Evidence map›Paper›PMID 26804166›Full record

ArticleOncogene2016

High expression of connective tissue growth factor accelerates dissemination of leukaemia.

J E Wells, M Howlett, H M Halse, J Heng, J Ford, L C Cheung, A L Samuels, M Crook, A K Charles, C H Cole and 1 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. The role of the CCN family of proteins in blood cancers.Journal of cell communication and signaling · 2016
    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

11 authors at 3 institutions in 1 country.

J E WellsTelethon Kids Institute, University of Western Australia, Perth, Western Australia, Australia.
M HowlettTelethon Kids Institute, University of Western Australia, Perth, Western Australia, Australia.
H M HalseTelethon Kids Institute, University of Western Australia, Perth, Western Australia, Australia.
J HengTelethon Kids Institute, University of Western Australia, Perth, Western Australia, Australia.
J FordTelethon Kids Institute, University of Western Australia, Perth, Western Australia, Australia.
L C CheungTelethon Kids Institute, University of Western Australia, Perth, Western Australia, Australia.
A L SamuelsTelethon Kids Institute, University of Western Australia, Perth, Western Australia, Australia.
M CrookPrincess Margaret Hospital for Children, Perth, Western Australia, Australia.
A K CharlesPrincess Margaret Hospital for Children, Perth, Western Australia, Australia.
C H ColeSchool of Paediatrics and Child Health, University of Western Australia, Perth, Western Australia, Australia.
U R KeesTelethon Kids Institute, University of Western Australia, Perth, Western Australia, Australia.
The Kids Research Institute Australia · AUUniversity of Western Australia · AUPrincess Margaret Hospital for Children · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To improve treatment of acute lymphoblastic leukaemia (ALL), a better understanding of disease development is needed to tailor new therapies. Connective tissue growth factor (CTGF/CCN2) is highly expressed in leukaemia cells from the majority of paediatric patients with B-lineage ALL (pre-B ALL). CTGF is a matricellular protein and plays a role in aggressive cancers. Here we have genetically engineered leukaemia cells to modulate CTGF expression levels. Elevated CTGF levels accelerated disease dissemination and reduced survival in NOD/SCID mice. In vitro studies showed that CTGF protein induces stromal cell proliferation, promotes adhesion of leukaemia cells to stromal cells and leads to overexpression of genes associated with cell cycle and synthesis of extracellular matrix (ECM). Corresponding data from our leukaemia xenograft models demonstrated that CTGF leads to increased proliferation of non-leukaemia cells and deposition of ECM in the bone marrow. We document for the first time a functional role of CTGF in altering disease progression in a lymphoid malignancy. The findings provide support for targeting the bone marrow microenvironment in aggressive forms of leukaemia.

Indexed as

AnimalsCell CycleCell DifferentiationCell ProliferationConnective Tissue Growth FactorDisease ProgressionExtracellular MatrixGene Expression Regulation, LeukemicGene Knockdown TechniquesHumansMicePrecursor Cell Lymphoblastic Leukemia-LymphomaStromal CellsXenograft Model Antitumor AssaysCCN2 protein, humanConnective Tissue Growth Factor

Identifiers

PMID26804166
OpenAlexW2273141996

What OpenQuestion holds

Textmetadata
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.