Pancreatic Ducts

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Axel Behrens - One of the best experts on this subject based on the ideXlab platform.

  • tissue curvature and apicobasal mechanical tension imbalance instruct cancer morphogenesis
    Nature, 2019
    Co-Authors: Hendrik A Messal, Rute M M Ferreira, Christopher Gribben, Victoria Wang, Corina Cotoi, Guillaume Salbreux, Axel Behrens
    Abstract:

    Tubular epithelia are a basic building block of organs and a common site of cancer occurrence1–4. During tumorigenesis, transformed cells overproliferate and epithelial architecture is disrupted. However, the biophysical parameters that underlie the adoption of abnormal tumour tissue shapes are unknown. Here we show in the pancreas of mice that the morphology of epithelial tumours is determined by the interplay of cytoskeletal changes in transformed cells and the existing tubular geometry. To analyse the morphological changes in tissue architecture during the initiation of cancer, we developed a three-dimensional whole-organ imaging technique that enables tissue analysis at single-cell resolution. Oncogenic transformation of Pancreatic Ducts led to two types of neoplastic growth: exophytic lesions that expanded outwards from the duct and endophytic lesions that grew inwards to the ductal lumen. Myosin activity was higher apically than basally in wild-type cells, but upon transformation this gradient was lost in both lesion types. Three-dimensional vertex model simulations and a continuum theory of epithelial mechanics, which incorporate the cytoskeletal changes observed in transformed cells, indicated that the diameter of the source epithelium instructs the morphology of growing tumours. Three-dimensional imaging revealed that—consistent with theory predictions—small Pancreatic Ducts produced exophytic growth, whereas large Ducts deformed endophytically. Similar patterns of lesion growth were observed in tubular epithelia of the liver and lung; this finding identifies tension imbalance and tissue curvature as fundamental determinants of epithelial tumorigenesis. Three-dimensional imaging of mouse Pancreatic Ducts before and after oncogenic transformation reveals that epithelial tumorigenesis is determined by the relationship between tissue curvature and apical–basal mechanical tension.

Corina Cotoi - One of the best experts on this subject based on the ideXlab platform.

  • tissue curvature and apicobasal mechanical tension imbalance instruct cancer morphogenesis
    Nature, 2019
    Co-Authors: Hendrik A Messal, Rute M M Ferreira, Christopher Gribben, Victoria Wang, Corina Cotoi, Guillaume Salbreux, Axel Behrens
    Abstract:

    Tubular epithelia are a basic building block of organs and a common site of cancer occurrence1–4. During tumorigenesis, transformed cells overproliferate and epithelial architecture is disrupted. However, the biophysical parameters that underlie the adoption of abnormal tumour tissue shapes are unknown. Here we show in the pancreas of mice that the morphology of epithelial tumours is determined by the interplay of cytoskeletal changes in transformed cells and the existing tubular geometry. To analyse the morphological changes in tissue architecture during the initiation of cancer, we developed a three-dimensional whole-organ imaging technique that enables tissue analysis at single-cell resolution. Oncogenic transformation of Pancreatic Ducts led to two types of neoplastic growth: exophytic lesions that expanded outwards from the duct and endophytic lesions that grew inwards to the ductal lumen. Myosin activity was higher apically than basally in wild-type cells, but upon transformation this gradient was lost in both lesion types. Three-dimensional vertex model simulations and a continuum theory of epithelial mechanics, which incorporate the cytoskeletal changes observed in transformed cells, indicated that the diameter of the source epithelium instructs the morphology of growing tumours. Three-dimensional imaging revealed that—consistent with theory predictions—small Pancreatic Ducts produced exophytic growth, whereas large Ducts deformed endophytically. Similar patterns of lesion growth were observed in tubular epithelia of the liver and lung; this finding identifies tension imbalance and tissue curvature as fundamental determinants of epithelial tumorigenesis. Three-dimensional imaging of mouse Pancreatic Ducts before and after oncogenic transformation reveals that epithelial tumorigenesis is determined by the relationship between tissue curvature and apical–basal mechanical tension.

Rute M M Ferreira - One of the best experts on this subject based on the ideXlab platform.

  • tissue curvature and apicobasal mechanical tension imbalance instruct cancer morphogenesis
    Nature, 2019
    Co-Authors: Hendrik A Messal, Rute M M Ferreira, Christopher Gribben, Victoria Wang, Corina Cotoi, Guillaume Salbreux, Axel Behrens
    Abstract:

    Tubular epithelia are a basic building block of organs and a common site of cancer occurrence1–4. During tumorigenesis, transformed cells overproliferate and epithelial architecture is disrupted. However, the biophysical parameters that underlie the adoption of abnormal tumour tissue shapes are unknown. Here we show in the pancreas of mice that the morphology of epithelial tumours is determined by the interplay of cytoskeletal changes in transformed cells and the existing tubular geometry. To analyse the morphological changes in tissue architecture during the initiation of cancer, we developed a three-dimensional whole-organ imaging technique that enables tissue analysis at single-cell resolution. Oncogenic transformation of Pancreatic Ducts led to two types of neoplastic growth: exophytic lesions that expanded outwards from the duct and endophytic lesions that grew inwards to the ductal lumen. Myosin activity was higher apically than basally in wild-type cells, but upon transformation this gradient was lost in both lesion types. Three-dimensional vertex model simulations and a continuum theory of epithelial mechanics, which incorporate the cytoskeletal changes observed in transformed cells, indicated that the diameter of the source epithelium instructs the morphology of growing tumours. Three-dimensional imaging revealed that—consistent with theory predictions—small Pancreatic Ducts produced exophytic growth, whereas large Ducts deformed endophytically. Similar patterns of lesion growth were observed in tubular epithelia of the liver and lung; this finding identifies tension imbalance and tissue curvature as fundamental determinants of epithelial tumorigenesis. Three-dimensional imaging of mouse Pancreatic Ducts before and after oncogenic transformation reveals that epithelial tumorigenesis is determined by the relationship between tissue curvature and apical–basal mechanical tension.

Ralph H Hruban - One of the best experts on this subject based on the ideXlab platform.

  • an illustrated consensus on the classification of Pancreatic intraepithelial neoplasia and intraductal papillary mucinous neoplasms
    The American Journal of Surgical Pathology, 2004
    Co-Authors: Ralph H Hruban, Volkan N Adsay, J Alboressaavedra, Carolyn C Compton, David S Klimstra, Kyoichi Takaori, Andrew V Biankin, Sandra A Biankin, Noriyoshi Fukushima, Toru Furukawa
    Abstract:

    Invasive Pancreatic ductal adenocarcinoma is an almost uniformly fatal disease. Several distinct noninvasive precursor lesions can give rise to invasive adenocarcinoma of the pancreas, and the prevention, detection, and treatment of these noninvasive lesions offers the potential to cure early Pancreatic cancers. Noninvasive precursors of invasive ductal adenocarcinoma of the pancreas include Pancreatic intraepithelial neoplasias (PanINs), intraductal papillary mucinous neoplasms (IPMNs), and mucinous cystic neoplasms. Diagnostic criteria, including a distinct ovarian-type stroma, and a consistent nomenclature are well established for mucinous cystic neoplasms. By contrast, consistent nomenclatures and diagnostic criteria have been more difficult to establish for PanINs and IPMNs. Because both PanINs and IPMNs consist of intraductal neoplastic proliferations of columnar, mucin-containing cells with a variable degree of papilla formation, the distinction between these two classes of precursor lesions remains problematic. Thus, considerable ambiguities still exist in the classification of noninvasive neoplasms in the Pancreatic Ducts. A meeting of international experts on precursor lesions of Pancreatic cancer was held at The Johns Hopkins Hospital from August 18 to 19, 2003. The purpose of this meeting was to define an international acceptable set of diagnostic criteria for PanINs and IPMNs and to address a number of ambiguities that exist in the previously reported classification systems for these neoplasms. We present a consensus classification of the precursor lesions in the Pancreatic Ducts, PanINs and IPMNs.

  • lymphoplasmacytic chronic cholecystitis and biliary tract disease in patients with lymphoplasmacytic sclerosing pancreatitis
    The American Journal of Surgical Pathology, 2003
    Co-Authors: Susan C Abraham, Ralph H Hruban, Marcia Cruzcorrea, Pedram Argani, Emma E Furth, John K Boitnott
    Abstract:

    Lymphoplasmacytic sclerosing pancreatitis (LPSP) represents a distinctive form of chronic pancreatitis characterized by diffuse fibroinflammatory infiltrates that can involve both the Pancreatic Ducts and acinar parenchyma. Several cases of inflammatory infiltrates within the gallbladder have been r

  • Pancreatic intraepithelial neoplasia a new nomenclature and classification system for Pancreatic duct lesions
    The American Journal of Surgical Pathology, 2001
    Co-Authors: Ralph H Hruban, Scott E Kern, N V Adsay, J Alboressaavedra, Carolyn C Compton, Elizabeth Garrett, Steven N Goodman, David S Klimstra, G Kloppel, Daniel S Longnecker
    Abstract:

    Proliferative epithelial lesions in the smaller caliber Pancreatic Ducts and ductules have been the subject of numerous morphologic, clinical, and genetic studies; however, a standard nomenclature and diagnostic criteria for classifying these lesion have not been established. To evaluate the uniform

  • genetic progression in the Pancreatic Ducts
    American Journal of Pathology, 2000
    Co-Authors: Ralph H Hruban, Robb E Wilentz, Scott E Kern
    Abstract:

    The genetic progression described by Yamano et al in this issue of The American Journal of Pathology helps establish a progression model for Pancreatic ductal carcinoma. This progression model has a number of important implications for the classification of lesions in the pancreas and for the future early detection and chemoprevention of Pancreatic carcinoma.

Susumu Shinoura - One of the best experts on this subject based on the ideXlab platform.

  • endosonographic finding of the simultaneous depiction of bile and Pancreatic Ducts can predict difficult biliary cannulation on endoscopic retrograde cholangiopancreatography
    PLOS ONE, 2020
    Co-Authors: Susumu Shinoura, Akihiro Tokushige, Kenji Chinen, Hideki Mori, Shin Kato, Shinichiro Ueda
    Abstract:

    Thus far, no curved linear array endoscopic ultrasound (CLAEUS) findings were established as predictors of difficult selective bile duct cannulation (SBDC). This study aimed to identify CLAEUS findings to predict endoscopic retrograde cholangiopancreatography (ERCP) cases with difficult SBDC. This single-center, retrospective cohort study was conducted between July 2014 and June 2017. This study included all consecutive patients who underwent CLAEUS prior to naive ERCP. A CLAEUS finding of the simultaneous depiction of bile and Pancreatic Ducts at the second portion of the duodenum (D2) (simultaneous depiction) was selected as a possible predictor of difficult SBDC, and the κ values in the evaluation of inter- and intra-observer variabilities for “simultaneous depiction” were 0.65 and 0.77, respectively, with substantial correlation. Among the 986 patients who underwent ERCP, 80 patients were relevant for evaluation. Logistic regression analysis revealed strong association between “simultaneous depiction” and difficult SBDC (odds ratio 15.4, 95% confidence interval 4.2–56.0; p<0.001). Among patients who underwent CLAEUS prior to naive ERCP, a strong correlation was observed between “simultaneous depiction” and the risk of difficult SBDC. An endoscopist can prepare for difficult SBDC by “simultaneous depiction.” The finding enables pertinent planning when performing ERCP, such as setting time limits and selecting alternative devices, techniques, and skilled endoscopists, for difficult SBDC with minimal complications including post-ERCP pancreatitis. However, a future prospective study is necessary to establish the procedure algorithm for suspected difficult SBDC cases based on CLAEUS.

  • Endosonographic finding of the simultaneous depiction of bile and Pancreatic Ducts can predict difficult biliary cannulation on endoscopic retrograde cholangiopancreatography.
    'Public Library of Science (PLoS)', 2020
    Co-Authors: Susumu Shinoura, Akihiro Tokushige, Kenji Chinen, Hideki Mori, Shin Kato, Shinichiro Ueda
    Abstract:

    Thus far, no curved linear array endoscopic ultrasound (CLAEUS) findings were established as predictors of difficult selective bile duct cannulation (SBDC). This study aimed to identify CLAEUS findings to predict endoscopic retrograde cholangiopancreatography (ERCP) cases with difficult SBDC. This single-center, retrospective cohort study was conducted between July 2014 and June 2017. This study included all consecutive patients who underwent CLAEUS prior to naïve ERCP. A CLAEUS finding of the simultaneous depiction of bile and Pancreatic Ducts at the second portion of the duodenum (D2) (simultaneous depiction) was selected as a possible predictor of difficult SBDC, and the κ values in the evaluation of inter- and intra-observer variabilities for "simultaneous depiction" were 0.65 and 0.77, respectively, with substantial correlation. Among the 986 patients who underwent ERCP, 80 patients were relevant for evaluation. Logistic regression analysis revealed strong association between "simultaneous depiction" and difficult SBDC (odds ratio 15.4, 95% confidence interval 4.2-56.0; p