Evidence map›Paper›PMID 22167754›Full record

ArticleBlood2012

Partial plasma cell differentiation as a mechanism of lost major histocompatibility complex class II expression in diffuse large B-cell lymphoma.

Sarah T Wilkinson, Kristie A Vanpatten, Diane R Fernandez, Patrick Brunhoeber, Karl E Garsha, Betty J Glinsmann-Gibson, Thomas M Grogan, Julie Teruya-Feldstein, Lisa M Rimsza

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

44 citing papers in PubMed, 61 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Cxcl9Communications biology · 2025
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  11. Quantum Dot-Based Nanosensors for In Vitro Detection ofNanomaterials (Basel, Switzerland) · 2024
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Mapping the dynamic genetic regulatory architecture ofmedRxiv : the preprint server for health sciences · 2023
    Article
  18. Review
  19. Article
  20. 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

9 authors at 3 institutions in 1 country.

Sarah T WilkinsonDepartment of Pathology, University of Arizona, 1501 N Campbell Avenue, Tucson, AZ 85724-5043, USA.
Kristie A Vanpatten
Diane R Fernandez
Patrick Brunhoeber
Karl E Garsha
Betty J Glinsmann-Gibson
Thomas M Grogan
Julie Teruya-Feldstein
Lisa M Rimsza
University of Arizona · USVentana Research Corporation (United States) · USMemorial Sloan Kettering Cancer Center · US

Funding

Integrative Cancer Scholars Training GrantT32CA009213 · NCI · UNIVERSITY OF ARIZONA · PI CAREW, JENNIFER S, CURIEL-LEWANDROWSKI, CLARA · 1985 to 2024
$8.6M
NCI NIH HHS NCI-T32 CA09213NCI NIH HHS T32 CA009213
6 · The paper itself

Abstract

Loss of major histocompatibility complex class II (MHC II) expression is associated with poor patient outcome in diffuse large B-cell lymphoma (DLBCL). As MHC II molecules are lost with plasmacytic differentiation in normal cells, we asked whether MHC II loss in DLBCL is associated with an altered differentiation state. We used gene expression profiling, quantum dots, and immunohistochemistry to study the relationship between MHC II and plasma cell markers in DLBCL and plasmablastic lymphoma (PBL). Results demonstrate that MHC II(-) DLBCL immunophenotypically overlap with PBL and demonstrate an inverse correlation between MHC II and plasma cell markers MUM1, PRDM1/Blimp1, and XBP1s. In addition, MHC II expression is significantly higher in germinal center-DLBCL than activated B cell-DLBCL. A minor subset of cases with an unusual pattern of mislocalized punctate MHC II staining and intermediate levels of mRNA is also described. Finally, we show that PBL is negative for MHC II. The results imply a spectrum of MHC II expression that is more frequently diminished in tumors derived from B cells at the later stages of differentiation (with complete loss in PBL). Our observations provide a possible unifying concept that may contribute to the poor outcome reported in all MHC II(-) B-cell tumors.

Indexed as

Analysis of VarianceAntigens, CD20Biomarkers, TumorCell DifferentiationDNA-Binding ProteinsGene Expression ProfilingGene Expression Regulation, NeoplasticHistocompatibility Antigens Class IIHLA-DR AntigensHumansImmunohistochemistryInterferon Regulatory Factor-4Interferon Regulatory FactorsLymphoma, B-CellLymphoma, Large B-Cell, DiffuseOligonucleotide Array Sequence AnalysisAntigens, CD20Biomarkers, TumorDNA-Binding ProteinsHistocompatibility Antigens Class IIHLA-DR AntigensInterferon Regulatory Factor-4Interferon Regulatory FactorsPositive Regulatory Domain I-Binding Factor 1PRDM1 protein, humanRegulatory Factor X Transcription FactorsRepressor ProteinsTranscription FactorsX-Box Binding Protein 1XBP1 protein, human

Identifiers

PMID22167754
PMCPMC3286210
OpenAlexW1978681820

What OpenQuestion holds

Textmetadata
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.