Evidence map›Paper›PMID 24569262›Full record

ArticleBlood2014

Novel anti-B-cell maturation antigen antibody-drug conjugate (GSK2857916) selectively induces killing of multiple myeloma.

Yu-Tzu Tai, Patrick A Mayes, Chirag Acharya, Mike Y Zhong, Michele Cea, Antonia Cagnetta, Jenny Craigen, John Yates, Louise Gliddon, William Fieles and 7 more

2 registry-linked trialsAbstract read
In one paragraph

Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 281 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
281citing papers in PubMed, 3 pooled it
12.8field-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.

NCT05297240 unknown statusnot on this mapstarted 2022, after this paper: background citation

Retrospective Study of the Use of Belantamab Mafodotin (Blenrep®) in Patients With Relapsed and/or Refractory Multiple Myeloma (RRMM) in Spain.

TypeobservationalSponsorPETHEMA FoundationRan2022 to 2022Enrolled170ConditionsRELAPSED AND/OR REFRACTORY MULTIPLE MYELOMAArmsBelantamab mafodotin
NCT07720843 phase1not yet recruitingnot on this mapstarted 2026, after this paper: background citation

TAlquetamab and BeLantamab Mafodotin in Relapsed/Refractory Multiple Myeloma (TaBleMM)

TypeinterventionalSponsorMontefiore Medical CenterRan2026 to 2032Enrolled50ConditionsRelapse Multiple Myeloma, Refractory Multiple MyelomaArmsTalquetamab, Belantamab mafodotin, Pomalidomide
3 · Its place in the literature

Who cites it

281 citing papers in PubMed, 3 syntheses or guidelines pooled it, 472 citations in OpenAlex.

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  14. Fc-engineering for improved cancer immunotherapy.Biochemical Society transactions · 2026
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221 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 5 institutions in 2 countries.

Yu-Tzu TaiThe Jerome Lipper Multiple Myeloma Center and LeBow Institute for Myeloma Therapeutics, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA;
Patrick A MayesOncology Research & Development, GlaxoSmithKline, Collegeville, PA;
Chirag AcharyaThe Jerome Lipper Multiple Myeloma Center and LeBow Institute for Myeloma Therapeutics, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA;
Mike Y ZhongThe Jerome Lipper Multiple Myeloma Center and LeBow Institute for Myeloma Therapeutics, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA;
Michele CeaThe Jerome Lipper Multiple Myeloma Center and LeBow Institute for Myeloma Therapeutics, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA;
Antonia CagnettaThe Jerome Lipper Multiple Myeloma Center and LeBow Institute for Myeloma Therapeutics, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA;
Jenny CraigenBiopharm Discovery, GlaxoSmithKline, Stevenage, United Kingdom;
John YatesBiopharm Discovery, GlaxoSmithKline, Stevenage, United Kingdom;
Louise GliddonBiopharm Discovery, GlaxoSmithKline, Stevenage, United Kingdom;
William FielesPlatform Technology & Science Research & Development, GlaxoSmithKline, Collegeville, PA;
Bao HoangPlatform Technology & Science Research & Development, GlaxoSmithKline, Collegeville, PA;
James TunsteadPlatform Technology & Science Research & Development, GlaxoSmithKline, Collegeville, PA;
Amanda L ChristieLurie Family Imaging Center, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA; and.
Andrew L KungDepartment of Pediatrics, Columbia University Medical Center, New York, NY.
Paul RichardsonThe Jerome Lipper Multiple Myeloma Center and LeBow Institute for Myeloma Therapeutics, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA;
Nikhil C MunshiThe Jerome Lipper Multiple Myeloma Center and LeBow Institute for Myeloma Therapeutics, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA;
Kenneth C AndersonThe Jerome Lipper Multiple Myeloma Center and LeBow Institute for Myeloma Therapeutics, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA;
Dana-Farber Cancer Institute · USGlaxoSmithKline (United States) · USGlaxoSmithKline (United Kingdom) · GBColumbia University Irving Medical Center · USImaging Center · US

Funding

Trageting the Multiple Myeloma EpigenomeP50CA100707 · NCI · DANA-FARBER CANCER INSTITUTE · PI ANDERSON, KENNETH C., MUNSHI, NIKHIL C. · 2003 to 2023
$45.0M
Targeting Genomic Instability and Evolution in MyelomaP01CA155258 · NCI · DANA-FARBER CANCER INST · PI Jill Corre · 2011 to 2026
$32.5M
NCI NIH HHS P01 CA155258NCI NIH HHS P50 CA100707NCI NIH HHS P50CA100707PHS HHS P01-78378PHS HHS R01 50947
6 · The paper itself

Abstract

B-cell maturation antigen (BCMA), highly expressed on malignant plasma cells in human multiple myeloma (MM), has not been effectively targeted with therapeutic monoclonal antibodies. We here show that BCMA is universally expressed on the MM cell surface and determine specific anti-MM activity of J6M0-mcMMAF (GSK2857916), a novel humanized and afucosylated antagonistic anti-BCMA antibody-drug conjugate via a noncleavable linker. J6M0-mcMMAF specifically blocks cell growth via G2/M arrest and induces caspase 3-dependent apoptosis in MM cells, alone and in coculture with bone marrow stromal cells or various effector cells. It strongly inhibits colony formation by MM cells while sparing surrounding BCMA-negative normal cells. J6M0-mcMMAF significantly induces effector cell-mediated lysis against allogeneic or autologous patient MM cells, with increased potency and efficacy compared with the wild-type J6M0 without Fc enhancement. The antibody-dependent cell-mediated cytotoxicity and apoptotic activity of J6M0-mcMMAF is further enhanced by lenalidomide. Importantly, J6M0-mcMMAF rapidly eliminates myeloma cells in subcutaneous and disseminated mouse models, and mice remain tumor-free up to 3.5 months. Furthermore, J6M0-mcMMAF recruits macrophages and mediates antibody-dependent cellular phagocytosis of MM cells. Together, these results demonstrate that GSK2857916 has potent and selective anti-MM activities via multiple cytotoxic mechanisms, providing a promising next-generation immunotherapeutic in this cancer.

Indexed as

AnimalsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedB-Cell Maturation AntigenB-LymphocytesCell Cycle CheckpointsCell Line, TumorCell ProliferationHumansImmunologic FactorsImmunotoxinsLenalidomideMiceMice, SCIDMultiple MyelomaThalidomideAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedB-Cell Maturation AntigenImmunologic FactorsImmunotoxinsLenalidomideThalidomide

Identifiers

PMID24569262
PMCPMC4023420
OpenAlexW1982877913

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.