Evidence map›Paper›PMID 25278152›Full record

ArticleNature communications2014

Diurnal suppression of EGFR signalling by glucocorticoids and implications for tumour progression and treatment.

Mattia Lauriola, Yehoshua Enuka, Amit Zeisel, Gabriele D'Uva, Lee Roth, Michal Sharon-Sevilla, Moshit Lindzen, Kirti Sharma, Nava Nevo, Morris Feldman and 10 more

Open access · hybridAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.0field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

42 citing papers in PubMed, 96 citations in OpenAlex.

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  7. Efficacy on symptoms and mortality day vs. night administration of EGFR-TKIs for advanced non-small cell lung cancer.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2024
    Article
  8. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors at 4 institutions in 4 countries.

Mattia Lauriola1] Department of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel [2] Unit of Histology, Embryology and Applied Biology, Department of Experimental, Diagnostic and Specialty Medicine, Bologna University, Bologna 40138, Italy.
Yehoshua EnukaDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel.
Amit ZeiselDepartment of Physics of Complex Systems, Weizmann Institute of Science, Rehovot 76100, Israel.
Gabriele D'UvaDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel.
Lee RothDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel.
Michal Sharon-SevillaDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel.
Moshit LindzenDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel.
Kirti SharmaDivision of Molecular Genome Analysis, German Cancer Research Centre (DKFZ), 69120 Heidelberg, Germany.
Nava NevoDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel.
Morris FeldmanDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel.
Silvia CarvalhoDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel.
Hadas Cohen-DvashiDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel.
Merav KedmiDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel.
Nir Ben-ChetritDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel.
Alon ChenDepartment of Neurobiology, Weizmann Institute of Science, Rehovot 76100, Israel.
Rossella SolmiUnit of Histology, Embryology and Applied Biology, Department of Experimental, Diagnostic and Specialty Medicine, Bologna University, Bologna 40138, Italy.
Stefan WiemannDivision of Molecular Genome Analysis, German Cancer Research Centre (DKFZ), 69120 Heidelberg, Germany.
Fernando Schmitt1] Department of Laboratory Medicine and Pathobiology, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada M5S 1A8 [2] Department of Pathology, University Health Network, Toronto, Ontario, Canada M5G 2C4 [3] IPATIMUP, University of Porto, Porto 4200-465, Portugal.
Eytan DomanyDepartment of Physics of Complex Systems, Weizmann Institute of Science, Rehovot 76100, Israel.
Yosef YardenDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel.
Weizmann Institute of Science · ILHeidelberg University · DEUniversity of Bologna · ITUniversity of Toronto · CA

Funding

LATERAL VERSUS VERTICAL SIGNALING BY ERBB2 ONCOPROTEINR01CA072981 · NCI · WEIZMANN INSTITUTE OF SCIENCE · PI YARDEN, YOSEF NONE · 1997 to 2004
$953k
NCI NIH HHS R01 CA072981
6 · The paper itself

Abstract

Signal transduction by receptor tyrosine kinases (RTKs) and nuclear receptors for steroid hormones is essential for body homeostasis, but the cross-talk between these receptor families is poorly understood. We observed that glucocorticoids inhibit signalling downstream of EGFR, an RTK. The underlying mechanism entails suppression of EGFR's positive feedback loops and simultaneous triggering of negative feedback loops that normally restrain EGFR. Our studies in mice reveal that the regulation of EGFR's feedback loops by glucocorticoids translates to circadian control of EGFR signalling: EGFR signals are suppressed by high glucocorticoids during the active phase (night-time in rodents), while EGFR signals are enhanced during the resting phase. Consistent with this pattern, treatment of animals bearing EGFR-driven tumours with a specific kinase inhibitor was more effective if administered during the resting phase of the day, when glucocorticoids are low. These findings support a circadian clock-based paradigm in cancer therapy.

Indexed as

Signal TransductionAnimalsCell Line, TumorCell MovementCircadian RhythmDisease ProgressionErbB ReceptorsFemaleGlucocorticoidsHumansLigandsMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, KnockoutNeoplasmsErbB ReceptorsGlucocorticoidsLigandsReceptors, Glucocorticoid

Identifiers

PMID25278152
PMCPMC4205848
OpenAlexW1991923050

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.