ArticleOncogene2016
Targeting tumor-stroma crosstalk: the example of the NT157 inhibitor.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 9 citations in OpenAlex.
- Cancer associated fibroblast derived gene signature determines cancer subtypes and prognostic model construction in head and neck squamous cell carcinomas.Cancer medicine · 2023Article
- NT157 has antineoplastic effects and inhibits IRS1/2 and STAT3/5 in JAK2Signal transduction and targeted therapy · 2020Article
- ConvPath: A software tool for lung adenocarcinoma digital pathological image analysis aided by a convolutional neural network.EBioMedicine · 2019Article
- Muc1 knockout potentiates murine lung carcinogenesis involving an epiregulin-mediated EGFR activation feedback loop.Carcinogenesis · 2017Article
- Multiscalar cellular automaton simulates in-vivo tumour-stroma patterns calibrated from in-vitro assay data.BMC medical informatics and decision making · 2017Article
- Capturing tumor complexity in vitro: Comparative analysis of 2D and 3D tumor models for drug discovery.Scientific reports · 2016Article
Corrections and comments
- Comment on
- Comment on
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Recent clinical research has provided evidence that cancer progression and therapy resistance is driven not only by tumor's genetic profile but also by complex paracrine interactions within the tumor microenvironment (TME). The role of TME in modulating tumor drug sensitivity is increasingly recognized and targeting TME has been the focus of novel therapeutic approaches. Two recent reports show that a new anti-cancer drug, the inhibitor NT157 has the potential to inhibit IGF-1R and STAT3 signaling pathways in cancer cells and stroma cells of TME leading to a decrease in cancer cell survival.
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.