EZH2 links pancreatitis to tissue regeneration and pancreatic cancer

Lasfargues, Charline; Pyronnet, Stéphane

doi:10.1016/j.clinre.2012.05.010

Cited by 5 publications

(4 citation statements)

References 3 publications

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“…Interestingly, the oncogenic mutant KRAS signal was found to increase the expression of EZH2 [41]. Furthermore, EZH2 suppresses the p16INK4 tumor suppressor gene, which is critical during injury-induced regeneration during pancreatitis and therefore, contributes to the progression to pancreatic cancer [42]. In addition, EZH2 has been characterized to directly affect the maintenance of the pancreatic cancer stem cell phenotype, which is also associated with its H3K27me3 catalytic activity [43].…”

Section: Nucleosome Remodeling Machines and Histone Modifying Enzymesmentioning

confidence: 99%

The Triple-Code Model for Pancreatic Cancer

Lomberk¹,

Urrutia²

2015

Surgical Clinics of North America

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Pancreatic adenocarcinoma (PDAC) is a lethal and painful disease, which has become one of the most frequent causes of death by malignant diseases around the world. Unfortunately, for the most part, this disease remains incurable. Significant advances in the field of genetics, particularly during the last two decades, has led to the proposal of a progression model, by which this cancer evolves by the accumulation of mutations and deletions in key oncogenes and tumor suppressor genes. This model has been remarkably useful for the development of tumor markers as well as elegant animal models. In spite of these strengths, this model does not take into consideration concepts and methodologies that have been derived from the field of epigenetics nor studies in the field of nuclear structure and function. Since our laboratory has been long been an advocate of these changes as critical for the pathobiology of pancreatic cancer, in this article, we describe an updated, more comprehensive model, which includes these concepts. With the widespread utilization of next generation sequencing for identifying both genetic and epigenetic changes genome-wide, we believe that the framework of this model will help to further identify and validate not only more but better markers for pancreatic cancer. In addition, as opposed to genetic changes, epigenetic alterations are amenable to pharmacological manipulations, consequently the familiarization with this model will help to better understand the potential beneficial effects of this type of therapy for this disease. Thus, we are optimistic that this new integrated paradigm will contribute to advance this field of research not only from a mechanistic point of view, but also from a translational one.

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Section: Nucleosome Remodeling Machines and Histone Modifying Enzymesmentioning

confidence: 99%

The Triple-Code Model for Pancreatic Cancer

Lomberk¹,

Urrutia²

2015

Surgical Clinics of North America

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“…One recent study demonstrated that loss of EZH2 results in impaired pancreatic regeneration and accelerates K‐ Ras (G12D)‐driven neoplasia, pancreatic intraepithelial neoplasia, in animal models . Those authors suggested that increased EZH2 expression in pancreatitis provided a mechanism of protection against progression to cancerous lesion, and loss of EZH2 in chronic pancreatitis initiates tumorigenesis . In a human study, however, only 33% of patients with chronic pancreatitis had some degree of EZH2 expression .…”

Section: Discussionmentioning

confidence: 99%

“…17 Those authors suggested that increased EZH2 expression in pancreatitis provided a mechanism of protection against progression to cancerous lesion, and loss of EZH2 in chronic pancreatitis initiates tumorigenesis. 17,18 In a human study, however, only 33% of patients with chronic pancreatitis had some degree of EZH2 expression. 11 Because the pancreatitis in the animal model was induced by cerulean, it may be different from chronic pancreatitis in humans.…”

Section: Cancer Cytopathologymentioning

confidence: 95%

Immunohistochemical analysis of E‐cadherin and zeste homolog 2 expression in endoscopic ultrasound‐guided fine‐needle aspiration of pancreatic adenocarcinoma

Gao

Antic

Hyjek

et al. 2013

Cancer Cytopathology

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“…Subsequently, acinar cell mass and function is finally restored through redifferentiation, which corresponds to restored basal levels of EZH2. EZH2 is involved therefore in homeostatic mechanisms that controls pancreatic regeneration, decreasing the risk of pancreatic cancer in patient with chronic pancreatic injury [156,184].…”

Section: Tumor Suppressor Roles Of Ezh2mentioning

confidence: 99%