Evidence map›Paper›PMID 32751699›Full record

ReviewCancers2020

Targeting Multiple Myeloma through the Biology of Long-Lived Plasma Cells.

Adam Utley, Brittany Lipchick, Kelvin P Lee, Mikhail A Nikiforov

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Anti-BCMA CAR-NK Cells Reveal Enhanced Cytolytic and Secretory Responses Against Myeloma Cells.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2026
    Article
  3. Why are long-lived plasma cells long-lived?Frontiers in immunology · 2026
    Review
  4. Review
  5. Targets for CAR Therapy in Multiple Myeloma.International journal of molecular sciences · 2025
    Review
  6. Review
  7. Multiple Myeloma: Genetic and Epigenetic Biomarkers with Clinical Potential.International journal of molecular sciences · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
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

4 authors at 2 institutions in 1 country.

Adam UtleyDepartment of Cancer Biology, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA.
Brittany LipchickDepartment of Cancer Biology, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA.
Kelvin P LeeDepartment of Immunology, Roswell Park Comprehensive Cancer Center, Buffalo, NY 14203, USA.
Mikhail A NikiforovDepartment of Cancer Biology, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA.
Wake Forest University · USRoswell Park Comprehensive Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma (MM) is a hematological malignancy of terminally differentiated bone marrow (BM) resident B lymphocytes known as plasma cells (PC). PC that reside in the bone marrow include a distinct population of long-lived plasma cells (LLPC) that have the capacity to live for very long periods of time (decades in the human population). LLPC biology is critical for understanding MM disease induction and progression because MM shares many of the same extrinsic and intrinsic survival programs as LLPC. Extrinsic survival signals required for LLPC survival include soluble factors and cellular partners in the bone marrow microenvironment. Intrinsic programs that enhance cellular fidelity are also required for LLPC survival including increased autophagy, metabolic fitness, the unfolded protein response (UPR), and enhanced responsiveness to endoplasmic reticulum (ER) stress. Targeting LLPC cell survival mechanisms have led to standard of care treatments for MM including proteasome inhibition (Bortezomib), steroids (Dexamethasone), and immunomodulatory drugs (Lenalidomide). MM patients that relapse often do so by circumventing LLPC survival pathways targeted by treatment. Understanding the mechanisms by which LLPC are able to survive can allow us insight into the treatment of MM, which allows for the enhancement of therapeutic strategies in MM both at diagnosis and upon patient relapse.

Indexed as

bone marrow microenvironment (BMME)long-lived plasma cell (LLPC)multiple myeloma (MM)

Identifiers

PMID32751699
PMCPMC7466116
OpenAlexW3046715843

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.