tbuckley/cabot-search huggingface dataset:
The Incidence of Breast Cancer Recurrence 10-32 Years After Primary Diagnosis
Authors: Rikke Nørgaard Pedersen, Buket Öztürk Esen, Lene Mellemkjær, Peer Christiansen, Bent Ejlertsen, Timothy Lee Lash, Mette Nørgaard, Deirdre Cronin-Fenton
Journal: JNCI Journal of the National Cancer Institute (2021)

Extended, more effective breast cancer treatments have increased the prevalence of long-term survivors. We investigated the risk of late breast cancer recurrence (BCR), 10 years or more after primary diagnosis, and associations between patient and tumor characteristics at primary diagnosis and late BCR up to 32 years after primary breast cancer diagnosis.Using the Danish Breast Cancer Group clinical database, we identified all women with an incident early breast cancer diagnosed during 1987-2004. We restricted to women who survived 10 years without a recurrence or second cancer (10-year disease-free survivors) and followed them from 10 years after breast cancer diagnosis date until late recurrence, death, emigration, second cancer, or December 31, 2018. We calculated incidence rates per 1000 person-years and cumulative incidences for late BCR, stratifying by patient and tumor characteristics. Using Cox regression, we calculated adjusted hazard ratios for late BCR accounting for competing risks.Among 36 924 women with breast cancer, 20 315 became 10-year disease-free survivors. Of these, 2595 developed late BCR (incidence rate = 15.53 per 1000 person-years, 95% confidence interval = 14.94 to 16.14; cumulative incidence = 16.6%, 95% confidence interval = 15.8% to 17.5%) from year 10 to 32 after primary diagnosis. Tumor size larger than 20 mm, lymph node-positive disease, and estrogen receptor-positive tumors were associated with increased cumulative incidences and hazards for late BCR.Recurrences continued to occur up to 32 years after primary diagnosis. Women with high lymph node burden, large tumor size, and estrogen receptor-positive tumors had increased risk of late recurrence. Such patients may warrant extended surveillance, more aggressive treatment, or new therapy approaches.
A Phase 1/1b Open-Label, Multicenter, Two-Part Study of SETD2 Inhibitor EZM0414 in Patients with Relapsed/Refractory Multiple Myeloma or Diffuse Large B-Cell Lymphoma
Authors: Paul G. Richardson, Ruben Niesvizky, Jay Yang, Neelu Yadav, Helen Hsu, Christopher R. Flowers
Journal: Blood (2021)
Flow Cytometric Analysis of Microbial Diversity in Patients with Aggressive Lymphoma Disease Undergoing Chemoimmunotherapy
Authors: Maren Schmiester, René Maier, René Riedel, Marco Frentsch, Robert R. Jenq, Christine B. Peterson, Liangliang Zhang, Lars Bullinger, Hyun-Dong Chang, Il-Kang Na
Journal: Blood (2021)
Abstract 10220: CSL112 (Apolipoprotein A-I (human)) Infusion Rapidly Increases ApoA-I Exchange Rate via Specific Serum Amyloid-Poor HDL Sub-Populations When Administered to Patients Post Myocardial Infarction
Authors: Svetlana A Didichenko, Elena Velkoska, Alexey V Navdaev, Brandon H Greene, Shuhui W Lorkowski, Jenny J Mears, Samuel D Wright, C M Gibson, Jonathan D Smith, Bronwyn A Kingwell
Journal: Circulation (2021)

Background: Apolipoprotein A-I (apoA-I) exchange rate (AER) into plasma high density lipoprotein (HDL) may represent a cell-free measure of HDL function, and predict recurrent major adverse cardiovascular events post-acute myocardial infarction (AMI). Purpose: To characterise the effects of CSL112 (apoA-I (human)) on AER and the relationships with specific HDL subpopulations when administered in the 90-day high-risk period post AMI. Methods: Patients from the AEGIS-I (ApoA-I Event Reducing in Ischemic Syndromes I) study received either placebo, 2g or 6g CSL112 post AMI. The rate of apoA-I exchange into HDL was measured in AEGIS-I plasma samples incubated with fluorescent apoA-I-NBD (7-nitrobenz-2-oxa-1,3-diazole) lipid-sensitive reporter for 30 min at 37°C. HDL particle size distribution was assessed by native gel electrophoresis followed by fluorescent imaging and detection of apoA-I and serum amyloid A (SAA1/SAA2) by western blotting. Results: CSL112 infusion increased AER peaking 2 h post infusion and returning to baseline by 24 h. AER was correlated with cholesterol efflux capacity, HDL-C, apoA-I and phosphatidylcholine (all p&lt;0.001). CSL112 infusion induced transient changes in HDL particle size distribution. Small remodelled HDL (S-HDL rem ) derived from CSL112 were detected in plasma 2-4 h after infusion. Large remodeled HDL species (L-HDL rem ) accumulated 2-12 h post infusion. The apoA-1-NBD reporter was confined to distinct HDL subpopulations that contained little SAA. In plasma samples characterized by the baseline pattern of HDL particle size distribution (0 h and 24-48 h post infusion), the apoA-I-NBD reporter predominantly exchanged into the HDL3 subpopulation, but not into large HDL2. Conclusion: Infusion of CSL112 increased AER via exchange into SAA-poor HDL particles. AER may represent a clinically amenable biomarker of HDL functionality. Figure: HDL particle remodelling and AER in a representative subject infused with 6g CSL112 .
NGS-Based MRD Quantitation: An Alternative to qPCR Validated on a Large Consecutive Cohort of Children with ALL
Authors: Michael Svaton, Aneta Skotnicova, Leona Reznickova, Andrea Rennerova, Tatana Valova, Michaela Kotrova, Vincent H.J. van der Velden, Monika Brüggemann, Nikos Darzentas, Anton W. Langerak, Jan Zuna, Jan Stary, Jan Trka, Eva Fronkova
Journal: Blood (2021)
Clinical correlation of miR-375 and alpha-fetoprotein in hepatocellular carcinoma: Comparison in mice and humans
Authors: Marta A. Kowalik, Giovanna M. Ledda-Columbano, Silvia Giordano, Amedeo Columbano
Journal: Hepatology (2011)

We read with great interest the letter by Cheng-Maw et al., commenting on our study about the increased expression levels of Yes-associated protein (YAP) in chemically induced mouse hepatocellular carcinomas (HCCs).1 These increased expression levels were associated with down-regulation of microRNA-375 (miR-375) expression, which is known to control YAP expression,2 and with enhanced levels of alpha-fetoprotein (AFP), which, in two independent studies, was found to be a target gene of YAP.3, 4 Cheng-Maw et al. in their letter show that in 157 HCC, divided into two groups on the basis of the mean levels of miR-375 expression, serum AFP levels were significantly higher in the group showing less reduction in miR-375 than in the group showing stronger reduction of miR-375. Based on these findings, the authors suggest that AFP expression in HCCs is not solely regulated by the axis of miR-375-YAP-AFP. We totally agree with this conclusion. Indeed, as shown in our article, while an anti-correlation exists between miR-375 and YAP expression, such an inverse relation could not be observed between miR and AFP, and nowhere in the text did we imply that a YAP increase could be the main mechanism responsible for AFP regulation. AFP is a well-known marker of HCC and its increase is considered the result of a loss of differentiation of cancer cells. Thus, it seems clear that the increased levels of AFP cannot be due simply to up-regulation of YAP, but rather to a general change in the several factors regulating this protein. Interestingly, the article that originally described AFP as a target gene of YAP was based on a transgenic mouse model where YAP overexpression was induced in newborn (3-week-old) animals.3 Thus, it is possible that the increased AFP expression observed in YAP-overexpressing mice could also be due to YAP-dependent alteration of hepatocyte differentiation. In conclusion, we agree with Cheng-Maw et al. that AFP expression in HCCs is not solely regulated by the axis of miR-375-YAP-AFP. As with most genes, many pathways and many mechanisms (both at the transcriptional, posttranscriptional, and posttranslational levels) can regulate the expression of a particular protein and this is surely true also for AFP. What we said in our article is that YAP is among the many factors that can contribute to this regulation. Marta A. Kowalik Ph.D.*, Giovanna M. Ledda-Columbano Ph.D.*, Silvia Giordano M.D., Ph.D. , Amedeo Columbano Ph.D.*, * Department of Toxicology, University of Cagliari, Italy, Institute for Cancer Research and Treatment, University of Torino, Italy.
Characterization of Atypical t(11;14) <i>CCND1/IGH</i> Translocations in Multiple Myeloma
Authors: James B Smadbeck, Neeraj Sharma, Nadine Abdallah, Hongwei Tang, Moritz Binder, Rafael Fonseca, P. Leif Bergsagel, Jess F Peterson, Rhett P. Ketterling, Patricia Greipp, S. Vincent Rajkumar, Shaji Kumar, Linda B Baughn
Journal: Blood (2021)
Acute-to-Chronic Glycemic Ratio as a Predictor of COVID-19 Severity and Mortality
Authors: Jordi Ramon, Gemma Llauradó, Roberto Güerri, Elisenda Climent, Silvia Ballesta, David Benaiges, Inmaculada López-Montesinos, Humberto Navarro, Natalia Fernández, Maria José Carrera, Dídac Mauricio, Juana A. Flores-Le Roux, Juan-José Chillarón
Journal: Diabetes Care (2021)

To evaluate the association between acute-to-chronic (A/C) glycemic ratio and mortality and severity outcomes for patients with type 2 diabetes (T2D) hospitalized with coronavirus disease 2019 (COVID-19).A total of 91 patients were included. We measured glycemia at admission and estimated the average chronic glucose levels to calculate the A/C glycemic ratio. The primary outcome was a composite of in-hospital mortality, intensive care unit admission, and mechanical ventilation.Thirty-five patients had a primary outcome event, presenting a significant association with the A/C glycemic ratio (hazard ratio [HR] 1.57 [95% CI 1.14-2.15], P = 0.005). In comparisons with the 2nd tertile, the 3rd tertile of the A/C glycemic ratio was associated with the primary outcome (HR 3.39 [95% CI 1.31-8.75], P = 0.012). In the multivariate analysis, after additional adjustment for age, sex, comorbidities, inflammatory markers, and corticosteroid therapy, the association for the 3rd tertile (HR 3.96 [95% CI 1.35-11.59], P = 0.012) remained significant.In patients with T2D hospitalized with COVID-19, the imbalance between acute glycemia at admission and chronic metabolic control is associated with worse prognosis.
New Rapid Helicobacter Pylori Blood Test Based on Dual Detection of FliD and CagA Antibodies for On-Site Testing
Authors: Christian Schulz, Behnam Kalali, Alexander Link, Markus Gerhard, Peter Malfertheiner
Journal: Clinical Gastroenterology and Hepatology (2021)

Helicobacter pylori is the most prevalent bacterial infection, affecting half of the world's population, with a high morbidity and mortality rate.1,2 Several invasive and noninvasive testing procedures are available, and their selective use serves the specific needs of diverse clinical scenarios. For gastric cancer prevention, mass screening is necessary and requires a noninvasive, rapid, accurate and cost-effective test. For this purpose H pylori serology currently seems to be the preferred noninvasive diagnostic method. Population-based testing and treatment for H pylori is cost effective in high-risk countries, but less effective in low- and medium-risk countries.3,4 Many serologic tests are available on the market, with inconsistent performance often being observed. Therefore, international guidelines recommend considering only serologic tests with high accuracy that have been validated in the respective local populations. To date, no rapid point-of-care test (POCT) has reached a sufficient degree of accuracy.
ZNF382 controls mouse neuropathic pain via silencer-based epigenetic inhibition of <i>Cxcl13</i> in DRG neurons
Authors: Longfei Ma, Lina Yu, Bao-Chun Jiang, Jingkai Wang, Xinying Guo, Yangyuxin Huang, Jinxuan Ren, Na Sun, Dave Schwinn Gao, Hao Ding, Jianan Lu, Hang Zhou, Lijing Zou, Yibo Gao, Lieju Wang, Kai Sun, Yue Ming, Zhipeng Meng, Yuan-Xiang Tao, Min Yan
Journal: The Journal of Experimental Medicine (2021)

Nerve injury–induced changes of gene expression in dorsal root ganglion (DRG) are critical for neuropathic pain genesis. However, how these changes occur remains elusive. Here we report the down-regulation of zinc finger protein 382 (ZNF382) in injured DRG neurons after nerve injury. Rescuing this down-regulation attenuates nociceptive hypersensitivity. Conversely, mimicking this down-regulation produces neuropathic pain symptoms, which are alleviated by C-X-C motif chemokine 13 (CXCL13) knockdown or its receptor CXCR5 knockout. Mechanistically, an identified cis-acting silencer at distal upstream of the Cxcl13 promoter suppresses Cxcl13 transcription via binding to ZNF382. Blocking this binding or genetically deleting this silencer abolishes the ZNF382 suppression on Cxcl13 transcription and impairs ZNF382-induced antinociception. Moreover, ZNF382 down-regulation disrupts the repressive epigenetic complex containing histone deacetylase 1 and SET domain bifurcated 1 at the silencer-promoter loop, resulting in Cxcl13 transcriptional activation. Thus, ZNF382 down-regulation is required for neuropathic pain likely through silencer-based epigenetic disinhibition of CXCL13, a key neuropathic pain player, in DRG neurons.
Oral Decitabine/Cedazuridine in Patients with Lower Risk Myelodysplastic Syndrome: A Longer-Term Follow-up of from the Ascertain Study
Authors: Guillermo Garcia-Manero, James K McCloskey, Elizabeth A. Griffiths, Karen Yee, Amer M. Zeidan, Aref Al-Kali, H. Joachim Deeg, Prapti Patel, Mitchell Sabloff, Mary-Margaret Keating, Kim-Hien Dao, Nancy Zhu, Nashat Y. Gabrail, Salman Fazal, Joseph Maly, Olatoyosi Odenike, Hagop Kantarjian, Amy E. DeZern, Casey L. O'Connell, Gail J. Roboz, Lambert Busque, Richard A. Wells, Harshad Amin, Jasleen K. Randhawa, Brian Leber, Yong Hao, Harold N. Keer, Mohammad Azab, Michael R. Savona
Journal: Blood (2021)
Ponatinib in Combination with FLAG-IDA Chemotherapy for Blast-Phase Chronic Myeloid Leukemia: Final Results of the Seamless Phase I/II Dose-Finding UK Trials Acceleration Programme (TAP) Matchpoint Trial
Authors: Mhairi Copland, Daniel Slade, Graham McIlroy, Gillian Horne, Jennifer Byrne, Kate Rothwell, Kristian Brock, Hugues De Lavallade, Charles Craddock, Richard Clark, Matthew Smith, Rachel Fletcher, Rebecca Bishop, Dragana Milojkovic, Christina Yap
Journal: Blood (2021)
CD47‐ and Integrin <i>α</i>4/<i>β</i>1‐Comodified‐Macrophage‐Membrane‐Coated Nanoparticles Enable Delivery of Colchicine to Atherosclerotic Plaque
Authors: Yuyu Li, Junyi Che, Lei Chang, Meng Guo, Xue Bao, Dan Mu, Xuan Sun, Xin Zhang, Wen Lu, Jun Xie
Journal: Advanced Healthcare Materials (2021)

Atherosclerosis is a chronic inflammatory disease and the major pathological factor of most cardiovascular diseases, leading to ≈1/3 of deaths worldwide. Improving local delivery of anti-inflammatory drugs to the site of atherosclerosis has significant promise to prevent the development of atherosclerotic plaque clinically. Here, a modified-macrophage-membrane-coated nanoparticle drug delivery able to transport colchicine to the atherosclerotic site is reported. This hybrid system efficiently targets endothelial cells under an inflammatory environment while escaping the endocytosis of macrophages. Furthermore, the anti-inflammatory effect of the modified-macrophage-membrane-coated nanoparticles on foam cells is studied. In vivo, the migration of the modified-macrophage-membrane-coated nanoparticles to atherosclerotic lesions is confirmed in a vulnerable atherosclerotic plaque mouse model. Intravenous injections of the hybrid system successfully reduce the lipid plaque load and improve the plaque stability. This strategy provides a potential therapeutic system for the targeted delivery of anti-inflammatory drugs to the atherosclerotic site for the treatment of atherosclerosis in cardiovascular diseases.
Impact of Sacubitril/Valsartan Versus Ramipril on Total Heart Failure Events in the PARADISE-MI Trial
Authors: Marc A. Pfeffer, Brian Claggett, Eldrin F. Lewis, Christopher B. Granger, Lars Køber, Aldo P. Maggioni, Douglas L. Mann, John J.V. McMurray, Jean-Lucien Rouleau, Scott D. Solomon, Philippe Gabriel Steg, Otavio Berwanger, Maja Cikes, Carmine G. De Pasquale, Alberto Fernandez, Gerasimos Filippatos, Karola Jering, Ulf Landmesser, Venugopal Menon, Béla Merkely, Mark C. Petrie, Ivo Petrov, Morten Schou, Michele Senni, David Sim, Peter van der Meer, Martin Lefkowitz, Yinong Zhou, Yi Wang, Eugene Braunwald
Journal: Circulation (2021)
T Cell Engaging Bispecific Antibodies Produce Durable Response in Mesothelin-Positive Patient-Derived Xenograft Models of Pediatric AML
Authors: Anilkumar Gopalakrishnapillai, Colin Correnti, Kristina Pilat, Ida Lin, Albe Man Kid Chan, Ashok D. Bandaranayake, Christopher Mehlin, Anne Kisielewski, Darcy Hamill, Allison Kaeding, Soheil Meshinchi, James Olson, E. Anders Kolb, Sonali P. Barwe
Journal: Blood (2021)
Minimal Role for the Alternative Pathway in Complement Activation By HIT Immune Complexes
Authors: Ayiesha Barnes, Sanjay Khandelwal, Simone Sartoretto, Grace M Lee, Sooho Myoung, Samuel Francis, Lubica Rauova, Douglas B. Cines, Brandon Garcia, Jon Skare, Charles Booth, Gowthami M. Arepally
Journal: Blood (2021)
P-Selectin Deficiency Reduces Acute Vascular Complications but Not Chronic Organ Damage in Sickle Cell Mice
Authors: Erica Sparkenbaugh, Malgorzata Kasztan, Megan D Miller, Elizabeth A Binning, Christina M Abrams, Brandi Reeves, Prithu Sundd, Rafal Pawlinski
Journal: Blood (2021)
Novel Induction Therapy for Newly Diagnosed Extranodal Natural Killer/T Cell Lymphoma (ENKTL) Treated By Anti-PD-1 Antibody Plus Histone Deacetylase Inhibitor Followed By P-GemOx Regimen
Authors: Gao Yan, Yujing Zhang, Xiaoxiao Wang, Bing Bai, Yuhua Huang, Haixia He, Liqin Ping, Yanxia He, Cheng Huang, Jibin Li, Jiaying Mao, Huiqiang Huang
Journal: Blood (2021)
Abstract 9170: Medication Reconciliation: Much Remains to Be Done
Authors: Anas Bizanti, Ahmad Al-abdouh, Sadam Haddadin, Mohammed Mohammed, Mina Michael, Roshniben Patel, Gina Patel, Samir Ahmed, Sapna Kuehl
Journal: Circulation (2021)

Introduction: Medication reconciliation had been a persistently national patient safety issue. Despite several efforts, the rate of error is still significantly high, and the measures that had been taken to improve this process are lacking data to prove their efficacy in reducing medication errors. In this retrospective study, we will measure the efficacy of medication grouping intervention on the discharge platform ion order to reduce medication error. The intervention was grouping medication according to pharmaceutical class, in addition, bundling home and inpatient medication. Methods: This retrospective study was conducted in a single-center teaching hospital. A multidisciplinary team changed the discharge medication platform. This intervention was done in July 2019. Afterwards a total of 1395 patients were screened. The control group were 760 patients, versus 635 patients in the intervention group. Patients who were not admitted under the medical team service were excluded, and patients who had less than 7 medications on admission were also excluded. After screening, the remaining patients were subjected to detailed charting for medication error, which was done in 179 subjects in the control group vs 176 intervention groups. The primary outcome was medication error on discharge, which was measured by 2 different independent physicians. Furthermore, a subgroup analysis was done comparing residents' vs hospitalists' medication reconciliation errors on discharge. Results: A total of 329 patients were studied. In the control group, the percentage of errors noted was 42/161 (26.08%), while in the intervention group errors were noted in 37/168 patients screened (22.02%) a significant reduction of 4.06% in the percentage of errors noted. Conclusion: The electronic intervention of grouping medication by pharmaceutical class and bundling home and inpatient medication resulted in a reduction of medication error upon discharge medication reconciliation.
A Comparison of Clinical Outcomes from Updated Zuma-5 (Axicabtagene Ciloleucel) and the International Scholar-5 External Control Cohort in Relapsed/Refractory Follicular Lymphoma (R/R FL)
Authors: M. Lia Palomba, Paola Ghione, Anik R. Patel, Kevin Deighton, Caron Jacobson, Myrna Nahas, A Scott Jung, Anthony J Hatswell, Steve Kanters, Eve Limbrick-Oldfield, Sally W Wade, Julia Thornton Snider, Sattva S. Neelapu, Maria Teresa Riberio, John Gribben, John Radford, Sabela Bobillo, Herve Ghesquieres
Journal: Blood (2021)
Comprehensive Genomic Characterization of <i>ASXL1</i> C.1934dupG (p.G646fs*12) Versus Other <i>ASXL1</i> mutations in Myeloid Neoplasia
Authors: Steven M. Johnson, Lori Ramkissoon, James Haberberger, Naomi L Ferguson, Jonathan Galeotti, Daniel R. Richardson, Matthew C. Foster, Jeffrey Ross, Shakti H. Ramkissoon, Joshua F. Zeidner, Daniel Duncan, Nathan Montgomery
Journal: Blood (2021)
Abstract 9937: Three Times Higher Risk of Stroke in Adult Congenital Heart Disease on a Median Follow-Up of Over a Decade: A Global Meta-Analysis
Authors: Rupak Desai, Zainab J Gandhi, Prerna Bansal, Umarani Badarabandi, Nayana Sasidharan, Khizran Agha, NFN Hiba Ambreen, Waleed Sultan, Rishabh Jindal, Akhil Jain
Journal: Circulation (2021)

Background: With the advent of medicine, there is an increasing number of congenital heart disease survivors, which mandates assessment of the long-term risk of stroke and outcomes. We aimed to systematically review the pooled global prevalence of stroke in adults with congenital heart disease (ACHD). Methods: PubMed/Medline, SCOPUS and EMBASE were reviewed until May 2021 to ascertain articles describing stroke rates in ACHD compared to non-ACHD patients over a long follow-up (at least ≥3 years). Random effects models were used to estimate the pooled prevalence of stroke in ACHD and risk of stroke in ACHD vs non ACHD. Heterogeneity was assessed using the I 2 statistics with &gt;75% value suggesting substantial heterogeneity, for which subgroup analysis was performed. Results: We included 14 studies comprising 96,626 participants with ACHD and 751,460 without ACHD. The overall pooled prevalence of stroke in ACHD was 3.7% (95CI 2.5%-5.0%, I 2 = 99%) over a median follow-up period of 11.5 years ( Fig. 1a ). The ACHD patients showed nearly 3 times higher risk of stroke [OR 3.11 (95% CI 2.09-4.63), I 2 =97.99%, p&lt;0.01] on 11.5 years median follow-up ( Fig. 1b ). On subgroup analysis, studies with older ACHD patients showed nearly two times higher rate of stroke compared to studies with younger patients (mean age&gt;40 years: 4.8% vs. mean age ≤40 years, 2.6%). Furthermore, the prevalence of stroke was higher among the ACHD cohorts with shorter median follow-up (&lt;10 years) vs. studies with a median follow-up of &gt;10 years [5.0% vs 3.0%]. Studies published from Denmark (4.5%) and Canada/USA (3.2%) revealed greater rates of stroke in ACHD than the studies from Sweden (2.8%). Conclusion: This meta-analysis found nearly three times higher risk of stroke in ACHD patients over a decade follow-up compared to controls. The demographic, chronological and regional variation of the stroke prevalence in ACHD indicates that the risk could be multifactorial and warrants further risk stratification measures