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  1. Article ; Online: An inflammatory transcriptional switch.

    Murtaugh, L Charles / MacDonald, Raymond J

    Nature

    2019  Volume 554, Issue 7693, Page(s) 470–472

    Language English
    Publishing date 2019-02-25
    Publishing country England
    Document type News
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/d41586-018-01262-4
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  2. Article ; Online: Putting GWAS to the functional test: NR5A2 and pancreatic cancer risk.

    Murtaugh, L Charles

    Gut

    2014  Volume 63, Issue 4, Page(s) 535–536

    MeSH term(s) Animals ; Carcinoma, Acinar Cell/physiopathology ; Carcinoma, Pancreatic Ductal/physiopathology ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/physiopathology ; Pancreatitis/genetics ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/physiology ; Receptors, Cytoplasmic and Nuclear/genetics ; Receptors, Cytoplasmic and Nuclear/physiology
    Chemical Substances Nr5a2 protein, mouse ; Receptors, Cytoplasmic and Nuclear ; Kras2 protein, mouse (EC 3.6.5.2) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
    Language English
    Publishing date 2014-04
    Publishing country England
    Document type Comment ; Journal Article
    ZDB-ID 80128-8
    ISSN 1468-3288 ; 0017-5749
    ISSN (online) 1468-3288
    ISSN 0017-5749
    DOI 10.1136/gutjnl-2013-305030
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: An inflammatory transcriptional switch.

    Murtaugh, L Charles / MacDonald, Raymond J

    Nature

    2018  Volume 554, Issue 7693, Page(s) 470–472

    MeSH term(s) Recombination, Genetic ; Transcription, Genetic
    Language English
    Publishing date 2018--22
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/d41586-018-01262-4
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  4. Article ; Online: Pathogenesis of pancreatic cancer: lessons from animal models.

    Murtaugh, L Charles

    Toxicologic pathology

    2013  Volume 42, Issue 1, Page(s) 217–228

    Abstract: The past several decades have seen great effort devoted to mimicking the key features of pancreatic ductal adenocarcinoma (PDAC) in animals and have produced 2 robust models of this deadly cancer. Carcinogen-treated Syrian hamsters develop PDAC with ... ...

    Abstract The past several decades have seen great effort devoted to mimicking the key features of pancreatic ductal adenocarcinoma (PDAC) in animals and have produced 2 robust models of this deadly cancer. Carcinogen-treated Syrian hamsters develop PDAC with genetic lesions, which reproduce those of human, including activation of the Kras oncogene, and early studies in this species validated nongenetic risk factors for PDAC including pancreatitis, obesity, and diabetes. More recently, PDAC research has been invigorated by the development of genetically engineered mouse models based on tissue-specific Kras activation and deletion of tumor suppressor genes. Surprisingly, mouse PDAC appears to arise from exocrine acinar rather than ductal cells, via a process of phenotypic reprogramming that is accelerated by inflammation. Studies in both models have uncovered molecular mechanisms by which inflammation promotes and sustains PDAC and identified targets for chemoprevention to suppress PDAC in high-risk individuals. The mouse model, in particular, has also been instrumental in developing new approaches to early detection as well as treatment of advanced disease. Together, animal models enable diverse approaches to basic and preclinical research on pancreatic cancer, the results of which will accelerate progress against this currently intractable cancer.
    MeSH term(s) Animals ; Carcinoma, Pancreatic Ductal/diagnosis ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/pathology ; Cricetinae ; Disease Models, Animal ; Humans ; Mice ; Pancreatic Neoplasms/diagnosis ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism ; Risk Factors
    Chemical Substances Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
    Language English
    Publishing date 2013-10-31
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 841009-4
    ISSN 1533-1601 ; 0192-6233
    ISSN (online) 1533-1601
    ISSN 0192-6233
    DOI 10.1177/0192623313508250
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  5. Article ; Online: Stem cells and β cells: the same, but different?

    Murtaugh, L Charles

    Cell stem cell

    2011  Volume 8, Issue 3, Page(s) 244–245

    Abstract: Researchers have long debated whether new pancreatic β cells derive from stem cells or from pre-existing β cells. A new study in this issue of Cell Stem Cell (Smukler et al., 2011) suggests that both sides may be right. ...

    Abstract Researchers have long debated whether new pancreatic β cells derive from stem cells or from pre-existing β cells. A new study in this issue of Cell Stem Cell (Smukler et al., 2011) suggests that both sides may be right.
    Language English
    Publishing date 2011-03-04
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 2375354-7
    ISSN 1875-9777 ; 1934-5909
    ISSN (online) 1875-9777
    ISSN 1934-5909
    DOI 10.1016/j.stem.2011.02.010
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  6. Article: Differentiation and Inflammation: 'Best Enemies' in Gastrointestinal Carcinogenesis.

    Krah, Nathan M / Murtaugh, L Charles

    Trends in cancer

    2016  Volume 2, Issue 12, Page(s) 723–735

    Abstract: While recent studies demonstrate that cancer can arise from mutant stem cells, this hypothesis does not explain why tissues without defined stem cell populations are susceptible to inflammation-driven tumorigenesis. We propose that chronic inflammatory ... ...

    Abstract While recent studies demonstrate that cancer can arise from mutant stem cells, this hypothesis does not explain why tissues without defined stem cell populations are susceptible to inflammation-driven tumorigenesis. We propose that chronic inflammatory diseases, such as colitis and pancreatitis, predispose to gastrointestinal (GI) adenocarcinoma by reprogramming differentiated cells. Focusing on colon and pancreas, we discuss recently discovered connections between inflammation and loss of cell differentiation, and propose that dysregulation of cell fate may be a novel rate-limiting step of tumorigenesis. We review studies identifying differentiation mechanisms that limit tumor initiation and that, upon reactivation, can prevent or revert the cancer cell transformed phenotype. Together, these findings suggest that differentiation-targeted treatments hold promise as a therapeutic strategy in GI cancer.
    Language English
    Publishing date 2016-12
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2852626-0
    ISSN 2405-8033 ; 2405-8025 ; 2405-8033
    ISSN (online) 2405-8033 ; 2405-8025
    ISSN 2405-8033
    DOI 10.1016/j.trecan.2016.11.005
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  7. Article ; Online: Matters arising: Insufficient evidence that pancreatic β cells are derived from adult ductal Neurog3-expressing progenitors.

    Magenheim, Judith / Maestro, Miguel Angel / Sharon, Nadav / Herrera, Pedro L / Murtaugh, L Charles / Kopp, Janel / Sander, Maike / Gu, Guoqiang / Melton, Douglas A / Ferrer, Jorge / Dor, Yuval

    Cell stem cell

    2023  Volume 30, Issue 4, Page(s) 488–497.e3

    Abstract: Understanding the origin of pancreatic β cells has profound implications for regenerative therapies in diabetes. For over a century, it was widely held that adult pancreatic duct cells act as endocrine progenitors, but lineage-tracing experiments ... ...

    Abstract Understanding the origin of pancreatic β cells has profound implications for regenerative therapies in diabetes. For over a century, it was widely held that adult pancreatic duct cells act as endocrine progenitors, but lineage-tracing experiments challenged this dogma. Gribben et al. recently used two existing lineage-tracing models and single-cell RNA sequencing to conclude that adult pancreatic ducts contain endocrine progenitors that differentiate to insulin-expressing β cells at a physiologically important rate. We now offer an alternative interpretation of these experiments. Our data indicate that the two Cre lines that were used directly label adult islet somatostatin-producing ∂ cells, which precludes their use to assess whether β cells originate from duct cells. Furthermore, many labeled ∂ cells, which have an elongated neuron-like shape, were likely misclassified as β cells because insulin-somatostatin coimmunolocalizations were not used. We conclude that most evidence so far indicates that endocrine and exocrine lineage borders are rarely crossed in the adult pancreas.
    MeSH term(s) Insulin-Secreting Cells ; Evidence Gaps ; Cell Differentiation ; Pancreas/physiology ; Pancreatic Ducts ; Insulin ; Somatostatin
    Chemical Substances Insulin ; Somatostatin (51110-01-1)
    Language English
    Publishing date 2023-04-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2375354-7
    ISSN 1875-9777 ; 1934-5909
    ISSN (online) 1875-9777
    ISSN 1934-5909
    DOI 10.1016/j.stem.2023.03.003
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  8. Article ; Online: Regeneration and repair of the exocrine pancreas.

    Murtaugh, L Charles / Keefe, Matthew D

    Annual review of physiology

    2015  Volume 77, Page(s) 229–249

    Abstract: Pancreatitis is caused by inflammatory injury to the exocrine pancreas, from which both humans and animal models appear to recover via regeneration of digestive enzyme-producing acinar cells. This regenerative process involves transient phases of ... ...

    Abstract Pancreatitis is caused by inflammatory injury to the exocrine pancreas, from which both humans and animal models appear to recover via regeneration of digestive enzyme-producing acinar cells. This regenerative process involves transient phases of inflammation, metaplasia, and redifferentiation, driven by cell-cell interactions between acinar cells, leukocytes, and resident fibroblasts. The NFκB signaling pathway is a critical determinant of pancreatic inflammation and metaplasia, whereas a number of developmental signals and transcription factors are devoted to promoting acinar redifferentiation after injury. Imbalances between these proinflammatory and prodifferentiation pathways contribute to chronic pancreatitis, characterized by persistent inflammation, fibrosis, and acinar dedifferentiation. Loss of acinar cell differentiation also drives pancreatic cancer initiation, providing a mechanistic link between pancreatitis and cancer risk. Unraveling the molecular bases of exocrine regeneration may identify new therapeutic targets for treatment and prevention of both of these deadly diseases.
    MeSH term(s) Acinar Cells/cytology ; Acinar Cells/physiology ; Animals ; Cell Differentiation/physiology ; Disease Models, Animal ; Humans ; Pancreas, Exocrine/cytology ; Pancreas, Exocrine/physiology ; Pancreatic Neoplasms/pathology ; Pancreatic Neoplasms/physiopathology ; Pancreatitis/pathology ; Pancreatitis/physiopathology ; Regeneration/physiology ; Signal Transduction/physiology
    Language English
    Publishing date 2015
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 207933-1
    ISSN 1545-1585 ; 0066-4278
    ISSN (online) 1545-1585
    ISSN 0066-4278
    DOI 10.1146/annurev-physiol-021014-071727
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  9. Article ; Online: Key transcriptional effectors of the pancreatic acinar phenotype and oncogenic transformation.

    Azevedo-Pouly, Ana / Hale, Michael A / Swift, Galvin H / Hoang, Chinh Q / Deering, Tye G / Xue, Jumin / Wilkie, Thomas M / Murtaugh, L Charles / MacDonald, Raymond J

    PloS one

    2023  Volume 18, Issue 10, Page(s) e0291512

    Abstract: Proper maintenance of mature cellular phenotypes is essential for stable physiology, suppression of disease states, and resistance to oncogenic transformation. We describe the transcriptional regulatory roles of four key DNA-binding transcription factors ...

    Abstract Proper maintenance of mature cellular phenotypes is essential for stable physiology, suppression of disease states, and resistance to oncogenic transformation. We describe the transcriptional regulatory roles of four key DNA-binding transcription factors (Ptf1a, Nr5a2, Foxa2 and Gata4) that sit at the top of a regulatory hierarchy controlling all aspects of a highly differentiated cell-type-the mature pancreatic acinar cell (PAC). Selective inactivation of Ptf1a, Nr5a2, Foxa2 and Gata4 individually in mouse adult PACs rapidly altered the transcriptome and differentiation status of PACs. The changes most emphatically included transcription of the genes for the secretory digestive enzymes (which conscript more than 90% of acinar cell protein synthesis), a potent anabolic metabolism that provides the energy and materials for protein synthesis, suppressed and properly balanced cellular replication, and susceptibility to transformation by oncogenic KrasG12D. The simultaneous inactivation of Foxa2 and Gata4 caused a greater-than-additive disruption of gene expression and uncovered their collaboration to maintain Ptf1a expression and control PAC replication. A measure of PAC dedifferentiation ranked the effects of the conditional knockouts as Foxa2+Gata4 > Ptf1a > Nr5a2 > Foxa2 > Gata4. Whereas the loss of Ptf1a or Nr5a2 greatly accelerated Kras-mediated transformation of mature acinar cells in vivo, the absence of Foxa2, Gata4, or Foxa2+Gata4 together blocked transformation completely, despite extensive dedifferentiation. A lack of correlation between PAC dedifferentiation and sensitivity to oncogenic KrasG12D negates the simple proposition that the level of differentiation determines acinar cell resistance to transformation.
    MeSH term(s) Mice ; Animals ; Acinar Cells/metabolism ; Pancreas, Exocrine ; Epithelium/metabolism ; Transcription Factors/genetics ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Phenotype ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism
    Chemical Substances Transcription Factors
    Language English
    Publishing date 2023-10-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0291512
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  10. Article: The what, where, when and how of Wnt/β-catenin signaling in pancreas development.

    Murtaugh, L Charles

    Organogenesis

    2008  Volume 4, Issue 2, Page(s) 81–86

    Abstract: The Wnt/β-catenin signaling pathway, conserved across the animal kingdom, is critical for the development of numerous tissues. Several recent studies have focused on the roles that this pathway plays at different stages of pancreatic organogenesis, ... ...

    Abstract The Wnt/β-catenin signaling pathway, conserved across the animal kingdom, is critical for the development of numerous tissues. Several recent studies have focused on the roles that this pathway plays at different stages of pancreatic organogenesis, including specification, proliferation, differentiation and function. Whereas, during early endoderm development, inhibition of the pathway is required for pancreatic specification, subsequent growth and differentiation of the fetal organ depends on the pathway being active. This appears especially true for exocrine acinar cells, the specification and differentiation of which also depend on β-catenin function. Whether the pathway plays an important role in development or function of endocrine islet cells, including insulin-producing β-cells, remains controversial. This question is particularly important in light of recent studies that implicate a downstream component of the pathway, TCF7L2, in human β-cell function. This review will cover recent work on Wnt/β-catenin signaling in pancreas development, emphasizing those points of controversy that most urgently require further investigation.
    Language English
    Publishing date 2008-10-09
    Publishing country United States
    Document type Journal Article
    ISSN 1547-6278
    ISSN 1547-6278
    DOI 10.4161/org.4.2.5853
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