Evidence map›Paper›PMID 30988157›Full record

ArticleMolecular and cellular biology2019

Uncoupling the Senescence-Associated Secretory Phenotype from Cell Cycle Exit via Interleukin-1 Inactivation Unveils Its Protumorigenic Role.

Lena Lau, Angelo Porciuncula, Alex Yu, Yoichiro Iwakura, Gregory David

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Transcriptional regulation in cardiovascular aging.Frontiers in cardiovascular medicine · 2026
    Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article

14 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 2 countries.

Lena LauDepartment of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York, USA.
Angelo PorciunculaDepartment of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York, USA.
Alex YuDepartment of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York, USA.
Yoichiro IwakuraResearch Institute for Biomedical Sciences, Tokyo University of Science, Yamazaki, Noda, Japan.
Gregory DavidDepartment of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York, USA gregory.david@nyulangone.org.
New York University · USTokyo University of Science · JP

Funding

Vaccine FacilityP30CA016087 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ADRIANA HEGUY · 1985 to 2026
$83.1M
Regulation of Cellular Senescence and Oncogenic Transformation by Sin3B.R01CA148639 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DAVID, GREGORY · 2011 to 2015
$2.0M
Role of cell cycle withdrawal in restricting pancreatic cancer progression.R21CA155736 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DAVID, GREGORY · 2012 to 2014
$590k
(PQ1) Cellular senescence as an initiating event in malignant transformationR21CA206013 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DAVID, GREGORY · 2017 to 2018
$373k
Function and Regulation of IL-1a in the Senescence-Associated Secretory PhenotypeF31CA206387 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI LAU, LENA · 2017 to 2019
$107k
NCI NIH HHS F31 CA206387NCI NIH HHS P30 CA016087NCI NIH HHS R01 CA148639NCI NIH HHS R21 CA155736NCI NIH HHS R21 CA206013
6 · The paper itself

Abstract

Cellular senescence has emerged as a potent tumor suppressor mechanism in numerous human neoplasias. Senescent cells secrete a distinct set of factors, collectively termed the senescence-associated secretory phenotype (SASP), which has been postulated to carry both pro- and antitumorigenic properties depending on tissue context. However, the

Indexed as

AnimalsCell CycleCell Line, TumorCellular SenescenceCytokinesGene Expression ProfilingGene Expression Regulation, NeoplasticHEK293 CellsHumansInterleukin-1MiceNeoplasm TransplantationNF-kappa BPancreatic NeoplasmsReceptors, Interleukin-1Signal TransductionCytokinesInterleukin-1NF-kappa BReceptors, Interleukin-1cancerinflammationinterleukin-1senescence

Identifiers

PMID30988157
PMCPMC6549465
OpenAlexW2937053683

What OpenQuestion holds

Textmetadata
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.