期刊
CANCER RESEARCH
卷 82, 期 21, 页码 3932-3949出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-22-0396
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资金
- Thermo Fisher Scientific
- European Cancer Moonshot Center Lund
- U.S. National Cancer Institutes International Cancer Proteogenome Consortium (ICPC)
- U.S.National Cancer Institute's Clinical Proteomic Tumor Analysis Consortium (CPTAC)
- Academy of Finland [307415, 324929]
- University of Helsinki
- Sigrid Juselius Foundation
- Fondation Leducq
- Jane and Aatos Erkko Foundation
- Emil Aaltonen Foundation
- Orion Research Foundation
- Ida Montin's Foundation
- Magnus Ehrnrooth Foundation
- Cancer Foundation Finland
- Helsinki University Hospital Research Funds
- Mary and Georg Ehrnrooth Foundation
- LENDULET-BIOMAG Grant [2018-342]
- European Regional Development Funds [GINOP-2.3.2-15201600006, GINOP-2.3.215201600026, GINOP-2.3.2-152016-00037]
- H2020 (ERAPERMED-COMPASS, DiscovAIR
- Chan Zuckerberg Initiative
- Berta Kamprad Foundation, Lund, Sweden [FBKS-2020-22, FBKS-2020-18]
Proteomic analyses of PDAC patients revealed widespread downregulation of pancreatic secretory functions in PDAC lesions.
Pancreatic ductal adenocarcinoma (PDAC) is among the deadliest malignancies and potentially curable only with radical surgical resection at early stages. The tumor microenvironment has been shown to be central to the development and progression of PDAC. A better understanding of how early human PDAC metabolically communicates with its environment and differs from healthy pancreas could help improve PDAC diagnosis and treatment. Here we performed deep proteomic analyses from diagnostic specimens of operable, treatment-narve PDAC patients (n = 14), isolating four tissue compartments by laser-capture microdissection: PDAC lesions, tumor-adjacent but morphologically benign exocrine glands, and connective tissues neighboring each of these compartments. Protein and pathway levels were compared between compartments and with control pancreatic proteomes. Selected targets were studied immunohistochemically in the 14 patients and in additional tumor microarrays, and lipid deposition was assessed by nonlinear label-free imaging (n = 16). Widespread downregulation of pancreatic secretory functions was observed, which was
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