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4. Preliminary Evidence for Progressions in Ownership Reasoning over the Preschool Period

Author

Nancekivell, Shaylene E., Davidson, Natalie S., Noles, Nicholaus S., and Gelman, Susan A.

Abstract

Defining developmental progressions can be an important step in identifying developmental precursors and mechanisms of change, within and across areas of reasoning. In one exploratory study, we examine whether the development of children's thinking about ownership follows a systematic progression wherein some components emerge reliably before others. We examine this issue in a sample of 72 children: 40 older 2-year-olds, M[subscript age] = 2.78 (0.14); R = 2.50-3.00, and 32 older 4-year-olds, M[subscript age] = 4.77 (0.16); R = 4.50-5.00, living in Michigan in the United States. We use a battery of four established ownership tasks that tested different aspects of children's ownership thinking. A Guttman test revealed a reliable sequence that explained 81.9% of children's performance. Namely, we discovered that identifying familiar owned objects emerged first, control of permission as a cue to ownership second, understanding ownership transfers third, and the tracking of sets of identical objects last. This ordering suggests two foundational ownership abilities on which more complex reasoning may be built: the ability to include information about familiar owners in children's mental models of objects and recognizing that control is central to ownership. The observed progression is an important first step toward developing a formal ownership scale. This study paves the way for mapping the conceptual and information-processing demands (e.g., executive functioning, memory) that likely underlie change in ownership thinking across childhood.

Published
2023
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7. Genomic basis for RNA alterations in cancer.

Author

PCAWG Transcriptome Core Group, Calabrese, Claudia, Davidson, Natalie R, Demircioğlu, Deniz, Fonseca, Nuno A, He, Yao, Kahles, André, Lehmann, Kjong-Van, Liu, Fenglin, Shiraishi, Yuichi, Soulette, Cameron M, Urban, Lara, Greger, Liliana, Li, Siliang, Liu, Dongbing, Perry, Marc D, Xiang, Qian, Zhang, Fan, Zhang, Junjun, Bailey, Peter, Erkek, Serap, Hoadley, Katherine A, Hou, Yong, Huska, Matthew R, Kilpinen, Helena, Korbel, Jan O, Marin, Maximillian G, Markowski, Julia, Nandi, Tannistha, Pan-Hammarström, Qiang, Pedamallu, Chandra Sekhar, Siebert, Reiner, Stark, Stefan G, Su, Hong, Tan, Patrick, Waszak, Sebastian M, Yung, Christina, Zhu, Shida, Awadalla, Philip, Creighton, Chad J, Meyerson, Matthew, Ouellette, BF Francis, Wu, Kui, Yang, Huanming, PCAWG Transcriptome Working Group, Brazma, Alvis, Brooks, Angela N, Göke, Jonathan, Rätsch, Gunnar, Schwarz, Roland F, Stegle, Oliver, Zhang, Zemin, and PCAWG Consortium

Subjects
PCAWG Transcriptome Core Group, PCAWG Transcriptome Working Group, PCAWG Consortium, Humans, Neoplasms, DNA, Neoplasm, RNA, Genomics, Gene Expression Regulation, Neoplastic, Genome, Human, DNA Copy Number Variations, Transcriptome, DNA, Neoplasm, Gene Expression Regulation, Neoplastic, Genome, Human, General Science & Technology
Abstract

Transcript alterations often result from somatic changes in cancer genomes1. Various forms of RNA alterations have been described in cancer, including overexpression2, altered splicing3 and gene fusions4; however, it is difficult to attribute these to underlying genomic changes owing to heterogeneity among patients and tumour types, and the relatively small cohorts of patients for whom samples have been analysed by both transcriptome and whole-genome sequencing. Here we present, to our knowledge, the most comprehensive catalogue of cancer-associated gene alterations to date, obtained by characterizing tumour transcriptomes from 1,188 donors of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA)5. Using matched whole-genome sequencing data, we associated several categories of RNA alterations with germline and somatic DNA alterations, and identified probable genetic mechanisms. Somatic copy-number alterations were the major drivers of variations in total gene and allele-specific expression. We identified 649 associations of somatic single-nucleotide variants with gene expression in cis, of which 68.4% involved associations with flanking non-coding regions of the gene. We found 1,900 splicing alterations associated with somatic mutations, including the formation of exons within introns in proximity to Alu elements. In addition, 82% of gene fusions were associated with structural variants, including 75 of a new class, termed 'bridged' fusions, in which a third genomic location bridges two genes. We observed transcriptomic alteration signatures that differ between cancer types and have associations with variations in DNA mutational signatures. This compendium of RNA alterations in the genomic context provides a rich resource for identifying genes and mechanisms that are functionally implicated in cancer.

Published
2020

10. EIF1AX and RAS mutations cooperate to drive thyroid tumorigenesis through ATF4 and c-MYC

Author

Krishnamoorthy, Gnana P, Davidson, Natalie R, Leach, Steven D, Zhao, Zhen, Lowe, Scott W, Lee, Gina, Landa, Iňigo, Nagarajah, James, Saqcena, Mahesh, Singh, Kamini, Wendel, Hans-Guido, Dogan, Snjezana, Tamarapu, Prasanna P, Blenis, John, Ghossein, Ronald A, Knauf, Jeffrey A, Rätsch, Gunnar, and Fagin, James A

Subjects
Rare Diseases, Genetics, Cancer, Aetiology, 2.1 Biological and endogenous factors, Activating Transcription Factor 4, Alternative Splicing, Animals, Apoptosis, Carcinogenesis, Cell Proliferation, Eukaryotic Initiation Factor-1, Female, Gene Expression Regulation, Neoplastic, Humans, Mice, Mice, Inbred NOD, Mice, SCID, Mutation, Phosphorylation, Protein Biosynthesis, Protein Kinase Inhibitors, TOR Serine-Threonine Kinases, Thyroid Neoplasms, Tumor Cells, Cultured, Xenograft Model Antitumor Assays, ras Proteins, Oncology and Carcinogenesis
Abstract

Translation initiation is orchestrated by the cap binding and 43S preinitiation complexes (PIC). Eukaryotic initiation factor 1A (EIF1A) is essential for recruitment of the ternary complex and for assembling the 43S PIC. Recurrent EIF1AX mutations in papillary thyroid cancers are mutually exclusive with other drivers, including RAS. EIF1AX mutations are enriched in advanced thyroid cancers, where they display a striking co-occurrence with RAS, which cooperates to induce tumorigenesis in mice and isogenic cell lines. The C-terminal EIF1AX-A113splice mutation is the most prevalent in advanced thyroid cancer. EIF1AX-A113splice variants stabilize the PIC and induce ATF4, a sensor of cellular stress, which is co-opted to suppress EIF2α phosphorylation, enabling a general increase in protein synthesis. RAS stabilizes c-MYC, an effect augmented by EIF1AX-A113splice. ATF4 and c-MYC induce expression of amino acid transporters and enhance sensitivity of mTOR to amino acid supply. These mutually reinforcing events generate therapeutic vulnerabilities to MEK, BRD4, and mTOR kinase inhibitors. SIGNIFICANCE: Mutations of EIF1AX, a component of the translation PIC, co-occur with RAS in advanced thyroid cancers and promote tumorigenesis. EIF1AX-A113splice drives an ATF4-induced dephosphorylation of EIF2α, resulting in increased protein synthesis. ATF4 also cooperates with c-MYC to sensitize mTOR to amino acid supply, thus generating vulnerability to mTOR kinase inhibitors. This article is highlighted in the In This Issue feature, p. 151.

Published
2019

12. Establishing standardized immune phenotyping of metastatic melanoma by digital pathology

Author

Sobottka, Bettina, Nowak, Marta, Frei, Anja Laura, Haberecker, Martina, Merki, Samuel, Levesque, Mitchell P., Dummer, Reinhard, Moch, Holger, Koelzer, Viktor Hendrik, Aebersold, Rudolf, Ak, Melike, Al-Quaddoomi, Faisal S., Albinus, Jonas, Alborelli, Ilaria, Andani, Sonali, Attinger, Per-Olof, Bacac, Marina, Baumhoer, Daniel, Beck-Schimmer, Beatrice, Beerenwinkel, Niko, Beisel, Christian, Bernasconi, Lara, Bertolini, Anne, Bodenmiller, Bernd, Bonilla, Ximena, Casanova, Ruben, Chevrier, Stéphane, Chicherova, Natalia, D'Costa, Maya, Danenberg, Esther, Davidson, Natalie, Drăganmoch, Monica-Andreea, Engler, Stefanie, Erkens, Martin, Eschbach, Katja, Esposito, Cinzia, Fedier, André, Ferreira, Pedro, Ficek, Joanna, Frey, Bruno, Goetze, Sandra, Grob, Linda, Gut, Gabriele, Günther, Detlef, Haeuptle, Pirmin, Heinzelmann-Schwarz, Viola, Herter, Sylvia, Holtackers, Rene, Huesser, Tamara, Irmisch, Anja, Jacob, Francis, Jacobs, Andrea, Jaeger, Tim M., Jahn, Katharina, James, Alva R., Jermann, Philip M., Kahles, André, Kahraman, Abdullah, Kuebler, Werner, Kuipers, Jack, Kunze, Christian P., Kurzeder, Christian, Lehmann, Kjong-Van, Lugert, Sebastian, Maass, Gerd, Manz, Markus G., Markolin, Philipp, Mena, Julien, Menzel, Ulrike, Metzler, Julian M., Miglino, Nicola, Milani, Emanuela S., Muenst, Simone, Murri, Riccardo, Ng, Charlotte K.Y., Nicolet, Stefan, Pedrioli, Patrick G.A., Pelkmans, Lucas, Piscuoglio, Salvatore, Prummer, Michael, Ritter, Mathilde, Rommel, Christian, Rosano-González, María L., Rätsch, Gunnar, Santacroce, Natascha, del Castillo, Jacobo Sarabia, Schlenker, Ramona, Schwalie, Petra C., Schwan, Severin, Schär, Tobias, Senti, Gabriela, Singer, Franziska, Sivapatham, Sujana, Snijder, Berend, Sreedharan, Vipin T., Stark, Stefan, Stekhoven, Daniel J., Theocharides, Alexandre P.A., Thomas, Tinu M., Tolnay, Markus, Tosevski, Vinko, Toussaint, Nora C., Tuncel, Mustafa A., Tusup, Marina, Van Drogen, Audrey, Vetter, Marcus, Vlajnic, Tatjana, Weber, Sandra, Weber, Walter P., Wegmann, Rebekka, Weller, Michael, Wendt, Fabian, Wey, Norbert, Wicki, Andreas, Wildschut, Mattheus HE, Wollscheid, Bernd, Yu, Shuqing, Ziegler, Johanna, Zimmermann, Marc, Zoche, Martin, and Zuend, Gregor

Published
2021
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15. Molecular subtypes of high-grade serous ovarian cancer across racial groups and gene expression platforms

Author

Davidson, Natalie R., primary, Barnard, Mollie E., additional, Hippen, Ariel A., additional, Campbell, Amy, additional, Johnson, Courtney E., additional, Way, Gregory P., additional, Dalley, Brian K., additional, Berchuck, Andrew, additional, Salas, Lucas A., additional, Peres, Lauren C., additional, Marks, Jeffrey R., additional, Schildkraut, Joellen M., additional, Greene, Casey S., additional, and Doherty, Jennifer A., additional

Published
2024
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17. Author Correction: Genomic basis for RNA alterations in cancer

Author

Calabrese, Claudia, Davidson, Natalie R., Demircioğlu, Deniz, Fonseca, Nuno A., He, Yao, Kahles, André, Lehmann, Kjong-Van, Liu, Fenglin, Shiraishi, Yuichi, Soulette, Cameron M., Urban, Lara, Greger, Liliana, Li, Siliang, Liu, Dongbing, Perry, Marc D., Xiang, Qian, Zhang, Fan, Zhang, Junjun, Bailey, Peter, Erkek, Serap, Hoadley, Katherine A., Hou, Yong, Huska, Matthew R., Kilpinen, Helena, Korbel, Jan O., Marin, Maximillian G., Markowski, Julia, Nandi, Tannistha, Pan-Hammarström, Qiang, Pedamallu, Chandra Sekhar, Siebert, Reiner, Stark, Stefan G., Su, Hong, Tan, Patrick, Waszak, Sebastian M., Yung, Christina, Zhu, Shida, Awadalla, Philip, Creighton, Chad J., Meyerson, Matthew, Ouellette, B. F. Francis, Wu, Kui, Yang, Huanming, Brazma, Alvis, Brooks, Angela N., Göke, Jonathan, Rätsch, Gunnar, Schwarz, Roland F., Stegle, Oliver, and Zhang, Zemin

Published
2023
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18. Human Rights Realism.

Author

Davidson, Natalie R.

Subjects
Torts (International law) -- Laws, regulations and rules -- Remedies -- Research, Legal realism -- Analysis -- Research, Damages -- Laws, regulations and rules -- Research, Immunities of foreign states -- Laws, regulations and rules -- Research, Crimes against humanity -- Laws, regulations and rules -- Remedies -- Research, Jurisdiction (International law) -- Laws, regulations and rules -- Research, Government regulation, Alien Tort Statute
Abstract

TABLE OF CONTENTS I. INTRODUCTION 33 II. LEGAL REALISM, RIGHTS AND REMEDIES 10 A. Legal Realism from Domestic to International Law 40 B. Legal Realism and the Right-Remedy Relationship 43 [...], In the aftermath of gross human rights abuses, when, if at all, should we forego legal accountability? Human rights scholars debated this question in the 1980s and 1990s, in what was referred to as the "peace versus justice" debate. The "justice" side won the day among human rights advocates, among whom the dominant position is that legal accountability is a necessary response to atrocity and cannot be limited by political considerations (a position this Article terms "human rights absolutism"). However, this question has resurfaced in the twenty-first century, in intense debates with interlocutors outside the field of human rights. Faced with the development of international criminal justice, Alien Tort Statute litigation, and regional human rights court jurisprudence on the right to a remedy, courts, state officials, and conservative scholars argue that legal accountability should be limited to avoid hampering states' control of their internal affairs and international relations (a position this Article terms "sovereigntism"). Some scholars take a middle ground and argue that legal responses to gross human rights abuses should be limited only to avoid harm to peace or democratic decision-making. However, the latter have not yet offered a persuasive justification for their position nor a rationale for distinguishing peace and democratic decision-making from other values advanced by sovereigntists as limits to accountability. This Article offers a new middle ground between sovereigntism and human rights absolutism, under a position it terms "human rights realism."Drawing on American legal realism and grounded in human rights values, this approach mandates limiting legal accountability to avoid those consequences that threaten certain core human rights, and the Article identifies armed conflict and economic inequality as relevant consequences. This approach overcomes both human rights absolutists' denial of the politics of accountability mechanisms and sovereigntists' subordination of accountability to values other than human rights. Moreover, drawing on legal realist writing on the right-remedy relationship, this Article offers a robust justification for accepting limitations to legal accountability across a wide range of mechanisms and a principled framework for considering such limitations in light of evolving empirical evidence. The argument is developed by revisiting the debate about universal civil jurisdiction and expanding the analysis to international criminal law and regional court jurisprudence. The Article shows that human rights realism offers not only a promising normative framework for integrating political considerations into human rights enforcement but also that it sheds new light on recent developments, such as African state threats of withdrawal from the International Criminal Court.

Published
2021

19. Legal Ethics in Authoritarian Legality.

Author

Bilsky, Leora and Davidson, Natalie R.

Subjects
Government attorneys -- Ethical aspects -- History -- Research, Authoritarianism -- Ethical aspects -- Research, Legal ethics -- History -- Research
Abstract

TABLE OF CONTENTS INTRODUCTION 666 I. LUBAN'S AGENTIST FRAMEWORK: THE DILEMMAS OF THE PUBLIC OFFICIAL 668 II. THE STRUCTURAL CHARACTER OF VIOLENCE UNDER AUTHORITARIANISM AND THE ROLE OF LAW 670 [...], In "Complicity and Lesser Evils: A Tale of Two Lawyers," David Luban considers the dilemma of a decent person employed by the government or offered a government position in an evil regime. Through an analysis of two legal advisors in the Third Reich, Bernhard Losener and Helmuth James von Moltke, who remained on the job and arguably saved lives, Luban challenges Hannah Arendt's contention that remaining in office in these conditions is necessarily to support the regime. In this response, we remain within Luban's primarily consequentialist perspective, and ask, like him, whether any good can be done by lawyers staying on the job. However, we challenge his analytical framework for being overly individualist and agentist. We argue that, if we expand our perspective to the structure of evil regimes and the ways they inflict harm, we will notice important consequences of remaining and leaving that Luban fails to take into account. In particular, we argue that understanding the complex part played by legal institutions and legal discourse in authoritarian and semi-authoritarian regimes would lead to the realization that lawyers face a particularly sharp dilemma in such regimes, as both their possibilities of doing good and of strengthening the regime are strong. We proceed in three steps. First, we show that Luban's analysis is narrowly focused on individual agency. We then draw on scholarship on the Third Reich, bureaucratic crimes, and authoritarian uses of law to outline the structural characteristics and legal foundations of authoritarian wrongs. Finally, equipped with this theoretical background, we analyze anew the lawyer's dilemma. Applying a structural perspective cognizant of the role of law in repression to the stories of Losener and Moltke as well as of two other lawyers in the Third Reich, Ernst Fraenkel and Georg Konrad Morgen, we argue that the lawyer's dilemma is more difficult to resolve than Luban suggests.

Published
2021

20. Genomic basis for RNA alterations in cancer

Author

Calabrese, Claudia, Davidson, Natalie R., Demircioglu, Deniz, Fonseca, Nuno A., He, Yao, Kahles, André, and Lehmann, Kjong-Van

Subjects
Nucleotide sequencing -- Identification and classification, Gene expression -- Identification and classification, DNA sequencing -- Identification and classification, RNA -- Health aspects, Cancer -- Genetic aspects -- Identification and classification, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Transcript alterations often result from somatic changes in cancer genomes.sup.1. Various forms of RNA alterations have been described in cancer, including overexpression.sup.2, altered splicing.sup.3 and gene fusions.sup.4; however, it is difficult to attribute these to underlying genomic changes owing to heterogeneity among patients and tumour types, and the relatively small cohorts of patients for whom samples have been analysed by both transcriptome and whole-genome sequencing. Here we present, to our knowledge, the most comprehensive catalogue of cancer-associated gene alterations to date, obtained by characterizing tumour transcriptomes from 1,188 donors of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA).sup.5. Using matched whole-genome sequencing data, we associated several categories of RNA alterations with germline and somatic DNA alterations, and identified probable genetic mechanisms. Somatic copy-number alterations were the major drivers of variations in total gene and allele-specific expression. We identified 649 associations of somatic single-nucleotide variants with gene expression in cis, of which 68.4% involved associations with flanking non-coding regions of the gene. We found 1,900 splicing alterations associated with somatic mutations, including the formation of exons within introns in proximity to Alu elements. In addition, 82% of gene fusions were associated with structural variants, including 75 of a new class, termed 'bridged' fusions, in which a third genomic location bridges two genes. We observed transcriptomic alteration signatures that differ between cancer types and have associations with variations in DNA mutational signatures. This compendium of RNA alterations in the genomic context provides a rich resource for identifying genes and mechanisms that are functionally implicated in cancer. Integrative analyses of transcriptome and whole-genome sequencing data for 1,188 tumours across 27 types of cancer are used to provide a comprehensive catalogue of RNA-level alterations in cancer., Author(s): Claudia Calabrese [sup.2] , Natalie R. Davidson [sup.3] [sup.4] [sup.5] [sup.6] [sup.7] , Deniz Demircioglu [sup.8] [sup.9] , Nuno A. Fonseca [sup.2] , Yao He [sup.10] , André Kahles [...]

Published
2020
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21. Building an international consortium for tracking coronavirus health status

Author

Segal, Eran, Zhang, Feng, Lin, Xihong, King, Gary, Shalem, Ophir, Shilo, Smadar, Allen, William E., Alquaddoomi, Faisal, Altae-Tran, Han, Anders, Simon, Balicer, Ran, Bauman, Tal, Bonilla, Ximena, Booman, Gisel, Chan, Andrew T., Cohen, Ori, Coletti, Silvano, Davidson, Natalie, Dor, Yuval, Drew, David A., Elemento, Olivier, Evans, Georgina, Ewels, Phil, Gale, Joshua, Gavrieli, Amir, Geiger, Benjamin, Grad, Yonatan H., Greene, Casey S., Hajirasouliha, Iman, Jerala, Roman, Kahles, Andre, Kallioniemi, Olli, Keshet, Ayya, Kocarev, Ljupco, Landua, Gregory, Meir, Tomer, Muller, Aline, Nguyen, Long H., Oresic, Matej, Ovchinnikova, Svetlana, Peterson, Hedi, Prodanova, Jana, Rajagopal, Jay, Rätsch, Gunnar, Rossman, Hagai, Rung, Johan, Sboner, Andrea, Sigaras, Alexandros, Spector, Tim, Steinherz, Ron, Stevens, Irene, Vilo, Jaak, and Wilmes, Paul

Published
2020
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25. Host response signature trends in persistent bacteraemia and metastatic infection due to Staphylococcus aureus and Gram-negative bacilli: a prospective multicentre observational study.

Author

Peri, Anna Maria, Rafiei, Nastaran, O'Callaghan, Kevin, Brischetto, Anna, Graves, Bianca, Sinclair, Holly, Eustace, Matthew, Lim, Karen, Parkes-Smith, Jill, Stewart, Adam, Davidson, Natalie, Tabah, Alexis, Bergh, Haakon, Chatfield, Mark D., Harris, Patrick N. A., and Paterson, David L.

Subjects
STAPHYLOCOCCUS aureus infections, BACTEREMIA, GRAM-negative bacteria, SCIENTIFIC observation, METASTASIS
Abstract

A prompt diagnosis of bacteraemia and sepsis is essential. Markers to predict the risk of persistent bacteraemia and metastatic infection are lacking. SeptiCyte RAPID is a host response assay stratifying patients according to the risk of infectious vs sterile inflammation through a scoring system (SeptiScore). In this study we explore the association between SeptiScore and persistent bacteraemia as well as metastatic and persistent infection in the context of a proven bacteraemia episode. This is a prospective multicentre observational 14-month study on patients with proven bacteraemia caused by Staphylococcus aureus or Gram-negative bacilli. Samples for assessment by SeptiCyte were collected with paired blood cultures for 4 consecutive days after the index blood culture. We included 86 patients in the study, 40 with S. aureus and 46 with Gram-negative bacilli bacteraemia. SeptiScores over the follow-up were higher in patients with Gram-negative compared to S. aureus bacteraemia (median 6.4, IQR 5.5–7.4 vs 5.6 IQR 5.1–6.2, p = 0.002). Higher SeptiScores were found to be associated with positive blood cultures at follow-up (AUC = 0.86, 95%CI 0.68–1.00) and with a diagnosis of metastatic infection at day 1 and 2 of follow-up (AUC = 0.79, 95%CI 0.57–1.00 and AUC = 0.82, 95%CI 0.63–1.00 respectively) in the context of Gram-negative bacteraemia while no association between SeptiScore and the outcomes of interest was observed in S. aureus bacteraemia. Mixed models confirmed the association of SeptiScore with positive blood cultures at follow-up (p = 0.04) and metastatic infection (p = 0.03) in the context of Gram-negative bacteraemia but not S. aureus bacteraemia after adjusting for confounders. SeptiScores differ in the follow-up of S. aureus and Gram-negative bacteraemia. In the setting of Gram-negative bacteraemia SeptiScore demonstrated a good negative predictive value for the outcomes of interest and might help rule out the persistence of infection defined as metastatic spread, lack of source control or persistent bacteraemia. [ABSTRACT FROM AUTHOR]

Published
2024
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26. Molecular subtypes of high-grade serous ovarian cancer across racial groups and gene expression platforms

Author

Davidson, Natalie R., primary, Barnard, Mollie E., additional, Hippen, Ariel A., additional, Campbell, Amy, additional, Johnson, Courtney E., additional, Way, Gregory P., additional, Dalley, Brian K., additional, Berchuck, Andrew, additional, Salas, Lucas A., additional, Peres, Lauren C., additional, Marks, Jeffrey R., additional, Schildkraut, Joellen M., additional, Greene, Casey S., additional, and Doherty, Jennifer A., additional

Published
2023
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27. Persistence of Detectable Pathogens by Culture-Independent Systems (T2 Magnetic Resonance) in Patients With Bloodstream Infection: Prognostic Role and Possible Clinical Implications

Author

Peri, Anna Maria, primary, O’Callaghan, Kevin, additional, Rafiei, Nastaran, additional, Graves, Bianca, additional, Sinclair, Holly, additional, Brischetto, Anna, additional, Lim, Karen, additional, Parkes-Smith, Jill, additional, Eustace, Matthew, additional, Davidson, Natalie, additional, Tabah, Alexis, additional, Stewart, Adam, additional, Chatfield, Mark D, additional, Harris, Patrick N A, additional, and Paterson, David L, additional

Published
2023
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32. Persistence of Detectable Pathogens by Culture-Independent Systems (T2 Magnetic Resonance) in Patients With Bloodstream Infection: Prognostic Role and Possible Clinical Implications.

Author

Peri, Anna Maria, O'Callaghan, Kevin, Rafiei, Nastaran, Graves, Bianca, Sinclair, Holly, Brischetto, Anna, Lim, Karen, Parkes-Smith, Jill, Eustace, Matthew, Davidson, Natalie, Tabah, Alexis, Stewart, Adam, Chatfield, Mark D, Harris, Patrick N A, and Paterson, David L

Subjects
BACTEREMIA, RESEARCH, BLOOD, PREDICTIVE tests, SCIENTIFIC observation, CONFIDENCE intervals, CELL culture, TIME, GRAM-negative bacteria, MAGNETIC resonance imaging, STAPHYLOCOCCAL diseases, DESCRIPTIVE statistics, STAPHYLOCOCCUS aureus, ODDS ratio, MICROBIAL sensitivity tests, LONGITUDINAL method
Abstract

Background Persistent Staphylococcus aureus bacteremia is associated with metastatic infection and adverse outcomes, whereas gram-negative bacteremia is normally transient and shorter course therapy is increasingly advocated for affected patients. Whether the prolonged detection of pathogen DNA in blood by culture-independent systems could have prognostic value and guide management decisions is unknown. Methods We performed a multicenter, prospective, observational study on 102 patients with bloodstream infection (BSI) to compare time to bloodstream clearance according to T2 magnetic resonance and blood cultures over a 4-day follow-up. We also explored the association between duration of detectable pathogens according to T2 magnetic resonance (magnetic resonance–DNAemia [MR-DNAemia]) and clinical outcomes. Results Time to bloodstream clearance according to T2 magnetic resonance was significantly longer than blood culture clearance (HR,.54; 95% CI,.39–.75) and did not differ according to the causative pathogen (P =.5). Each additional day of MR-DNAemia increased the odds of persistent infection (defined as metastatic infection or delayed source control) both in the overall population (OR, 1.98; 95% CI, 1.45–2.70) and in S. aureus (OR, 1.92; 95% CI, 1.12–3.29) and gram-negative bacteremia (OR, 2.21; 95% CI, 1.35–3.60). MR-DNAemia duration was also associated with no improvement in Sequential Organ Failure Assessment score at day 7 from infection onset (OR, 1.76; 95% CI, 1.21–2.56). Conclusions T2 magnetic resonance may help diagnose BSI in patients on antimicrobials with negative blood cultures as well as to identify patients with metastatic infection, source control failure, or adverse short-term outcome. Future studies may inform its usefulness within the setting of antimicrobial stewardship programs. [ABSTRACT FROM AUTHOR]

Published
2024
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33. Vibrio species bloodstream infections in Queensland, Australia.

Author

Davidson, Natalie, Edwards, Felicity, Harris, Patrick N. A., and Laupland, Kevin B.

Subjects
*BACTEREMIA, *BLOOD, *PATHOLOGICAL laboratories, *CELL culture, *AGE distribution, *DISEASE incidence, *POPULATION geography, *VIBRIO infections, *RISK assessment, *SEASONS, *SEX distribution, *VIBRIO, *PATIENT education, *MICROBIAL sensitivity tests, *COMORBIDITY, *HEALTH promotion, *CLIMATE change, *DISEASE risk factors
Abstract

Background: Vibrio species bloodstream infections have been associated with significant mortality and morbidity. Limited information is available regarding the epidemiology of bloodstream infections because of Vibrio species in the Australian context. Aims: The objective of this study was to define the incidence and risk factors for developing Vibrio species bloodstream infections and compare differences between different species. Methods: All patients with Vibrio spp. isolated from positive blood cultures between 1 January 2000 and 31 December 2019 were identified by the state‐wide Pathology Queensland laboratory. Demographics, clinical foci of infections and comorbid conditions were collected in addition to antimicrobial susceptibility results. Results: About 100 cases were identified between 2000 and 2019 with an incidence of 1.2 cases/1 million person‐years. Seasonal and geographical variation occurred with the highest incidence in the summer months and in the tropical north. Increasing age, male sex and multiple comorbidities were identified as risk factors. Vibrio vulnificus was isolated most frequently and associated with the most severe disease. Overall case fatality was 19%. Conclusions: There is potential for increasing cases of Vibrio species infections globally with ageing populations and climate change. Ongoing clinical awareness is required to ensure optimal patient outcomes. [ABSTRACT FROM AUTHOR]

Published
2024
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34. Abstract 3506: High-grade serous ovarian cancer somatic mutational signatures in Black and White individuals

Author

Lawson-Michod, Katherine A., primary, Nix, David, additional, Collin, Lindsay, additional, Davidson, Natalie, additional, Hippen, Ariel, additional, Huff, Chad, additional, Atkinson, Aaron, additional, Salas, Lucas A., additional, Peres, Lauren, additional, Greene, Casey, additional, Schildkraut, Joellen, additional, Marks, Jeffrey, additional, and Doherty, Jennifer A., additional

Published
2023
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35. Data from EIF1AX and RAS Mutations Cooperate to Drive Thyroid Tumorigenesis through ATF4 and c-MYC

Author

Krishnamoorthy, Gnana P., primary, Davidson, Natalie R., primary, Leach, Steven D., primary, Zhao, Zhen, primary, Lowe, Scott W., primary, Lee, Gina, primary, Landa, Iňigo, primary, Nagarajah, James, primary, Saqcena, Mahesh, primary, Singh, Kamini, primary, Wendel, Hans-Guido, primary, Dogan, Snjezana, primary, Tamarapu, Prasanna P., primary, Blenis, John, primary, Ghossein, Ronald A., primary, Knauf, Jeffrey A., primary, Rätsch, Gunnar, primary, and Fagin, James A., primary

Published
2023
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36. Supplementary Data from EIF1AX and RAS Mutations Cooperate to Drive Thyroid Tumorigenesis through ATF4 and c-MYC

Author

Krishnamoorthy, Gnana P., primary, Davidson, Natalie R., primary, Leach, Steven D., primary, Zhao, Zhen, primary, Lowe, Scott W., primary, Lee, Gina, primary, Landa, Iňigo, primary, Nagarajah, James, primary, Saqcena, Mahesh, primary, Singh, Kamini, primary, Wendel, Hans-Guido, primary, Dogan, Snjezana, primary, Tamarapu, Prasanna P., primary, Blenis, John, primary, Ghossein, Ronald A., primary, Knauf, Jeffrey A., primary, Rätsch, Gunnar, primary, and Fagin, James A., primary

Published
2023
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37. Supplementary Table S3 from EIF1AX and RAS Mutations Cooperate to Drive Thyroid Tumorigenesis through ATF4 and c-MYC

Author

Krishnamoorthy, Gnana P., primary, Davidson, Natalie R., primary, Leach, Steven D., primary, Zhao, Zhen, primary, Lowe, Scott W., primary, Lee, Gina, primary, Landa, Iňigo, primary, Nagarajah, James, primary, Saqcena, Mahesh, primary, Singh, Kamini, primary, Wendel, Hans-Guido, primary, Dogan, Snjezana, primary, Tamarapu, Prasanna P., primary, Blenis, John, primary, Ghossein, Ronald A., primary, Knauf, Jeffrey A., primary, Rätsch, Gunnar, primary, and Fagin, James A., primary

Published
2023
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40. Participants' and implementors' views on the adaptation of the Parenting for Lifelong Health Teen Programme to address both violence against children and violence against women

Author

Davidson, Natalie and Ward, Catherine

Subjects
Psychology
Abstract

This study collected views about how the Parenting for Lifelong Health (PLH) Teen programme might be adapted to include a more explicit focus on preventing VAW (in addition to its current strength in preventing VAC) and engagement of fathers for the Zimbabwean context. Violence against women (VAW) and violence against children (VAC) intersect in various and damaging ways. Parenting programmes have been identified as a potentially successful way to deal with both simultaneously, given the effect of violence in the family on parenting and the importance of parenting as a key point of intervention to prevent present and future violence. Participants were caregiver and teen (10-17 years) participants of the PLH Teen programme and fathers, mothers and teens (10-17 years) who were not PLH participants; as well as PLH facilitators, from the Mazowe district, Zimbabwe. Qualitative data were collected via Zoom for the individual interviews with the facilitators of the PLH programme and WhatsApp for focus group discussions for the rest of the participants, given the current global pandemic. The findings of this study and a review of relevant literature suggest that a gender-transformative approach, the inclusion of a community focus and the active recruitment and engagement of fathers is needed in terms of the process for the adapted programme. In terms of the content for the adapted programme, the study's findings suggest that there is a need to strengthen and expand the existing communication and conflict resolution skills to consider the couple and the parent-teen relationships and interactions. They also suggest that the budgeting and saving component in the current PLH Teen Programme could perhaps include business skills. Lastly, this study suggests that there is potential for the future use of virtual data collection in low- and middle income countries where there is limited access to video conferencing. This study contributes both to the important work preventing VAW and VAC in one programme as well as the future use of messaging services such as WhatsApp as a data collection tool.

Published
2023

41. A deep learning system accurately classifies primary and metastatic cancers using passenger mutation patterns

Author

Jiao, Wei, Atwal, Gurnit, Polak, Paz, Karlic, Rosa, Cuppen, Edwin, Al-Shahrour, Fatima, Bailey, Peter J, Biankin, Andrew V, Boutros, Paul C, Campbell, Peter J, Chang, David K, Cooke, Susanna L, Deshpande, Vikram, Faltas, Bishoy M, Faquin, William C, Garraway, Levi, Getz, Gad, Grimmond, Sean M, Haider, Syed, Hoadley, Katherine A, Kaiser, Vera B, Kato, Mamoru, Kübler, Kirsten, Lazar, Alexander J, Li, Constance H, Louis, David N, Margolin, Adam, Martin, Sancha, Nahal-Bose, Hardeep K, Nielsen, G Petur, Nik-Zainal, Serena, Omberg, Larsson, P’ng, Christine, Perry, Marc D, Rheinbay, Esther, Rubin, Mark A, Semple, Colin A, Sgroi, Dennis C, Shibata, Tatsuhiro, Siebert, Reiner, Smith, Jaclyn, Stein, Lincoln D, Stobbe, Miranda D, Sun, Ren X, Thai, Kevin, Wright, Derek W, Wu, Chin-Lee, Yuan, Ke, Zhang, Junjun, Danyi, Alexandra, de Ridder, Jeroen, van Herpen, Carla, Lolkema, Martijn P, Steeghs, Neeltje, Morris, Quaid D, Aaltonen, Lauri A, Abascal, Federico, Abeshouse, Adam, Aburatani, Hiroyuki, Adams, David J, Agrawal, Nishant, Ahn, Keun Soo, Ahn, Sung-Min, Aikata, Hiroshi, Akbani, Rehan, Akdemir, Kadir C, Al-Ahmadie, Hikmat, Al-Sedairy, Sultan T, Alawi, Malik, Albert, Monique, Aldape, Kenneth, Alexandrov, Ludmil B, Ally, Adrian, Alsop, Kathryn, Alvarez, Eva G, Amary, Fernanda, Amin, Samirkumar B, Aminou, Brice, Ammerpohl, Ole, Anderson, Matthew J, Ang, Yeng, Antonello, Davide, Anur, Pavana, Aparicio, Samuel, Appelbaum, Elizabeth L, Arai, Yasuhito, Aretz, Axel, Arihiro, Koji, Ariizumi, Shun-ichi, Armenia, Joshua, Arnould, Laurent, Asa, Sylvia, Assenov, Yassen, Aukema, Sietse, Auman, J Todd, Aure, Miriam RR, Awadalla, Philip, Aymerich, Marta, Bader, Gary D, Baez-Ortega, Adrian, Bailey, Matthew H, Balasundaram, Miruna, Balu, Saianand, Bandopadhayay, Pratiti, Banks, Rosamonde E, Barbi, Stefano, Barbour, Andrew P, Barenboim, Jonathan, Barnholtz-Sloan, Jill, Barr, Hugh, Barrera, Elisabet, Bartlett, John, Bartolome, Javier, Bassi, Claudio, Bathe, Oliver F, Baumhoer, Daniel, Bavi, Prashant, Baylin, Stephen B, Bazant, Wojciech, Beardsmore, Duncan, Beck, Timothy A, Behjati, Sam, Behren, Andreas, Niu, Beifang, Bell, Cindy, Beltran, Sergi, Benz, Christopher, Berchuck, Andrew, Bergmann, Anke K, Bergstrom, Erik N, Berman, Benjamin P, Berney, Daniel M, Bernhart, Stephan H, Beroukhim, Rameen, Berrios, Mario, Bersani, Samantha, Bertl, Johanna, Betancourt, Miguel, Bhandari, Vinayak, Bhosle, Shriram G, Bieg, Matthias, Bigner, Darell, Binder, Hans, Birney, Ewan, Birrer, Michael, Biswas, Nidhan K, Bjerkehagen, Bodil, Bodenheimer, Tom, Boice, Lori, Bonizzato, Giada, De Bono, Johann S, Boot, Arnoud, Bootwalla, Moiz S, Borg, Ake, Borkhardt, Arndt, Boroevich, Keith A, Borozan, Ivan, Borst, Christoph, Bosenberg, Marcus, Bosio, Mattia, Boultwood, Jacqueline, Bourque, Guillaume, Bova, G Steven, Bowen, David T, Bowlby, Reanne, Bowtell, David DL, Boyault, Sandrine, Boyce, Rich, Boyd, Jeffrey, Brazma, Alvis, Brennan, Paul, Brewer, Daniel S, Brinkman, Arie B, Bristow, Robert G, Broaddus, Russell R, Brock, Jane E, Brock, Malcolm, Broeks, Annegien, Brooks, Angela N, Brooks, Denise, Brors, Benedikt, Brunak, Søren, Bruxner, Timothy JC, Bruzos, Alicia L, Buchanan, Alex, Buchhalter, Ivo, Buchholz, Christiane, Bullman, Susan, Burke, Hazel, Burkhardt, Birgit, Burns, Kathleen H, Busanovich, John, Bustamante, Carlos D, Butler, Adam P, Butte, Atul J, Byrne, Niall J, Børresen-Dale, Anne-Lise, Caesar-Johnson, Samantha J, Cafferkey, Andy, Cahill, Declan, Calabrese, Claudia, Caldas, Carlos, Calvo, Fabien, Camacho, Niedzica, Campo, Elias, Cantù, Cinzia, Cao, Shaolong, Carey, Thomas E, Carlevaro-Fita, Joana, Carlsen, Rebecca, Cataldo, Ivana, Cazzola, Mario, Cebon, Jonathan, Cerfolio, Robert, Chadwick, Dianne E, Chakravarty, Dimple, Chalmers, Don, Chan, Calvin Wing Yiu, Chan, Kin, Chan-Seng-Yue, Michelle, Chandan, Vishal S, Chanock, Stephen J, Chantrill, Lorraine A, Chateigner, Aurélien, Chatterjee, Nilanjan, Chayama, Kazuaki, Chen, Hsiao-Wei, Chen, Jieming, Chen, Ken, Chen, 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Demeulemeester, Jonas, Demidov, German M, Demircioğlu, Deniz, Dennis, Nening M, Denroche, Robert E, Dentro, Stefan C, Desai, Nikita, Deshwar, Amit G, Desmedt, Christine, Deu-Pons, Jordi, Dhalla, Noreen, Dhani, Neesha C, Dhingra, Priyanka, Dhir, Rajiv, DiBiase, Anthony, Diamanti, Klev, Ding, Li, Ding, Shuai, Dinh, Huy Q, Dirix, Luc, Doddapaneni, HarshaVardhan, Donmez, Nilgun, Dow, Michelle T, Drapkin, Ronny, Drechsel, Oliver, Drews, Ruben M, Serge, Serge, Dudderidge, Tim, Dueso-Barroso, Ana, Dunford, Andrew J, Dunn, Michael, Dursi, Lewis Jonathan, Duthie, Fraser R, Dutton-Regester, Ken, Eagles, Jenna, Easton, Douglas F, Edmonds, Stuart, Edwards, Paul A, Edwards, Sandra E, Eeles, Rosalind A, Ehinger, Anna, Eils, Juergen, Eils, Roland, El-Naggar, Adel, Eldridge, Matthew, Ellrott, Kyle, Erkek, Serap, Escaramis, Georgia, Espiritu, Shadrielle MG, Estivill, Xavier, Etemadmoghadam, Dariush, Eyfjord, Jorunn E, Fan, Daiming, Fan, Yu, Farcas, Claudiu, Fassan, Matteo, Fatima, Aquila, Favero, Francesco, Fayzullaev, Nodirjon, Felau, Ina, Fereday, Sian, Ferguson, Martin L, Ferretti, Vincent, Feuerbach, Lars, Field, Matthew A, Fink, J Lynn, Finocchiaro, Gaetano, Fisher, Cyril, Fittall, Matthew W, Fitzgerald, Anna, Fitzgerald, Rebecca C, Flanagan, Adrienne M, Fleshner, Neil E, Flicek, Paul, Foekens, John A, Fong, Kwun M, Fonseca, Nuno A, Foster, Christopher S, Fox, Natalie S, Fraser, Michael, Frazer, Scott, Frenkel-Morgenstern, Milana, Friedman, William, Frigola, Joan, Fronick, Catrina C, Fujimoto, Akihiro, Fujita, Masashi, Fukayama, Masashi, Fulton, Lucinda A, Fulton, Robert S, Furuta, Mayuko, Futreal, P Andrew, Füllgrabe, Anja, Gabriel, Stacey B, Gallinger, Steven, Gambacorti-Passerini, Carlo, Gao, Jianjiong, Gao, Shengjie, Garred, Øystein, Garrison, Erik, Garsed, Dale W, Gehlenborg, Nils, Gelpi, Josep LL, George, Joshy, Gerhard, Daniela S, Gerhauser, Clarissa, Gershenwald, Jeffrey E, Gerstein, Mark, Gerstung, Moritz, Ghori, Mohammed, Ghossein, Ronald, Giama, Nasra H, Gibbs, Richard A, Gibson, Bob, Gill, Anthony J, Gill, Pelvender, Giri, Dilip D, Glodzik, Dominik, Gnanapragasam, Vincent J, Goebler, Maria Elisabeth, Goldman, Mary J, Gomez, Carmen, Gonzalez, Santiago, Gonzalez-Perez, Abel, Gordenin, Dmitry A, Gossage, James, Gotoh, Kunihito, Govindan, Ramaswamy, Grabau, Dorthe, Graham, Janet S, Grant, Robert C, Green, Anthony R, Green, Eric, Greger, Liliana, Grehan, Nicola, Grimaldi, Sonia, Grossman, Robert L, Grundhoff, Adam, Gundem, Gunes, Guo, Qianyun, Gupta, Manaswi, Gupta, Shailja, Gut, Ivo G, Gut, Marta, Göke, Jonathan, Ha, Gavin, Haake, Andrea, Haan, David, Haas, Siegfried, Haase, Kerstin, Haber, James E, Habermann, Nina, Hach, Faraz, Hama, Natsuko, Hamdy, Freddie C, Hamilton, Anne, Hamilton, Mark P, Han, Leng, Hanna, George B, Hansmann, Martin, Haradhvala, Nicholas J, Harismendy, Olivier, Harliwong, Ivon, Harmanci, Arif O, Harrington, Eoghan, Hasegawa, Takanori, Haussler, David, Hawkins, Steve, Hayami, Shinya, Hayashi, Shuto, Hayes, D Neil, Hayes, Stephen J, Hayward, Nicholas K, Hazell, Steven, He, Yao, Heath, Allison P, Heath, Simon C, Hedley, David, Hegde, Apurva M, Heiman, David I, Heinold, Michael C, Heins, Zachary, Heisler, Lawrence E, Hellstrom-Lindberg, Eva, Helmy, Mohamed, Heo, Seong Gu, Hepperla, Austin J, Heredia-Genestar, José María, Herrmann, Carl, Hersey, Peter, Hess, Julian M, Hilmarsdottir, Holmfridur, Hinton, Jonathan, Hirano, Satoshi, Hiraoka, Nobuyoshi, Hobolth, Asger, Hodzic, Ermin, Hoell, Jessica I, Hoffmann, Steve, Hofmann, Oliver, Holbrook, Andrea, Holik, Aliaksei Z, Hollingsworth, Michael A, Holmes, Oliver, Holt, Robert A, Hong, Chen, Hong, Eun Pyo, Hong, Jongwhi H, Hooijer, Gerrit K, Hornshøj, Henrik, Hosoda, Fumie, Hou, Yong, Hovestadt, Volker, Howat, William, Hoyle, Alan P, Hruban, Ralph H, Hu, Jianhong, Hu, Taobo, Hua, Xing, Huang, Kuan-lin, Huang, Mei, Huang, Mi Ni, Huang, Vincent, Huang, Yi, Huber, Wolfgang, Hudson, Thomas J, Hummel, Michael, Hung, Jillian A, Huntsman, David, Hupp, Ted R, Huse, Jason, Huska, Matthew R, Hutter, Barbara, Hutter, Carolyn M, Hübschmann, Daniel, Iacobuzio-Donahue, Christine A, Imbusch, Charles David, Imielinski, Marcin, Imoto, Seiya, Isaacs, William B, Isaev, Keren, Ishikawa, Shumpei, Iskar, Murat, Islam, SM Ashiqul, Ittmann, Michael, Ivkovic, Sinisa, Izarzugaza, Jose MG, Jacquemier, Jocelyne, Jakrot, Valerie, Jamieson, Nigel B, Jang, Gun Ho, Jang, Se Jin, Jayaseelan, Joy C, Jayasinghe, Reyka, Jefferys, Stuart R, Jegalian, Karine, Jennings, Jennifer L, Jeon, Seung-Hyup, Jerman, Lara, Ji, Yuan, Johansson, Peter A, Johns, Amber L, Johns, Jeremy, Johnson, Rory, Johnson, Todd A, Jolly, Clemency, Joly, Yann, Jonasson, Jon G, Jones, Corbin D, Jones, David R, Jones, David TW, Jones, Nic, Jones, Steven JM, Jonkers, Jos, Ju, Young Seok, Juhl, Hartmut, Jung, Jongsun, Juul, Malene, Juul, Randi Istrup, Juul, Sissel, Jäger, Natalie, Kabbe, Rolf, Kahles, Andre, Kahraman, Abdullah, Kakavand, Hojabr, Kalimuthu, Sangeetha, von Kalle, Christof, Kang, Koo Jeong, Karaszi, Katalin, Karlan, Beth, Karlić, Rosa, Karsch, Dennis, Kasaian, Katayoon, Kassahn, Karin S, Katai, Hitoshi, Katoh, Hiroto, Kawakami, Yoshiiku, Kay, Jonathan D, Kazakoff, Stephen H, Kazanov, Marat D, Keays, Maria, Kebebew, Electron, Kefford, Richard F, Kellis, Manolis, Kench, James G, Kennedy, Catherine J, Kerssemakers, Jules NA, Khoo, David, Khoo, Vincent, Khuntikeo, Narong, Khurana, Ekta, Kilpinen, Helena, Kim, Hark Kyun, Kim, Hyung-Lae, Kim, Hyung-Yong, Kim, Hyunghwan, Kim, Jaegil, Kim, Jihoon, Kim, Jong K, Kim, Youngwook, King, Tari A, Klapper, Wolfram, Kleinheinz, Kortine, Klimczak, Leszek J, Knappskog, Stian, Kneba, Michael, Knoppers, Bartha M, Koh, Youngil, Komorowski, Jan, Komura, Daisuke, Komura, Mitsuhiro, Kong, Gu, Kool, Marcel, Korbel, Jan O, Korchina, Viktoriya, Korshunov, Andrey, Koscher, Michael, Koster, Roelof, Kote-Jarai, Zsofia, Koures, Antonios, Kovacevic, Milena, Kremeyer, Barbara, Kretzmer, Helene, Kreuz, Markus, Krishnamurthy, Savitri, Kube, Dieter, Kumar, Kiran, Kumar, Pardeep, Kumar, Sushant, Kumar, Yogesh, Kundra, Ritika, Küppers, Ralf, Lagergren, Jesper, Lai, Phillip H, Laird, Peter W, Lakhani, Sunil R, Lalansingh, Christopher M, Lalonde, Emilie, Lamaze, Fabien C, Lambert, Adam, Lander, Eric, Landgraf, Pablo, Landoni, Luca, Langerød, Anita, Lanzós, Andrés, Larsimont, Denis, Larsson, Erik, Lathrop, Mark, Lau, Loretta MS, Lawerenz, Chris, Lawlor, Rita T, Lawrence, Michael S, Lazic, Ana Mijalkovic, Le, Xuan, Lee, Darlene, Lee, Donghoon, Lee, Eunjung Alice, Lee, Hee Jin, Lee, Jake June-Koo, Lee, Jeong-Yeon, Lee, Juhee, Lee, Ming Ta Michael, Lee-Six, Henry, Lehmann, Kjong-Van, Lehrach, Hans, Lenze, Dido, Leonard, Conrad R, Leongamornlert, Daniel A, Leshchiner, Ignaty, Letourneau, Louis, Letunic, Ivica, Levine, Douglas A, Lewis, Lora, Ley, Tim, Li, Chang, Li, Haiyan Irene, Li, Jun, Li, Lin, Li, Shantao, Li, Siliang, Li, Xiaobo, Li, Xiaotong, Li, Xinyue, Li, Yilong, Liang, Han, Liang, Sheng-Ben, Lichter, Peter, Lin, Pei, Lin, Ziao, Linehan, 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Karen, Musgrove, Elizabeth A, Mustonen, Ville, Mutch, David, Muyas, Francesc, Muzny, Donna M, Muñoz, Alfonso, Myers, Jerome, Myklebost, Ola, Möller, Peter, Nagae, Genta, Nagrial, Adnan M, Nakagama, Hitoshi, Nakagawa, Hidewaki, Nakamura, Hiromi, Nakamura, Toru, Nakano, Kaoru, Nandi, Tannistha, Nangalia, Jyoti, Nastic, Mia, Navarro, Arcadi, Navarro, Fabio CP, Neal, David E, Nettekoven, Gerd, Newell, Felicity, Newhouse, Steven J, Newton, Yulia, Ng, Alvin Wei Tian, Ng, Anthony, Nicholson, Jonathan, Nicol, David, Nie, Yongzhan, Nielsen, Morten Muhlig, Noble, Michael S, Nones, Katia, Northcott, Paul A, Notta, Faiyaz, O’Connor, Brian D, O’Donnell, Peter, O’Donovan, Maria, O’Meara, Sarah, O’Neill, Brian Patrick, O’Neill, J Robert, Ocana, David, Ochoa, Angelica, Oesper, Layla, Ogden, Christopher, Ohdan, Hideki, Ohi, Kazuhiro, Ohno-Machado, Lucila, Oien, Karin A, Ojesina, Akinyemi I, Ojima, Hidenori, Okusaka, Takuji, Ong, Choon Kiat, Ossowski, Stephan, Ott, German, Ouellette, BF Francis, 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Deurzen, Carolien HM, van de Vijver, Marc J, Veer, L van’t, and von Mering, Christian

Subjects
Human Biology & Physiology, Ecology,Evolution & Ethology, Tumour Biology, Genetics & Genomics, Structural Biology & Biophysics, Computational & Systems Biology
Abstract

In cancer, the primary tumour’s organ of origin and histopathology are the strongest determinants of its clinical behaviour, but in 3% of cases a patient presents with a metastatic tumour and no obvious primary. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, we train a deep learning classifier to predict cancer type based on patterns of somatic passenger mutations detected in whole genome sequencing (WGS) of 2606 tumours representing 24 common cancer types produced by the PCAWG Consortium. Our classifier achieves an accuracy of 91% on held-out tumor samples and 88% and 83% respectively on independent primary and metastatic samples, roughly double the accuracy of trained pathologists when presented with a metastatic tumour without knowledge of the primary. Surprisingly, adding information on driver mutations reduced accuracy. Our results have clinical applicability, underscore how patterns of somatic passenger mutations encode the state of the cell of origin, and can inform future strategies to detect the source of circulating tumour DNA.

Published
2023
Full Text
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42. Combined burden and functional impact tests for cancer driver discovery using DriverPower

Author

Shuai, Shimin, Abascal, Federico, Amin, Samirkumar B, Bader, Gary D, Bandopadhayay, Pratiti, Barenboim, Jonathan, Beroukhim, Rameen, Bertl, Johanna, Boroevich, Keith A, Brunak, Søren, Campbell, Peter J, Carlevaro-Fita, Joana, Chakravarty, Dimple, Chan, Calvin Wing Yiu, Chen, Ken, Choi, Jung Kyoon, Deu-Pons, Jordi, Dhingra, Priyanka, Diamanti, Klev, Feuerbach, Lars, Fink, J Lynn, Fonseca, Nuno A, Frigola, Joan, Gambacorti-Passerini, Carlo, Garsed, Dale W, Gerstein, Mark, Getz, Gad, Guo, Qianyun, Gut, Ivo G, Haan, David, Hamilton, Mark P, Haradhvala, Nicholas J, Harmanci, Arif O, Helmy, Mohamed, Herrmann, Carl, Hess, Julian M, Hobolth, Asger, Hodzic, Ermin, Hong, Chen, Hornshøj, Henrik, Isaev, Keren, Izarzugaza, Jose MG, Johnson, Rory, Johnson, Todd A, Juul, Malene, Juul, Randi Istrup, Kahles, Andre, Kahraman, Abdullah, Kellis, Manolis, Khurana, Ekta, Kim, Jaegil, Kim, Jong K, Kim, Youngwook, Komorowski, Jan, Korbel, Jan O, Kumar, Sushant, Lanzós, Andrés, Larsson, Erik, Lawrence, Michael S, Lee, Donghoon, Lehmann, Kjong-Van, Li, Shantao, Li, Xiaotong, Lin, Ziao, Liu, Eric Minwei, Lochovsky, Lucas, Lou, Shaoke, Madsen, Tobias, Marchal, Kathleen, Martincorena, Iñigo, Martinez-Fundichely, Alexander, Maruvka, Yosef E, McGillivray, Patrick D, Meyerson, William, Muiños, Ferran, Mularoni, Loris, Nakagawa, Hidewaki, Nielsen, Morten Muhlig, Paczkowska, Marta, Park, Keunchil, Park, Kiejung, Pedersen, Jakob Skou, Pons, Tirso, Pulido-Tamayo, Sergio, Raphael, Benjamin J, Reimand, Jüri, Reyes-Salazar, Iker, Reyna, Matthew A, Rheinbay, Esther, Rubin, Mark A, Rubio-Perez, Carlota, Sahinalp, S Cenk, Saksena, Gordon, Salichos, Leonidas, Sander, Chris, Schumacher, Steven E, Shackleton, Mark, Shapira, Ofer, Shen, Ciyue, Shrestha, Raunak, Sidiropoulos, Nikos, Sieverling, Lina, Sinnott-Armstrong, Nasa, Stein, Lincoln D, Stuart, Joshua M, Tamborero, David, Tiao, Grace, Tsunoda, Tatsuhiko, Umer, Husen M, Uusküla-Reimand, Liis, Valencia, Alfonso, Vazquez, Miguel, Verbeke, Lieven PC, Wadelius, 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Subjects
Human Biology & Physiology, Ecology,Evolution & Ethology, Tumour Biology, Genetics & Genomics, Structural Biology & Biophysics, Computational & Systems Biology
Abstract

The discovery of driver mutations is one of the key motivations for cancer genome sequencing. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancers across 38 tumour types, we describe DriverPower, a software package that uses mutational burden and functional impact evidence to identify driver mutations in coding and non-coding sites within cancer whole genomes. Using a total of 1373 genomic features derived from public sources, DriverPower’s background mutation model explains up to 93% of the regional variance in the mutation rate across multiple tumour types. By incorporating functional impact scores, we are able to further increase the accuracy of driver discovery. Testing across a collection of 2583 cancer genomes from the PCAWG project, DriverPower identifies 217 coding and 95 non-coding driver candidates. Comparing to six published methods used by the PCAWG Drivers and Functional Interpretation Working Group, DriverPower has the highest F1 score for both coding and non-coding driver discovery. This demonstrates that DriverPower is an effective framework for computational driver discovery.

Published
2023
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43. Integrative pathway enrichment analysis of multivariate omics data

Author

Paczkowska, Marta, Barenboim, Jonathan, Sintupisut, Nardnisa, Fox, Natalie S, Zhu, Helen, Abd-Rabbo, Diala, Mee, Miles W, Boutros, Paul C, Abascal, Federico, Amin, Samirkumar B, Bader, Gary D, Beroukhim, Rameen, Bertl, Johanna, Boroevich, Keith A, Brunak, Søren, Campbell, Peter J, Carlevaro-Fita, Joana, Chakravarty, Dimple, Chan, Calvin Wing Yiu, Chen, Ken, Choi, Jung Kyoon, Deu-Pons, Jordi, Dhingra, Priyanka, Diamanti, Klev, Feuerbach, Lars, Fink, J Lynn, Fonseca, Nuno A, Frigola, Joan, Gambacorti-Passerini, Carlo, Garsed, Dale W, Gerstein, Mark, Getz, Gad, Gonzalez-Perez, Abel, Guo, Qianyun, Gut, Ivo G, Haan, David, Hamilton, Mark P, Haradhvala, Nicholas J, Harmanci, Arif O, Helmy, Mohamed, Herrmann, Carl, Hess, Julian M, Hobolth, Asger, Hodzic, Ermin, Hong, Chen, Hornshøj, Henrik, Isaev, Keren, Izarzugaza, Jose MG, Johnson, Rory, Johnson, Todd A, Juul, Malene, Juul, Randi Istrup, Kahles, Andre, Kahraman, Abdullah, Kellis, Manolis, Khurana, Ekta, Kim, Jaegil, Kim, Jong K, Kim, Youngwook, Komorowski, Jan, Korbel, Jan O, Kumar, Sushant, Lanzós, Andrés, Lawrence, Michael S, Lee, Donghoon, Lehmann, Kjong-Van, Li, Shantao, Li, Xiaotong, Lin, Ziao, Liu, Eric Minwei, Lochovsky, Lucas, Lou, Shaoke, Madsen, Tobias, Marchal, Kathleen, Martincorena, Iñigo, Martinez-Fundichely, Alexander, Maruvka, Yosef E, McGillivray, Patrick D, Meyerson, William, Muiños, Ferran, Mularoni, Loris, Nakagawa, Hidewaki, Nielsen, Morten Muhlig, Park, Keunchil, Park, Kiejung, Pedersen, Jakob Skou, Pich, Oriol, Pons, Tirso, Pulido-Tamayo, Sergio, Raphael, Benjamin J, Reyes-Salazar, Iker, Reyna, Matthew A, Rheinbay, Esther, Rubin, Mark A, Rubio-Perez, Carlota, Sabarinathan, Radhakrishnan, Sahinalp, S Cenk, Saksena, Gordon, Salichos, Leonidas, Sander, Chris, Schumacher, Steven E, Shackleton, Mark, Shapira, Ofer, Shen, Ciyue, Shrestha, Raunak, Shuai, Shimin, Sidiropoulos, Nikos, Sieverling, Lina, Sinnott-Armstrong, Nasa, Stein, Lincoln D, Stuart, Joshua M, Tamborero, David, Tiao, Grace, Tsunoda, 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Vijver, Marc J, and Veer, L van’t

Subjects
Human Biology & Physiology, Ecology,Evolution & Ethology, Tumour Biology, Genetics & Genomics, Structural Biology & Biophysics, Computational & Systems Biology
Abstract

Multi-omics datasets represent distinct aspects of the central dogma of molecular biology. Such high-dimensional molecular profiles pose challenges to data interpretation and hypothesis generation. ActivePathways is an integrative method that discovers significantly enriched pathways across multiple datasets using statistical data fusion, rationalizes contributing evidence and highlights associated genes. As part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancers across 38 tumor types, we integrated genes with coding and non-coding mutations and revealed frequently mutated pathways and additional cancer genes with infrequent mutations. We also analyzed prognostic molecular pathways by integrating genomic and transcriptomic features of 1780 breast cancers and highlighted associations with immune response and anti-apoptotic signaling. Integration of ChIP-seq and RNA-seq data for master regulators of the Hippo pathway across normal human tissues identified processes of tissue regeneration and stem cell regulation. ActivePathways is a versatile method that improves systems-level understanding of cellular organization in health and disease through integration of multiple molecular datasets and pathway annotations.

Published
2023
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44. Pathway and network analysis of more than 2500 whole cancer genomes

Author

Reyna, Matthew A, Haan, David, Paczkowska, Marta, Verbeke, Lieven PC, Vazquez, Miguel, Kahraman, Abdullah, Pulido-Tamayo, Sergio, Barenboim, Jonathan, Wadi, Lina, Dhingra, Priyanka, Shrestha, Raunak, Getz, Gad, Lawrence, Michael S, Pedersen, Jakob Skou, Rubin, Mark A, Wheeler, David A, Brunak, Søren, Izarzugaza, Jose MG, Khurana, Ekta, Marchal, Kathleen, von Mering, Christian, Sahinalp, S Cenk, Valencia, Alfonso, Abascal, Federico, Amin, Samirkumar B, Bader, Gary D, Bandopadhayay, Pratiti, Beroukhim, Rameen, Bertl, Johanna, Boroevich, Keith A, Busanovich, John, Campbell, Peter J, Carlevaro-Fita, Joana, Chakravarty, Dimple, Chan, Calvin Wing Yiu, Chen, Ken, Choi, Jung Kyoon, Deu-Pons, Jordi, Diamanti, Klev, Feuerbach, Lars, Fink, J Lynn, Fonseca, Nuno A, Frigola, Joan, Gambacorti-Passerini, Carlo, Garsed, Dale W, Gerstein, Mark, Guo, Qianyun, Gut, Ivo G, Hamilton, Mark P, Haradhvala, Nicholas J, Harmanci, Arif O, Helmy, Mohamed, Herrmann, Carl, Hess, Julian M, Hobolth, Asger, Hodzic, Ermin, Hong, Chen, Hornshøj, Henrik, Isaev, Keren, Johnson, Rory, Johnson, Todd A, Juul, Malene, Juul, Randi Istrup, Kahles, Andre, Kellis, Manolis, Kim, Jaegil, Kim, Jong K, Kim, Youngwook, Komorowski, Jan, Korbel, Jan O, Kumar, Sushant, Lanzós, Andrés, Larsson, Erik, Lee, Donghoon, Lehmann, Kjong-Van, Li, Shantao, Li, Xiaotong, Lin, Ziao, Liu, Eric Minwei, Lochovsky, Lucas, Lou, Shaoke, Madsen, Tobias, Martincorena, Iñigo, Martinez-Fundichely, Alexander, Maruvka, Yosef E, McGillivray, Patrick D, Meyerson, William, Muiños, Ferran, Mularoni, Loris, Nakagawa, Hidewaki, Nielsen, Morten Muhlig, Park, Keunchil, Park, Kiejung, Pons, Tirso, Reyes-Salazar, Iker, Rheinbay, Esther, Rubio-Perez, Carlota, Saksena, Gordon, Salichos, Leonidas, Sander, Chris, Schumacher, Steven E, Shackleton, Mark, Shapira, Ofer, Shen, Ciyue, Shuai, Shimin, Sidiropoulos, Nikos, Sieverling, Lina, Sinnott-Armstrong, Nasa, Stein, Lincoln D, Tamborero, David, Tiao, Grace, Tsunoda, Tatsuhiko, Umer, Husen M, 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Subjects
Human Biology & Physiology, Ecology,Evolution & Ethology, Tumour Biology, Genetics & Genomics, Structural Biology & Biophysics, Computational & Systems Biology
Abstract

The catalog of cancer driver mutations in protein-coding genes has greatly expanded in the past decade. However, non-coding cancer driver mutations are less well-characterized and only a handful of recurrent non-coding mutations, most notably TERT promoter mutations, have been reported. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancer across 38 tumor types, we perform multi-faceted pathway and network analyses of non-coding mutations across 2583 whole cancer genomes from 27 tumor types compiled by the ICGC/TCGA PCAWG project that was motivated by the success of pathway and network analyses in prioritizing rare mutations in protein-coding genes. While few non-coding genomic elements are recurrently mutated in this cohort, we identify 93 genes harboring non-coding mutations that cluster into several modules of interacting proteins. Among these are promoter mutations associated with reduced mRNA expression in TP53, TLE4, and TCF4. We find that biological processes had variable proportions of coding and non-coding mutations, with chromatin remodeling and proliferation pathways altered primarily by coding mutations, while developmental pathways, including Wnt and Notch, altered by both coding and non-coding mutations. RNA splicing is primarily altered by non-coding mutations in this cohort, and samples containing non-coding mutations in well-known RNA splicing factors exhibit similar gene expression signatures as samples with coding mutations in these genes. These analyses contribute a new repertoire of possible cancer genes and mechanisms that are altered by non-coding mutations and offer insights into additional cancer vulnerabilities that can be investigated for potential therapeutic treatments.

Published
2023
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45. Divergent mutational processes distinguish hypoxic and normoxic tumours

Author

Bhandari, Vinayak, Li, Constance H, Bristow, Robert G, Boutros, Paul C, Aaltonen, Lauri A, Abascal, Federico, Abeshouse, Adam, Aburatani, Hiroyuki, Adams, David J, Agrawal, Nishant, Ahn, Keun Soo, Ahn, Sung-Min, Aikata, Hiroshi, Akbani, Rehan, Akdemir, Kadir C, Al-Ahmadie, Hikmat, Al-Sedairy, Sultan T, Al-Shahrour, Fatima, Alawi, Malik, Albert, Monique, Aldape, Kenneth, Alexandrov, Ludmil B, Ally, Adrian, Alsop, Kathryn, Alvarez, Eva G, Amary, Fernanda, Amin, Samirkumar B, Aminou, Brice, Ammerpohl, Ole, Anderson, Matthew J, Ang, Yeng, Antonello, Davide, Anur, Pavana, Aparicio, Samuel, Appelbaum, Elizabeth L, Arai, Yasuhito, Aretz, Axel, Arihiro, Koji, Ariizumi, Shun-ichi, Armenia, Joshua, Arnould, Laurent, Asa, Sylvia, Assenov, Yassen, Atwal, Gurnit, Aukema, Sietse, Auman, J Todd, Aure, Miriam RR, Awadalla, Philip, Aymerich, Marta, Bader, Gary D, Baez-Ortega, Adrian, Bailey, Matthew H, Bailey, Peter J, Balasundaram, Miruna, Balu, Saianand, Bandopadhayay, Pratiti, Banks, Rosamonde E, 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Yamamoto, Shogo, Yamaue, Hiroki, Yang, Fan, Yang, Huanming, Yang, Jean Y, Yang, Liming, Yang, Lixing, Yang, Shanlin, Yang, Tsun-Po, Yang, Yang, Yao, Xiaotong, Yaspo, Marie-Laure, Yates, Lucy, Yau, Christina, Ye, Chen, Ye, Kai, Yellapantula, Venkata D, Yoon, Christopher J, Yoon, Sung-Soo, Yousif, Fouad, Yu, Jun, Yu, Kaixian, Yu, Willie, Yu, Yingyan, Yuan, Ke, Yuan, Yuan, Yuen, Denis, Yung, Christina K, Zaikova, Olga, Zamora, Jorge, Zapatka, Marc, Zenklusen, Jean C, Zenz, Thorsten, Zeps, Nikolajs, Zhang, Cheng-Zhong, Zhang, Fan, Zhang, Hailei, Zhang, Hongwei, Zhang, Hongxin, Zhang, Jiashan, Zhang, Jing, Zhang, Junjun, Zhang, Xiuqing, Zhang, Xuanping, Zhang, Yan, Zhang, Zemin, Zhao, Zhongming, Zheng, Liangtao, Zheng, Xiuqing, Zhou, Wanding, Zhou, Yong, Zhu, Bin, Zhu, Hongtu, Zhu, Jingchun, Zhu, Shida, Zou, Lihua, Zou, Xueqing, deFazio, Anna, van As, Nicholas, van Deurzen, Carolien HM, van de Vijver, Marc J, Veer, L van’t, and von Mering, Christian

Subjects
Human Biology & Physiology, Ecology,Evolution & Ethology, Tumour Biology, Genetics & Genomics, Structural Biology & Biophysics, Computational & Systems Biology
Abstract

Many primary tumours have low levels of molecular oxygen (hypoxia), and hypoxic tumours respond poorly to therapy. Pan-cancer molecular hallmarks of tumour hypoxia remain poorly understood, with limited comprehension of its associations with specific mutational processes, non-coding driver genes and evolutionary features. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancers across 38 tumour types, we quantify hypoxia in 1188 tumours spanning 27 cancer types. Elevated hypoxia associates with increased mutational load across cancer types, irrespective of underlying mutational class. The proportion of mutations attributed to several mutational signatures of unknown aetiology directly associates with the level of hypoxia, suggesting underlying mutational processes for these signatures. At the gene level, driver mutations in TP53, MYC and PTEN are enriched in hypoxic tumours, and mutations in PTEN interact with hypoxia to direct tumour evolutionary trajectories. Overall, hypoxia plays a critical role in shaping the genomic and evolutionary landscapes of cancer.

Published
2023
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46. Genomic footprints of activated telomere maintenance mechanisms in cancer

Author

Sieverling, Lina, Hong, Chen, Koser, Sandra D, Ginsbach, Philip, Kleinheinz, Kortine, Hutter, Barbara, Braun, Delia M, Cortés-Ciriano, Isidro, Xi, Ruibin, Kabbe, Rolf, Park, Peter J, Eils, Roland, Schlesner, Matthias, Akdemir, Kadir C, Alvarez, Eva G, Baez-Ortega, Adrian, Beroukhim, Rameen, Boutros, Paul C, Bowtell, David DL, Brors, Benedikt, Burns, Kathleen H, Campbell, Peter J, Chan, Kin, Chen, Ken, Dueso-Barroso, Ana, Dunford, Andrew J, Edwards, Paul A, Estivill, Xavier, Etemadmoghadam, Dariush, Feuerbach, Lars, Fink, J Lynn, Frenkel-Morgenstern, Milana, Garsed, Dale W, Gerstein, Mark, Gordenin, Dmitry A, Haan, David, Haber, James E, Hess, Julian M, Imielinski, Marcin, Jones, David TW, Ju, Young Seok, Kazanov, Marat D, Klimczak, Leszek J, Koh, Youngil, Korbel, Jan O, Kumar, Kiran, Lee, Eunjung Alice, Lee, Jake June-Koo, Li, Yilong, Lynch, Andy G, Macintyre, Geoff, Markowetz, Florian, Martincorena, Iñigo, Martinez-Fundichely, Alexander, Meyerson, Matthew, Miyano, Satoru, Nakagawa, 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Christian

Subjects
Human Biology & Physiology, Ecology,Evolution & Ethology, Tumour Biology, Genetics & Genomics, Structural Biology & Biophysics, Computational & Systems Biology
Abstract

Cancers require telomere maintenance mechanisms for unlimited replicative potential. They achieve this through TERT activation or alternative telomere lengthening associated with ATRX or DAXX loss. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, we dissect whole-genome sequencing data of over 2500 matched tumor-control samples from 36 different tumor types aggregated within the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium to characterize the genomic footprints of these mechanisms. While the telomere content of tumors with ATRX or DAXX mutations (ATRX/DAXXtrunc) is increased, tumors with TERT modifications show a moderate decrease of telomere content. One quarter of all tumor samples contain somatic integrations of telomeric sequences into non-telomeric DNA. This fraction is increased to 80% prevalence in ATRX/DAXXtrunc tumors, which carry an aberrant telomere variant repeat (TVR) distribution as another genomic marker. The latter feature includes enrichment or depletion of the previously undescribed singleton TVRs TTCGGG and TTTGGG, respectively. Our systematic analysis provides new insight into the recurrent genomic alterations associated with telomere maintenance mechanisms in cancer.

Published
2023
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47. Publisher Correction: Building an international consortium for tracking coronavirus health status

Author

Segal, Eran, Zhang, Feng, Lin, Xihong, King, Gary, Shalem, Ophir, Shilo, Smadar, Allen, William E., Alquaddoomi, Faisal, Altae-Tran, Han, Anders, Simon, Balicer, Ran, Bauman, Tal, Bonilla, Ximena, Booman, Gisel, Chan, Andrew T., Cohen, Ori, Coletti, Silvano, Davidson, Natalie, Dor, Yuval, Drew, David A., Elemento, Olivier, Evans, Georgina, Ewels, Phil, Gale, Joshua, Gavrieli, Amir, Geiger, Benjamin, Grad, Yonatan H., Greene, Casey S., Hajirasouliha, Iman, Jerala, Roman, Kahles, Andre, Kallioniemi, Olli, Keshet, Ayya, Kocarev, Ljupco, Landua, Gregory, Meir, Tomer, Muller, Aline, Nguyen, Long H., Oresic, Matej, Ovchinnikova, Svetlana, Peterson, Hedi, Prodanova, Jana, Rajagopal, Jay, Rätsch, Gunnar, Rossman, Hagai, Rung, Johan, Sboner, Andrea, Sigaras, Alexandros, Spector, Tim, Steinherz, Ron, Stevens, Irene, Vilo, Jaak, and Wilmes, Paul

Published
2020
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50. Conceptual Influences on Category-Based Induction

Author

Gelman, Susan A. and Davidson, Natalie S.

Abstract

One important function of categories is to permit rich inductive inferences. Prior work shows that children use category labels to guide their inductive inferences. However, there are competing theories to explain this phenomenon, differing in the roles attributed to conceptual information vs. perceptual similarity. Seven experiments with 4- to 5-year-old children and adults (N=344) test these theories by teaching categories for which category membership and perceptual similarity are in conflict, and varying the conceptual basis of the novel categories. Results indicate that for non-natural kind categories that have little conceptual coherence, children make inferences based on perceptual similarity, whereas adults make inferences based on category membership. In contrast, for basic- and ontological-level categories that have a principled conceptual basis, children and adults alike make use of category membership more than perceptual similarity as the basis of their inferences. These findings provide evidence in favor of the role of conceptual information in preschoolers' inferences, and further demonstrate that labeled categories are not all equivalent; they differ in their inductive potential. (Contains 2 figures and 4 tables.)

Published
2013
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