Evidence map›Paper›PMID 23423860›Full record

ReviewCancer2013

Modulation of c-Met signaling and cellular sensitivity to radiation: potential implications for therapy.

Vikas Bhardwaj, Tina Cascone, Maria Angelica Cortez, Arya Amini, Jaden Evans, Ritsuko U Komaki, John V Heymach, James W Welsh

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.5field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Clinical Perspectives in Brain Metastasis.Cold Spring Harbor perspectives in medicine · 2020
    Review
  8. Article
  9. Article
  10. Article
  11. Journal of experimental pharmacology · 2020
    Review
  12. Article
  13. Targeting the cMET pathway augments radiation response without adverse effect on hearing in NF2 schwannoma models.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  14. Developmentally regulated signaling pathways in glioma invasion.Cellular and molecular life sciences : CMLS · 2018
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Vikas BhardwajDepartment of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Tina Cascone
Maria Angelica Cortez
Arya Amini
Jaden Evans
Ritsuko U Komaki
John V Heymach
James W Welsh
The University of Texas MD Anderson Cancer Center · USTexas Tech University · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI GIBBONS, DON LYNN · 1996 to 2024
$57.4M
X-RAY BEAM SPECTRA MEASUREMENTP01CA006294 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ANG, K KIAN · 1985 to 2009
$11.0M
Personalizing NSCLC Therapy: Exploiting KRAS activated pathwaysR01CA155196 · NCI · YALE UNIVERSITY · PI HERBST, ROY S, PAPADIMITRAKOPOULOU, VASSILIKI · 2011 to 2015
$2.8M
Inhibiting oncogenic KRAS for cancer therapyR01CA160398 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI POWIS, GARTH · 2012 to 2016
$1.9M
Markers and therapeutic strategies for overcoming chemoradiotherapy resistanceR01CA168484 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HEYMACH, JOHN V. · 2011 to 2015
$1.4M
NCI NIH HHS CA016672NCI NIH HHS CA155196NCI NIH HHS CA160398NCI NIH HHS CA168484NCI NIH HHS P01 CA006294NCI NIH HHS P01CA06294NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA070907NCI NIH HHS R01 CA155196NCI NIH HHS R01 CA160398NCI NIH HHS R01 CA168484PHS HHS K12 11111246
6 · The paper itself

Abstract

The c-Met/hepatocyte growth factor receptor and its family members are known to promote cancer cell migration and invasion. Signaling within and beyond this pathway contributes to the systemic spread of metastases through induction of the epithelial-mesenchymal transition, a process also implicated in mediating resistance to current anticancer therapies, including radiation. Induction of c-Met has also been observed after irradiation, suggesting that c-Met participates in radiation-induced disease progression through the epithelial-mesenchymal transition. Therefore, c-Met inhibition is an attractive target for potentially mitigating radiation resistance. This article summarizes key findings regarding crosstalk between radiotherapy and c-Met and discusses studies performed to date in which c-Met inhibition was used as a strategy to increase cellular radiosensitivity.

Indexed as

AnilidesAnimalsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntineoplastic AgentsCell MovementDNA DamageEpithelial-Mesenchymal TransitionErlotinib HydrochlorideGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessNeoplasmsNeovascularization, PathologicProto-Oncogene Proteins c-metPyridinesAnilidesAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntineoplastic AgentsARQ 197cabozantinibErlotinib HydrochlorideMET protein, humanProto-Oncogene Proteins c-metPyridinesPyrrolidinonesQuinazolinesQuinolinesrilotumumab

Identifiers

PMID23423860
PMCPMC3648606
OpenAlexW2080282656

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.