ReviewOncotarget2017
Breaking the crosstalk of the cellular tumorigenic network: Hypothesis for addressing resistances to targeted therapies in advanced NSCLC.
Review in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 10 citations in OpenAlex.
- Breaking the crosstalk of the Cellular Tumorigenic Network by low-dose combination therapy in lung cancer patient-derived xenografts.Communications biology · 2022Article
- Cancer-Associated Fibroblasts Differentiated by Exosomes Isolated from Cancer Cells Promote Cancer Cell Invasion.International journal of molecular sciences · 2020Article
- Interaction between CXCR4 and EGFR and downstream PI3K/AKT pathway in lung adenocarcinoma A549 cells and transplanted tumor in nude mice.International journal of clinical and experimental pathology · 2020Article
- Combination Strategies Using EGFR-TKi in NSCLC Therapy: Learning from the Gap between Pre-Clinical Results and Clinical Outcomes.International journal of biological sciences · 2018Review
- Metapristone (RU486 metabolite) suppresses NSCLC by targeting EGFR-mediated PI3K/AKT pathway.Oncotarget · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the light of current treatment developments for non-small cell lung cancer (NSCLC), the idea of a plastic cellular tumorigenic network bound by key paracrine signaling pathways mediating resistances to targeted therapies is brought forward. Based on a review of available preclinical and clinical data in NSCLC combinational approaches to address drivers of this network with marketed drugs are discussed. Five criteria for selecting drug combination regimens aiming at its disruption and thereby overcoming resistances are postulated.
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.