04 cm vs 0.71±0.02 cm, p&lt;0.0001), end-diastolic LV enlargement (4.24±0.16 cm vs 3.34±0.09 cm, p&lt;0.0001), and depressed ejection fraction (29.7±4.9% vs 61.7±4.0%, p&lt;0.0001) compared to P7 shams (n=16). While LV tissue modulus for P1 MI and sham mice were similar (460.9±46.4 kPa vs 527.1±61.2 kPa, p=0.40, Fig 1C), the modulus for P7 MI mice was significantly elevated compared to that for P7 shams (1099.6±175.1 kPa vs 616.0±95.2 kPa, p=0.02, Fig 1D). Conclusion: In a neonatal mouse MI model, regenerated LV muscle has similar biomechanical properties as native LV muscle.
High Response Rate in Relapsed/Refractory Follicular Lymphoma Following Personalised Immunotherapy with Intranodal IFN-Alfa-Dendritic-Cell and Rituximab
Authors: M. Christina Christina Cox, Carmela Rozera, Mauro Mattei, Elena Muraro, Eleonora Aricò, Arianna Di Napoli, Antonio Pavan, Francesca Di Landro, Laura Santodonato, Debora Martorelli, Giuseppina D'Agostino, Caterina Lapenta, Stefan Hohaus, Annarosa Cuccaro, Maria Cantonetti, Valerio Zoli, Cinzia Berdini, Borgioni Sonia, Livio Pupo, Daniela Prosperi, Simona Donati, Mariarosaria Napolitano, Cangemi Michela, Enrica Montefiore, Davide Carlei, Domenica Monque, Luigi Ruco, Agostino Tafuri, Riccardo Dolcetti, Stefano Maria Santini, Imerio Capone, Filippo Belardelli
Journal: Blood (2018)
Abstract 184: Cardioprotective Effects of Brain-derived Neurotrophic Factor rs6265 Polymorphism in Duchenne Cardiomyopathy
Authors: Frank J Raucci, Anand P Singh, Jonathan H Soslow, Lin Zhong, Wejdan Aljafar, Natasja Lessiohadi, Cassandra P Awgulewitsch, Prachi Umbarkar, Qinkun Zhang, Holly M Smith, Presley L Cannon, Erica J Carrier, Antonis K Hatzopoulos, Hind Lal, Cristi L Galindo
Journal: Circulation Research (2019)

We previously identified brain-derived neurotrophic factor (BDNF) as a putative cardiac-specific biomarker for preserved cardiac function in Duchenne Muscular Dystrophy (DMD). BDNF has cardioprotective qualities that may attenuate dilated cardiomyopathy, and a common, functional BDNF single nucleotide polymorphism rs6265 (Val66-Met) may be correlated with increased risk of cardiovascular events. We hypothesized that BDNF is protective in the setting of DMD and that BDNF’s beneficial effects are diminished in rs6265 allelic carriers. We compared circulating BDNF levels with cardiovascular and skeletal muscle functional parameters in DMD patients stratified by carrier status. Positive association of circulating BDNF with left ventricular ejection fraction in DMD patients was restricted to non-carriers of the rs6265 allele, whereas carriers exhibited worse cardiac function with increased BDNF, more fibrosis and worse skeletal muscle function. To more directly assess association of rs6265 with cardiac function, we used mice with knock-in of BDNF polymorphic Val66Met allele. RNASeq showed higher expression of extracellular matrix genes in Val66Met hearts, and there was a negative correlation of cardiac BDNF protein levels with fibrosis. Additionally, there were baseline echocardiographic and ECG differences, and isolated cardiomyocytes had decreased contractility. This overall cardiac phenotype was substantially enhanced when Val66Met mice were crossed with muscular dystrophy mice. Considered together, our results indicate that BDNF plays a protective role in the dystrophic heart and may represent a novel therapeutic candidate for DMD cardiomyopathy.
Anaesthetic depth and complications after major surgery: an international, randomised controlled trial
Authors: Timothy G Short, Douglas Campbell, Christopher Frampton, Matthew T V Chan, Paul S Myles, Tomás B Corcoran, Daniel I Sessler, Gary H Mills, Juan P Cata, Thomas Painter, Kelly Byrne, Ruquan Han, Mandy H M Chu, Davina J McAllister, Kate Leslie, M Shulman, S Wallace, C Farrington, W Gallagher, A Ditoro, P Peyton, S Baulch, A Dalyell, S Sidiropoulos, J Reynolds, J Rowley, N Tan, D McCallum, E O'Loughlin, S Wong, K Owen, I-K Sim, L Glazov, P Coutts, M Pushpanathan, V Findlay, M Paech, D Cavill, A Chuan, L Pope, J Lucas, B Robinson, A Millard, S Allen, M Allen, S McKeown, P Sivalingam, T Wilkes, C Jowett, A Kearney, M Bennett, J-P Favero, S Sawhney, K Drummond, S Osborn, A Wing, J Taylor, M Edwards, H Reynolds, C Town, N Terblanche, M Challis, R Seale, K Button, R Cotter, M Stewart, N Zingerle, S Hannon, D Middleton, C Edgley, S March, T McCulloch, G Wong, S Jeong, K Connell, K Kramer, G Henderson, V Ward, Y Buller, N Hird, D Scott, L Evered, G Snyder, B Silbert, P Corcoran, E Fitzgerald, S Said, A Watson, D Baby, S Bolsin, A Marriott, K Ives, B-J Wakefeld, A Jeffreys, S Bates, R Halliwell, D Elliott, L Cope, R Paranthoiene, P Peng, X Liu, X Zhou, X Jin, H Liu, L An, W Cui, L Zhang, B Jia, J Fang, E Koo, E Lo, B Fung, M Tsang, L Lam, E Pang, V Lau, G Choi, M Tsang, B Fung, R Kwok, K Yau, B Cheng, C Lam, E Lee, D Buggy, H Keane, K Byrne, C Connolly, M Ali, A Cervantes, K Kumar, S Dandy, L Ritchie, R Kennedy, M McKellow, C Read, D France, H Truong, C Chapman, S Walker, S Olliff, H Houston, M Scott, I Minchin, A Moniwa, J McAlpine, M Chaddock, L Gray, C Czepanski, S Vinish, U Buehner, E Williams, C Zhou, L Goodman, J Bermaat, G Mans, A Garden, R Franks, J Deiterle, J Barrett, S Roubos, F van Lier, S Verbrugge, C Kalkman, J Dieleman, J Verdam-Veldkamp, A van Kampen, A Pai, A Sevillano, J Yeung, T Melody, K Atterbury, M Hough, S Dukes, S Williams, Z Milan, G Kunst, K Bhatia, W MacNab, E Weaver, R Moulding, P Doble, P Klepsch, J Self, T Howes, B Rees, B Faulkner, J Blackburn, N Crombie, L Cooper, A Nair, G Bell, R Longfellow, C Nicholas, T Garratt, M Pollard, G Brown, G Morrison, A Lang, H Dawson, M MacDonald, T Martin, E Niebrzegowska, P Dias, R Rao Baikady, S Jhanji, N Siddaiah, L Bird, R Mittal, P Nalawaya, J Sonksen, R Gidda, I Wrench, N Craw, L Pippard, S Davies, M Wright, M Turan, K Maheshwari, B Cohen, W Saasouh, P Singh, S Govindarajan, E Cuko, F Marcano, R Babazade, S Leung, S Raza, E Reville, C Hanline, S Ayad, M Buttar, Z Akhtar, A Niazi, P Saha, A Morris, C Lokhande, M Hassan, H Honar, G Bairacharya, J Saxon, D Chelnick, R Carlson, J Ruiz, J Wilks, W Williams, L Dangler, I Ifeanyi-Pillette, J Suarez, R Erfe, A Perez, R Veselis, G Yang, M Mehta, K Pryor, L Rubin, J Malhotra, M Steinkamp, F Cooke, R Friedlander
Journal: The Lancet (2019)
BRCA1 Deficiency Upregulates NNMT, Which Reprograms Metabolism and Sensitizes Ovarian Cancer Cells to Mitochondrial Metabolic Targeting Agents
Authors: Arun Kanakkanthara, Kiran Kurmi, Thomas L. Ekstrom, Xiaonan Hou, Emma R. Purfeerst, Ethan P. Heinzen, Cristina Correia, Catherine J. Huntoon, Daniel O'Brien, Andrea E. Wahner Hendrickson, Sean C. Dowdy, Hu Li, Ann L. Oberg, Taro Hitosugi, Scott H. Kaufmann, S. John Weroha, Larry M. Karnitz
Journal: Cancer Research (2019)

BRCA1 plays a key role in homologous recombination (HR) DNA repair. Accordingly, changes that downregulate BRCA1, including BRCA1 mutations and reduced BRCA1 transcription, due to promoter hypermethylation or loss of the BRCA1 transcriptional regulator CDK12, disrupt HR in multiple cancers. In addition, BRCA1 has also been implicated in the regulation of metabolism. Here, we show that reducing BRCA1 expression, either by CDK12 or BRCA1 depletion, led to metabolic reprogramming of ovarian cancer cells, causing decreased mitochondrial respiration and reduced ATP levels. BRCA1 depletion drove this reprogramming by upregulating nicotinamide N-methyltransferase (NNMT). Notably, the metabolic alterations caused by BRCA1 depletion and NNMT upregulation sensitized ovarian cancer cells to agents that inhibit mitochondrial metabolism (VLX600 and tigecycline) and to agents that inhibit glucose import (WZB117). These observations suggest that inhibition of energy metabolism may be a potential strategy to selectively target BRCA1-deficient high-grade serous ovarian cancer, which is characterized by frequent BRCA1 loss and NNMT overexpression. SIGNIFICANCE: Loss of BRCA1 reprograms metabolism, creating a therapeutically targetable vulnerability in ovarian cancer.
Interferon-alfa2 Treatment of Patients with Polycythemia Vera and Related Neoplasms Influences Deregulated Inflammation and Immune Genes in Polycythemia Vera and Allied Neoplasms
Authors: Vibe Skov, Caroline Riley, Mads Thomassen, Lasse Kjær, Thomas Stauffer Larsen, Ole Weis Bjerrum, Torben A Kruse, Hans Carl Hasselbalch
Journal: Blood (2018)
Prevalence and risk factors of small airway dysfunction and its association with smoking in China: a national cross-sectional study of 50 479 adults
Authors: Dan Xiao, Zhengming Chen, Sinan Wu, Kewu Huang, Jianying Xu, Lan Yang, Yongjian Xu, Xiangyan Zhang, Chunxue Bai, Jian Kang, Peixin Ran, Huahao Shen, Fuqiang Wen, Wanzhen Yao, Tieying Sun, Guangliang Shan, Ting Yang, Yingxiang Lin, Jianguo Zhu, Ruiying Wang, Zhihong Shi, Jianping Zhao, Xianwei Ye, Yuanlin Song, Qiuyue Wang, Yumin Zhou, Liren Ding, Ting Yang, Yahong Chen, Yanfei Guo, Fei Xiao, Yong Lu, Xiaoxia Peng, Biao Zhang, Zuomin Wang, Hong Zhang, Xiaoning Bu, Xiaolei Zhang, Li An, Shu Zhang, Zhixin Cao, Qingyuan Zhan, Yuanhua Yang, Lirong Liang, Zhao Liu, Xinran Zhang, Anqi Cheng, Haoxiang Lin, Bin Cao, Huaping Dai, Jiang He, Chen Wang
Journal: The Lancet (2019)