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  1. AU="Roberts, Nicholas J"
  2. AU="Chauhan, Gaurav B"
  3. AU=Hanjaya-Putra Donny
  4. AU=Powell James
  5. AU="Russell, Todd"
  6. AU=Forth Scott
  7. AU="Kreutzer, Susanne" AU="Kreutzer, Susanne"
  8. AU="St John, Maie"
  9. AU=Gerhardy A
  10. AU="Qi, Huixin"
  11. AU="Dobosiewicz, May"
  12. AU="Srivastava, Rakesh"
  13. AU="Grevtsov K.I."

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  1. Artikel ; Online: Understanding familial risk of pancreatic ductal adenocarcinoma.

    Paranal, Raymond M / Wood, Laura D / Klein, Alison P / Roberts, Nicholas J

    Familial cancer

    2024  

    Abstract: Pancreatic ductal adenocarcinoma (PDAC) is a deadly disease that is the result of an accumulation of sequential genetic alterations. These genetic alterations can either be inherited, such as pathogenic germline variants that are associated with an ... ...

    Abstract Pancreatic ductal adenocarcinoma (PDAC) is a deadly disease that is the result of an accumulation of sequential genetic alterations. These genetic alterations can either be inherited, such as pathogenic germline variants that are associated with an increased risk of cancer, or acquired, such as somatic mutations that occur during the lifetime of an individual. Understanding the genetic basis of inherited risk of PDAC is essential to advancing patient care and outcomes through improved clinical surveillance, early detection initiatives, and targeted therapies. In this review we discuss factors associated with an increased risk of PDAC, the prevalence of genetic variants associated with an increased risk in patients with PDAC, estimates of PDAC risk in carriers of pathogenic germline variants in genes associated with an increased risk of PDAC. The role of common variants in pancreatic cancer risk will also be discussed.
    Sprache Englisch
    Erscheinungsdatum 2024-04-12
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Review
    ZDB-ID 1502496-9
    ISSN 1573-7292 ; 1389-9600
    ISSN (online) 1573-7292
    ISSN 1389-9600
    DOI 10.1007/s10689-024-00383-2
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Temporal and probabilistic comparisons of epidemic interventions.

    Boudreau, Mariah C / Allen, Andrea J / Roberts, Nicholas J / Allard, Antoine / Hébert-Dufresne, Laurent

    ArXiv

    2024  

    Abstract: Forecasting disease spread is a critical tool to help public health officials design and plan public health interventions.However, the expected future state of an epidemic is not necessarily well defined as disease spread is inherently stochastic, ... ...

    Abstract Forecasting disease spread is a critical tool to help public health officials design and plan public health interventions.However, the expected future state of an epidemic is not necessarily well defined as disease spread is inherently stochastic, contact patterns within a population are heterogeneous, and behaviors change. In this work, we use time-dependent probability generating functions (PGFs) to capture these characteristics by modeling a stochastic branching process of the spread of a disease over a network of contacts in which public health interventions are introduced over time. To achieve this, we define a general transmissibility equation to account for varying transmission rates (e.g. masking), recovery rates (e.g. treatment), contact patterns (e.g. social distancing) and percentage of the population immunized (e.g. vaccination). The resulting framework allows for a temporal and probabilistic analysis of an intervention's impact on disease spread, which match continuous-time stochastic simulations that are much more computationally expensive.To aid policy making, we then define several metrics over which temporal and probabilistic intervention forecasts can be compared: Looking at the expected number of cases and the worst-case scenario over time, as well as the probability of reaching a critical level of cases and of not seeing any improvement following an intervention.Given that epidemics do not always follow their average expected trajectories and that the underlying dynamics can change over time, our work paves the way for more detailed short-term forecasts of disease spread and more informed comparison of intervention strategies.
    Sprache Englisch
    Erscheinungsdatum 2024-01-18
    Erscheinungsland United States
    Dokumenttyp Preprint
    ISSN 2331-8422
    ISSN (online) 2331-8422
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: Functional characterization of all

    Kimura, Hirokazu / Lahouel, Kamel / Tomasetti, Cristian / Roberts, Nicholas J

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Interpretation of variants identified during genetic testing is a significant clinical challenge. In this study, we developed a high-throughput CDKN2A functional assay and characterized all ... ...

    Abstract Interpretation of variants identified during genetic testing is a significant clinical challenge. In this study, we developed a high-throughput CDKN2A functional assay and characterized all possible
    Sprache Englisch
    Erscheinungsdatum 2023-12-28
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2023.12.28.573507
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: ATM

    Nanda, Neha / Roberts, Nicholas J

    Genes

    2020  Band 11, Heft 1

    Abstract: Next-generation sequencing has led to the recent discovery of several novel pancreatic cancer susceptibility genes. These genes include ataxia telangiectasia mutated ( ...

    Abstract Next-generation sequencing has led to the recent discovery of several novel pancreatic cancer susceptibility genes. These genes include ataxia telangiectasia mutated (
    Mesh-Begriff(e) Animals ; Ataxia Telangiectasia Mutated Proteins/genetics ; Ataxia Telangiectasia Mutated Proteins/metabolism ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/metabolism ; Carcinoma, Pancreatic Ductal/pathology ; DNA Repair ; Germ-Line Mutation ; Humans ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Pancreas/metabolism ; Pancreas/pathology ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Risk Factors
    Chemische Substanzen Neoplasm Proteins ; ATM protein, human (EC 2.7.11.1) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2020-01-17
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2527218-4
    ISSN 2073-4425 ; 2073-4425
    ISSN (online) 2073-4425
    ISSN 2073-4425
    DOI 10.3390/genes11010108
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel: ATM Serine/Threonine Kinase and its Role in Pancreatic Risk

    Nanda, Neha / Roberts, Nicholas J

    Genes. 2020 Jan. 17, v. 11, no. 1

    2020  

    Abstract: Next-generation sequencing has led to the recent discovery of several novel pancreatic cancer susceptibility genes. These genes include ataxia telangiectasia mutated (ATM), a serine/threonine kinase that is an integral component of DNA repair. Pathogenic ...

    Abstract Next-generation sequencing has led to the recent discovery of several novel pancreatic cancer susceptibility genes. These genes include ataxia telangiectasia mutated (ATM), a serine/threonine kinase that is an integral component of DNA repair. Pathogenic germline ATM variants are frequently identified in patients with pancreatic ductal adenocarcinoma (PDAC) with and without a family history of the disease. Loss of ATM is also a frequent somatic event in the development of PDAC. These discoveries have advanced our understanding of the genetic basis of pancreatic cancer risk and will impact patient care through appropriate patient–risk stratification; personalized screening and early detection efforts; and, for some, targeted therapy.
    Schlagwörter DNA repair ; adenocarcinoma ; ataxia (disorder) ; genes ; germ cells ; high-throughput nucleotide sequencing ; pancreatic neoplasms ; patient care ; patients ; protein-serine-threonine kinases ; risk ; screening ; therapeutics
    Sprache Englisch
    Erscheinungsverlauf 2020-0117
    Erscheinungsort Multidisciplinary Digital Publishing Institute
    Dokumenttyp Artikel
    ZDB-ID 2527218-4
    ISSN 2073-4425
    ISSN 2073-4425
    DOI 10.3390/genes11010108
    Datenquelle NAL Katalog (AGRICOLA)

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  6. Artikel ; Online: Temporal and Probabilistic Comparisons of Epidemic Interventions.

    Boudreau, Mariah C / Allen, Andrea J / Roberts, Nicholas J / Allard, Antoine / Hébert-Dufresne, Laurent

    Bulletin of mathematical biology

    2023  Band 85, Heft 12, Seite(n) 118

    Abstract: Forecasting disease spread is a critical tool to help public health officials design and plan public health interventions. However, the expected future state of an epidemic is not necessarily well defined as disease spread is inherently stochastic, ... ...

    Abstract Forecasting disease spread is a critical tool to help public health officials design and plan public health interventions. However, the expected future state of an epidemic is not necessarily well defined as disease spread is inherently stochastic, contact patterns within a population are heterogeneous, and behaviors change. In this work, we use time-dependent probability generating functions (PGFs) to capture these characteristics by modeling a stochastic branching process of the spread of a disease over a network of contacts in which public health interventions are introduced over time. To achieve this, we define a general transmissibility equation to account for varying transmission rates (e.g. masking), recovery rates (e.g. treatment), contact patterns (e.g. social distancing) and percentage of the population immunized (e.g. vaccination). The resulting framework allows for a temporal and probabilistic analysis of an intervention's impact on disease spread, which match continuous-time stochastic simulations that are much more computationally expensive. To aid policy making, we then define several metrics over which temporal and probabilistic intervention forecasts can be compared: Looking at the expected number of cases and the worst-case scenario over time, as well as the probability of reaching a critical level of cases and of not seeing any improvement following an intervention. Given that epidemics do not always follow their average expected trajectories and that the underlying dynamics can change over time, our work paves the way for more detailed short-term forecasts of disease spread and more informed comparison of intervention strategies.
    Mesh-Begriff(e) Models, Biological ; Mathematical Concepts ; Epidemics/prevention & control ; Public Health ; Forecasting
    Sprache Englisch
    Erscheinungsdatum 2023-10-19
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
    ZDB-ID 184905-0
    ISSN 1522-9602 ; 0007-4985 ; 0092-8240
    ISSN (online) 1522-9602
    ISSN 0007-4985 ; 0092-8240
    DOI 10.1007/s11538-023-01220-w
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Germline sequence analysis of RABL3 in a large series of pancreatic ductal adenocarcinoma patients reveals no evidence of deleterious variants.

    Roberts, Nicholas J / Grant, Robert C / Gallinger, Steven / Klein, Alison P

    Genes, chromosomes & cancer

    2021  Band 60, Heft 8, Seite(n) 559–564

    Abstract: Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with a 5-year survival rate of less than 10%. Individuals with a pathogenic germline variant in a pancreatic cancer susceptibility gene are at an increased risk of developing pancreatic cancer. ... ...

    Abstract Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with a 5-year survival rate of less than 10%. Individuals with a pathogenic germline variant in a pancreatic cancer susceptibility gene are at an increased risk of developing pancreatic cancer. Understanding the inherited genetic basis of pancreatic tumor development provides a unique opportunity to improve patient care and outcomes. For example, relatives of a patients with PDAC who have a pathogenic germline variant in a pancreatic cancer susceptibility gene are eligible for disease surveillance where cancers may be detected early, and 5-year survival greatly improved. Furthermore, for some patients with PDAC and a pathogenic germline variant in a pancreatic cancer susceptibility gene, their tumors may be susceptible to specific anti-cancer therapies. Recently, RABL3 was identified as a pancreatic cancer susceptibility gene. To validate these findings and inform clinical translation, we determined the prevalence of deleterious RABL3 variants in a large cohort of 1037 patients with PDAC that had undergone either whole genome or whole exome germline sequencing. We identified two synonymous variants and four missense variants classified as variants of unknown significance. We found no pathogenic RABL3 variants, indicating that the maximum prevalence of such variants in patients with PDAC is less than 0.36% (minor allele frequency 0, 97.5% one-sided confidence interval: 0-0.0036). This finding has important implications for germline genetic testing of patients with PDAC.
    Mesh-Begriff(e) Adult ; Aged ; Aged, 80 and over ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/pathology ; Female ; Germ-Line Mutation ; Humans ; Male ; Middle Aged ; Mutation, Missense ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; rab GTP-Binding Proteins/genetics
    Chemische Substanzen Rabl3 protein, human (EC 3.6.1.-) ; rab GTP-Binding Proteins (EC 3.6.5.2)
    Sprache Englisch
    Erscheinungsdatum 2021-04-01
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1018988-9
    ISSN 1098-2264 ; 1045-2257
    ISSN (online) 1098-2264
    ISSN 1045-2257
    DOI 10.1002/gcc.22947
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: The Role of Inherited Pathogenic CDKN2A Variants in Susceptibility to Pancreatic Cancer.

    Kimura, Hirokazu / Klein, Alison P / Hruban, Ralph H / Roberts, Nicholas J

    Pancreas

    2021  Band 50, Heft 8, Seite(n) 1123–1130

    Abstract: Abstract: CDKN2A is cell cycle negative regulator, and the role of CDKN2A in the development of pancreatic ductal adenocarcinoma, which continues to be a lethal cancer, is well-established. Somatic loss of CDKN2A is considered one of the major drivers ... ...

    Abstract Abstract: CDKN2A is cell cycle negative regulator, and the role of CDKN2A in the development of pancreatic ductal adenocarcinoma, which continues to be a lethal cancer, is well-established. Somatic loss of CDKN2A is considered one of the major drivers of pancreatic tumorigenesis. CDKN2A gene is one of the pancreatic cancer susceptibility gene; in addition to melanoma, pathogenic germline CDKN2A variants have been identified in up to 3.3% patients with pancreatic ductal adenocarcinoma depending on family history of disease. Carriers of a known pathogenic germline CDKN2A variant have up to a 12.3-fold increased risk of developing pancreatic cancer. Recently, several studies have demonstrated the benefit of clinical surveillance in patients with pathogenic germline CDKN2A variants. Therefore, identification of patients with a pathogenic germline CDKN2A variant is important for screening of at-risk relatives for pancreatic cancer. It has the potential to lead to the detection of early, potentially curable pancreatic cancer and precursor neoplasms, and reduce mortality. Furthermore, patients with a germline pathogenic CDKN2A variant and somatic loss of CDKN2A may benefit in the future from treatment with targeted therapies, such as a CDK4/6 inhibitor.
    Mesh-Begriff(e) Carcinoma, Pancreatic Ductal/diagnosis ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/therapy ; Cyclin-Dependent Kinase Inhibitor p16/genetics ; Genetic Predisposition to Disease ; Genetic Variation ; Germ-Line Mutation ; Humans ; Pancreatic Neoplasms/diagnosis ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/therapy ; Risk
    Chemische Substanzen CDKN2A protein, human ; Cyclin-Dependent Kinase Inhibitor p16
    Sprache Englisch
    Erscheinungsdatum 2021-10-29
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Review
    ZDB-ID 632831-3
    ISSN 1536-4828 ; 0885-3177
    ISSN (online) 1536-4828
    ISSN 0885-3177
    DOI 10.1097/MPA.0000000000001888
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Evolutionary History Mediates Population Response to Rapid Environmental Change through Within-Generational and Transgenerational Plasticity.

    Clement, Dale T / Neylan, Isabelle P / Roberts, Nicholas J / Schreiber, Sebastian J / Trimmer, Pete C / Sih, Andrew

    The American naturalist

    2023  Band 201, Heft 5, Seite(n) E90–E109

    Abstract: AbstractRapid environmental change is affecting many organisms; some are coping well, but many species are in decline. A key mechanism for facilitating success following environmental change is phenotypic plasticity. Organisms use cues to respond ... ...

    Abstract AbstractRapid environmental change is affecting many organisms; some are coping well, but many species are in decline. A key mechanism for facilitating success following environmental change is phenotypic plasticity. Organisms use cues to respond phenotypically to environmental conditions; many incorporate recent information (within-generation plasticity) and information from previous generations (transgenerational plasticity). We extend an existing evolutionary model where organisms utilize within-generational plasticity, transgenerational plasticity, and bet hedging to include changes in environmental regime. We show how when rapid evolution of plasticity is not possible, the effect of environmental change (altering the environment mean, variance, or autocorrelation or cue reliability) on population growth rate depends on the population's evolutionary history and past evolutionary responses to historical environmental conditions. We then evaluate the predictions that populations adapted to highly variable environments or with greater within-generational plasticity are more likely to successfully respond to environmental change. We identify when these predictions fail and show that environmental change is most detrimental when previously reliable cues become unreliable. When multiple cues become unreliable, environmental change can cause deleterious effects regardless of the population's evolutionary history. Overall, this work provides a general framework for understanding the role of plasticity in population responses to rapid environmental change.
    Mesh-Begriff(e) Reproducibility of Results ; Adaptation, Physiological ; Cues ; Adaptation, Psychological ; Biological Evolution ; Phenotype
    Sprache Englisch
    Erscheinungsdatum 2023-03-29
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
    ZDB-ID 207092-3
    ISSN 1537-5323 ; 0003-0147
    ISSN (online) 1537-5323
    ISSN 0003-0147
    DOI 10.1086/723624
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: Nickel-Catalyzed O-Arylation of Primary or Secondary Aliphatic Alcohols with (Hetero)aryl Chlorides: A Comparison of Ni(I) and Ni(II) Precatalysts.

    Morrison, Kathleen M / Roberts, Nicholas J / Dudra, Samantha L / Tassone, Joseph P / Ferguson, Michael J / Johnson, Erin R / Stradiotto, Mark

    The Journal of organic chemistry

    2023  

    Abstract: A comparative experimental and computational study examining the interplay of the ancillary ligand structure and Ni oxidation state in the Ni-catalyzed C( ... ...

    Abstract A comparative experimental and computational study examining the interplay of the ancillary ligand structure and Ni oxidation state in the Ni-catalyzed C(sp
    Sprache Englisch
    Erscheinungsdatum 2023-12-13
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 123490-0
    ISSN 1520-6904 ; 0022-3263
    ISSN (online) 1520-6904
    ISSN 0022-3263
    DOI 10.1021/acs.joc.3c01584
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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