tbuckley/cabot-search huggingface dataset:
Single-cell analysis of somatic mutations in human bronchial epithelial cells in relation to aging and smoking
Authors: Zhenqiu Huang, Shixiang Sun, Moonsook Lee, Alexander Y. Maslov, Miao Shi, Spencer Waldman, Ava Marsh, Taha Siddiqui, Xiao Dong, Yakov Peter, Ali Sadoughi, Chirag Shah, Kenny Ye, Simon D. Spivack, Jan Vijg
Journal: Nature Genetics (2022)
Demographic Differences Among US Department of Veterans Affairs Patients Referred for Genetic Consultation to a Centralized VA Telehealth Program, VA Medical Centers, or the Community
Authors: Maren T. Scheuner, Alexis K. Huynh, Catherine Chanfreau-Coffinier, Barbara Lerner, Alicia R. Gable, Martin Lee, Alissa Simon, Randall Coeshott, Alison B. Hamilton, Olga V. Patterson, Scott DuVall, Marcia M. Russell
Journal: JAMA Network Open (2022)

Telehealth enables access to genetics clinicians, but impact on care coordination is unknown.
CCR2/CCR5 inhibitor permits the radiation-induced effector T cell infiltration in pancreatic adenocarcinoma
Authors: Jianxin Wang, May Tun Saung, Keyu Li, Juan Fu, Kenji Fujiwara, Nan Niu, Stephen Muth, Junke Wang, Yao Xu, Noah Rozich, Haley Zlomke, Sophia Chen, Birginia Espinoza, MacKenzie Henderson, Vanessa Funes, Brian Herbst, Ding Ding, Christina Twyman-Saint Victor, Qihong Zhao, Amol Narang, Jin He, Lei Zheng
Journal: The Journal of Experimental Medicine (2022)

The resistance of pancreatic ductal adenocarcinoma (PDAC) to immune checkpoint inhibitors (ICIs) is attributed to the immune-quiescent and -suppressive tumor microenvironment (TME). We recently found that CCR2 and CCR5 were induced in PDAC following treatment with anti-PD-1 antibody (αPD-1); thus, we examined PDAC vaccine or radiation therapy (RT) as T cell priming mechanisms together with BMS-687681, a dual antagonist of CCR2 and CCR5 (CCR2/5i), in combination with αPD-1 as new treatment strategies. Using PDAC mouse models, we demonstrated that RT followed by αPD-1 and prolonged treatment with CCR2/5i conferred better antitumor efficacy than other combination treatments tested. The combination of RT + αPD-1 + CCR2/5i enhanced intratumoral effector and memory T cell infiltration but suppressed regulatory T cell, M2-like tumor-associated macrophage, and myeloid-derived suppressive cell infiltration. RNA sequencing showed that CCR2/5i partially inhibited RT-induced TLR2/4 and RAGE signaling, leading to decreased expression of immunosuppressive cytokines including CCL2/CCL5, but increased expression of effector T cell chemokines such as CCL17/CCL22. This study thus supports the clinical development of CCR2/5i in combination with RT and ICIs for PDAC treatment.
COVID-19 Vaccine Uptake and Intentions Following US Food and Drug Administration Approval of the Pfizer-BioNTech COVID-19 Vaccine
Authors: Aaron M. Scherer, Andrew M. Parker, Courtney A. Gidengil, Amber M. Gedlinske, Natoshia M. Askelson, Christine A. Petersen, Megan C. Lindley
Journal: JAMA Internal Medicine (2022)

This survey study assesses vaccination intentions of unvaccinated US adults in response to full US Food and Drug Administration (FDA) approval of the BNT162b2 (Pfizer-BioNTech) COVID-19 vaccine and any demographic characteristics associated with those intentions.
SREBP1c-PARP1 axis tunes anti-senescence activity of adipocytes and ameliorates metabolic imbalance in obesity
Authors: Gung Lee, Ye Young Kim, Hagoon Jang, Ji Seul Han, Hahn Nahmgoong, Yoon Jeong Park, Sang Mun Han, Changyun Cho, Sangsoo Lim, Jung-Ran Noh, Won Keun Oh, Chul-Ho Lee, Sun Kim, Jae Bum Kim
Journal: Cell Metabolism (2022)
Psychosocial Interventions for the Treatment of Functional Abdominal Pain Disorders in Children
Authors: Morris Gordon, Vassiliki Sinopoulou, Merit Tabbers, Robyn Rexwinkel, Clara de Bruijn, Terence Dovey, Marco Gasparetto, Helen Vanker, Marc Benninga
Journal: JAMA Pediatrics (2022)

Functional abdominal pain disorders (FAPDs) can severely affect the life of children and their families, with symptoms carrying into adulthood. Management of FADP symptoms is also a financial and time burden to clinicians and health care systems.
Targeting Podoplanin for the Treatment of Osteosarcoma
Authors: Ai Takemoto, Satoshi Takagi, Takao Ukaji, Nobuhiko Gyobu, Mamoru Kakino, Miho Takami, Asami Kobayashi, Marie Lebel, Tokuichi Kawaguchi, Minoru Sugawara, Kazue Tsuji-Takayama, Kenji Ichihara, Yuki Funauchi, Keisuke Ae, Seiichi Matsumoto, Yoshiya Sugiura, Kengo Takeuchi, Tetsuo Noda, Ryohei Katayama, Naoya Fujita
Journal: Clinical Cancer Research (2022)

Abstract Purpose: Osteosarcoma, the most common bone malignancy in children, has a poor prognosis, especially when the tumor metastasizes to the lungs. Therefore, novel therapeutic strategies targeting both proliferation and metastasis of osteosarcoma are required. Podoplanin (PDPN) is expressed by various tumors and is associated with tumor-induced platelet activation via its interaction with C-type lectin-like receptor 2 (CLEC-2) on platelets. We previously found that PDPN contributed to osteosarcoma growth and metastasis through platelet activation; thus, in this study, we developed an anti-PDPN humanized antibody and evaluated its effect on osteosarcoma growth and metastasis. Experimental Design: Nine osteosarcoma cell lines and two osteosarcoma patient-derived cells were collected, and we evaluated the efficacy of the anti-DPN-neutralizing antibody PG4D2 and the humanized anti-PDPN antibody AP201, which had IgG4 framework region. The antitumor and antimetastasis effect of PG4D2 and AP201 were examined in vitro and in vivo. In addition, growth signaling by the interaction between PDPN and CLEC-2 was analyzed using phospho-RTK (receptor tyrosine kinase) array, growth assay, or immunoblot analysis under the supression of RTKs by knockout and inhibitor treatment. Results: We observed that PG4D2 treatment significantly suppressed tumor growth and pulmonary metastasis in osteosarcoma xenograft models highly expressing PDPN. The contribution of PDGFR activation by activated platelet releasates to osteosarcoma cell proliferation was confirmed, and the humanized antibody, AP201, suppressed in vivo osteosarcoma growth and metastasis without significant adverse events. Conclusions: Targeting PDPN with a neutralizing antibody against PDPN–CLEC-2 without antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity is a novel therapeutic strategy for PDPN-positive osteosarcoma.
Impact of Allocation on Survival During Intermittent Chemotherapy Shortages: A Modeling Analysis
Authors: Andrew Hantel, Michael L. McManus, Martha Wadleigh, Michael Cotugno, Gregory A. Abel
Journal: Journal of the National Comprehensive Cancer Network (2022)

Background: Intermittent shortages of chemotherapeutics used to treat curable malignancies are a worldwide problem that increases patient mortality. Although multiple strategies have been proposed for managing these shortages (eg, prioritizing patients by age, scarce treatment efficacy per volume, alternative treatment efficacy difference), critical clinical dilemmas arise when selecting a management strategy and understanding its impact. Patients and Methods: We developed a model to compare the impact of different allocation strategies on overall survival during intermittent chemotherapy shortages and tested it using vincristine, which was recently scarce for 9 months in the United States. Demographic and treatment data were abstracted from 1,689 previously treated patients in our tertiary-care system; alternatives were abstracted from NCCN Clinical Practice Guidelines in Oncology for each disease and survival probabilities from the studies cited therein. Modeled survival was validated using SEER data. Nine-month shortages were modeled for all possible supply levels. Pairwise differences in 3-year survival and risk reductions were calculated for each strategy compared with standard practice (first-come, first-served) for each 50-mg supply increment, as were supply thresholds above which each strategy maintained survival similar to scenarios without shortages. Results: A strategy prioritizing by higher vincristine efficacy per volume and greater alternative treatment efficacy difference performed best, improving survival significantly ( P &lt;.01) across 86.5% of possible shortages (relative risk reduction, 8.3%; 99% CI, 8.0–8.5) compared with standard practice. This strategy also maintained survival rates similar to a model without shortages until supply fell below 72.2% of the amount required to treat all patients, compared with 94.3% for standard practice. Conclusions: During modeled vincristine shortages, prioritizing patients by higher efficacy per volume and alternative treatment efficacy difference significantly improved survival over standard practice. This approach can help optimize allocation as intermittent chemotherapy shortages continue to arise.
ROS-responsive 18β-glycyrrhetic acid-conjugated polymeric nanoparticles mediate neuroprotection in ischemic stroke through HMGB1 inhibition and microglia polarization regulation
Authors: Lulu Jin, Zhixin Zhu, Liangjie Hong, Zhefeng Qian, Fang Wang, Zhengwei Mao
Journal: Bioactive Materials (2022)

Ischemic stroke is an acute and serious cerebral vascular disease, which greatly affects people's health and brings huge economic burden to society. Microglia, as important innate immune components in central nervous system (CNS), are double-edged swords in the battle of nerve injury, considering their polarization between pro-inflammatory M1 or anti-inflammatory M2 phenotypes. High mobility group box 1 (HMGB1) is one of the potent pro-inflammatory mediators that promotes the M1 polarization of microglia. 18β-glycyrrhetinic acid (GA) is an effective intracellular inhibitor of HMGB1, but of poor water solubility and dose-dependent toxicity. To overcome the shortcomings of GA delivery and to improve the efficacy of cerebral ischemia therapy, herein, we designed reactive oxygen species (ROS) responsive polymer-drug conjugate nanoparticles (DGA) to manipulate microglia polarization by suppressing the translocation of nuclear HMGB1. DGA presented excellent therapeutic efficacy in stroke mice, as evidenced by the reduction of infarct volume, recovery of motor function, suppressed of M1 microglia activation and enhanced M2 activation, and induction of neurogenesis. Altogether, our work demonstrates a close association between HMGB1 and microglia polarization, suggesting potential strategies for coping with inflammatory microglia-related diseases.
2D Molybdenum Sulfide‐Based Materials for Photo‐Excited Antibacterial Application
Authors: Fangqian Chen, Yue Luo, Xiangmei Liu, Yufeng Zheng, Yong Han, Dapeng Yang, Shuilin Wu
Journal: Advanced Healthcare Materials (2022)

Abstract Bacterial infections have seriously threatened human health and the abuse of natural or artificial antibiotics leads to bacterial resistance, so development of a new generation of antibacterial agents and treatment methods is urgent. 2D molybdenum sulfide (MoS 2 ) has good biocompatibility, high specific surface area to facilitate surface modification and drug loading, adjustable energy bandgap, and high near‐infrared photothermal conversion efficiency (PCE), so it is often used for antibacterial application through its photothermal or photodynamic effects. This review comprehensively summarizes and discusses the fabrication processes, structural characteristics, antibacterial performance, and the corresponding mechanisms of MoS 2 ‐based materials as well as their representative antibacterial applications. In addition, the outlooks on the remaining challenges that should be addressed in the field of MoS 2 are also proposed.
Meaningful Evidence for Anticoagulation in the Gray (Elder) Zone
Authors: Karen P. Alexander
Journal: JAMA Cardiology (2022)

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Tracking of lung function from 10 to 35 years after being born extremely preterm or with extremely low birth weight
Authors: Tonje Bårdsen, Ola Drange Røksund, Merete Røineland Benestad, Karl Ove Hufthammer, Hege Havstad Clemm, Ingvild Bruun Mikalsen, Knut Øymar, Trond Markestad, Thomas Halvorsen, Maria Vollsæter
Journal: Thorax (2022)

Background Lifelong pulmonary consequences of being born extremely preterm or with extremely low birth weight remain unknown. We aimed to describe lung function trajectories from 10 to 35 years of age for individuals born extremely preterm, and address potential cohort effects over a period that encompassed major changes in perinatal care. Methods We performed repeated spirometry in three population-based cohorts born at gestational age ≤28 weeks or with birth weight ≤1000 g during 1982–85, 1991–92 and 1999–2000, referred to as extremely preterm-born, and in term-born controls matched for age and gender. Examinations were performed at 10, 18, 25 and 35 years. Longitudinal data were analysed using mixed models regression, with the extremely preterm-born stratified by bronchopulmonary dysplasia (BPD). Results We recruited 148/174 (85%) eligible extremely preterm-born and 138 term-born. Compared with term-born, the extremely preterm-born had lower z-scores for forced expiratory volume in 1 s (FEV 1 ) at most assessments, the main exceptions were in the groups without BPD in the two youngest cohorts. FEV 1 trajectories were largely parallel for the extremely preterm- and term-born, also during the period 25–35 years that includes the onset of the age-related decline in lung function. Extremely preterm-born had lower peak lung function than term-born, but z-FEV 1 values improved for each consecutive decade of birth (p = 0.009). More extremely preterm—than term-born fulfilled the spirometry criteria for chronic obstructive pulmonary disease, 44/148 (30%) vs 7/138 (5%), p &lt; 0.001. Conclusions Lung function after extremely preterm birth tracked in parallel, but significantly below the trajectories of term-born from 10 to 35 years, including the incipient age-related decline from 25 to 35 years. The deficits versus term-born decreased with each decade of birth from 1980 to 2000.
Discovery, Preclinical Characterization, and Early Clinical Activity of JDQ443, a Structurally Novel, Potent, and Selective Covalent Oral Inhibitor of KRASG12C
Authors: Andreas Weiss, Edwige Lorthiois, Louise Barys, Kim S. Beyer, Claudio Bomio-Confaglia, Heather Burks, Xueying Chen, Xiaoming Cui, Ruben de Kanter, Lekshmi Dharmarajan, Carmine Fedele, Marc Gerspacher, Daniel Alexander Guthy, Victoria Head, Ashley Jaeger, Eloísa Jiménez Núñez, Jeffrey D. Kearns, Catherine Leblanc, Sauveur-Michel Maira, Jason Murphy, Helen Oakman, Nils Ostermann, Johannes Ottl, Pascal Rigollier, Danielle Roman, Christian Schnell, Richard Sedrani, Toshio Shimizu, Rowan Stringer, Andrea Vaupel, Hans Voshol, Peter Wessels, Toni Widmer, Rainer Wilcken, Kun Xu, Frederic Zecri, Anna F. Farago, Simona Cotesta, Saskia M. Brachmann
Journal: Cancer Discovery (2022)

Covalent inhibitors of KRASG12C have shown antitumor activity against advanced/metastatic KRASG12C-mutated cancers, though resistance emerges and additional strategies are needed to improve outcomes. JDQ443 is a structurally unique covalent inhibitor of GDP-bound KRASG12C that forms novel interactions with the switch II pocket. JDQ443 potently inhibits KRASG12C-driven cellular signaling and demonstrates selective antiproliferative activity in KRASG12C-mutated cell lines, including those with G12C/H95 double mutations. In vivo, JDQ443 induces AUC exposure-driven antitumor efficacy in KRASG12C-mutated cell-derived (CDX) and patient-derived (PDX) tumor xenografts. In PDX models, single-agent JDQ443 activity is enhanced by combination with inhibitors of SHP2, MEK, or CDK4/6. Notably, the benefit of JDQ443 plus the SHP2 inhibitor TNO155 is maintained at reduced doses of either agent in CDX models, consistent with mechanistic synergy. JDQ443 is in clinical development as monotherapy and in combination with TNO155, with both strategies showing antitumor activity in patients with KRASG12C-mutated tumors. JDQ443 is a structurally novel covalent KRASG12C inhibitor with a unique binding mode that demonstrates potent and selective antitumor activity in cell lines and in vivo models. In preclinical models and patients with KRASG12C-mutated malignancies, JDQ443 shows potent antitumor activity as monotherapy and in combination with the SHP2 inhibitor TNO155. This article is highlighted in the In This Issue feature, p. 1397.
Patchwork Cancer Predisposition
Authors: L. Alexander Liggett, Vijay G. Sankaran
Journal: Cancer Discovery (2022)

Summary: Inherited genetic variation is increasingly identified as an important predisposing factor to a variety of cancers. In this issue of Cancer Discovery, Pareja and colleagues developed a method of reliably detecting mosaic cancer susceptibility mutations in patients who have been sequenced as part of the MSK-IMPACT tumor profiling platform. This led to the identification of a number of mosaic mutations in cancer susceptibility alleles that are generally found in the germline, suggesting that many predisposition variants may be missed through conventional testing. See related article by Pareja et al., p. 949 (6).
Glucocorticoid receptor modulates myeloid-derived suppressor cell function via mitochondrial metabolism in immune thrombocytopenia
Authors: Yu Hou, Jie Xie, Shuwen Wang, Daqi Li, Lingjun Wang, Haoyi Wang, Xiaofei Ni, Shaoqiu Leng, Guosheng Li, Ming Hou, Jun Peng
Journal: Cellular and Molecular Immunology (2022)
Impaired neurogenesis alters brain biomechanics in a neuroprogenitor-based genetic subtype of congenital hydrocephalus
Authors: Phan Q. Duy, Stefan C. Weise, Claudia Marini, Xiao-Jun Li, Dan Liang, Peter J. Dahl, Shaojie Ma, Ana Spajic, Weilai Dong, Jane Juusola, Emre Kiziltug, Adam J. Kundishora, Sunil Koundal, Maysam Z. Pedram, Lucia A. Torres-Fernández, Kristian Händler, Elena De Domenico, Matthias Becker, Thomas Ulas, Stefan A. Juranek, Elisa Cuevas, Le Thi Hao, Bettina Jux, André M. M. Sousa, Fuchen Liu, Suel-Kee Kim, Mingfeng Li, Yiying Yang, Yutaka Takeo, Alvaro Duque, Carol Nelson-Williams, Yonghyun Ha, Kartiga Selvaganesan, Stephanie M. Robert, Amrita K. Singh, Garrett Allington, Charuta G. Furey, Andrew T. Timberlake, Benjamin C. Reeves, Hannah Smith, Ashley Dunbar, Tyrone DeSpenza, June Goto, Arnaud Marlier, Andres Moreno-De-Luca, Xin Yu, William E. Butler, Bob S. Carter, Evelyn M. R. Lake, R. Todd Constable, Pasko Rakic, Haifan Lin, Engin Deniz, Helene Benveniste, Nikhil S. Malvankar, Juvianee I. Estrada-Veras, Christopher A. Walsh, Seth L. Alper, Joachim L. Schultze, Katrin Paeschke, Angelika Doetzlhofer, F. Gregory Wulczyn, Sheng Chih Jin, Richard P. Lifton, Nenad Sestan, Waldemar Kolanus, Kristopher T. Kahle
Journal: Nature Neuroscience (2022)
Nosocomial septicemia in COVID-19 nosocomial K. pneumoniae, A. baumannii, and Elizabethkingia meningoseptica septicemia in a patient of COVID-19
Authors: Jie Ywi Ong, Cheng-Hui Wang, Yi-San Tsai, Fu-Lun Chen, Chih-Hsin Lee, Tsong-Yih Ou
Journal: Journal of Infection (2022)
Leveraging fine-mapping and multipopulation training data to improve cross-population polygenic risk scores
Authors: Omer Weissbrod, Masahiro Kanai, Huwenbo Shi, Steven Gazal, Wouter J. Peyrot, Amit V. Khera, Yukinori Okada, Koichi Matsuda, Yuji Yamanashi, Yoichi Furukawa, Takayuki Morisaki, Yoshinori Murakami, Yoichiro Kamatani, Kaori Muto, Akiko Nagai, Wataru Obara, Ken Yamaji, Kazuhisa Takahashi, Satoshi Asai, Yasuo Takahashi, Takao Suzuki, Nobuaki Sinozaki, Hiroki Yamaguchi, Shiro Minami, Shigeo Murayama, Kozo Yoshimori, Satoshi Nagayama, Daisuke Obata, Masahiko Higashiyama, Akihide Masumoto, Yukihiro Koretsune, Alicia R. Martin, Hilary K. Finucane, Alkes L. Price
Journal: Nature Genetics (2022)
TCTAP C-056 Front Door, Back Door? Keep Knocking Until One Door Opens: Percutaneous Coronary Angioplasty to a Chronically Occluded Right Coronary Artery Via Multiple Antegrade and Retrograde Approaches
Authors: Khai Chih Teh, Siti Dalila Adnan, Jayakhanthan Kolanthaivelu, Shaiful Azmi Yahaya
Journal: Journal of the American College of Cardiology (2022)
Fuzuloparib Maintenance Therapy in Patients With Platinum-Sensitive, Recurrent Ovarian Carcinoma (FZOCUS-2): A Multicenter, Randomized, Double-Blind, Placebo-Controlled, Phase III Trial
Authors: Ning Li, Youzhong Zhang, Jing Wang, Jianqing Zhu, Li Wang, Xiaohua Wu, Desheng Yao, Qiang Wu, Jihong Liu, Junying Tang, Rutie Yin, Ge Lou, Ruifang An, Guonan Zhang, Xiaoping Xia, Qingshui Li, Yaping Zhu, Hong Zheng, Xinfeng Yang, Yuanjing Hu, Xin Zhang, Min Hao, Yi Huang, Zhongqiu Lin, Dong Wang, Xiaoqing Guo, Shuzhong Yao, Xiaoyun Wan, Huaijun Zhou, Liangqing Yao, Xielan Yang, Heng Cui, Yuanguang Meng, Songling Zhang, Jing Qu, Ben Zhang, Jianjun Zou, Lingying Wu
Journal: Journal of Clinical Oncology (2022)

This phase III trial aimed to explore the efficacy and safety of fuzuloparib (formerly fluzoparib) versus placebo as a maintenance treatment after response to second- or later-line platinum-based chemotherapy in patients with high-grade, platinum-sensitive, recurrent ovarian cancer.Patients with platinum-sensitive, recurrent ovarian cancer previously treated with at least two platinum-based regimens were assigned (2:1) to receive fuzuloparib (150 mg, twice daily) or matching placebo for 28-day cycles. The primary end points were progression-free survival (PFS) assessed by blinded independent review committee (BIRC) in the overall population and PFS by BIRC in the subpopulation with germline BRCA 1/2 mutation.Between April 30, 2019, and January 10, 2020, 252 patients were randomly assigned to the fuzuloparib (n = 167) or placebo (n = 85). As of July 1, 2020, the median PFS per BIRC assessment in the overall population was significantly improved with fuzuloparib treatment (hazard ratio [HR], 0.25; 95% CI, 0.17 to 0.36; one-sided P < .0001) compared with that with placebo. The HR derived from a prespecified subgroup analysis showed a consistent trend of benefit in patients with germline BRCA 1/2 mutations (HR, 0.14; 95% CI, 0.07 to 0.28) or in those without mutations (HR, 0.46; 95% CI, 0.29 to 0.74). The most common grade ≥ 3 treatment-emergent adverse events reported in the fuzuloparib group were anemia (25.1%), decreased platelet count (16.8%), and decreased neutrophil count (12.6%). Only one patient (0.6%) discontinued fuzuloparib because of treatment-related toxicity (concurrent decreased white blood cell count and neutrophil count).Fuzuloparib as maintenance therapy achieved a statistically significant and clinically meaningful improvement in PFS for patients with platinum-sensitive, recurrent ovarian cancer versus placebo, regardless of germline BRCA 1/2 mutation, and showed a manageable safety profile.