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The effect of a germline mutation in the APC gene on β-catenin in human embryonic stem cells

Overview of attention for article published in BMC Cancer, December 2016
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About this Attention Score

  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (93rd percentile)
  • High Attention Score compared to outputs of the same age and source (97th percentile)

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2 news outlets
blogs
1 blog
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10 X users
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2 Facebook pages
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1 Google+ user
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1 Redditor

Citations

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9 Dimensions

Readers on

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31 Mendeley
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Title
The effect of a germline mutation in the APC gene on β-catenin in human embryonic stem cells
Published in
BMC Cancer, December 2016
DOI 10.1186/s12885-016-2809-9
Pubmed ID
Authors

Nofar Yedid, Yael Kalma, Mira Malcov, Ami Amit, Revital Kariv, Michal Caspi, Rina Rosin-Arbesfeld, Dalit Ben-Yosef

Abstract

Most cases of colorectal cancer (CRC) are initiated by inactivation mutations in the APC gene, which is a negative regulator of the Wnt-β-catenin pathway. Patients with familial adenomatous polyposis (FAP) inherit a germline mutation in one APC allele, and loss of the second allele leads to the development of polyps that will turn malignant if not removed. It is not fully understood which molecular mechanisms are activated by APC loss and when the loss of the second APC allele occurs. Two FAP human embryonic stem cell (hESCs) lines were derived from APC mutated embryos following pre-implantation genetic diagnosis (PGD) for FAP. These FAP-hESCs were cultured in vitro and following extended culture: 1) β-catenin expression was analyzed by Western blot analysis; 2) Wnt-β-catenin/TCF-mediated transcription luciferase assay was performed; 3) cellular localization of β-catenin was evaluated by immunoflorecence confocal microscopy; and 4) DNA sequencing of the APC gene was performed. We have established a novel human in-vitro model for studying malignant transformation, using hESCs that carry a germline mutation in the APC gene following PGD for FAP. Extended culturing of FAP1 hESCs led to activation of the Wnt signaling pathway, as demonstrated by enhanced β-catenin/TCF-mediated activity. Additionally, β-catenin showed a distinct perinuclear distribution in most (91 %) of the FAP1 hESCs high passage colonies. DNA sequencing of the whole gene detected several polymorphisms in FAP1 hESCs, however, no somatic mutations were discovered in the APC gene. On the other hand, no changes in β-catenin were detected in the FAP2 hESCs, demonstrating the natural diversity of the human FAP population. Our results describe the establishment of novel hESC lines from FAP patients with a predisposition for cancer mutation. These cells can be maintained in culture for long periods of time and may serve as a platform for studying the initial molecular and cellular changes that occur during early stages of malignant transformation.

X Demographics

X Demographics

The data shown below were collected from the profiles of 10 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 31 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 31 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 6 19%
Student > Ph. D. Student 4 13%
Student > Master 4 13%
Student > Bachelor 3 10%
Professor > Associate Professor 2 6%
Other 3 10%
Unknown 9 29%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 11 35%
Agricultural and Biological Sciences 6 19%
Medicine and Dentistry 3 10%
Unknown 11 35%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 28. 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 09 January 2017.
All research outputs
#1,352,036
of 24,995,564 outputs
Outputs from BMC Cancer
#185
of 8,839 outputs
Outputs of similar age
#27,817
of 431,849 outputs
Outputs of similar age from BMC Cancer
#4
of 108 outputs
Altmetric has tracked 24,995,564 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 94th percentile: it's in the top 10% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 8,839 research outputs from this source. They receive a mean Attention Score of 4.6. This one has done particularly well, scoring higher than 97% 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 431,849 tracked outputs that were published within six weeks on either side of this one in any source. This one has done particularly well, scoring higher than 93% of its contemporaries.
We're also able to compare this research output to 108 others from the same source and published within six weeks on either side of this one. This one has done particularly well, scoring higher than 97% of its contemporaries.