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CCL2 and CCL5 are novel therapeutic targets for estrogen-dependent breast cancer.

Overview of attention for article published in Clinical Cancer Research, April 2015
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3 tweeters

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45 Mendeley
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Title
CCL2 and CCL5 are novel therapeutic targets for estrogen-dependent breast cancer.
Published in
Clinical Cancer Research, April 2015
DOI 10.1158/1078-0432.ccr-15-0204
Pubmed ID
Authors

Susanne Svensson, Annelie Abrahamsson, Gabriela Vazquez Rodriguez, Anna-Karin Olsson, Lasse Jensen, Yihai Cao, Charlotta Dabrosin

Abstract

Novel therapeutic targets of estrogen receptor (ER)-positive breast cancers are urgently needed because current anti-estrogen therapy causes severe adverse effects, nearly 50% of patients are intrinsically resistant, and the majority of recurrences have maintained ER expression. We investigated the role of estrogen dependent chemokine expression and subsequent cancer growth in human tissues and experimental breast cancer models. For in vivo sampling of human chemokines microdialysis was used in breast cancers of women or normal human breast tissue before and after tamoxifen therapy. Estrogen exposure and targeted therapies were assessed in immune competent PyMT murine breast cancer, orthotopic human breast cancers in nude mice, cell culture of cancer cells, and freshly isolated human macrophages. Cancer cell dissemination was investigated using zebrafish. ER+ cancers in women produced high levels of extracellular CCL2 and CCL5 in vivo, which was associated with infiltration of tumor-associated macrophages. In experimental breast cancer, estradiol enhanced macrophage influx and angiogenesis through increased release of CCL2, CCL5, and vascular endothelial growth factor. These effects were inhibited by anti-CCL2 or anti-CCL5 therapy, which resulted in potent inhibition of cancer growth. In addition, estradiol induced a pro-tumorigenic activation of the macrophages. In a zebrafish model, macrophages increased cancer cell dissemination via CCL2 and CCL5 in the presence of estradiol, which was inhibited with anti-CCL2 and anti-CCL5 treatment. Our findings shed new light on the mechanisms underlying the progression of ER+ breast cancer and indicate the potential of novel therapies targeting CCL2 and CCL5 pathways.

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 %
United Kingdom 1 2%
Brazil 1 2%
China 1 2%
Turkey 1 2%
Unknown 41 91%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 9 20%
Student > Bachelor 8 18%
Researcher 8 18%
Student > Master 6 13%
Student > Postgraduate 3 7%
Other 11 24%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 16 36%
Medicine and Dentistry 11 24%
Agricultural and Biological Sciences 9 20%
Unspecified 3 7%
Immunology and Microbiology 2 4%
Other 4 9%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. 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 27 April 2015.
All research outputs
#3,322,539
of 5,028,598 outputs
Outputs from Clinical Cancer Research
#3,064
of 4,255 outputs
Outputs of similar age
#104,837
of 154,715 outputs
Outputs of similar age from Clinical Cancer Research
#175
of 218 outputs
Altmetric has tracked 5,028,598 research outputs across all sources so far. This one is in the 29th percentile – i.e., 29% of other outputs scored the same or lower than it.
So far Altmetric has tracked 4,255 research outputs from this source. They receive a mean Attention Score of 4.1. This one is in the 21st percentile – i.e., 21% of its peers scored the same or lower than it.
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 154,715 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 27th percentile – i.e., 27% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 218 others from the same source and published within six weeks on either side of this one. This one is in the 14th percentile – i.e., 14% of its contemporaries scored the same or lower than it.