Evidence map›Paper›PMID 21903859›Full record

ArticleEndocrine-related cancer2012

mTOR is a selective effector of the radiation therapy response in androgen receptor-positive prostate cancer.

Matthew J Schiewer, Robert Den, David T Hoang, Michael A Augello, Yaacov R Lawrence, Adam P Dicker, Karen E Knudsen

Open access · bronzeAbstract read
In one paragraph

Article in Endocrine-related cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Augmenting the therapeutic window of radiotherapy: A perspective on molecularly targeted therapies and nanomaterials.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2020
    Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Genome-wide association study identifies a region on chromosome 11q14.3 associated with late rectal bleeding following radiation therapy for prostate cancer.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2013
    Article
  13. Article
  14. Article
  15. Article
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

7 authors at 2 institutions in 1 country.

Matthew J SchiewerKimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
Robert Den
David T Hoang
Michael A Augello
Yaacov R Lawrence
Adam P Dicker
Karen E Knudsen
Thomas Jefferson University · USSidney Kimmel Cancer Center · US

Funding

Cyclin D1: repercussions of AR control and alternative splicing in prostate canceR01CA099996 · NCI · UNIVERSITY OF CINCINNATI · PI KNUDSEN, KAREN E · 2003 to 2013
$2.6M
Role of BAF57 in AR control and prostate cancer growthR01CA116777 · NCI · UNIVERSITY OF CINCINNATI · PI KNUDSEN, KAREN E · 2006 to 2010
$1.3M
NCI NIH HHS CA099996NCI NIH HHS CA116777
6 · The paper itself

Abstract

Ionizing radiation (IR) is used frequently in the management of multiple tumor types, including both organ-confined and locally advanced prostate cancer (PCa). Enhancing tumor radiosensitivity could both reduce the amount of radiation required for definitive treatment and improve clinical outcome. Androgen suppression therapy improves clinical outcomes when combined with radiation therapy but is associated with significant acute and chronic toxicities; hence, there is a clear need for alternative means to increase the therapeutic window of radiotherapy. Herein, it is demonstrated that the mammalian target of rapamycin (mTOR) inhibitors rapamycin (sirolimus) and temsirolimus limit both hormone therapy (HT)-sensitive and castration-resistant PCa (CRPC) cell proliferation as single agents and have a profound radiosensitization effect when used in combination with IR. Importantly, the observed radiosensitization was influenced by the treatment schedule, in which adjuvant administration of mTOR inhibitors was most effective in limiting PCa cell population doubling. This schedule-dependent influence on in vitro treatment outcome was determined to be the result of relative effects on the cell cycle kinetics. Finally, adjuvant administration of either mTOR inhibitor tested after IR significantly decreased clonogenic cell survival of both HT-sensitive and CRPC cells compared with IR alone. Taken together, these data demonstrate that inhibition of mTOR confers a radiosensitization phenotype that is dependent on relative cell cycle kinetics and provide a foundation for clinical assessment.

Indexed as

Antineoplastic AgentsCell CycleCell Line, TumorCell SurvivalHumansMaleProstatic NeoplasmsRadiation-Sensitizing AgentsReceptors, AndrogenSirolimusTOR Serine-Threonine KinasesX-RaysAntineoplastic AgentsMTOR protein, humanRadiation-Sensitizing AgentsReceptors, AndrogenSirolimustemsirolimusTOR Serine-Threonine Kinases

Identifiers

PMID21903859
PMCPMC3253653
OpenAlexW2170460353

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.