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BMP9, but not BMP10, acts as a quiescence factor on tumor growth, vessel normalization and metastasis in a mouse model of breast cancer

Overview of attention for article published in Journal of Experimental & Clinical Cancer Research, August 2018
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Title
BMP9, but not BMP10, acts as a quiescence factor on tumor growth, vessel normalization and metastasis in a mouse model of breast cancer
Published in
Journal of Experimental & Clinical Cancer Research, August 2018
DOI 10.1186/s13046-018-0885-1
Pubmed ID
Authors

Marie Ouarné, Claire Bouvard, Gabriela Boneva, Christine Mallet, Johnny Ribeiro, Agnès Desroches-Castan, Emmanuelle Soleilhac, Emmanuelle Tillet, Olivier Peyruchaud, Sabine Bailly

Abstract

Angiogenesis has become an attractive target for cancer therapy. However, despite the initial success of anti-VEGF (Vascular endothelial growth factor) therapies, the overall survival appears only modestly improved and resistance to therapy often develops. Other anti-angiogenic targets are thus urgently needed. The predominant expression of the type I BMP (bone morphogenetic protein) receptor ALK1 (activin receptor-like kinase 1) in endothelial cells makes it an attractive target, and phase I/II trials are currently being conducted. ALK1 binds with strong affinity to two ligands that belong to the TGF-ß family, BMP9 and BMP10. In the present work, we addressed their specific roles in tumor angiogenesis, cancer development and metastasis in a mammary cancer model. For this, we used knockout (KO) mice for BMP9 (constitutive Gdf2-deficient), for BMP10 (inducible Bmp10-deficient) and double KO mice (Gdf2 and Bmp10) in a syngeneic immunocompetent orthotopic mouse model of spontaneous metastatic breast cancer (E0771). Our studies demonstrate a specific role for BMP9 in the E0771 mammary carcinoma model. Gdf2 deletion increased tumor growth while inhibiting vessel maturation and tumor perfusion. Gdf2 deletion also increased the number and the mean size of lung metastases. On the other hand, Bmp10 deletion did not significantly affect the E0771 mammary model and the double deletion (Gdf2 and Bmp10) did not lead to a stronger phenotype than the single Gdf2 deletion. Altogether, our data show that in a tumor environment BMP9 and BMP10 play different roles and thus blocking their shared receptor ALK1 is maybe not appropriate. Indeed, BMP9, but not BMP10, acts as a quiescence factor on tumor growth, lung metastasis and vessel normalization. Our results also support that activating rather than blocking the BMP9 pathway could be a new strategy for tumor vessel normalization in order to treat breast cancer.

Twitter Demographics

The data shown below were collected from the profiles of 3 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 45 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 45 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 9 20%
Student > Bachelor 8 18%
Researcher 5 11%
Student > Postgraduate 4 9%
Other 3 7%
Other 5 11%
Unknown 11 24%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 9 20%
Medicine and Dentistry 7 16%
Agricultural and Biological Sciences 5 11%
Engineering 4 9%
Pharmacology, Toxicology and Pharmaceutical Science 3 7%
Other 3 7%
Unknown 14 31%

Attention Score in Context

This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 20 October 2018.
All research outputs
#10,644,921
of 18,097,951 outputs
Outputs from Journal of Experimental & Clinical Cancer Research
#406
of 1,527 outputs
Outputs of similar age
#145,810
of 284,541 outputs
Outputs of similar age from Journal of Experimental & Clinical Cancer Research
#1
of 1 outputs
Altmetric has tracked 18,097,951 research outputs across all sources so far. This one is in the 40th percentile – i.e., 40% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,527 research outputs from this source. They receive a mean Attention Score of 2.8. This one has gotten more attention than average, scoring higher than 71% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 284,541 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 47th percentile – i.e., 47% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 1 others from the same source and published within six weeks on either side of this one. This one has scored higher than all of them