tbuckley/cabot-search huggingface dataset:
COVID-19 among fit patients with CLL treated with venetoclax-based combinations
Authors: Moritz Fürstenau, Petra Langerbeins, Nisha De Silva, Anna Maria Fink, Sandra Robrecht, Julia von Tresckow, Florian Simon, Karin Hohloch, Jolanda Droogendijk, Marjolein van der Klift, Ellen van der Spek, Thomas Illmer, Björn Schöttker, Kirsten Fischer, Clemens M. Wendtner, Eugen Tausch, Stephan Stilgenbauer, Carsten U. Niemann, Michael Gregor, Arnon P. Kater, Michael Hallek, Barbara Eichhorst
Journal: Leukemia (2020)
Transcriptome analysis reveals two distinct endotypes and putative immune pathways in tonsils from children with periodic fever, aphthous stomatitis, pharyngitis, and cervical adenitis syndrome
Authors: Mariko Hara, Noriko Morimoto, Noriomi Suzuki, Nana Tsuchihashi, Manabu Komori, Keisuke Yoshihama, Kae Fujii, Sota Yamaguchi, Mayumi Tsunoda, Syuta Tomisato, Nozomi Takahashi, Koichiro Oyake, Yuzuru Okuba, Mikiya Fujieda, Kenji Matsumoto
Journal: Allergy (2020)

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Identification of Recurrent TERT Promoter Mutations in Intrathyroid Thymic Carcinomas
Authors: Ippei Tahara, Naoki Oishi, Kunio Mochizuki, Toshio Oyama, Kazuyuki Miyata, Akira Miyauchi, Mitsuyoshi Hirokawa, Ryohei Katoh, Tetsuo Kondo
Journal: Endocrine Pathology (2020)
A Single Load of Fructose Attenuates the Risk of Exercise-Induced Hypoglycemia in Adults With Type 1 Diabetes on Ultra-Long-Acting Basal Insulin: A Randomized, Open-Label, Crossover Proof-of-Principle Study
Authors: Christophe Kosinski, David Herzig, Céline Isabelle Laesser, Christos T. Nakas, Andreas Melmer, Andreas Vogt, Bruno Vogt, Markus Laimer, Lia Bally, Christoph Stettler
Journal: Diabetes Care (2020)

While the adjustment of insulin is an established strategy to reduce the risk of exercise-associated hypoglycemia for individuals with type 1 diabetes, it is not easily feasible for those treated with ultra-long-acting basal insulin. The current study determined whether pre-exercise intake of fructose attenuates the risk of exercise-induced hypoglycemia in individuals with type 1 diabetes using insulin degludec.Fourteen male adults with type 1 diabetes completed two 60-min aerobic cycling sessions with or without prior intake (30 min) of 20 g of fructose, in a randomized two-period crossover design. Exercise was performed in the morning in a fasted state without prior insulin reduction and after 48 h of standardized diet. The primary outcome was time to hypoglycemia (plasma glucose ≤3.9 mmol/L) during exercise.Intake of fructose resulted in one hypoglycemic event at 60 min compared with six hypoglycemic events at 27.5 ± 9.4 min of exercise in the control condition, translating into a risk reduction of 87.8% (hazard ratio 0.12 [95% CI 0.02, 0.66]; P = 0.015). Mean plasma glucose during exercise was 7.3 ± 1.4 mmol/L with fructose and 5.5 ± 1.1 mmol/L in the control group (P < 0.001). Lactate levels were higher at rest in the 30 min following fructose intake (P < 0.001) but were not significantly different from the control group during exercise (P = 0.32). Substrate oxidation during exercise did not significantly differ between the conditions (P = 0.73 for carbohydrate and P = 0.48 for fat oxidation). Fructose was well tolerated.Pre-exercise intake of fructose is an easily feasible, effective, and well-tolerated strategy to alleviate the risk of exercise-induced hypoglycemia while avoiding hyperglycemia in individuals with type 1 diabetes on ultra-long-acting insulin.
Recent Common Origin, Reduced Population Size, and Marked Admixture Have Shaped European Roma Genomes
Authors: Erica Bianco, Guillaume Laval, Neus Font-Porterias, Carla García-Fernández, Begoña Dobon, Rubén Sabido-Vera, Emilija Sukarova Stefanovska, Vaidutis Kučinskas, Halyna Makukh, Horolma Pamjav, Lluis Quintana-Murci, Mihai G Netea, Jaume Bertranpetit, Francesc Calafell, David Comas
Journal: Molecular Biology and Evolution (2020)

Abstract The Roma Diaspora—traditionally known as Gypsies—remains among the least explored population migratory events in historical times. It involved the migration of Roma ancestors out-of-India through the plateaus of Western Asia ultimately reaching Europe. The demographic effects of the Diaspora—bottlenecks, endogamy, and gene flow—might have left marked molecular traces in the Roma genomes. Here, we analyze the whole-genome sequence of 46 Roma individuals pertaining to four migrant groups in six European countries. Our analyses revealed a strong, early founder effect followed by a drastic reduction of ∼44% in effective population size. The Roma common ancestors split from the Punjabi population, from Northwest India, some generations before the Diaspora started, &amp;lt;2,000 years ago. The initial bottleneck and subsequent endogamy are revealed by the occurrence of extensive runs of homozygosity and identity-by-descent segments in all Roma populations. Furthermore, we provide evidence of gene flow from Armenian and Anatolian groups in present-day Roma, although the primary contribution to Roma gene pool comes from non-Roma Europeans, which accounts for &amp;gt;50% of their genomes. The linguistic and historical differentiation of Roma in migrant groups is confirmed by the differential proportion, but not a differential source, of European admixture in the Roma groups, which shows a westward cline. In the present study, we found that despite the strong admixture Roma had in their diaspora, the signature of the initial bottleneck and the subsequent endogamy is still present in Roma genomes.
U.S. Phase I First-in-human Study of Taletrectinib (DS-6051b/AB-106), a ROS1/TRK Inhibitor, in Patients with Advanced Solid Tumors
Authors: Kyriakos P. Papadopoulos, Erkut Borazanci, Alice T. Shaw, Ryohei Katayama, Yuki Shimizu, Viola W. Zhu, Thomas Yang Sun, Heather A. Wakelee, Russell Madison, Alexa B. Schrock, Giorgio Senaldi, Naoki Nakao, Hiroyuki Hanzawa, Masaya Tachibana, Takeshi Isoyama, Kenji Nakamaru, Chenhui Deng, Meijing Li, Frank Fan, Qinying Zhao, Yanfei Gao, Takashi Seto, Pasi A. Jänne, Sai-Hong Ignatius Ou
Journal: Clinical Cancer Research (2020)

Taletrectinib (DS-6051b/AB-106) is an oral, tyrosine kinase inhibitor of ROS1 and NTRK with potent preclinical activity against ROS1 G2032R solvent-front mutation among others. We report the first-in-human U.S. phase I results of taletrectinib.Patients ≥18 years old with neuroendocrine tumors, with tumor-induced pain, or tumors harboring ROS1/NTRK rearrangements were eligible. Accelerated titration followed by modified continuous reassessment method and escalation with overdose control was used (50-1,200 mg once daily or 400 mg twice daily). Primary objectives were safety/tolerability, and MTD determination. Secondary objectives were food-effect pharmacokinetics and antitumor activity.A total of 46 patients were enrolled. Steady-state peak concentration (Cmax) and exposure (AUC0-8) increased dose dependently from 50-mg to 800-mg once-daily doses. The ratio of the geometric mean of AUC0-24 between low-fat-diet-fed/fasted state was 123% (90% confidence interval, 104%-149%). Dose-limiting toxicities (grade 3 transaminases increase) occurred in two patients (1,200-mg once-daily dose). MTD was 800 mg once daily. Most common treatment-related adverse events were nausea (47.8%), diarrhea (43.5%), and vomiting (32.6%). Pain score reductions were observed in the 800-mg once-daily dose cohort. Confirmed objective response rate was 33.3% among the six patients with RECIST-evaluable crizotinib-refractory ROS1+ NSCLC. One patient with TPM3-NTRK1 differentiated thyroid cancer achieving a confirmed partial response of 27 months at data cutoff. We identified a cabozantinib-sensitive ROS1 L2086F as an acquired taletrectinib-resistance mutation.Taletrectinib has manageable toxicities at the MTD of 800 mg daily. Preliminary efficacy was observed in patients with crizotinib-refractory ROS1+ NSCLC.
A CLN6-CLN8 complex recruits lysosomal enzymes at the ER for Golgi transfer
Authors: Lakshya Bajaj, Jaiprakash Sharma, Alberto di Ronza, Pengcheng Zhang, Aiden Eblimit, Rituraj Pal, Dany Roman, John R. Collette, Clarissa Booth, Kevin T. Chang, Richard N. Sifers, Sung Y. Jung, Jill M. Weimer, Rui Chen, Randy W. Schekman, Marco Sardiello
Journal: Journal of Clinical Investigation (2020)

Lysosomal enzymes are synthesized in the endoplasmic reticulum (ER) and transferred to the Golgi complex by interaction with the Batten disease protein CLN8 (ceroid lipofuscinosis, neuronal, 8). Here we investigated the relationship of this pathway with CLN6, an ER-associated protein of unknown function that is defective in a different Batten disease subtype. Experiments focused on protein interaction and trafficking identified CLN6 as an obligate component of a CLN6-CLN8 complex (herein referred to as EGRESS: ER-to-Golgi relaying of enzymes of the lysosomal system), which recruits lysosomal enzymes at the ER to promote their Golgi transfer. Mutagenesis experiments showed that the second luminal loop of CLN6 is required for the interaction of CLN6 with the enzymes but dispensable for interaction with CLN8. In vitro and in vivo studies showed that CLN6 deficiency results in inefficient ER export of lysosomal enzymes and diminished levels of the enzymes at the lysosome. Mice lacking both CLN6 and CLN8 did not display aggravated pathology compared with the single deficiencies, indicating that the EGRESS complex works as a functional unit. These results identify CLN6 and the EGRESS complex as key players in lysosome biogenesis and shed light on the molecular etiology of Batten disease caused by defects in CLN6.
International Consensus on Antineutrophil Cytoplasm Antibodies Testing in Eosinophilic Granulomatosis with Polyangiitis
Authors: Sergey Moiseev, Xavier Bossuyt, Yoshihiro Arimura, Daniel Blockmans, Elena Csernok, Jan Damoiseaux, Giacomo Emmi, Luis Felipe Flores-Suárez, Bernhard Hellmich, David Jayne, J. Charles Jennette, Mark A. Little, Aladdin J. Mohammad, Frank Moosig, Pavel Novikov, Christian Pagnoux, Antonella Radice, Ken-ei Sada, Mårten Segelmark, Yehuda Shoenfeld, Renato A. Sinico, Ulrich Specks, Benjamin Terrier, Athanasios G. Tzioufas, Augusto Vaglio, Ming-Hui Zhao, Jan Willem Cohen Tervaert, Fabian Arndt, Allyson Egan, Jean-Emmanuel Kahn, Anna Kernder, Alfred Mahr, Julian Mahrhold, Chiara Marvisi, Thomas Neumann, Domenico Prisco, Carlo Salvarani, Franco Schiavon, Arianna Troilo, Maria L. Urban, Nils Venhoff
Journal: American Journal of Respiratory and Critical Care Medicine (2020)

Section:ChooseTop of pageAbstract <<Table of ContentsMethodsPrevalence of ANCA in Pat...Clinical Value of ANCA in...MPO-ANCA as a Classificat...MPO-ANCA as a Guide for T...ANCA MonitoringConclusionsReferencesCITING ARTICLES
Low-dose L-NAME induces salt sensitivity associated with sustained increased blood volume and sodium-chloride cotransporter activity in rodents
Authors: Conghui Wang, Fumiko Kawakami-Mori, Lei Kang, Nobuhiro Ayuzawa, Sayoko Ogura, Suang Suang Koid, Latapati Reheman, Alimila Yeerbolati, Beibei Liu, Yutaka Yatomi, Xiangmei Chen, Toshiro Fujita, Tatsuo Shimosawa
Journal: Kidney International (2020)

To investigate the cause of salt sensitivity in a normotensive animal model, we treated rats with a low-dose of the nitric oxide synthase inhibitor, L-NAME, that does not elevate blood pressure per se or induce kidney fibrosis. A high salt diet increased the circulating blood volume both in L-NAME-treated and nontreated animals for the first 24 hours. Thereafter, the blood volume increase persisted only in the L-NAME-treated rats. Blood pressure was higher in the L-NAME-treated group from the start of high salt diet exposure. Within the first 24 hours of salt loading, the L-NAME treated animals failed to show vasodilation and maintained high systemic vascular resistance in response to blood volume expansion. After four weeks on the high salt diet, the slope of the pressure-natriuresis curve was blunted in the L-NAME-treated group. An increase in natriuresis was observed after treatment with hydrochlorothiazide, but not amiloride, a change observed in parallel with increased phosphorylated sodium-chloride cotransporter (NCC). In contrast, a change in blood pressure was not observed in L-NAME-treated NCC-deficient mice fed a high salt diet. Moreover, direct L-NAME-induced NCC activation was demonstrated in cells of the mouse distal convoluted tubule. The vasodilatator, sodium nitroprusside, downregulated phosphorylated NCC expression. The effect of L-NAME on phosphorylated NCC was blocked by both the SPAK inhibitor STOCK2S-26016 and the superoxide dismutase mimetic TEMPO which also attenuated salt-induced hypertension. These results suggest that the initiation of salt sensitivity in normotensive rodents could be due to hyporeactivity of the vasculature and that maintaining blood pressure could result in a high circulating volume due to inappropriate NCC activity in the low-dose L-NAME model. Thus, even slightly impaired nitric oxide production may be important in salt sensitivity regulation in healthy rodents.
Epithelial-derived gasdermin D mediates nonlytic IL-1β release during experimental colitis
Authors: Katarzyna Bulek, Junjie Zhao, Yun Liao, Nitish Rana, Daniele Corridoni, Agne Antanaviciute, Xing Chen, Han Wang, Wen Qian, William A. Miller-Little, Shadi Swaidani, Fangqiang Tang, Belinda B. Willard, Keith McCrae, Zizhen Kang, George R. Dubyak, Fabio Cominelli, Alison Simmons, Theresa T. Pizarro, Xiaoxia Li
Journal: Journal of Clinical Investigation (2020)

Gasdermin D (GSDMD) induces pyroptosis via the pore-forming activity of its N-terminal domain, cleaved by activated caspases associated with the release of IL-1β. Here, we report a nonpyroptotic role of full-length GSDMD in guiding the release of IL-1β-containing small extracellular vesicles (sEVs) from intestinal epithelial cells (IECs). In response to caspase-8 inflammasome activation, GSDMD, chaperoned by Cdc37/Hsp90, recruits the E3 ligase, NEDD4, to catalyze polyubiquitination of pro-IL-1β, serving as a signal for cargo loading into secretory vesicles. GSDMD and IL-1β colocalize with the exosome markers CD63 and ALIX intracellularly, and GSDMD and NEDD4 are required for release of CD63+ sEVs containing IL-1β, GSDMD, NEDD4, and caspase-8. Importantly, increased expression of epithelial-derived GSDMD is observed both in patients with inflammatory bowel disease (IBD) and those with experimental colitis. While GSDMD-dependent release of IL-1β-containing sEVs is detected in cultured colonic explants from colitic mice, GSDMD deficiency substantially attenuates disease severity, implicating GSDMD-mediated release of IL-1β sEVs in the pathogenesis of intestinal inflammation, such as that observed in IBD.
Impaired pulmonary function in discharged patients with COVID-19: more work ahead
Authors: Ruchong Chen, Yi Gao, Mu Chen, Wenhua Jian, Chunliang Lei, Jinping Zheng, Shiyue Li
Journal: European Respiratory Journal (2020)

<b>Impairment of diffusion capacity is the most common abnormality in discharged patients with COVID-19. Both decreased alveolar volume and <i>K</i><sub>CO</sub> contribute to the pathogenesis of impaired diffusion capacity. More follow-up work is needed.</b>https://bit.ly/2YL2eaK
Pre-existing immunity to influenza virus hemagglutinin stalk might drive selection for antibody-escape mutant viruses in a human challenge model
Authors: Jae-Keun Park, Yongli Xiao, Mitchell D. Ramuta, Luz Angela Rosas, Sharon Fong, Alexis M. Matthews, Ashley D. Freeman, Monica A. Gouzoulis, Natalia A. Batchenkova, Xingdong Yang, Kelsey Scherler, Li Qi, Susan Reed, Rani Athota, Lindsay Czajkowski, Alison Han, David M. Morens, Kathie-Anne Walters, Matthew J. Memoli, John C. Kash, Jeffery K. Taubenberger
Journal: Nature Medicine (2020)
iRhom2 Promotes Hepatic Steatosis by Activating MAP3K7‐Dependent Pathway
Authors: Minxuan Xu, Chenxu Ge, Liancai Zhu, Yuting Qin, Chengjiang Du, Deshuai Lou, Qiang Li, Linfeng Hu, Yan Sun, Xianling Dai, Mingxin Xiong, Tingting Long, Jianxia Zhan, Qin Kuang, Huanhuan Li, Qiufeng Yang, Ping Huang, Xuepeng Teng, Jing Feng, Yekuan Wu, Wei Dong, Bochu Wang, Jun Tan
Journal: Hepatology (2020)

Background and Aims Nonalcoholic fatty liver disease (NAFLD) has been widely recognized as a precursor to metabolic complications. Elevated inflammation levels are predictive of NAFLD‐associated metabolic disorder. Inactive rhomboid‐like protein 2 (iRhom2) is regarded as a key regulator in inflammation. However, the precise mechanisms by which iRhom2‐regulated inflammation promotes NAFLD progression remain to be elucidated. Approach and Results Here, we report that insulin resistance, hepatic steatosis, and specific macrophage inflammatory activation are significantly alleviated in iRhom2 ‐deficient (knockout [KO]) mice, but aggravated in iRhom2 overexpressing mice. We further show that, mechanistically, in response to a high‐fat diet (HFD), iRhom2 KO mice and mice with iRhom2 deficiency in myeloid cells only showed less severe hepatic steatosis and insulin resistance than controls. Inversely, transplantation of bone marrow cells from healthy mice to iRhom2 KO mice expedited the severity of insulin resistance and hepatic dyslipidemia. Of note, in response to HFD, hepatic iRhom2 binds to mitogen‐activated protein kinase kinase kinase 7 (MAP3K7) to facilitate MAP3K7 phosphorylation and nuclear factor kappa B cascade activation, thereby promoting the activation of c‐Jun N‐terminal kinase/insulin receptor substrate 1 signaling, but disturbing AKT/glycogen synthase kinase 3β–associated insulin signaling. The iRhom2/MAP3K7 axis is essential for iRhom2‐regulated liver steatosis. Conclusions iRhom2 may represent a therapeutic target for the treatment of HFD‐induced hepatic steatosis and insulin resistance.
FGFR4 regulates tumor subtype differentiation in luminal breast cancer and metastatic disease
Authors: Susana Garcia-Recio, Aatish Thennavan, Michael P. East, Joel S. Parker, Juan M. Cejalvo, Joseph P. Garay, Daniel P. Hollern, Xiaping He, Kevin R. Mott, Patricia Galván, Cheng Fan, Sara R. Selitsky, Alisha R. Coffey, David Marron, Fara Brasó-Maristany, Octavio Burgués, Joan Albanell, Federico Rojo, Ana Lluch, Eduardo Martinez de Dueñas, Jeffery M. Rosen, Gary L. Johnson, Lisa A. Carey, Aleix Prat, Charles M. Perou
Journal: Journal of Clinical Investigation (2020)

Mechanisms driving tumor progression from less aggressive subtypes to more aggressive states represent key targets for therapy. We identified a subset of luminal A primary breast tumors that give rise to HER2-enriched (HER2E) subtype metastases, but remain clinically HER2 negative (cHER2–). By testing the unique genetic and transcriptomic features of these cases, we developed the hypothesis that FGFR4 likely participates in this subtype switching. To evaluate this, we developed 2 FGFR4 genomic signatures using a patient-derived xenograft (PDX) model treated with an FGFR4 inhibitor, which inhibited PDX growth in vivo. Bulk tumor gene expression analysis and single-cell RNA sequencing demonstrated that the inhibition of FGFR4 signaling caused molecular switching. In the Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) breast cancer cohort, FGFR4-induced and FGFR4-repressed signatures each predicted overall survival. Additionally, the FGFR4-induced signature was an independent prognostic factor beyond subtype and stage. Supervised analysis of 77 primary tumors with paired metastases revealed that the FGFR4-induced signature was significantly higher in luminal/ER+ tumor metastases compared with their primaries. Finally, multivariate analysis demonstrated that the FGFR4-induced signature also predicted site-specific metastasis for lung, liver, and brain, but not for bone or lymph nodes. These data identify a link between FGFR4-regulated genes and metastasis, suggesting treatment options for FGFR4-positive patients, whose high expression is not caused by mutation or amplification.
A Pygopus 2-Histone Interaction Is Critical for Cancer Cell Dedifferentiation and Progression in Malignant Breast Cancer
Authors: Meera Saxena, Ravi K.R. Kalathur, Natalia Rubinstein, Andrea Vettiger, Nami Sugiyama, Melanie Neutzner, Mairene Coto-Llerena, Venkatesh Kancherla, Caner Ercan, Salvatore Piscuoglio, Jonas Fischer, Ernesta Fagiani, Claudio Cantù, Konrad Basler, Gerhard Christofori
Journal: Cancer Research (2020)

Abstract Pygopus 2 (Pygo2) is a coactivator of Wnt/β-catenin signaling that can bind bi- or trimethylated lysine 4 of histone-3 (H3K4me2/3) and participate in chromatin reading and writing. It remains unknown whether the Pygo2–H3K4me2/3 association has a functional relevance in breast cancer progression in vivo. To investigate the functional relevance of histone-binding activity of Pygo2 in malignant progression of breast cancer, we generated a knock-in mouse model where binding of Pygo2 to H3K4me2/3 was rendered ineffective. Loss of Pygo2–histone interaction resulted in smaller, differentiated, and less metastatic tumors, due, in part, to decreased canonical Wnt/β-catenin signaling. RNA- and ATAC-sequencing analyses of tumor-derived cell lines revealed downregulation of TGFβ signaling and upregulation of differentiation pathways such as PDGFR signaling. Increased differentiation correlated with a luminal cell fate that could be reversed by inhibition of PDGFR activity. Mechanistically, the Pygo2–histone interaction potentiated Wnt/β-catenin signaling, in part, by repressing the expression of Wnt signaling antagonists. Furthermore, Pygo2 and β-catenin regulated the expression of miR-29 family members, which, in turn, repressed PDGFR expression to promote dedifferentiation of wild-type Pygo2 mammary epithelial tumor cells. Collectively, these results demonstrate that the histone binding function of Pygo2 is important for driving dedifferentiation and malignancy of breast tumors, and loss of this binding activates various differentiation pathways that attenuate primary tumor growth and metastasis formation. Interfering with the Pygo2–H3K4me2/3 interaction may therefore serve as an attractive therapeutic target for metastatic breast cancer. Significance: Pygo2 represents a potential therapeutic target in metastatic breast cancer, as its histone-binding capability promotes β-catenin–mediated Wnt signaling and transcriptional control in breast cancer cell dedifferentiation, EMT, and metastasis.
Corrigendum to: “Impaired endothelial autophagy promotes liver fibrosis by aggravating the oxidative stress response during acute liver injury” [J Hepatol (2019) 458-469]
Authors: Maria Ruart, Laia Chavarria, Genís Campreciós, Nuria Suárez-Herrera, Carla Montironi, Sergi Guixé-Muntet, Jaume Bosch, Scott L. Friedman, Juan Carlos Garcia-Pagán, Virginia Hernández-Gea
Journal: Journal of Hepatology (2020)
ZBP1: A STARGᐰTE to decode the biology of Z-nucleic acids in disease
Authors: Sannula Kesavardhana, Thirumala-Devi Kanneganti
Journal: The Journal of Experimental Medicine (2020)

ZBP1 triggers NLRP3 inflammasome activation/pyroptosis, apoptosis, and necroptosis; the specific ligand for ZBP1 activation remains ambiguous. Recent studies, including Devos et al. in this issue of JEM (https://doi.org/10.1084/jem.20191913), collectively suggest that ZBP1 sensing Z-nucleic acids is critical for cell death/inflammatory disease.
Phytochemicals in cancer cell chemosensitization: Current knowledge and future perspectives
Authors: Elina Khatoon, Kishore Banik, Choudhary Harsha, Bethsebie Lalduhsaki Sailo, Krishan Kumar Thakur, Amrita Devi Khwairakpam, Rajesh Vikkurthi, Thengujam Babita Devi, Subash C Gupta, Ajaikumar B Kunnumakkara
Journal: Seminars in Cancer Biology (2020)