ArticleOncogene2012
A KrasG12D-driven genetic mouse model of pancreatic cancer requires glypican-1 for efficient proliferation and angiogenesis.
Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
49 citing papers in PubMed, 78 citations in OpenAlex.
- Tumor promotion or suppression: Revisiting the role of EXT1 and Heparan sulfate.Histology and histopathology · 2026Review
- Defining the extracellular matrix for targeted immunotherapy in adult and pediatric brain cancer.NPJ precision oncology · 2025Article
- Development of CAR-T Therapies and Personalized Vaccines for the Treatment of Cholangiocarcinoma: Current Progress, Mechanisms of Action, and Challenges.The American journal of pathology · 2025Review
- KRAS Mutation Subtypes and Their Association with Other Driver Mutations in Oncogenic Pathways.Cells · 2024Review
- Clinical Evaluation of the Pancreatic Cancer Microenvironment: Opportunities and Challenges.Cancers · 2024Review
- The next "sweet" spot for pancreatic ductal adenocarcinoma: Glycoprotein for early detection.Mass spectrometry reviews · 2023Review
- Cells function as a ternary logic gate to decide migration direction under integrated chemical and fluidic cues.Lab on a chip · 2023Article
- Upregulated miR-194-5p suppresses retinal microvascular endothelial cell dysfunction and mitigates the symptoms of hypertensive retinopathy in mice by targeting SOX17 and VEGF signaling.Cell cycle (Georgetown, Tex.) · 2023Article
- Heparan sulfate proteoglycans in cancer: Pathogenesis and therapeutic potential.Advances in cancer research · 2023Article
- Signal processing capacity of the cellular sensory machinery regulates the accuracy of chemotaxis under complex cues.iScience · 2021Article
- Role of glypican-1 in regulating multiple cellular signaling pathways.American journal of physiology. Cell physiology · 2021Review
- The Glypican-1/HGF/C-Met and Glypican-1/VEGF/VEGFR2 Ternary Complexes Regulate Hair Follicle Angiogenesis.Frontiers in cell and developmental biology · 2021Article
- Radioimmunotherapy for solid tumors: spotlight on Glypican-1 as a radioimmunotherapy target.Therapeutic advances in medical oncology · 2021Article
- Sry-related High Mobility Group Box 17 Functions as a Tumor Suppressor by Antagonizing the Wingless-related Integration Site Pathway.Journal of cancer prevention · 2020Review
- The Role of Glypicans in Cancer Progression and Therapy.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020Review
- An engineered pancreatic cancer model with intra-tumoral heterogeneity of driver mutations.Lab on a chip · 2020Article
- Roles of Proteoglycans and Glycosaminoglycans in Cancer Development and Progression.International journal of molecular sciences · 2020Review
- Article
- Elevated microRNA-125b inhibits cytotrophoblast invasion and impairs endothelial cell function in preeclampsia.Cell death discovery · 2020Article
- Glypican-3: A New Target for Diagnosis and Treatment of Hepatocellular Carcinoma.Journal of Cancer · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Pancreatic ductal adenocarcinomas (PDACs) exhibit multiple molecular alterations and overexpress heparin-binding growth factors (HBGFs) and glypican-1 (GPC1), a heparan sulfate proteoglycan that promotes efficient signaling by HBGFs. It is not known, however, whether GPC1 has a role in genetic mouse models of PDAC. Therefore, we generated a GPC1 null mouse that combines pancreas-specific Cre-mediated activation of oncogenic Kras (Kras(G12D)) with deletion of a conditional INK4A/Arf allele (Pdx1-Cre;LSL-Kras(G12D);INK4A/Arf(lox/lox);GPC1(-/-) mice). By comparison with Pdx1-Cre;LSL-Kras(G12D);INK4A/Arf(lox/lox) mice that were wild type for GPC1, the Pdx1-Cre;LSL-Kras(G12D);INK4A/Arf(lox/lox);GPC1(-/-) mice exhibited attenuated pancreatic tumor growth and invasiveness, decreased cancer cell proliferation and mitogen-activated protein kinase activation. These mice also exhibited suppressed angiogenesis in conjunction with decreased expression of messenger RNAs encoding several pro-angiogenic factors and molecules, including vascular endothelial growth factor-A (VEGF-A), SRY-box containing gene (SOX17), chemokine C-X3-C motif ligand 1 (CX3CL1) and integrin β3 (ITGB3). Moreover, pancreatic cancer cells isolated from the tumors of GPC1(-/-) mice were not as invasive in response to fibroblast growth factor-2 (FGF-2) as cancer cells isolated from wild-type mice, and formed smaller tumors that exhibited an attenuated metastatic potential. Similarly, VEGF-A and FGF-2 did not enhance the migration of hepatic endothelial cells and immortalized murine embryonic fibroblasts isolated from GPC1 null mice. These data demonstrate in an oncogenic Kras-driven genetic mouse model of PDAC that tumor growth, angiogenesis and invasion are enhanced by GPC1, and suggest that suppression of GPC1 may be an important component of therapeutic strategies in PDAC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.