Evidence map›Paper›PMID 31595181›Full record

ArticleOncotarget2019

Therapeutic inhibition of Mcl-1 blocks cell survival in estrogen receptor-positive breast cancers.

Michelle M Williams, David L Elion, Bushra Rahman, Donna J Hicks, Violeta Sanchez, Rebecca S Cook

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Modeling the Binding of Anticancer Peptides and Mcl-1.International journal of molecular sciences · 2024
    Article
  4. Review
  5. Review
  6. Bcl-xL inhibition radiosensitizesCancer research communications · 2022
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. BH3-mimetics: recent developments in cancer therapy.Journal of experimental & clinical cancer research : CR · 2021
    Review
  12. Targeting MCL-1 in cancer: current status and perspectives.Journal of hematology & oncology · 2021
    Review
  13. Article
  14. Review
  15. Article
  16. 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

6 authors at 2 institutions in 1 country.

Michelle M WilliamsProgram in Cancer Biology, Vanderbilt University, Nashville, TN 37232, USA.
David L ElionProgram in Cancer Biology, Vanderbilt University, Nashville, TN 37232, USA.
Bushra RahmanDepartment of Cell and Developmental Biology, Vanderbilt University, Nashville, TN 37232, USA.
Donna J HicksDepartment of Cell and Developmental Biology, Vanderbilt University, Nashville, TN 37232, USA.
Violeta SanchezDepartment of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Rebecca S CookProgram in Cancer Biology, Vanderbilt University, Nashville, TN 37232, USA.
Vanderbilt University · USVanderbilt University Medical Center · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI STACIE B DUSETZINA · 1995 to 2026
$172.8M
TISSUE CoreP50CA098131 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PARK, BEN HO, PIETENPOL, JENNIFER A · 2003 to 2024
$48.7M
The Vanderbilt Institute for Clinical and Translational Research (VICTR)UL1TR000445 · NCATS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BERNARD, GORDON RAPHAEL · 2012 to 2016
$41.4M
Vanderbilt/Meharry Initiative for Minority Student DvptR25GM062459 · NIGMS · VANDERBILT UNIVERSITY · PI VELEZ EDWARDS, DIGNA R · 2002 to 2020
$10.4M
Mcl-1 drives resistance of luminal breast cancers to targeted therapiesF31CA195989 · NCI · VANDERBILT UNIVERSITY · PI WILLIAMS, MICHELLE M · 2015 to 2016
$57k
NCATS NIH HHS UL1 TR000445NCI NIH HHS F31 CA195989NCI NIH HHS P30 CA068485NCI NIH HHS P50 CA098131NIGMS NIH HHS R25 GM062459
6 · The paper itself

Abstract

Cancers often overexpress anti-apoptotic Bcl-2 proteins for cell death evasion, a recognized hallmark of cancer progression. While estrogen receptor (ER)-α+ breast cancers express high levels of three anti-apoptotic Bcl-2 family members (Bcl-2, Bcl-xL, and Mcl-1), pharmacological inhibition of Bcl-2 and/or Bcl-xL fails to induce cell death in ERα+ breast cancer cell lines, due to rapid and robust Mcl-1 upregulation. The mechanisms of acute Mcl-1 upregulation in response to Bcl-2/Bcl-xL inhibition remain undefined in in ERα+ breast cancers. We report here that blockade of Bcl-2 or Bcl-xL, alone or together, rapidly induced mTOR signaling in ERα+ breast cancer cells, rapidly increasing cap-dependent Mcl-1 translation. Cells treated with a pharmacological inhibitor of cap-dependent translation, or with the mTORC1 inhibitor RAD001/everolimus, displayed reduced protein levels of Mcl-1 under basal conditions, and failed to upregulate Mcl-1 protein expression following treatment with ABT-263, a pharmacological inhibitor of Bcl-2 and Bcl-xL. Although treatment with ABT-263 alone did not sustain apoptosis in tumor cells in culture or

Indexed as

ABT-263 resistanceluminal breast cancersMcl-1mTORC1 signaling

Identifiers

PMID31595181
PMCPMC6739218
OpenAlexW2989293326

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.