Abstract
The study identifies an opportunity to discover a PKA-independent pathway downstream of oncogene GNAS for managing IPMN lesions and their progression to PDAC.
©2024 American Association for Cancer Research.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Acinar Cells / metabolism
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Acinar Cells / pathology
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Carcinoma, Pancreatic Ductal / genetics
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Carcinoma, Pancreatic Ductal / metabolism
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Carcinoma, Pancreatic Ductal / pathology
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Cell Proliferation*
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Chromogranins* / genetics
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Chromogranins* / metabolism
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Cyclic AMP-Dependent Protein Kinases* / genetics
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Cyclic AMP-Dependent Protein Kinases* / metabolism
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GTP-Binding Protein alpha Subunits, Gs* / genetics
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GTP-Binding Protein alpha Subunits, Gs* / metabolism
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Humans
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Organoids* / metabolism
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Organoids* / pathology
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Pancreatic Ducts / cytology
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Pancreatic Ducts / metabolism
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Pancreatic Ducts / pathology
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Pancreatic Neoplasms* / genetics
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Pancreatic Neoplasms* / metabolism
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Pancreatic Neoplasms* / pathology
Substances
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GNAS protein, human
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GTP-Binding Protein alpha Subunits, Gs
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Chromogranins
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Cyclic AMP-Dependent Protein Kinases