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EGFR isoforms and gene regulation in human endometrial cancer cells

Overview of attention for article published in Molecular Cancer, June 2010
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2 patents

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70 Mendeley
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Title
EGFR isoforms and gene regulation in human endometrial cancer cells
Published in
Molecular Cancer, June 2010
DOI 10.1186/1476-4598-9-166
Pubmed ID
Authors

Lina Albitar, Gavin Pickett, Marilee Morgan, Jason A Wilken, Nita J Maihle, Kimberly K Leslie

Abstract

Epidermal growth factor (EGF) and its receptor (EGFR) constitute a principal growth-promoting pathway in endometrial cancer cells. Pre-clinical studies were undertaken to compare the expression of EGFR isoforms and the downstream effects of activating or blocking EGFR function in Ishikawa H cells, derived from a moderately differentiated type I endometrioid adenocarcinoma, or in Hec50co cells, derived from a poorly differentiated type II adenocarcinoma with papillary serous sub-differentiation. We investigated whether EGFR mutations are present in the tyrosine kinase domain (exons 18-22) of EGFR and also whether EGFR isoforms are expressed in the Ishikawa H or Hec50co cell lines. Sequence of the EGFR tyrosine kinase domain proved to be wild type in both cell lines. While both cell lines expressed full-length EGFR (isoform A), EGFR and sEGFR (isoform D) were expressed at significantly lower levels in Hec50co cells compared to Ishikawa H cells. Analysis of gene expression following EGF vs. gefitinib treatment (a small molecule EGFR tyrosine kinase inhibitor) was performed. Early growth response 1, sphingosine kinase 2, dual specificity phosphatase 6, and glucocorticoid receptor DNA binding factor 1 are members of a cluster of genes downstream of EGFR that are differentially regulated by treatment with EGF compared to gefitinib in Ishikawa H cells, but not in Hec50co cells. Type I Ishikawa H and type II Hec50co endometrial carcinoma cells both express EGFR and sEGFR, but differ markedly in their responsiveness to the EGFR inhibitor gefitinib. This difference is paralleled by differences in the expression of sEGFR and EGFR, as well as in their transcriptional response following treatment with either EGF or gefitinib. The small cluster of differently regulated genes reported here in these type I vs. type II endometrial cancer-derived cell lines may identify candidate biomarkers useful for predicting sensitivity to EGFR blockade.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 70 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Malaysia 1 1%
Spain 1 1%
Germany 1 1%
Brazil 1 1%
Unknown 66 94%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 19 27%
Researcher 12 17%
Student > Master 7 10%
Student > Postgraduate 5 7%
Student > Bachelor 4 6%
Other 11 16%
Unknown 12 17%
Readers by discipline Count As %
Agricultural and Biological Sciences 25 36%
Biochemistry, Genetics and Molecular Biology 14 20%
Medicine and Dentistry 10 14%
Computer Science 4 6%
Pharmacology, Toxicology and Pharmaceutical Science 1 1%
Other 1 1%
Unknown 15 21%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 3. 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 12 February 2020.
All research outputs
#7,475,808
of 22,854,458 outputs
Outputs from Molecular Cancer
#547
of 1,722 outputs
Outputs of similar age
#33,616
of 94,335 outputs
Outputs of similar age from Molecular Cancer
#10
of 25 outputs
Altmetric has tracked 22,854,458 research outputs across all sources so far. This one is in the 44th percentile – i.e., 44% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,722 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.7. This one has gotten more attention than average, scoring higher than 55% 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 94,335 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 23rd percentile – i.e., 23% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 25 others from the same source and published within six weeks on either side of this one. This one is in the 12th percentile – i.e., 12% of its contemporaries scored the same or lower than it.