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Oncogenic hijacking of the stress response machinery in T cell acute lymphoblastic leukemia

Overview of attention for article published in Nature Medicine, July 2018
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About this Attention Score

  • In the top 5% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (99th percentile)
  • High Attention Score compared to outputs of the same age and source (93rd percentile)

Mentioned by

news
56 news outlets
blogs
1 blog
twitter
45 tweeters
facebook
4 Facebook pages

Citations

dimensions_citation
54 Dimensions

Readers on

mendeley
74 Mendeley
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Title
Oncogenic hijacking of the stress response machinery in T cell acute lymphoblastic leukemia
Published in
Nature Medicine, July 2018
DOI 10.1038/s41591-018-0105-8
Pubmed ID
Authors

Nikos Kourtis, Charalampos Lazaris, Kathryn Hockemeyer, Juan Carlos Balandrán, Alejandra R. Jimenez, Jasper Mullenders, Yixiao Gong, Thomas Trimarchi, Kamala Bhatt, Hai Hu, Liza Shrestha, Alberto Ambesi-Impiombato, Michelle Kelliher, Elisabeth Paietta, Gabriela Chiosis, Monica L. Guzman, Adolfo A. Ferrando, Aristotelis Tsirigos, Iannis Aifantis

Abstract

Cellular transformation is accompanied by extensive rewiring of many biological processes leading to augmented levels of distinct types of cellular stress, including proteotoxic stress. Cancer cells critically depend on stress-relief pathways for their survival. However, the mechanisms underlying the transcriptional initiation and maintenance of the oncogenic stress response remain elusive. Here, we show that the expression of heat shock transcription factor 1 (HSF1) and the downstream mediators of the heat shock response is transcriptionally upregulated in T cell acute lymphoblastic leukemia (T-ALL). Hsf1 ablation suppresses the growth of human T-ALL and eradicates leukemia in mouse models of T-ALL, while sparing normal hematopoiesis. HSF1 drives a compact transcriptional program and among the direct HSF1 targets, specific chaperones and co-chaperones mediate its critical role in T-ALL. Notably, we demonstrate that the central T-ALL oncogene NOTCH1 hijacks the cellular stress response machinery by inducing the expression of HSF1 and its downstream effectors. The NOTCH1 signaling status controls the levels of chaperone/co-chaperone complexes and predicts the response of T-ALL patient samples to HSP90 inhibition. Our data demonstrate an integral crosstalk between mediators of oncogene and non-oncogene addiction and reveal critical nodes of the heat shock response pathway that can be targeted therapeutically.

Twitter Demographics

The data shown below were collected from the profiles of 45 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 74 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 74 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 18 24%
Researcher 11 15%
Student > Master 6 8%
Student > Bachelor 6 8%
Student > Doctoral Student 5 7%
Other 13 18%
Unknown 15 20%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 24 32%
Agricultural and Biological Sciences 17 23%
Medicine and Dentistry 7 9%
Immunology and Microbiology 4 5%
Chemistry 2 3%
Other 3 4%
Unknown 17 23%

Attention Score in Context

This research output has an Altmetric Attention Score of 463. 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 19 May 2020.
All research outputs
#46,372
of 22,489,892 outputs
Outputs from Nature Medicine
#280
of 8,419 outputs
Outputs of similar age
#1,105
of 301,479 outputs
Outputs of similar age from Nature Medicine
#8
of 108 outputs
Altmetric has tracked 22,489,892 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 99th percentile: it's in the top 5% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 8,419 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 95.6. This one has done particularly well, scoring higher than 96% 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 301,479 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 99% 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 93% of its contemporaries.