Evidence map›Paper›PMID 21730367›Full record

ArticleOncotarget2011

Involvement of Akt-1 and mTOR in sensitivity of breast cancer to targeted therapy.

Melissa L Sokolosky, Kristin M Stadelman, William H Chappell, Stephen L Abrams, Alberto M Martelli, Franca Stivala, Massimo Libra, Ferdinando Nicoletti, Lyudmyla B Drobot, Richard A Franklin and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Oncotarget, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

50 citing papers in PubMed, 81 citations in OpenAlex.

  1. Trial
  2. The cross-talk between GSK-3β, RKIP, and PTEN as potential targets for therapeutic implications in cancer: a comprehensive insight.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Statins and endocrine resistance in breast cancer.Cancer drug resistance (Alhambra, Calif.) · 2021
    Review
  7. miR-18a Inhibitor Suppresses Leukemia Cell Proliferation by Upregulation of PTEN Expression.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  8. Overexpression of 14-3-3BioMed research international · 2020
    Article
  9. Review
  10. Article
  11. Article
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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

12 authors at 4 institutions in 3 countries.

Melissa L SokoloskyDepartment of Microbiology and Immunology Brody School of Medicine at East Carolina University Greenville, NC 27858 USA.
Kristin M Stadelman
William H Chappell
Stephen L Abrams
Alberto M Martelli
Franca Stivala
Massimo Libra
Ferdinando Nicoletti
Lyudmyla B Drobot
Richard A Franklin
Linda S Steelman
James A McCubrey
East Carolina University · USUniversity of Catania · ITIstituto Nazionale di Fisica Nucleare, Sezione di Bologna · ITNational Academy of Sciences of Ukraine · UA

Funding

Ras/Raf &PI3K/Akt Induced Breast Cancer Drug ResistanceR01CA098195 · NCI · EAST CAROLINA UNIVERSITY · PI MC CUBREY, JAMES A · 2003 to 2007
$1.5M
NCI NIH HHS R01 CA098195NCI NIH HHS R01CA098195
6 · The paper itself

Abstract

Elucidating the response of breast cancer cells to chemotherapeutic and hormonal based drugs is clearly important as these are frequently used therapeutic approaches. A signaling pathway often involved in chemo- and hormonal-resistance is the Ras/PI3K/PTEN/Akt/mTOR cascades. In the studies presented in this report, we have examined the effects of constitutive activation of Akt on the sensitivity of MCF-7 breast cancer cells to chemotherapeutic- and hormonal-based drugs as well as mTOR inhibitors. MCF-7 cells which expressed a constitutively-activated Akt-1 gene [∆Akt-1(CA)] were more resistant to doxorubicin, etoposide and 4-OH-tamoxifen (4HT) than cells lacking ∆Akt-1(CA). Cells which expressed ∆Akt-1(CA) were hypersensitive to the mTOR inhibitor rapamycin. Furthermore, rapamycin lowered the IC50s for doxorubicin, etoposide and 4HT in the cells which expressed ∆Akt-1(CA), demonstrating a potential improved method for treating certain breast cancers which have deregulated PI3K/PTEN/Akt/mTOR signaling. Understanding how breast cancers respond to chemo- and hormonal-based therapies and the mechanisms by which they can become drug resistant may enhance our ability to treat breast cancer. These results also document the potential importance of knowledge of the mutations present in certain cancers which may permit more effective therapies.

Indexed as

Drug Resistance, NeoplasmMolecular Targeted TherapyAntineoplastic AgentsBreast NeoplasmsCell Line, TumorCell ProliferationDoxorubicinEtoposideFemaleHumansProto-Oncogene Proteins c-aktSignal TransductionSirolimusTamoxifenTOR Serine-Threonine KinasesAKT1 protein, humanAntineoplastic AgentsDoxorubicinEtoposideMTOR protein, humanProto-Oncogene Proteins c-aktSirolimusTamoxifenTOR Serine-Threonine Kinases

Identifiers

PMID21730367
PMCPMC3248182
OpenAlexW1754519356

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.