ArticleNeoplasia (New York, N.Y.)2011
Ectopic overexpression of Sonic Hedgehog (Shh) induces stromal expansion and metaplasia in the adult murine pancreas.
Article in Neoplasia (New York, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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.
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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.
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Who cites it
22 citing papers in PubMed, 43 citations in OpenAlex.
- Hedgehog signaling drives glial cell plasticity and oncogenic reprogramming in gastroenteropancreatic neuroendocrine neoplasms.Molecular cancer · 2026Article
- Mechanisms and therapeutic potential of the hedgehog signaling pathway in cancer.Cell death discovery · 2025Review
- Cancer-associated fibroblasts as therapeutic targets for cancer: advances, challenges, and future prospects.Journal of biomedical science · 2025Review
- Developmental function of Piezo1 in mouse submandibular gland morphogenesis.Histochemistry and cell biology · 2023Article
- A Quick Guide to CAF Subtypes in Pancreatic Cancer.Cancers · 2023Review
- Review
- Forebrain Shh overexpression improves cognitive function and locomotor hyperactivity in an aneuploid mouse model of Down syndrome and its euploid littermates.Acta neuropathologica communications · 2021Article
- Inhibition of Hedgehog Signaling Alters Fibroblast Composition in Pancreatic Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- Review
- Inflammatory and Senescent Phenotype of Pancreatic Stellate Cells Induced by Sqstm1 Downregulation Facilitates Pancreatic Cancer Progression.International journal of biological sciences · 2019Article
- The Stromal Niche for Epithelial Stem Cells: A Template for Regeneration and a Brake on Malignancy.Cancer cell · 2017Review
- A sesquiterpene lactone fromOncology letters · 2016Article
- Article
- SMO expression in colorectal cancer: associations with clinical, pathological, and molecular features.Annals of surgical oncology · 2014Article
- Mirk kinase inhibition blocks the in vivo growth of pancreatic cancer cells.Genes & cancer · 2014Article
- Stromal response to Hedgehog signaling restrains pancreatic cancer progression.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Inhibition of Hedgehog signaling in the gastrointestinal tract: targeting the cancer microenvironment.Cancer treatment reviews · 2014Review
- Cancer subclonal genetic architecture as a key to personalized medicine.Neoplasia (New York, N.Y.) · 2013Article
- Mechanistic insights into self-reinforcing processes driving abnormal histogenesis during the development of pancreatic cancer.The American journal of pathology · 2013Review
- Overcoming intratumor heterogeneity of polygenic cancer drug resistance with improved biomarker integration.Neoplasia (New York, N.Y.) · 2012Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Ligand-dependent activation of the Hedgehog (Hh) signaling pathway has been implicated in both tumor initiation and metastasis of pancreatic ductal adenocarcinoma (PDAC). Prior studies in genetically engineered mouse models (GEMMs) have assessed the role of Hh signaling by cell autonomous expression of a constitutively active Gli2 within epithelial cells. On the contrary, aberrant pathway reactivation in the human exocrine pancreas occurs principally as a consequence of Sonic Hh ligand (Shh) overexpression from epithelial cells. To recapitulate the cognate pathophysiology of Hh signaling observed in the human pancreas, we examined GEMM where Hh ligand is conditionally overexpressed within the mature exocrine pancreas using a tamoxifen-inducible Elastase-Cre promoter (Ela-CreERT2;LSL-mShh). We also facilitated potential cell autonomous epithelial responsiveness to secreted Hh ligand by generating compound transgenic mice with concomitant expression of the Hh receptor Smoothened (Ela-CreERT2;LSL-mShh;LSL-mSmo). Of interest, none of these mice developed intraductal precursor lesions or PDAC during the follow-up period of up to 12 months after tamoxifen induction. Instead, all animals demonstrated marked expansion of stromal cells, consistent with the previously described epithelial-to-stromal paracrine Hh signaling. Hh responsiveness was mirrored by the expression of primary cilia within the expanded mesenchymal compartment and the absence within mature acinar cells. In the absence of cooperating mutations, Hh ligand overexpression in the mature exocrine pancreas is insufficient to induce neoplasia, even when epithelial cells coexpress the Smo receptor. This autochthonous model serves as a platform for studying epithelial stromal interactions in pancreatic carcinogenesis.
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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.