ArticlePloS one2012
Concomitant targeting of EGF receptor, TGF-beta and SRC points to a novel therapeutic approach in pancreatic cancer.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 19 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
19 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- Retraction: Concomitant Targeting of EGF Receptor, TGF-beta and Src Points to a Novel Therapeutic Approach in Pancreatic Cancer.PloS one · 2020Article
- A phase I study of gemcitabine + dasatinib (gd) or gemcitabine + dasatinib + cetuximab (GDC) in refractory solid tumors.Cancer chemotherapy and pharmacology · 2019Article
- Regulation of transforming growth factor β-mediated epithelial-mesenchymal transition of lens epithelial cells by c-Src kinase under high glucose conditions.Experimental and therapeutic medicine · 2018Article
- Blocking fibrotic signaling in fibroblasts from patients with carpal tunnel syndrome.Journal of cellular physiology · 2018Review
- Functional Genome-wide Screening Identifies Targets and Pathways Sensitizing Pancreatic Cancer Cells to Dasatinib.Journal of Cancer · 2018Article
- The critical role of EGF-β-catenin signaling in the epithelial-mesenchymal transition in human glioblastoma.OncoTargets and therapy · 2017Article
- SMAD4 loss enables EGF, TGFβ1 and S100A8/A9 induced activation of critical pathways to invasion in human pancreatic adenocarcinoma cells.Oncotarget · 2016Article
- Prevention of pancreatic cancer in a hamster model by cAMP decrease.Oncotarget · 2016Article
- ATRA modulates mechanical activation of TGF-β by pancreatic stellate cells.Scientific reports · 2016Article
- Immunotherapy of Malignant Tumors in the Brain: How Different from Other Sites?Frontiers in oncology · 2016Review
- Article
- TGF-β signaling and its targeting for glioma treatment.American journal of cancer research · 2015Review
- Thiol-ene hydrogels as desmoplasia-mimetic matrices for modeling pancreatic cancer cell growth, invasion, and drug resistance.Biomaterials · 2014Article
- SIBLINGs and SPARC families: their emerging roles in pancreatic cancer.World journal of gastroenterology · 2014Review
- A mathematical model for pancreatic cancer growth and treatments.Journal of theoretical biology · 2014Article
- Inhibition of TGF-β and EGF pathway gene expression and migration of oral carcinoma cells by mucosa-associated lymphoid tissue 1.British journal of cancer · 2013Article
- Targeting TGF-β signaling in cancer.Expert opinion on therapeutic targets · 2013Review
- The influence of matrix properties on growth and morphogenesis of human pancreatic ductal epithelial cells in 3D.Biomaterials · 2013Article
Corrections and comments
- Retraction · 2020-05-13Concerns/Issues about Data · Duplication of/in Article · Original Data and/or Images not Provided and/or not Available ·
- Retracted
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
To test the hypothesis that concomitant targeting of the epidermal growth factor receptor (EGFR) and transforming growth factor-beta (TGF-β) may offer a novel therapeutic approach in pancreatic cancer, EGFR silencing by RNA interference (shEGFR) was combined with TGF-β sequestration by soluble TGF-β receptor II (sTβRII). Effects on colony formation in 3-dimensional culture, tumor formation in nude mice, and downstream signaling were monitored. In both ASPC-1 and T3M4 cells, either shEGFR or sTβRII significantly inhibited colony formation. However, in ASPC-1 cells, combining shEGFR with sTβRII reduced colony formation more efficiently than either approach alone, whereas in T3M4 cells, shEGFR-mediated inhibition of colony formation was reversed by sTβRII. Similarly, in vivo growth of ASPC-1-derived tumors was attenuated by either shEGFR or sTβRII, and was markedly suppressed by both vectors. By contrast, T3M4-derived tumors either failed to form or were very small when EGFR alone was silenced, and these effects were reversed by sTβRII due to increased cancer cell proliferation. The combination of shEGFR and sTβRII decreased phospho-HER2, phospho-HER3, phoshpo-ERK and phospho-src (Tyr416) levels in ASPC-1 cells but increased their levels in T3M4 cells. Moreover, inhibition of both EGFR and HER2 by lapatinib or of src by SSKI-606, PP2, or dasatinib, blocked the sTβRII-mediated antagonism of colony formation in T3M4 cells. Together, these observations suggest that concomitantly targeting EGFR, TGF-β, and src may constitute a novel therapeutic approach in PDAC that prevents deleterious cross-talk between EGFR family members and TGF-β-dependent pathways.
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.