Evidence map›Paper›PMID 29127189›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2018

Autophagy promotes escape from phosphatidylinositol 3-kinase inhibition in estrogen receptor-positive breast cancer.

Wei Yang, Sarah R Hosford, Nicole A Traphagen, Kevin Shee, Eugene Demidenko, Stephanie Liu, Todd W Miller

Open access · bronzeAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 37 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Wei YangDepartment of Molecular and Systems Biology, Norris Cotton Cancer Center, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire, USA.
Sarah R HosfordDepartment of Molecular and Systems Biology, Norris Cotton Cancer Center, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire, USA.
Nicole A TraphagenDepartment of Molecular and Systems Biology, Norris Cotton Cancer Center, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire, USA.
Kevin SheeDepartment of Molecular and Systems Biology, Norris Cotton Cancer Center, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire, USA.
Eugene DemidenkoCommunity and Family Medicine, Norris Cotton Cancer Center, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire, USA; and.
Stephanie LiuDepartment of Molecular and Systems Biology, Norris Cotton Cancer Center, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire, USA.
Todd W MillerDepartment of Molecular and Systems Biology, Norris Cotton Cancer Center, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire, USA.
Dartmouth College · USDartmouth Psychiatric Research Center · US

Funding

Translational Engineering in Cancer (TEC)P30CA023108 · NCI · DARTMOUTH COLLEGE · PI Steven D Leach · 1985 to 2026
$91.3M
A precision medicine basis for estrogen therapy for advanced breast cancerR01CA200994 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI Todd W. Miller · 2017 to 2026
$3.7M
Timing is everything: applications in precision oncology for ER+ breast cancerR01CA211869 · NCI · DARTMOUTH COLLEGE · PI MILLER, TODD W. · 2017 to 2021
$2.1M
Microenvironmental FGF2-mediated resistance to anti-estrogen and PI3K/mTOR pathway therapeutics in ER+ breast cancerF30CA216966 · NCI · DARTMOUTH COLLEGE · PI SHEE, KEVIN · 2017 to 2020
$176k
NCI NIH HHS F30 CA216966NCI NIH HHS P30 CA023108NCI NIH HHS R01 CA200994NCI NIH HHS R01 CA211869
6 · The paper itself

Abstract

Hyperactivation of the PI3K pathway has been implicated in resistance to antiestrogen therapies in estrogen receptor α (ER)-positive breast cancer, prompting the development of therapeutic strategies to inhibit this pathway. Autophagy has tumor-promoting and -suppressing roles and has been broadly implicated in resistance to anticancer therapies, including antiestrogens. Chloroquine (CQ) is an antimalarial and amebicidal drug that inhibits autophagy in mammalian cells and human tumors. Herein, we observed that CQ inhibited proliferation and autophagy in ER

Indexed as

AutophagyPhosphoinositide-3 Kinase InhibitorsAnimalsAntimalarialsApoptosisBreast NeoplasmsCell ProliferationChloroquineFemaleHumansMiceMice, Inbred NODMice, SCIDProto-Oncogene Proteins c-aktReceptors, EstrogenSignal TransductionAntimalarialsChloroquinePhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktReceptors, EstrogenBH3-only proteinschloroquineERGDC-0941PI3K

Identifiers

PMID29127189
PMCPMC5892720
OpenAlexW2767476370

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.