Evidence map›Paper›PMID 36765430›Full record

ArticleJournal of translational medicine2023

Cellular senescence in the response of HR

Vanessa Klapp, Aitziber Buqué, Norma Bloy, Ai Sato, Takahiro Yamazaki, Xi Kathy Zhou, Silvia C Formenti, Lorenzo Galluzzi, Giulia Petroni

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
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

9 authors at 1 institution in 3 countries.

Vanessa KlappDepartment of Radiation Oncology, Weill Cornell Medical College, New York, NY, USA.
Aitziber BuquéDepartment of Radiation Oncology, Weill Cornell Medical College, New York, NY, USA.
Norma BloyDepartment of Radiation Oncology, Weill Cornell Medical College, New York, NY, USA.
Ai SatoDepartment of Radiation Oncology, Weill Cornell Medical College, New York, NY, USA.
Takahiro YamazakiDepartment of Radiation Oncology, Weill Cornell Medical College, New York, NY, USA.
Xi Kathy ZhouHealthcare Policy and Research, Weill Cornell Medical College, New York, NY, USA.
Silvia C FormentiDepartment of Radiation Oncology, Weill Cornell Medical College, New York, NY, USA.
Lorenzo GalluzziDepartment of Radiation Oncology, Weill Cornell Medical College, New York, NY, USA. deadoc80@gmail.com.
Giulia PetroniDepartment of Radiation Oncology, Weill Cornell Medical College, New York, NY, USA. giuliapetroni@gmail.com.ORCID 0000-0002-0558-5322
Cornell University · US

Funding

Radiation Effect on Immune Cells and the MicrobiomeU54CA274291 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI Joseph O Deasy · 2022 to 2026
$9.1M
NCI NIH HHS U54 CA274291
6 · The paper itself

Abstract

backgroundPreclinical evidence from us and others demonstrates that the anticancer effects of cyclin-dependent kinase 4/6 (CDK4/6) inhibitors can be enhanced with focal radiation therapy (RT), but only when RT is delivered prior to (rather than after) CDK4/6 inhibition. Depending on tumor model, cellular senescence (an irreversible proliferative arrest that is associated with the secretion of numerous bioactive factors) has been attributed beneficial or detrimental effects on response to treatment. As both RT and CDK4/6 inhibitors elicit cellular senescence, we hypothesized that a differential accumulation of senescent cells in the tumor microenvironment could explain such an observation, i.e., the inferiority of CDK4/6 inhibition with palbociclib (P) followed by RT (P→RT) as compared to RT followed by palbociclib (RT→P).

methodsThe impact of cellular senescence on the interaction between RT and P was assessed by harnessing female INK-ATTAC mice, which express a dimerizable form of caspase 8 (CASP8) under the promoter of cyclin dependent kinase inhibitor 2A (Cdkn2a, coding for p16

resultsIn vivo depletion of p16

conclusionsPending validation in other experimental systems, these findings suggest that a program of cellular senescence in malignant cells may explain (at least partially) the inferiority of P→RT versus RT→P in preclinical models of HR

Indexed as

Breast NeoplasmsAnimalsCarcinogenesisCarrier ProteinsCellular SenescenceCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6FemaleHumansMiceTumor MicroenvironmentCarrier ProteinsCDK4 protein, humanCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6INK-ATTAC miceMCF7 cellsMDA-MB-231 cellsMPA/DMBA-driven mammary carcinogenesisTS/A cellsβ-galactosidase

Identifiers

PMID36765430
PMCPMC9921325
OpenAlexW4319948476

What Socratic 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 Socratic graph.