Evidence map›Paper›PMID 32204955›Full record

ReviewBlood reviews2020

Targeting MCL-1 in hematologic malignancies: Rationale and progress.

Andrew H Wei, Andrew W Roberts, Andrew Spencer, Aaron Seth Rosenberg, David Siegel, Roland B Walter, Sean Caenepeel, Paul Hughes, Zach McIver, Khalid Mezzi and 2 more

Open access · hybridAbstract readReview
In one paragraph

Review in Blood reviews, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 1 pooled it
18.2field-weighted citation impact, top 1% 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

124 citing papers in PubMed, 1 synthesis or guideline pooled it, 205 citations in OpenAlex.

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  14. MNT: a new target for AML.Blood neoplasia · 2025
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64 more citing papers are in PubMed but not listed here.

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 7 institutions in 2 countries.

Andrew H WeiAlfred Hospital and Monash University, Melbourne, VIC, Australia. Electronic address: Andrew.wei@monash.edu.
Andrew W RobertsUniversity of Melbourne, Royal Melbourne Hospital, Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, Australia.
Andrew SpencerAlfred Hospital, Monash University, Australian Centre for Blood Diseases, Melbourne, VIC, Australia.
Aaron Seth RosenbergUniversity of California Davis School of Medicine, Sacramento, CA, USA.
David SiegelJohn Theurer Cancer Center at Hackensack University Medical Center, Hackensack, NJ, USA.
Roland B WalterClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA.
Sean CaenepeelAmgen Inc., Thousand Oaks, CA, USA.
Paul HughesAmgen Inc., Thousand Oaks, CA, USA.
Zach McIverAmgen Inc., Thousand Oaks, CA, USA.
Khalid MezziAmgen Inc., Thousand Oaks, CA, USA.
Phuong Khanh MorrowAmgen Inc., Thousand Oaks, CA, USA.
Anthony SteinGehr Family Center for Leukemia, City of Hope Medical Center, Duarte, CA, USA.
Amgen (United States) · USMonash University · AUCity of Hope · USFred Hutch Cancer Center · USHackensack University Medical Center · USUniversity of California, Davis · USUniversity of Melbourne · AU

Funding

Staff InvestigatorsP30CA093373 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI Gina M Dayton · 2002 to 2026
$84.9M
UC Davis Paul Calabresi K12 Clinical Oncology Research Career Development ProgramK12CA138464 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BIRKELAND, ANDREW CHARLES, LARA, PRIMO N. · 2011 to 2025
$11.4M
NCI NIH HHS K12 CA138464NCI NIH HHS P30 CA093373
6 · The paper itself

Abstract

Myeloid cell leukemia sequence 1 (MCL-1) is an antiapoptotic protein that plays a key role in promoting cell survival in multiple myeloma (MM), acute myeloid leukemia (AML), and non-Hodgkin lymphoma (NHL). Overexpression of MCL-1 is associated with treatment resistance and poor prognosis; thus, MCL-1 inhibitors are rational therapeutic options for malignancies depending on MCL-1. Several MCL-1 inhibitors have entered clinical trials, including AZD5991, S64315, AMG 176, and AMG 397. A key area of investigation is whether MCL-1 inhibitors will complement the activity of BCL-2 inhibitors, such as venetoclax, and synergistically enhance anti-tumor efficacy when given in combination with other anti-cancer drugs. Another important question is whether a safe therapeutic window can be found for this new class of inhibitors. In summary, inhibition of MCL-1 shows potential as a treatment for hematologic malignancies and clinical evaluation of MCL-1 inhibitors is currently underway.

Indexed as

AnimalsAntineoplastic AgentsGene Expression Regulation, NeoplasticHematologic NeoplasmsHumansLeukemia, Myeloid, AcuteMolecular Targeted TherapyMultiple MyelomaMyeloid Cell Leukemia Sequence 1 ProteinSignal TransductionUp-RegulationAntineoplastic AgentsMCL1 protein, humanMyeloid Cell Leukemia Sequence 1 ProteinAcute myeloid leukemiaBH3-mimeticMCL-1 inhibitorMultiple myelomaNon-Hodgkin lymphoma

Identifiers

PMID32204955
PMCPMC7442684
OpenAlexW3006985196

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.