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1. von Furstenberg RJ, Li J, Stolarchuk C, Feder R, Campbell A, Kruger L, Gonzalez LM, Blikslager AT, Cardona DM, McCall SJ, Henning SJ, Garman KS: Porcine Esophageal Submucosal Gland Culture Model Shows Capacity for Proliferation and Differentiation. Cell Mol Gastroenterol Hepatol; 2017 Nov;4(3):385-404
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  • BACKGROUND & AIMS: Although cells comprising esophageal submucosal glands (ESMGs) represent a potential progenitor cell niche, new models are needed to understand their capacity to proliferate and differentiate.
  • METHODS: We evaluated proliferation in human ESMGs from normal and diseased tissue by proliferating cell nuclear antigen immunohistochemistry.
  • CONCLUSIONS: Our results suggest that the activated ESMG state, seen in both human disease and our porcine model, may provide a source of cells to repopulate damaged epithelium in a normal manner (squamous) or abnormally (columnar epithelium).

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  • (PMID = 28936470.001).
  • [ISSN] 2352-345X
  • [Journal-full-title] Cellular and molecular gastroenterology and hepatology
  • [ISO-abbreviation] Cell Mol Gastroenterol Hepatol
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK098528; United States / NCI NIH HHS / CA / P30 CA014236; United States / NIDDK NIH HHS / DK / P30 DK034987
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; 3D Culture / 3D, 3-dimensional / ANOVA, analysis of variance / Acinar Ductal Metaplasia / Adult Stem Cell / BE, Barrett’s esophagus / Barrett’s Esophagus / CK7, cytokeratin 7 / DMSO, dimethyl sulfoxide / EAC, esophageal adenocarcinoma / EGF, epidermal growth factor / ESMG, esophageal submucosal gland / EdU, 5-ethynyl-2′-deoxyuridine / Esophagus / IHC, immunohistochemistry / PBS, phosphate-buffered saline / PCNA, proliferating cell nuclear antigen / RFA, radiofrequency ablation
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2. Matthaei H, Semaan A, Hruban RH: The genetic classification of pancreatic neoplasia. J Gastroenterol; 2015 May;50(5):520-32
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  • The recent decline in the cost of DNA sequencing has allowed tumor sequencing to be conducted on a large scale, which, in turn, has led to an unprecedented understanding of the genetic events that drive neoplasia.
  • [MeSH-major] Adenocarcinoma, Mucinous / genetics. Biomarkers, Tumor / genetics. Carcinoma, Acinar Cell / genetics. Carcinoma, Pancreatic Ductal / genetics. Mutation. Pancreatic Neoplasms / genetics. Sequence Analysis, DNA

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  • (PMID = 25605630.001).
  • [ISSN] 1435-5922
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA62924
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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3. Morris JP 4th, Cano DA, Sekine S, Wang SC, Hebrok M: Beta-catenin blocks Kras-dependent reprogramming of acini into pancreatic cancer precursor lesions in mice. J Clin Invest; 2010 Feb;120(2):508-20
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  • WT mouse acinar cells rapidly regenerate following injury that mimics acute pancreatitis, a process characterized by transient reactivation of pathways involved in embryonic pancreatic development.
  • In contrast, such injury promotes the development of pancreatic ductal adenocarcinoma (PDA) precursor lesions in mice expressing a constitutively active form of the GTPase, Kras, in the exocrine pancreas.
  • The molecular environment that mediates acinar regeneration versus the development of PDA precursor lesions is poorly understood.
  • Here, we used genetically engineered mice to demonstrate that mutant Kras promotes acinar-to-ductal metaplasia (ADM) and pancreatic cancer precursor lesion formation by blocking acinar regeneration following acute pancreatitis.
  • Our results indicate that beta-catenin is required for efficient acinar regeneration.
  • In addition, canonical beta-catenin signaling, a pathway known to regulate embryonic acinar development, is activated following acute pancreatitis.
  • This regeneration-associated activation of beta-catenin signaling was not observed during the initiation of Kras-induced acinar-to-ductal reprogramming.
  • Therefore, these results suggest that beta-catenin signaling is a critical determinant of acinar plasticity and that it is inhibited during Kras-induced fate decisions that specify PDA precursors, highlighting the importance of temporal regulation of embryonic signaling pathways in the development of neoplastic cell fates.


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4. Zhang J, Shao J, Zhu L, Zhao R, Xing J, Wang J, Guo X, Tu S, Han B, Yu K: Molecular profiling identifies prognostic markers of stage IA lung adenocarcinoma. Oncotarget; 2017 Sep 26;8(43):74846-74855
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  • [Title] Molecular profiling identifies prognostic markers of stage IA lung adenocarcinoma.
  • We previously showed that different pathologic subtypes were associated with different prognostic values in patients with stage IA lung adenocarcinoma (AC).
  • We hypothesize that differential gene expression profiles of different subtypes may be valuable factors for prognosis in stage IA lung adenocarcinoma.
  • We performed microarray gene expression profiling on tumor tissues micro-dissected from patients with acinar and solid predominant subtypes of stage IA lung adenocarcinoma.
  • We performed the Gene Set Enrichment Analysis (GSEA) analysis to look for gene expression signatures associated with tumor subtypes.
  • The histologic subtypes of all patients were classified according to the 2015 WHO lung Adenocarcinoma classification.
  • Further, we identified a list of genes that may serve as prognostic markers for stage IA lung adenocarcinoma.
  • Validation in the TCGA database shows that these genes are correlated with survival, suggesting that they are novel prognostic factors for stage IA lung adenocarcinoma.
  • In conclusion, we have uncovered novel prognostic factors for stage IA lung adenocarcinoma using gene expression profiling in combination with histopathology subtyping.

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  • (PMID = 29088828.001).
  • [ISSN] 1949-2553
  • [Journal-full-title] Oncotarget
  • [ISO-abbreviation] Oncotarget
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; acinar / differently expressed genes (DEGs) / gene expression profiling / lung adenocarcinoma / solid
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5. Lotan TL, Gupta NS, Wang W, Toubaji A, Haffner MC, Chaux A, Hicks JL, Meeker AK, Bieberich CJ, De Marzo AM, Epstein JI, Netto GJ: ERG gene rearrangements are common in prostatic small cell carcinomas. Mod Pathol; 2011 Jun;24(6):820-8
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  • [Title] ERG gene rearrangements are common in prostatic small cell carcinomas.
  • Small cell carcinoma of the prostate is a rare subtype with an aggressive clinical course.
  • Despite the frequent occurrence of ERG gene rearrangements in acinar carcinoma, the incidence of these rearrangements in prostatic small cell carcinoma is unclear.
  • In addition, molecular markers to distinguish prostatic small cell carcinomas from lung and bladder small cell carcinomas may be clinically useful.
  • We examined the occurrence of ERG gene rearrangements by fluorescence in situ hybridization in prostatic, bladder and lung small cell carcinomas.
  • Overall, 45% (10/22) of prostatic small cell carcinoma cases harbored ERG rearrangements, whereas no cases of bladder or lung small cell carcinomas showed ERG rearrangement (0/12 and 0/13, respectively).
  • Of prostatic small cell carcinoma cases, 80% (8/10) showed ERG deletion and 20% (2/10) showed ERG translocation.
  • In 83% (5/6) of prostatic small cell carcinoma cases in which a concurrent conventional prostatic acinar carcinoma component was available for analysis, there was concordance for the presence/absence of ERG gene rearrangement between the different subtypes.
  • ERG, AR and NKX3-1 protein expression was detected in a minority of prostatic small cell carcinoma cases (23, 27 and 18%, respectively), while these markers were positive in the majority of concurrent acinar carcinoma cases (66, 83 and 83%, respectively).
  • The presence of ERG rearrangements in nearly half of the prostatic small cell carcinomas is a similar rate of rearrangement to that found in prostatic acinar carcinomas.
  • Furthermore, the high concordance rate of ERG rearrangement between the small cell and acinar components in a given patient supports a common origin for these two subtypes of prostate cancer.
  • Finally, the absence of ERG rearrangement in bladder or lung small cell carcinomas highlights the utility of detecting ERG rearrangement in small cell carcinomas of unknown primary for establishing prostatic origin.
  • [MeSH-major] Carcinoma, Small Cell / pathology. Gene Rearrangement. Homeodomain Proteins / genetics. Prostatic Neoplasms / pathology. Trans-Activators / genetics. Transcription Factors / genetics

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  • (PMID = 21336263.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA058236
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / ERG protein, human; 0 / Homeodomain Proteins; 0 / NKX3-1 protein, human; 0 / Receptors, Androgen; 0 / Trans-Activators; 0 / Transcription Factors
  • [Other-IDs] NLM/ NIHMS403696; NLM/ PMC3484363
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6. Wong CH, Li YJ, Chen YC: Therapeutic potential of targeting acinar cell reprogramming in pancreatic cancer. World J Gastroenterol; 2016 Aug 21;22(31):7046-57
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  • [Title] Therapeutic potential of targeting acinar cell reprogramming in pancreatic cancer.
  • Pancreatic ductal adenocarcinoma (PDAC) is a common pancreatic cancer and the fourth leading cause of cancer death in the United States.
  • Treating this life-threatening disease remains challenging due to the lack of effective prognosis, diagnosis and therapy.
  • Apart from pancreatic duct cells, acinar cells may also be the origin of PDAC.
  • During pancreatitis or combined with activating KRas(G12D) mutation, acinar cells lose their cellular identity and undergo a transdifferentiation process called acinar-to-ductal-metaplasia (ADM), forming duct cells which may then transform into pancreatic intraepithelial neoplasia (PanIN) and eventually PDAC.
  • During ADM, the activation of mitogen-activated protein kinases, Wnt, Notch and phosphatidylinositide 3-kinases/Akt signaling inhibits the transcription of acinar-specific genes, including Mist and amylase, but promotes the expression of ductal genes, such as cytokeratin-19.
  • In addition, the transdifferentiated cells regain acinar identity, indicating ADM may be a reversible process.
  • [MeSH-major] Acinar Cells / pathology. Cellular Reprogramming. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Carcinoma, Pancreatic Ductal / pathology. Humans. Intercellular Signaling Peptides and Proteins / physiology. MAP Kinase Signaling System / physiology. Metaplasia. NFATC Transcription Factors / physiology. SOX9 Transcription Factor / physiology. TRPP Cation Channels / physiology. Wnt Signaling Pathway

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  • (PMID = 27610015.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DKK3 protein, human; 0 / Intercellular Signaling Peptides and Proteins; 0 / NFATC Transcription Factors; 0 / NFATC1 protein, human; 0 / SOX9 Transcription Factor; 0 / SOX9 protein, human; 0 / TRPP Cation Channels; 0 / polycystic kidney disease 1 protein
  • [Other-IDs] NLM/ PMC4988312
  • [Keywords] NOTNLM ; Acinar cells / Acinar-to-ductal metaplasia / Pancreatic ductal adenocarcinoma / Reprogramming / Signal transduction
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7. Saloman JL, Albers KM, Li D, Hartman DJ, Crawford HC, Muha EA, Rhim AD, Davis BM: Ablation of sensory neurons in a genetic model of pancreatic ductal adenocarcinoma slows initiation and progression of cancer. Proc Natl Acad Sci U S A; 2016 Mar 15;113(11):3078-83
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  • [Title] Ablation of sensory neurons in a genetic model of pancreatic ductal adenocarcinoma slows initiation and progression of cancer.
  • Pancreatic ductal adenocarcinoma (PDAC) is characterized by an exuberant inflammatory desmoplastic response.
  • Here, we show that sensory neurons, an under-studied cohort of the pancreas tumor stroma, play a significant role in the initiation and progression of the early stages of PDAC.
  • Also at the PanIN2 stage, pancreas acinar-derived cells frequently invade along sensory neurons into the spinal cord and migrate caudally to the lower thoracic and upper lumbar regions.
  • Thus, pancreatic sensory neurons comprise an important stromal cell population that supports the initiation and progression of PDAC and may represent a potential target for prevention in high-risk populations.
  • [MeSH-major] Capsaicin / therapeutic use. Carcinoma, Pancreatic Ductal / prevention & control. Denervation. Pancreas / innervation. Pancreatic Neoplasms / prevention & control. Sensory Receptor Cells / physiology
  • [MeSH-minor] Adenocarcinoma in Situ / pathology. Adenocarcinoma in Situ / physiopathology. Afferent Pathways. Animals. Animals, Newborn. Ceruletide / toxicity. Disease Progression. Female. Ganglia, Sympathetic / physiopathology. Genes, ras. Humans. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Myelitis / complications. Myelitis / genetics. Myelitis / physiopathology. Neoplasm Invasiveness. Pancreatitis / chemically induced. Pancreatitis / complications. Pancreatitis / physiopathology. Precancerous Conditions / chemically induced. Precancerous Conditions / complications. Precancerous Conditions / physiopathology. Spinal Cord / physiopathology. Spinothalamic Tracts / physiopathology. Thoracic Vertebrae

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  • (PMID = 26929329.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / P30-DK034933; United States / NIDDK NIH HHS / DK / K08 DK088945; United States / NCI NIH HHS / CA / R01-CA177857; United States / NIDDK NIH HHS / DK / P30 DK050306; United States / NIDDK NIH HHS / DK / K08-DK088945; United States / NIDDK NIH HHS / DK / P30 DK034933; United States / NCI NIH HHS / CA / R01 CA159222; United States / NINDS NIH HHS / NS / T32 NS086749; United States / NCI NIH HHS / CA / L30 CA136450; United States / NIDDK NIH HHS / DK / P30-DK050306; United States / NCI NIH HHS / CA / R01 CA177857
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 888Y08971B / Ceruletide; S07O44R1ZM / Capsaicin
  • [Other-IDs] NLM/ PMC4801275
  • [Keywords] NOTNLM ; PanIN / inflammation / pancreatic ductal adenocarcinoma / sensory neuron / tumorigenesis
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8. Wu J, Liu X, Nayak SG, Pitarresi JR, Cuitiño MC, Yu L, Hildreth BE 3rd, Thies KA, Schilling DJ, Fernandez SA, Leone G, Ostrowski MC: Generation of a pancreatic cancer model using a Pdx1-Flp recombinase knock-in allele. PLoS One; 2017;12(9):e0184984
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  • The contribution of the tumor microenvironment to the development of pancreatic adenocarcinoma (PDAC) is unclear.
  • The LSL-KrasG12D/+;LSL-p53R172H/+;Pdx-1-Cre (KPC) tumor model, which is widely utilized to faithfully recapitulate human pancreatic cancer, depends on Cre-mediated recombination in the epithelial lineage to drive tumorigenesis.
  • Therefore, specific Cre-loxP recombination in stromal cells cannot be applied in this model, limiting the in vivo investigation of stromal genetics in tumor initiation and progression.
  • This mouse specifically recombines Frt loci in pancreatic epithelial cells, including acinar, ductal, and islet cells.
  • When combined with the Frt-STOP-Frt KrasG12D and p53Frt mouse lines, simultaneous Pdx1FlpO activation of mutant Kras and deletion of p53 results in the spectrum of pathologic changes seen in PDAC, including PanIN lesions and ductal carcinoma.
  • This will provide an excellent in vivo tool to study the roles of genes in different cell types and multiple cell compartments within the pancreatic tumor microenvironment.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. DNA Nucleotidyltransferases / metabolism. Disease Models, Animal. Homeodomain Proteins / physiology. Pancreatic Neoplasms / pathology. Trans-Activators / physiology
  • [MeSH-minor] Animals. Disease Progression. Female. Male. Mice. Mice, Inbred C57BL. Proto-Oncogene Proteins p21(ras) / genetics. Signal Transduction. Tumor Microenvironment. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 28934293.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA097189
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Trans-Activators; 0 / Tumor Suppressor Protein p53; 0 / pancreatic and duodenal homeobox 1 protein; EC 2.7.7.- / DNA Nucleotidyltransferases; EC 2.7.7.- / FLP recombinase; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
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9. Yamada S, Nabeshima A, Noguchi H, Nawata A, Nishii H, Guo X, Wang KY, Hisaoka M, Nakayama T: Coincidence between malignant perivascular epithelioid cell tumor arising in the gastric serosa and lung adenocarcinoma. World J Gastroenterol; 2015 Jan 28;21(4):1349-56
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Coincidence between malignant perivascular epithelioid cell tumor arising in the gastric serosa and lung adenocarcinoma.
  • Since biopsy samples from the lung and abdomen revealed poorly differentiated adenocarcinoma and malignant tumor, clinicians first interpreted the abdominal mass as metastatic carcinoma, and a right lower lobectomy with following resection of the mass was performed.
  • On microscopic examination, the lung tumor was composed of a proliferation of highly atypical epithelial cells having abundant eosinophilic cytoplasm, predominantly arranged in an acinar or solid growth pattern with vessel permeation, while the abdominal tumor consisted of sheets or nests with markedly atypical epithelioid cells having pleomorphic nuclei and abundant eosinophilic to clear cytoplasm focally in a radial perivascular or infiltrative growth pattern.
  • Therefore, we finally made a diagnosis of malignant perivascular epithelioid cell tumor (PEComa) arising in the gastric serosa, combined with primary lung adenocarcinoma.
  • Furthermore, small papillary carcinoma of the thyroid gland was identified.
  • The current case describes the coincidence of malignant PEComa with other carcinomas, posing a challenge in distinction from metastatic tumor disease.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Neoplasms, Multiple Primary / pathology. Perivascular Epithelioid Cell Neoplasms / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Abdominal Pain / etiology. Adult. Back Pain / etiology. Biomarkers, Tumor / analysis. Biopsy. Carcinoma / pathology. Diagnosis, Differential. Gastrectomy. Humans. Immunohistochemistry. Male. Pneumonectomy. Predictive Value of Tests. Thyroid Neoplasms / pathology. Tomography, X-Ray Computed

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  • (PMID = 25632212.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; Adenocarcinoma of lung; Thyroid cancer, papillary
  • [Other-IDs] NLM/ PMC4306183
  • [Keywords] NOTNLM ; Gastric serosa / Lung adenocarcinoma / Malignant / Metastatic carcinoma / Perivascular epithelioid cell tumor
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10. Gomez-Chou SB, Swidnicka-Siergiejko AK, Badi N, Chavez-Tomar M, Lesinski GB, Bekaii-Saab T, Farren MR, Mace TA, Schmidt C, Liu Y, Deng D, Hwang RF, Zhou L, Moore T, Chatterjee D, Wang H, Leng X, Arlinghaus RB, Logsdon CD, Cruz-Monserrate Z: Lipocalin-2 Promotes Pancreatic Ductal Adenocarcinoma by Regulating Inflammation in the Tumor Microenvironment. Cancer Res; 2017 May 15;77(10):2647-2660
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  • [Title] Lipocalin-2 Promotes Pancreatic Ductal Adenocarcinoma by Regulating Inflammation in the Tumor Microenvironment.
  • Lipocalin-2 (LCN2) promotes malignant development in many cancer types.
  • LCN2 is upregulated in patients with pancreatic ductal adenocarcinoma (PDAC) and in obese individuals, but whether it contributes to PDAC development is unclear.
  • Mice with acinar cell-specific expression of Kras<sup>G12D</sup> were crossed with Lcn2-depleted animals and fed isocaloric diets with varying amounts of fat content.
  • We also used a syngeneic orthotopic PDAC mouse model to study tumor growth in the presence or absence of Lcn2 expression.
  • Depletion of Lcn2 diminished extracellular matrix deposition, immune cell infiltration, PanIN formation, and tumor growth.
  • LCN2 modulated the secretion of proinflammatory cytokines in PSC of the PDAC tumor microenvironment, whereas downregulation of LCN2-specific receptor SLC22A17 blocked these effects.
  • Our results reveal how LCN2 acts in the tumor microenvironment links obesity, inflammation, and PDAC development.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Carcinoma, Pancreatic Ductal / pathology. Lipocalin-2 / metabolism. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. Tumor Microenvironment
  • [MeSH-minor] Animals. Cytokines / blood. Cytokines / metabolism. Disease Models, Animal. Gene Expression Regulation, Neoplastic. Gene Knockdown Techniques. Humans. Inflammation Mediators / blood. Inflammation Mediators / metabolism. Kaplan-Meier Estimate. Mice. Mice, Knockout. Mice, Transgenic. Prognosis. RNA, Small Interfering / genetics

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  • [Copyright] ©2017 American Association for Cancer Research.
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  • (PMID = 28249896.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / P30 CA016672; United States / NIDDK NIH HHS / DK / R01 DK052067
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Inflammation Mediators; 0 / Lipocalin-2; 0 / RNA, Small Interfering; Pancreatic Carcinoma
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