Evidence map›Paper›PMID 25541151›Full record

ReviewLeukemia2015

You eat what you are: autophagy inhibition as a therapeutic strategy in leukemia.

A R Sehgal, H Konig, D E Johnson, D Tang, R K Amaravadi, M Boyiadzis, M T Lotze

Open access · bronzeAbstract readReview
In one paragraph

Review in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
6.4field-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

57 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
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  3. Mitochondria-ER crosstalk via MAMS: Bridging cellular homeostasis and cancer progression.Apoptosis : an international journal on programmed cell death · 2026
    Review
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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 4 institutions in 1 country.

A R SehgalDepartment of Medicine, Division of Hematology/Oncology, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA, USA.
H KonigDepartment of Medicine, Division of Hematology and Medical Oncology, Indiana University Simon Cancer Center, Indianapolis, IN, USA.
D E JohnsonDepartment of Medicine, Division of Hematology/Oncology, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA, USA.
D TangDepartment of Surgery, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA, USA.
R K AmaravadiDepartment of Medicine, Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA, USA.
M BoyiadzisDepartment of Medicine, Division of Hematology/Oncology, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA, USA.
M T LotzeDepartment of Surgery, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA, USA.
UPMC Hillman Cancer Center · USIndiana University – Purdue University Indianapolis · USUniversity of Pennsylvania · USUniversity of Pittsburgh · US

Funding

Targeting HMGB1-mediated Autophagy in Cancer TherapyR01CA160417 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI TANG, DAOLIN · 2012 to 2023
$3.0M
HLTF gene silencing: a novel determinant of sensitivity to autophagy inhibitionR01CA169134 · NCI · UNIVERSITY OF PENNSYLVANIA · PI AMARAVADI, RAVI K · 2013 to 2017
$1.7M
Pancreatic Ductal Adenocarcinoma is a disease of constitutive autophagyR01CA181450 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LOTZE, MICHAEL T, ZEH, HERBERT J · 2014 to 2018
$1.6M
Molecular Targeting Strategies in HNSCCR01CA137260 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI JOHNSON, DANIEL E · 2010 to 2014
$1.5M
NCI NIH HHS R01 CA137260NCI NIH HHS R01CA137260NCI NIH HHS R01 CA160417NCI NIH HHS R01CA160417NCI NIH HHS R01 CA169134NCI NIH HHS R01 CA181450NCI NIH HHS R01CA181450
6 · The paper itself

Abstract

A deeper understanding of the role of autophagy, literally 'self-eating', in normal and cancer cell biology has emerged over the last few years. Autophagy serves as a vehicle for cells to respond to various stressors including genomic, hypoxic and nutrient stress, and to oppose mechanisms of 'programmed' cell death. Here, we review not only mechanisms of cell death and cell survival but also the early successes in applying autophagy inhibition strategies in solid tumors using the only currently available clinical inhibitor, oral hydroxychloroquine. In acute leukemia, currently available chemotherapy drugs promote cell death and demonstrate clinical benefit, but relapse and subsequent chemotherapy resistance is common. Increasing preclinical data suggest that autophagy is active in leukemia as a means of promoting cell survival in response to chemotherapy. We propose coupling autophagy inhibition strategies with current cytotoxic chemotherapy and discuss synergistic combinations of available anti-leukemic therapies with autophagy inhibition. Furthermore, novel autophagy inhibitors are in development and promise to provide new therapeutic opportunities for patients with leukemia.

Indexed as

Antineoplastic AgentsAutophagyBoronic AcidsBortezomibCell SurvivalClinical Trials as TopicDrug Resistance, NeoplasmGene ExpressionHMGB1 ProteinHumansHydroxychloroquineLeukemiaLeukocytesLysosomesPhagosomesPyrazinesAntineoplastic AgentsBoronic AcidsBortezomibHMGB1 ProteinHMGB1 protein, humanHydroxychloroquinePyrazinesSirolimustemsirolimus

Identifiers

PMID25541151
PMCPMC4825874
OpenAlexW2027418572

What OpenQuestion holds

Textmetadata
LicenceTDM
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.