Evidence map›Paper›PMID 41935039›Full record

ArticleBlood cancer journal2026

Dynamics of BCMA expression in patients with relapsed/refractory multiple myeloma receiving BCMA-directed CAR-T therapy.

Masooma Shifa Rana, Sebastian Fernandez-Pol, Alexandria Jensen, Vanna Hovanky, Arash Velayati, Jean S Oak, Oscar Silva, Erik Ames, Lori S Muffly, Bita Sahaf and 16 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Blood cancer journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

26 authors.

Masooma Shifa RanaDivision of Blood and Marrow Transplantation & Cellular Therapy, Stanford University, Stanford, CA, USA.ORCID 0000-0003-1731-085X
Sebastian Fernandez-PolDepartment of Pathology, Stanford University, Stanford, CA, USA.
Alexandria JensenQuantitative Sciences Unit, Stanford School of Medicine, Stanford, CA, USA.ORCID 0000-0001-6337-9079
Vanna HovankyDivision of Blood and Marrow Transplantation & Cellular Therapy, Stanford University, Stanford, CA, USA.
Arash VelayatiDivision of Blood and Marrow Transplantation & Cellular Therapy, Stanford University, Stanford, CA, USA.
Jean S OakDepartment of Pathology, Stanford University, Stanford, CA, USA.
Oscar SilvaDepartment of Pathology, Stanford University, Stanford, CA, USA.
Erik AmesDepartment of Pathology, Stanford University, Stanford, CA, USA.
Lori S MufflyDivision of Blood and Marrow Transplantation & Cellular Therapy, Stanford University, Stanford, CA, USA.ORCID 0000-0002-9887-6136
Bita SahafStanford University School of Medicine, Cancer Correlative Science Unit, Stanford Cancer Institute, Stanford, CA, USA.
Sally AraiDivision of Blood and Marrow Transplantation & Cellular Therapy, Stanford University, Stanford, CA, USA.ORCID 0000-0003-1993-4172
Vanessa E KennedyDivision of Blood and Marrow Transplantation & Cellular Therapy, Stanford University, Stanford, CA, USA.
Sushma BharadwajDivision of Blood and Marrow Transplantation & Cellular Therapy, Stanford University, Stanford, CA, USA.
David J IberriDivision of Hematology, Stanford University, Stanford, CA, USA.
Michaela LiedtkeDivision of Hematology, Stanford University, Stanford, CA, USA.
Yasodha NatkunamDepartment of Pathology, Stanford University, Stanford, CA, USA.ORCID 0000-0002-9816-1018
Parveen ShirazDivision of Blood and Marrow Transplantation & Cellular Therapy, Stanford University, Stanford, CA, USA.ORCID 0000-0002-6721-0358
Wen-Kai WengDivision of Blood and Marrow Transplantation & Cellular Therapy, Stanford University, Stanford, CA, USA.
Melody SmithDivision of Blood and Marrow Transplantation & Cellular Therapy, Stanford University, Stanford, CA, USA.
Matthew J FrankDivision of Blood and Marrow Transplantation & Cellular Therapy, Stanford University, Stanford, CA, USA.
Crystal L MackallDivision of Blood and Marrow Transplantation & Cellular Therapy, Stanford University, Stanford, CA, USA.
Saurabh DahiyaDivision of Blood and Marrow Transplantation & Cellular Therapy, Stanford University, Stanford, CA, USA.
Lekha MikkilineniDivision of Blood and Marrow Transplantation & Cellular Therapy, Stanford University, Stanford, CA, USA.
David B MiklosDivision of Blood and Marrow Transplantation & Cellular Therapy, Stanford University, Stanford, CA, USA.ORCID 0000-0003-0717-4305
Hitomi HosoyaDivision of Blood and Marrow Transplantation & Cellular Therapy, Stanford University, Stanford, CA, USA.
Surbhi SidanaDivision of Blood and Marrow Transplantation & Cellular Therapy, Stanford University, Stanford, CA, USA. Surbhi.Sidana@stanford.edu.ORCID 0000-0003-3288-7614

Funding

U.S. Department of Health & Human Services | National Institutes of Health (NIH) 2P30CA124435-16U.S. Department of Health & Human Services | National Institutes of Health (NIH) CA04960529A1
6 · The paper itself

Abstract

There is limited systemic data on the dynamics of BCMA-target antigen expression with BCMA CAR-T at relapse. We analyzed 76 patients receiving standard-of-care BCMA-directed CAR-T who underwent real-time BCMA expression evaluation at baseline (n = 50), relapse (6), or both (20) using flow cytometry (FC) and/or immunohistochemistry (IHC). BCMA was universally expressed at baseline with significant heterogeneity in expression level. No concordance was seen between FC and IHC in categorizing high vs. low expression (Spearman: 0.07, Cohen kappa: 0). Plasma cell BCMA expression by FC correlated with clinical outcomes, whereas IHC did not. High BCMA expression by FC was associated with increased likelihood for VGPR/CR (p = 0.007) and longer time to progression (p = 0.005), including the ciltacabtagene autoleucel cohort (median: 23.0 vs. 7.7 months, p = 0.02). Relapsed patients retained BCMA expression by FC, though 29% (5/16) had BCMA loss by IHC, with 4/5 showing concurrent positive BCMA expression by FC. BCMA expression at relapse by FC was significantly lower than baseline (p = 0.04); downregulation (≥25% decrease) occurred in 50% (8/16) with paired samples. Higher BCMA expression by FC correlated with higher likelihood of deep, durable responses following BCMA-directed CAR-T. While BCMA loss is rare, decreased expression is common at relapse, with implications for sequencing BCMA-directed therapies.

Indexed as

B-Cell Maturation AntigenImmunotherapy, AdoptiveMultiple MyelomaReceptors, Chimeric AntigenAdultAgedFemaleHumansMaleMiddle AgedNeoplasm Recurrence, LocalRecurrenceB-Cell Maturation AntigenReceptors, Chimeric AntigenTNFRSF17 protein, human

Identifiers

PMID41935039
PMCPMC13186958

What Socratic holds

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LicenceCC BY-NC-ND
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 Socratic graph.