Evidence map›Paper›PMID 37074033›Full record

ArticleLeukemia & lymphoma2023

AMG176, an MCL-1 inhibitor, is active in pre-clinical models of aggressive B-cell lymphomas.

Pallawi Torka, Tara Russell, Cory Mavis, Juan Gu, Paola Ghione, Matthew Barth, Francisco J Hernandez-Ilizaliturri

Open access · greenAbstract read
In one paragraph

Article in Leukemia & lymphoma, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 42% 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

2 citing papers in PubMed, 1 citations in OpenAlex.

  1. Article
  2. 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

7 authors at 1 institution in 1 country.

Pallawi TorkaDepartments of Medicine, Immunology, and Pediatrics, Roswell Park Comprehensive Cancer Center, State University of New York, Buffalo, NY, USA.
Tara RussellDepartments of Medicine, Immunology, and Pediatrics, Roswell Park Comprehensive Cancer Center, State University of New York, Buffalo, NY, USA.
Cory MavisDepartments of Medicine, Immunology, and Pediatrics, Roswell Park Comprehensive Cancer Center, State University of New York, Buffalo, NY, USA.
Juan GuDepartments of Medicine, Immunology, and Pediatrics, Roswell Park Comprehensive Cancer Center, State University of New York, Buffalo, NY, USA.
Paola GhioneDepartments of Medicine, Immunology, and Pediatrics, Roswell Park Comprehensive Cancer Center, State University of New York, Buffalo, NY, USA.
Matthew BarthDepartments of Medicine, Immunology, and Pediatrics, Roswell Park Comprehensive Cancer Center, State University of New York, Buffalo, NY, USA.
Francisco J Hernandez-IlizaliturriDepartments of Medicine, Immunology, and Pediatrics, Roswell Park Comprehensive Cancer Center, State University of New York, Buffalo, NY, USA.
Roswell Park Comprehensive Cancer Center · US

Funding

Targeting the proteasome to overcome therapy resistance in B-NHLR01CA136907 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI CZUCZMAN, MYRON S · 2009 to 2013
$1.8M
NCI NIH HHS R01 CA136907
6 · The paper itself

Abstract

Upregulation of the anti-apoptotic protein MCL-1 has been implicated in chemotherapy resistance and poor clinical outcomes in B-cell lymphoma (BCL). We report the activity of AMG176, a direct, selective MCL-1 inhibitor, in preclinical models of BCL. A panel of cell lines representing diffuse large B-cell lymphoma (DLBCL), double-hit lymphoma (DHL) and Burkitt's lymphoma (BL) was selected. AMG176 induced apoptotic cell death in a dose- and time-dependent manner in all BCL cell lines. Baseline MCL-1 expression was not predictive of response. AMG176 exhibited impressive synergy with venetoclax and chemotherapeutic agents, less so with proteasomal inhibitors, and antagonism with anti-CD20 monoclonal antibodies. The activity of AMG176 could not be confirmed in murine models of BCL. Combination therapy targeting MCL-1 and BCL-2 may provide an alternative therapeutic approach in BCL, however optimal patient selection will remain the key to obtaining high response rates and tolerability.

Indexed as

Antineoplastic AgentsBurkitt LymphomaLymphoma, Large B-Cell, DiffuseAnimalsCell Line, TumorHumansMiceMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene Proteins c-bcl-2Antineoplastic AgentsMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene Proteins c-bcl-2burkitt lymphomadiffuse large B-cell lymphomadouble hit lymphomaMCL-1 inhibitornon-hodgkin lymphomavenetoclax

Identifiers

PMID37074033
PMCPMC10860744
OpenAlexW4366351747

What OpenQuestion holds

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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.