Evidence map›Paper›PMID 27911437›Full record

ReviewBlood cancer journal2016

The role of the proteasome in AML.

C M Csizmar, D-H Kim, Z Sachs

Open access · goldAbstract readReview
In one paragraph

Review in Blood cancer journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 61 citations in OpenAlex.

  1. A Phase I/II Trial of MEC (Mitoxantrone, Etoposide, Cytarabine) in Combination with Ixazomib for Relapsed Refractory Acute Myeloid Leukemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Trial
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  12. Oncotarget · 2024
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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

3 authors at 1 institution in 1 country.

C M CsizmarDepartment of Medicinal Chemistry, University of Minnesota, Minneapolis, MN, USA.
D-H KimDepartment of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, MN, USA.
Z SachsDepartment of Medicine, Division of Hematology, Oncology and Transplantation, University of Minnesota, Minneapolis, MN, USA.
University of Minnesota · US

Funding

University of Minnesota Clinical and Translational Science Institute (UMN CTSI)UL1TR000114 · NCATS · UNIVERSITY OF MINNESOTA · PI BLAZAR, BRUCE R · 2012 to 2015
$35.0M
UNIVERSITY OF MINNESOTA CLINICAL AND TRANSLATIONAL SCIENCE INSTITUTE (UMN CTSI)UL1RR033183 · NCRR · UNIVERSITY OF MINNESOTA · PI BLAZAR, BRUCE R · 2011 to 2011
$8.9M
University of Minnesota Clinical and Translational Science Institute (UMN CTSI)KL2TR000113 · NCATS · UNIVERSITY OF MINNESOTA · PI BLAZAR, BRUCE R · 2012 to 2015
$5.4M
Mechanisms of mTOR signaling to early and late stages of autophagyR01GM097057 · NIGMS · UNIVERSITY OF MINNESOTA · PI KIM, DO-HYUNG · 2011 to 2018
$2.7M
Engineering Reversible Cell-Cell Interactions with Chemically Self-Assembled CARsF30CA210345 · NCI · UNIVERSITY OF MINNESOTA · PI CSIZMAR, CLIFFORD MICHAEL · 2016 to 2019
$144k
NCATS NIH HHS KL2 TR000113NCATS NIH HHS UL1 TR000114NCI NIH HHS F30 CA210345NCRR NIH HHS UL1 RR033183NIGMS NIH HHS R01 GM097057
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is deadly hematologic malignancy. Despite a well-characterized genetic and molecular landscape, targeted therapies for AML have failed to significantly improve clinical outcomes. Over the past decade, proteasome inhibition has been demonstrated to be an effective therapeutic strategy in several hematologic malignancies. Proteasome inhibitors, such as bortezomib and carfilzomib, have become mainstays of treatment for multiple myeloma and mantle cell lymphoma. In light of this success, there has been a surge of literature exploring both the role of the proteasome and the effects of proteasome inhibition in AML. Pre-clinical studies have demonstrated that proteasome inhibition disrupts proliferative cell signaling pathways, exhibits cytotoxic synergism with other chemotherapeutics and induces autophagy of cancer-related proteins. Meanwhile, clinical trials incorporating bortezomib into combination chemotherapy regimens have reported a range of responses in AML patients, with complete remission rates >80% in some cases. Taken together, this preclinical and clinical evidence suggests that inhibition of the proteasome may be efficacious in this disease. In an effort to focus further investigation into this area, these recent studies and their findings are reviewed here.

Indexed as

AutophagyBortezomibCell ProliferationHumansLeukemia, Myeloid, AcuteOligopeptidesProteasome Endopeptidase ComplexProteasome InhibitorsSignal TransductionBortezomibcarfilzomibOligopeptidesProteasome Endopeptidase ComplexProteasome Inhibitors

Identifiers

PMID27911437
PMCPMC5223148
OpenAlexW2558732778

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.