Heike Döppler
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View article: Coxsackievirus and adenovirus receptor expression facilitates enteroviral infections to drive the development of pancreatic cancer
Coxsackievirus and adenovirus receptor expression facilitates enteroviral infections to drive the development of pancreatic cancer Open
The development of pancreatic cancer requires both, acquisition of an oncogenic mutation in KRAS as well as an inflammatory insult. However, the physiological causes for pancreatic inflammation are less defined. We show here that oncogenic…
View article: Macrophage-induced reactive oxygen species in the initiation of pancreatic cancer: a mini-review
Macrophage-induced reactive oxygen species in the initiation of pancreatic cancer: a mini-review Open
Pancreatic inflammation is a risk factor for the development of pancreatic cancer. Increased presence of inflammatory macrophages can be found in response to a KRAS mutation in acinar cells or in response to experimentally-induced pancreat…
View article: Inflammatory and alternatively activated macrophages independently induce metaplasia but cooperatively drive pancreatic precancerous lesion growth
Inflammatory and alternatively activated macrophages independently induce metaplasia but cooperatively drive pancreatic precancerous lesion growth Open
The innate immune system has a key role in pancreatic cancer initiation, but the specific contribution of different macrophage populations is still ill-defined. While inflammatory (M1) macrophages have been shown to drive acinar-to-ductal …
View article: Supplementary Figure S2 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions
Supplementary Figure S2 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions Open
Supplementary Figure S2 shows analysis for macrophages in cytokeratin-19 positive regions of ADM (A), and analysis for ICAM-1, macrophages and cytokeratin-19 in PanIN lesions (B).
View article: Data from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions
Data from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions Open
Desmoplasia and an inflammatory environment are defining features of pancreatic cancer. Unclear is how pancreatic cells that undergo oncogenic transformation can cross-talk with immune cells and how this contributes to the development of p…
View article: Supplementary Figure S3 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions
Supplementary Figure S3 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions Open
Supplementary Figure S3 shows analysis for microvascularization (A), alcian blue staining of tissue sections (B), and ICAM-1 expression in human samples (C).
View article: Supplementary Methods from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions
Supplementary Methods from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions Open
Supplementary Methods
View article: Supplementary Figure S5 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions
Supplementary Figure S5 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions Open
Supplementary Figure S5 shows the treatment schedule (A), additional controls (B), basic complete blood count tests (C), and analysis for T-cells and neutrophils (D) for Figure 3F.
View article: Supplementary Figure S6 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions
Supplementary Figure S6 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions Open
Supplementary Figure S6 shows an analysis of ADM events in 3D explant culture in presence of the MMP inhibitor GM6001.
View article: Data from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions
Data from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions Open
Desmoplasia and an inflammatory environment are defining features of pancreatic cancer. Unclear is how pancreatic cells that undergo oncogenic transformation can cross-talk with immune cells and how this contributes to the development of p…
View article: Supplementary Figure S4 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions
Supplementary Figure S4 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions Open
Supplementary Figure S4 shows controls for Figure 3A (A, B), data supporting Figure 3B (C), analysis of Raw264.7 cells for polarization markers (D), and controls for polarization of primary macrophages (E,F).
View article: Supplementary Methods from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions
Supplementary Methods from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions Open
Supplementary Methods
View article: Supplementary Figure S2 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions
Supplementary Figure S2 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions Open
Supplementary Figure S2 shows analysis for macrophages in cytokeratin-19 positive regions of ADM (A), and analysis for ICAM-1, macrophages and cytokeratin-19 in PanIN lesions (B).
View article: Supplementary Figure S6 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions
Supplementary Figure S6 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions Open
Supplementary Figure S6 shows an analysis of ADM events in 3D explant culture in presence of the MMP inhibitor GM6001.
View article: Supplementary Figure S4 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions
Supplementary Figure S4 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions Open
Supplementary Figure S4 shows controls for Figure 3A (A, B), data supporting Figure 3B (C), analysis of Raw264.7 cells for polarization markers (D), and controls for polarization of primary macrophages (E,F).
View article: Supplementary Figure S1 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions
Supplementary Figure S1 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions Open
Supplementary Figure S1 shows the treatment scheme for GdCl3 (A), and analysis of tissue for T-cells and neutrophils (B), or for presence of PanIN lesions (C).
View article: Supplementary Figure S1 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions
Supplementary Figure S1 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions Open
Supplementary Figure S1 shows the treatment scheme for GdCl3 (A), and analysis of tissue for T-cells and neutrophils (B), or for presence of PanIN lesions (C).
View article: Supplementary Figure S5 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions
Supplementary Figure S5 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions Open
Supplementary Figure S5 shows the treatment schedule (A), additional controls (B), basic complete blood count tests (C), and analysis for T-cells and neutrophils (D) for Figure 3F.
View article: Supplementary Figure S3 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions
Supplementary Figure S3 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions Open
Supplementary Figure S3 shows analysis for microvascularization (A), alcian blue staining of tissue sections (B), and ICAM-1 expression in human samples (C).
View article: Ym1+ macrophages orchestrate fibrosis, lesion growth, and progression during development of murine pancreatic cancer
Ym1+ macrophages orchestrate fibrosis, lesion growth, and progression during development of murine pancreatic cancer Open
Desmoplasia around pancreatic lesions is a barrier for immune cells and a hallmark of developing and established pancreatic cancer. However, the contribution of the innate immune system to this process is ill-defined. Using the KC mouse mo…
View article: Generation of Hydrogen Peroxide and Downstream Protein Kinase D1 Signaling Is a Common Feature of Inducers of Pancreatic Acinar-to-Ductal Metaplasia
Generation of Hydrogen Peroxide and Downstream Protein Kinase D1 Signaling Is a Common Feature of Inducers of Pancreatic Acinar-to-Ductal Metaplasia Open
Pancreatic acinar-to-ductal metaplasia (ADM) is a reversible process that occurs after pancreatic injury, but becomes permanent and leads to pancreatic lesions in the presence of an oncogenic mutation in KRAS,. While inflammatory macrophag…
View article: Dysfunctional EGFR and oxidative stress-induced PKD1 signaling drive formation of DCLK1+ pancreatic stem cells
Dysfunctional EGFR and oxidative stress-induced PKD1 signaling drive formation of DCLK1+ pancreatic stem cells Open
View article: Sangivamycin and its derivatives inhibit Haspin-Histone H3-survivin signaling and induce pancreatic cancer cell death
Sangivamycin and its derivatives inhibit Haspin-Histone H3-survivin signaling and induce pancreatic cancer cell death Open
View article: The phosphorylation status of PIP5K1C at serine 448 can be predictive for invasive ductal carcinoma of the breast
The phosphorylation status of PIP5K1C at serine 448 can be predictive for invasive ductal carcinoma of the breast Open
Phosphatidylinositol-4-phosphate 5-kinase type-1C (PIP5K1C) is a lipid kinase that regulates focal adhesion dynamics and cell attachment through site-specific formation of phosphatidylinositol-4,5-bisphosphate (PI4,5P2). By comp…
View article: Src-mediated tyrosine phosphorylation of Protein Kinase D2 at focal adhesions regulates cell adhesion
Src-mediated tyrosine phosphorylation of Protein Kinase D2 at focal adhesions regulates cell adhesion Open
Dependent on their cellular localization, Protein Kinase D (PKD) enzymes regulate different processes including Golgi transport, cell signaling and response to oxidative stress. The localization of PKD within cells is mediated by interacti…
View article: The Presence of Interleukin-13 at Pancreatic ADM/PanIN Lesions Alters Macrophage Populations and Mediates Pancreatic Tumorigenesis
The Presence of Interleukin-13 at Pancreatic ADM/PanIN Lesions Alters Macrophage Populations and Mediates Pancreatic Tumorigenesis Open
View article: Differential regulation of PKD isoforms in oxidative stress conditions through phosphorylation of a conserved Tyr in the P+1 loop
Differential regulation of PKD isoforms in oxidative stress conditions through phosphorylation of a conserved Tyr in the P+1 loop Open
Protein kinases are essential molecules in life and their crucial function requires tight regulation. Many kinases are regulated via phosphorylation within their activation loop. This loop is embedded in the activation segment, which addit…
View article: Mitochondrial and Oxidative Stress-Mediated Activation of Protein Kinase D1 and Its Importance in Pancreatic Cancer
Mitochondrial and Oxidative Stress-Mediated Activation of Protein Kinase D1 and Its Importance in Pancreatic Cancer Open
Due to alterations in their metabolic activity and decreased mitochondrial efficiency, cancer cells often show increased generation of reactive oxygen species (ROS), but at the same time, to avoid cytotoxic signaling and to facilitate tumo…
View article: Protein Kinase D1 regulates focal adhesion dynamics and cell adhesion through Phosphatidylinositol-4-phosphate 5-kinase type-l γ
Protein Kinase D1 regulates focal adhesion dynamics and cell adhesion through Phosphatidylinositol-4-phosphate 5-kinase type-l γ Open
View article: The PRKD1 promoter is a target of the KRas-NF-κB pathway in pancreatic cancer
The PRKD1 promoter is a target of the KRas-NF-κB pathway in pancreatic cancer Open