Evidence map›Paper›PMID 21447745›Full record

ReviewCancer research2011

BRAF(V600E) and microenvironment in thyroid cancer: a functional link to drive cancer progression.

Carmelo Nucera, Jack Lawler, Sareh Parangi

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 96 citations in OpenAlex.

  1. Review
  2. Review
  3. BRAF mutation and tumor immune microenvironment in new era.American journal of cancer research · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
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  11. Article
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  13. Article
  14. BRAFBiomedicines · 2022
    Article
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  16. Article
  17. Review
  18. Article
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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

3 authors at 2 institutions in 1 country.

Carmelo NuceraThyroid Cancer Research Laboratory, Endocrine Surgery Unit, Massachusetts General Hospital, Harvard Medical School, and Division of Cancer Biology and Angiogenesis, Department of Pathology, Harvard Medical School, Boston, Massachusetts, USA.
Jack Lawler
Sareh Parangi
Harvard University · USMassachusetts General Hospital · US

Funding

The Role of BRAF Mutation in Thyroid Cancer InvasionR01CA149738 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI PARANGI, SAREH · 2011 to 2015
$1.6M
Inhibition of angiogenesis by thrombospondin-1 (A2)R01CA130895 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LAWLER, JOHN W · 2009 to 2012
$1.4M
NCI NIH HHS CA130895NCI NIH HHS R01 CA130895NCI NIH HHS R01 CA149738
6 · The paper itself

Abstract

Papillary thyroid cancer (PTC) rates continue to increase in the United States and Europe, and, although most patients do well, some recur and die of their disease. Patients with PTC harboring the BRAF(V600E) mutation seem to display a more aggressive clinical behavior, but little is known about the role of this mutation in crucial processes in the tumor microenvironment, such as tumor adhesion, migration, invasion, and metastasis. The extracellular matrix (ECM) microenvironment is not merely a structural scaffold for the cellular elements of the epithelial and stromal microenvironment, but it also elicits a profound influence on cell behavior affecting viability, proliferation, adhesion, and motility. The effects of BRAF(V600E) on cell surface receptors (i.e., integrins) and ECM noncellular components [i.e., thrombospondin-1 (TSP-1) and fibronectin (FN)] seem to trigger different pathologic biological processes in a cell context-dependent manner. This review focuses on the recent progress in understanding the role of BRAF(V600E) in the regulation of some ECM noncellular components and trans-membrane receptors of the microenvironment in PTC in order to design novel targeted therapies directed at the BRAF(V600E) multifaceted signaling cascades. Some of these targeted therapeutics, such as ATP-competitive BRAF(V600E) inhibitors (i.e., orally bioavailable PLX4720 and PLX4032 compounds), are already under investigation.

Indexed as

AnimalsDisease ProgressionHumansProtein Kinase InhibitorsProto-Oncogene Proteins B-rafThyroid NeoplasmsTumor MicroenvironmentProtein Kinase InhibitorsProto-Oncogene Proteins B-raf

Identifiers

PMID21447745
PMCPMC3913061
OpenAlexW2122505925

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.