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TrkA is amplified in malignant melanoma patients and induces an anti-proliferative response in cell lines

Overview of attention for article published in BMC Cancer, October 2015
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  • Above-average Attention Score compared to outputs of the same age (55th percentile)
  • Good Attention Score compared to outputs of the same age and source (69th percentile)

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Title
TrkA is amplified in malignant melanoma patients and induces an anti-proliferative response in cell lines
Published in
BMC Cancer, October 2015
DOI 10.1186/s12885-015-1791-y
Pubmed ID
Authors

Luigi Pasini, Angela Re, Toma Tebaldi, Gianluca Ricci, Sebastiana Boi, Valentina Adami, Mattia Barbareschi, Alessandro Quattrone

Abstract

The nerve growth factor (NGF) receptor tyrosine-kinase TrkA is a well-known determinant of the melanocytic lineage, through modulation of the MAPK and AKT cascades. While TrkA gene is frequently rearranged in cancers, its involvement in malignant melanoma (MM) development is still unclear. We analyzed a dataset of primary cutaneous MM (n = 31) by array comparative genomic hybridization (aCGH), to identify genomic amplifications associated with tumor progression. The analysis was validated by genomic quantitative PCR (qPCR) on an extended set of cases (n = 64) and the results were correlated with the clinical outcome. To investigate TrkA molecular pathways and cellular function, we generated inducible activation of the NGF-TrkA signaling in human MM cell lines. We identified amplification of 1q23.1, where the TrkA locus resides, as a candidate hotspot implicated in the progression of MM. Across 40 amplicons detected, segmental amplification of 1q23.1 showed the strongest association with tumor thickness. By validation of the analysis, TrkA gene amplification emerged as a frequent event in primary melanomas (50 % of patients), and correlated with worse clinical outcome. However, experiments in cell lines revealed that induction of the NGF-TrkA signaling produced a phenotype of dramatic suppression of cell proliferation through inhibition of cell division and pronounced intracellular vacuolization, in a way straightly dependent on NGF activation of TrkA. These events were triggered via MAPK activity but not via AKT, and involved p21(cip1) protein increase, compatibly with a mechanism of oncogene-induced growth arrest. Taken together, our findings point to TrkA as a candidate oncogene in MM and support a model in which the NGF-TrkA-MAPK pathway may mediate a trade-off between neoplastic transformation and adaptive anti-proliferative response.

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X Demographics

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 30 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 30 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 10 33%
Other 4 13%
Student > Bachelor 4 13%
Student > Ph. D. Student 2 7%
Student > Master 2 7%
Other 2 7%
Unknown 6 20%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 8 27%
Agricultural and Biological Sciences 6 20%
Medicine and Dentistry 4 13%
Pharmacology, Toxicology and Pharmaceutical Science 3 10%
Psychology 2 7%
Other 1 3%
Unknown 6 20%
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 03 November 2015.
All research outputs
#12,877,483
of 22,830,751 outputs
Outputs from BMC Cancer
#2,700
of 8,306 outputs
Outputs of similar age
#125,476
of 283,725 outputs
Outputs of similar age from BMC Cancer
#69
of 225 outputs
Altmetric has tracked 22,830,751 research outputs across all sources so far. This one is in the 43rd percentile – i.e., 43% of other outputs scored the same or lower than it.
So far Altmetric has tracked 8,306 research outputs from this source. They receive a mean Attention Score of 4.3. This one has gotten more attention than average, scoring higher than 67% 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 283,725 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 55% of its contemporaries.
We're also able to compare this research output to 225 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 69% of its contemporaries.