tbuckley/cabot-search huggingface dataset:
Carboplatin During Craniospinal Radiotherapy for Children With Group 3 Medulloblastoma—A New Standard of Care?—Reply
Authors: Sarah E. S. Leary, Yimei Li, James M. Olson
Journal: JAMA Oncology (2021)

In Reply We thank Karajannis et al for their comments on our Original Investigation1 and bringing up what is the quintessential question for many of us as both clinical researchers and practicing pediatric oncologists: What evidence provides us with justification to change standard practice?
Functional Mapping of AKT Signaling and Biomarkers of Response from the FAIRLANE Trial of Neoadjuvant Ipatasertib plus Paclitaxel for Triple-Negative Breast Cancer
Authors: Zhen Shi, Julia Wulfkuhle, Malgorzata Nowicka, Rosa I. Gallagher, Cristina Saura, Paolo G. Nuciforo, Isabel Calvo, Jay Andersen, José Luis Passos-Coelho, Miguel J. Gil-Gil, Begoña Bermejo, Debra A. Pratt, Eva M. Ciruelos, Patricia Villagrasa, Matthew J. Wongchenko, Emanuel F. Petricoin, Mafalda Oliveira, Steven J. Isakoff
Journal: Clinical Cancer Research (2021)

Abstract Purpose: Despite extensive genomic and transcriptomic profiling, it remains unknown how signaling pathways are differentially activated and how tumors are differentially sensitized to certain perturbations. Here, we aim to characterize AKT signaling activity and its association with other genomic or IHC-based PI3K/AKT pathway biomarkers as well as the clinical activity of ipatasertib (AKT inhibitor) in the FAIRLANE trial. Experimental Design: In FAIRLANE, 151 patients with early triple-negative breast cancer (TNBC) were randomized 1:1 to receive paclitaxel with ipatasertib or placebo for 12 weeks prior to surgery. Adding ipatasertib did not increase pathologic complete response rate and numerically improved overall response rate by MRI. We used reverse-phase protein microarrays (RPPA) to examine the total level and/or phosphorylation states of over 100 proteins in various signaling or cell processes including PI3K/AKT and mTOR signaling. One hundred and twenty-five baseline and 127 on-treatment samples were evaluable by RPPA, with 110 paired samples at both time points. Results: Tumors with genomic/protein alterations in PIK3CA/AKT1/PTEN were associated with higher levels of AKT phosphorylation. In addition, phosphorylated AKT (pAKT) levels exhibited a significant association with enriched clinical benefit of ipatasertib, and identified patients who received benefit in the absence of PIK3CA/AKT1/PTEN alterations. Ipatasertib treatment led to a downregulation of AKT/mTORC1 signaling, which was more pronounced among the tumors with PIK3CA/AKT1/PTEN alterations or among the responders to the treatment. Conclusions: We showed that the high baseline pAKT levels are associated with the alterations of PI3K/AKT pathway components and enriched benefit of ipatasertib in TNBC.
ImmunoPET of Ovarian and Pancreatic Cancer with AR9.6, a Novel MUC16-Targeted Therapeutic Antibody
Authors: Sai Kiran Sharma, Kyeara N. Mack, Alessandra Piersigilli, Jacob Pourat, Kimberly J. Edwards, Outi Keinänen, Maria S. Jiao, Huiyong Zhao, Brandy White, Cory L. Brooks, Elisa de Stanchina, Madi R. Madiyalakan, Michael A. Hollingsworth, Prakash Radhakrishnan, Jason S. Lewis, Brian M. Zeglis
Journal: Clinical Cancer Research (2021)

Advances in our understanding of the contribution of aberrant glycosylation to the pro-oncogenic signaling and metastasis of tumor cells have reinvigorated the development of mucin-targeted therapies. Here, we validate the tumor-targeting ability of a novel monoclonal antibody (mAb), AR9.6, that binds MUC16 and abrogates downstream oncogenic signaling to confer a therapeutic response.The in vitro and ex vivo validation of the binding of AR9.6 to MUC16 was achieved via flow cytometry, radioligand binding assay (RBA), and immunohistochemistry (IHC). The in vivo MUC16 targeting of AR9.6 was validated by creating a 89Zr-labeled radioimmunoconjugate of the mAb and utilizing immunoPET and ex vivo biodistribution studies in xenograft models of human ovarian and pancreatic cancer.Flow cytometry, RBA, and IHC revealed that AR9.6 binds to ovarian and pancreatic cancer cells in an MUC16-dependent manner. The in vivo radiopharmacologic profile of 89Zr-labeled AR9.6 in mice bearing ovarian and pancreatic cancer xenografts confirmed the MUC16-dependent tumor targeting by the radioimmunoconjugate. Radioactivity uptake was also observed in the distant lymph nodes (LNs) of mice bearing xenografts with high levels of MUC16 expression (i.e., OVCAR3 and Capan-2). IHC analyses of these PET-positive LNs highlighted the presence of shed antigen as well as necrotic, phagocytized, and actively infiltrating neoplastic cells. The humanization of AR9.6 did not compromise its ability to target MUC16-expressing tumors.The unique therapeutic mechanism of AR9.6 combined with its excellent in vivo tumor targeting makes it a highly promising theranostic agent. huAR9.6 is poised for clinical translation to impact the management of metastatic ovarian and pancreatic cancers.
New Treatment for Rare Blood Disorder
Authors: Rita Rubin
Journal: JAMA (2021)

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Multiomics analysis identifies BIRC3 as a novel glucocorticoid response–associated gene
Authors: Mengyuan Kan, Avantika R. Diwadkar, Haoyue Shuai, Jaehyun Joo, Alberta L. Wang, Mei-Sing Ong, Joanne E. Sordillo, Carlos Iribarren, Meng X. Lu, Natalia Hernandez-Pacheco, Javier Perez-Garcia, Mario Gorenjak, Uroš Potočnik, Esteban G. Burchard, Maria Pino-Yanes, Ann Chen Wu, Blanca E. Himes
Journal: Journal of Allergy and Clinical Immunology (2021)
HMGA2 facilitates colorectal cancer progression via STAT3-mediated tumor-associated macrophage recruitment
Authors: Xin Wang, Jian Wang, Jiahui Zhao, Hao Wang, Jing Chen, Jingjing Wu
Journal: Theranostics (2021)

Rationale: Tumor-associated macrophages (TAMs), generally displaying the pro-tumor M2-like phenotype, strongly influence the progression of colorectal cancer (CRC) via their immunosuppressive activities. The high-mobility gene group A2 (HMGA2), an oncoprotein, is aberrantly overexpressed in CRC cells. However, the mechanisms by which tumor-derived HMGA2 modulates tumor microenvironment in CRC remain poorly understood. Methods:In vivo subcutaneous tumor xenograft model, azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced tumor mouse model and in vitro co-culture assays were used to investigate the Hmga2 role in TAM recruitment and polarization. Luciferase and chromatin immunoprecipitation (ChIP) assays were applied to examine the mechanism of HMGA2-mediated transcriptional regulation of signal transducer and activator of transcription 3 (STAT3). The CD68 correlation with patient outcome was analyzed in 167 human CRC tissues. Results: We found that HMGA2 in cancer cells promoted macrophage recruitment and M2 polarization in vitro and in vivo. HMGA2 directly bound to the STAT3 promoter to activate its transcription and subsequently induced CCL2 secretion, thus promoting macrophage recruitment. Our results from human CRC specimens also revealed a strong positive association between HMGA2 expression in tumor cells and CD68 expression in the stroma. We further showed that patients with an elevated CD68 expression had an unfavorable overall survival in all of the patients or in the subgroup with negative distant metastasis. Conclusion: Our work uncovers new insight into the link between the HMGA2/STAT3/CCL2 axis and macrophage recruitment in CRC. These findings provide a novel therapeutic option for targeting the HMGA2/STAT3/CCL2 axis in CRC.
对于生物治疗方案的新决策方法, 银屑病患者会关注哪些信息?
Journal: British Journal of Dermatology (2021)

银屑病是一种常见的炎症性皮肤病, 英国境内患者超过一百万人。一类被称作“生物制剂”的药物是患者的治疗选择之一, 但它们并不适用于所有银屑病患者。研究人员正在寻找新的方法来帮助医生开具生物制剂处方。这些新方法会使用大量患者信息, 包括他们的遗传特征, 以确定是否使用生物制剂, 如果要使用, 还能确定哪种生物制剂最适合该患者。这种过程被称作“药物分层”。
The Gut Microbiome and Hepatocellular Carcinoma: Implications for Early Diagnostic Biomarkers and Novel Therapies
Authors: Yongbo Kang, Yue Cai, Ying Yang
Journal: Liver Cancer (2021)

Hepatocellular carcinoma (HCC) ranks the third place among all causes inducing cancer-associated mortality, worldwide. HCC nearly exclusively occurs in cases suffering from chronic liver disease (CLD), which results from the vicious cycle of liver damage, inflammation, and regeneration possibly lasting for dozens of years. Recently, more and more investigation on microbiome-gut-liver axis enhances our understanding toward how gut microbiota promotes liver disease and even HCC development. In this review, we summarize the mechanisms underlying the effect of gut microbiota on promoting HCC occurrence, with the focus on key pathways such as bacterial dysbiosis, leaky gut, bacterial metabolites, and microorganism-related molecular patterns, which promote liver inflammation, genotoxicity, and fibrosis that finally lead to cancer occurrence. Furthermore, we discuss gut microbiota’s important potential to be the early diagnostic biomarker for HCC. Gut microbiota may be the candidate targets to simultaneously prevent CLD and HCC occurrence among advanced liver disease cases. We outlook the gut microbiota-targeting treatments in detail to prevent CLD and HCC progression.
Development and Use of a Calculator to Measure Pediatric Low-Value Care Delivered in US Children’s Hospitals
Authors: Samantha A. House, Matthew Hall, Shawn L. Ralston, Jennifer R. Marin, Eric R. Coon, Alan R. Schroeder, Heidi Gruhler De Souza, Amber Davidson, Patti Duda, Timmy Ho, Marquita C. Genies, Marcos Mestre, Mario A. Reyes
Journal: JAMA Network Open (2021)

The scope of low-value care in children's hospitals is poorly understood.
Corrigendum to “The prevention of titanium-particle-induced osteolysis by OA-14 through the suppression of the p38 signaling pathway and inhibition of osteoclastogenesis” [Biomaterials 35 (32) (2014) 8937–8950]
Authors: Bo Tian, Tao Jiang, Zhanying Shao, Zanjing Zhai, Haowei Li, Qiming Fan, Xuqiang Liu, Zhengxiao Ouyang, Tingting Tang, Qing Jiang, Minghao Zheng, Kerong Dai, An Qin, Yongping Yu, Zhenan Zhu
Journal: Biomaterials (2021)
172P Phenotypic and functional heterogeneity of tissue resident memory T-cells in colorectal cancer liver metastasis
Authors: S. Abdeljaoued, M. Kroemer, M. Ben Khelil, J. Viot, A. Bouard, F. Monnien, V. Mougey, R. Loyon, A. Doussot, B. Heyd, C. Borg
Journal: Annals of Oncology (2021)
An AAV gene therapy computes over multiple cellular inputs to enable precise targeting of multifocal hepatocellular carcinoma in mice
Authors: Bartolomeo Angelici, Linling Shen, Joerg Schreiber, Anthony Abraham, Yaakov Benenson
Journal: Science Translational Medicine (2021)

Gene therapy that regulates an antitumor gene via a multi-input biomolecular logic module treats multifocal tumors in a mouse model of liver cancer.
Aggressive Afterload Lowering to Improve the Right Ventricle: A New Target for Medical Therapy in Pulmonary Arterial Hypertension?
Authors: Carmine Dario Vizza, Irene M. Lang, Roberto Badagliacca, Raymond L. Benza, Stephan Rosenkranz, R. James White, Yochai Adir, Arne K. Andreassen, Vijay Balasubramanian, Sonja Bartolome, Isabel Blanco, Robert C. Bourge, Jørn Carlsen, Rafael Enrique Conde Camacho, Michele D’Alto, Harrison W. Farber, Robert P. Frantz, H. James Ford, Stefano Ghio, Mardi Gomberg-Maitland, Marc Humbert, Robert Naeije, Stylianos E. Orfanos, Ronald J. Oudiz, Sergio V. Perrone, Oksana A. Shlobin, Marc A. Simon, Olivier Sitbon, Fernando Torres, Jean Luc Vachiery, Kuo-Yang Wang, Magdi H. Yacoub, Yan Liu, Gil Golden, Hiromi Matsubara
Journal: American Journal of Respiratory and Critical Care Medicine (2021)

Section:ChooseTop of pageAbstract <<The Pathophysiology of RV...Clinical Importance of RV...Effect of PAH Therapies o...RV Morphology, Function, ...Open Questions and IssuesConclusionsOptimizing Knowledge: Cal...ReferencesCITING ARTICLES
Correspondence on "G-CSF as a suitable alternative to GM-CSF to boost dinutuximab-mediated neutrophil cytotoxicity in neuroblastoma treatment" by Martinez Sanz <i>et al</i>
Authors: Jaume Mora, Guillermo L Chantada
Journal: Journal for ImmunoTherapy of Cancer (2021)

Dear Editor, We read with great interest the work by Martinez Sanz et al [1][1] 'G-CSF as a suitable alternative to GM-CSF to boost dinutuximab-mediated neutrophil cytotoxicity in neuroblastoma treatment,' published in the Journal for ImmunoTherapy of Cancer on May 28, 2021. The authors note
RTK-Dependent Inducible Degradation of Mutant PI3Kα Drives GDC-0077 (Inavolisib) Efficacy
Authors: Kyung W. Song, Kyle A. Edgar, Emily J. Hanan, Marc Hafner, Jason Oeh, Mark Merchant, Deepak Sampath, Michelle A. Nannini, Rebecca Hong, Lilian Phu, William F. Forrest, Eric Stawiski, Stephen Schmidt, Nicholas Endres, Jane Guan, Jeffrey J. Wallin, Jonathan Cheong, Emile G. Plise, Gail D. Lewis Phillips, Laurent Salphati, Timothy P. Heffron, Alan G. Olivero, Shiva Malek, Steven T. Staben, Donald S. Kirkpatrick, Anwesha Dey, Lori S. Friedman
Journal: Cancer Discovery (2021)

Abstract PIK3CA is one of the most frequently mutated oncogenes; the p110a protein it encodes plays a central role in tumor cell proliferation. Small-molecule inhibitors targeting the PI3K p110a catalytic subunit have entered clinical trials, with early-phase GDC-0077 studies showing antitumor activity and a manageable safety profile in patients with PIK3CA-mutant breast cancer. However, preclinical studies have shown that PI3K pathway inhibition releases negative feedback and activates receptor tyrosine kinase signaling, reengaging the pathway and attenuating drug activity. Here we discover that GDC-0077 and taselisib more potently inhibit mutant PI3K pathway signaling and cell viability through unique HER2-dependent mutant p110a degradation. Both are more effective than other PI3K inhibitors at maintaining prolonged pathway suppression. This study establishes a new strategy for identifying inhibitors that specifically target mutant tumors by selective degradation of the mutant oncoprotein and provide a strong rationale for pursuing PI3Kα degraders in patients with HER2-positive breast cancer. Significance: The PI3K inhibitors GDC-0077 and taselisib have a unique mechanism of action; both inhibitors lead to degradation of mutant p110a protein. The inhibitors that have the ability to trigger specific degradation of mutant p110a without significant change in wild-type p110a protein may result in improved therapeutic index in PIK3CA-mutant tumors. See related commentary by Vanhaesebroeck et al., p. 20. This article is highlighted in the In This Issue feature, p. 1
HER3 Augmentation via Blockade of EGFR/AKT Signaling Enhances Anticancer Activity of HER3-Targeting Patritumab Deruxtecan in EGFR-Mutated Non–Small Cell Lung Cancer
Authors: Kimio Yonesaka, Junko Tanizaki, Osamu Maenishi, Koji Haratani, Hisato Kawakami, Kaoru Tanaka, Hidetoshi Hayashi, Kazuko Sakai, Yasutaka Chiba, Asuka Tsuya, Hiroki Goto, Eri Otsuka, Hiroaki Okida, Maki Kobayashi, Ryoto Yoshimoto, Masanori Funabashi, Yuuri Hashimoto, Kenji Hirotani, Takashi Kagari, Kazuto Nishio, Kazuhiko Nakagawa
Journal: Clinical Cancer Research (2021)

EGFR-tyrosine kinase inhibitor (TKI) is a standard first-line therapy for activated EGFR-mutated non-small cell lung cancer (NSCLC). Treatment options for patients with acquired EGFR-TKI resistance are limited. HER3 mediates EGFR-TKI resistance. Clinical trials of the HER3-targeting antibody-drug conjugate patritumab deruxtecan (HER3-DXd) demonstrated its anticancer activity in EGFR-mutated NSCLC; however, the mechanisms that regulate HER3 expression are unknown. This study was conducted with the aim to clarify the mechanisms underlying HER3 regulation in EGFR-mutated NSCLC tumors and explored the strategy for enhancing the anticancer activity of HER3-DXd in EGFR-mutated NSCLC.Paired tumor samples were obtained from 48 patients with EGFR-mutated NSCLC treated with EGFR-TKI(s). HER3 expression was immunohistochemically quantified with H-score, and genomic alteration and transcriptomic signature were tested in tumors from pretreatment to post-EGFR-TKI resistance acquisition. The anticancer efficacy of HER3-DXd and osimertinib was evaluated in EGFR-mutated NSCLC cells.We showed augmented HER3 expression in EGFR-mutated tumors with acquired EGFR-TKI resistance compared with paired pretreatment samples. RNA sequencing revealed that repressed PI3K/AKT/mTOR signaling was associated with HER3 augmentation, especially in tumors from patients who received continuous EGFR-TKI therapy. An in vitro study also showed that EGFR-TKI increased HER3 expression, repressed AKT phosphorylation in multiple EGFR-mutated cancers, and enhanced the anticancer activity of HER3-DXd.Our findings help clarify the mechanisms of HER3 regulation in EGFR-mutated NSCLC tumors and highlight a rationale for combination therapy with HER3-DXd and EGFR-TKI in EGFR-mutated NSCLC.
23P A comprehensive analysis of the mucosal melanoma immune microenvironment
Authors: J. Vos, J.J.H. Traets, X. Qiao, I.M. Seignette, M. Wouters, E. Hooijberg, A. Broeks, J.E. Van Der Wal, M. Klop, P. Schreuder, B. Karakullukcu, M. van Poelgeest, E. Kapiteijn, C.U. Blank, J.B.A.G. Haanen, C. Zuur
Journal: Annals of Oncology (2021)
Definition of competence standards for optical diagnosis of diminutive colorectal polyps: European Society of Gastrointestinal Endoscopy (ESGE) Position Statement
Authors: Britt B. S. L. Houwen, Cesare Hassan, Veerle M. H. Coupé, Marjolein J. E. Greuter, Yark Hazewinkel, Jasper L. A. Vleugels, Giulio Antonelli, Marco Bustamante-Balén, Emmanuel Coron, George A. Cortas, Mario Dinis-Ribeiro, Daniela E. Dobru, James E. East, Marietta Iacucci, Rodrigo Jover, Roman Kuvaev, Helmut Neumann, Maria Pellisé, Ignasi Puig, Matthew D. Rutter, Brian Saunders, David J. Tate, Yuichi Mori, Gaius Longcroft-Wheaton, Raf Bisschops, Evelien Dekker
Journal: Endoscopy (2021)

BACKGROUND : The European Society of Gastrointestinal Endoscopy (ESGE) has developed a core curriculum for high quality optical diagnosis training for practice across Europe. The development of easy-to-measure competence standards for optical diagnosis can optimize clinical decision-making in endoscopy. This manuscript represents an official Position Statement of the ESGE aiming to define simple, safe, and easy-to-measure competence standards for endoscopists and artificial intelligence systems performing optical diagnosis of diminutive colorectal polyps (1 - 5 mm). METHODS : A panel of European experts in optical diagnosis participated in a modified Delphi process to reach consensus on Simple Optical Diagnosis Accuracy (SODA) competence standards for implementation of the optical diagnosis strategy for diminutive colorectal polyps. In order to assess the clinical benefits and harms of implementing optical diagnosis with different competence standards, a systematic literature search was performed. This was complemented with the results from a recently performed simulation study that provides guidance for setting alternative competence standards for optical diagnosis. Proposed competence standards were based on literature search and simulation study results. Competence standards were accepted if at least 80 % agreement was reached after a maximum of three voting rounds. RECOMMENDATION 1: In order to implement the leave-in-situ strategy for diminutive colorectal lesions (1-5 mm), it is clinically acceptable if, during real-time colonoscopy, at least 90 % sensitivity and 80 % specificity is achieved for high confidence endoscopic characterization of colorectal neoplasia of 1-5 mm in the rectosigmoid. Histopathology is used as the gold standard.Level of agreement 95 %. RECOMMENDATION 2: In order to implement the resect-and-discard strategy for diminutive colorectal lesions (1-5 mm), it is clinically acceptable if, during real-time colonoscopy, at least 80 % sensitivity and 80 % specificity is achieved for high confidence endoscopic characterization of colorectal neoplasia of 1-5 mm. Histopathology is used as the gold standard.Level of agreement 100 %. CONCLUSION : The developed SODA competence standards define diagnostic performance thresholds in relation to clinical consequences, for training and for use when auditing the optical diagnosis of diminutive colorectal polyps.
Multiple omics study identifies an interspecies conserved driver for nonalcoholic steatohepatitis
Authors: Xiao-Jing Zhang, Zhi-Gang She, Junyong Wang, Dating Sun, Li-Jun Shen, Hui Xiang, Xu Cheng, Yan-Xiao Ji, Yong-Ping Huang, Peng-Long Li, Xia Yang, Yanjie Cheng, Jun-Peng Ma, Hai-Ping Wang, Yufeng Hu, Fengjiao Hu, Song Tian, Han Tian, Peng Zhang, Guang-Nian Zhao, Lin Wang, Man-Li Hu, Qin Yang, Li-Hua Zhu, Jingjing Cai, Juan Yang, Xin Zhang, Xinliang Ma, Qingbo Xu, Rhian M. Touyz, Peter P. Liu, Rohit Loomba, Yibin Wang, Hongliang Li
Journal: Science Translational Medicine (2021)

ALOX12 drives NASH by inhibiting ACC1 lysosomal degradation across multiple species.
Copycat
Authors: Brett W. Dietz, Lisa G. Winston, Jane E. Koehler, Mary Margaretten
Journal: New England Journal of Medicine (2021)

A 75-year-old man with a history of an untreated hepatitis C virus infection presented with a 4-day history of a pruritic rash on his lower legs. He noted generalized malaise and an unintentional weight loss of 7 kg over the past 2 months. A video showing aortic vegetation is available at NEJM.org.
Error in the First Paragraph
Journal: JAMA Cardiology (2021)

Error in the First Paragraph: In the Editorial titled, "The Potential and Pitfalls of Coronary Artery Calcium Scoring," 1 which published online October 27, 2021, the following sentence is incorrect: "Beyond this recommendation, however, some investigators have called for even more aggressive de-risking of patients with a CAC score of 0, suggesting that even those with familial hypercholesterolemia and a CAC score of 0 may not need statins."The sentence has been updated to the following: "Beyond this recommendation, however, some investigators have called for broader de-risking of patients with a CAC score of 0, suggesting that even those with familial hypercholesterolemia and a CAC score of 0 may not need add-on therapy beyond statins and ezetimibe."This article was corrected online.
Reply to ‘Paracetamol use in pregnancy — caution over causal inference from available data’; ‘Handle with care — interpretation, synthesis and dissemination of data on paracetamol in pregnancy’
Authors: Ann Z. Bauer, Shanna H. Swan, David Kriebel, Zeyan Liew, Hugh S. Taylor, Carl-Gustaf Bornehag, Anderson M. Andrade, Jørn Olsen, Rigmor H. Jensen, Rod T. Mitchell, Niels E. Skakkebaek, David M. Kristensen
Journal: Nature Reviews Endocrinology (2021)