Evidence map›Paper›PMID 26888257›Full record

ArticleBlood2016

Galectin-1 drives lymphoma CD20 immunotherapy resistance: validation of a preclinical system to identify resistance mechanisms.

Jacquelyn M Lykken, Mayuka Horikawa, Veronique Minard-Colin, Masahiro Kamata, Tomomitsu Miyagaki, Jonathan C Poe, Thomas F Tedder

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

  1. Circulating galectin-1 delineates response to bevacizumab in melanoma patients and reprograms endothelial cell biology.Proceedings of the National Academy of Sciences of the United States of America · 2023
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  18. Role of Galectins in Tumors and in Clinical Immunotherapy.International journal of molecular sciences · 2018
    Review
  19. Role of Galectins in Multiple Myeloma.International journal of molecular sciences · 2017
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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.

Jacquelyn M LykkenDepartment of Immunology, Duke University Medical Center, Durham, NC.
Mayuka HorikawaDepartment of Immunology, Duke University Medical Center, Durham, NC.
Veronique Minard-ColinDepartment of Immunology, Duke University Medical Center, Durham, NC.
Masahiro KamataDepartment of Immunology, Duke University Medical Center, Durham, NC.
Tomomitsu MiyagakiDepartment of Immunology, Duke University Medical Center, Durham, NC.
Jonathan C PoeDepartment of Immunology, Duke University Medical Center, Durham, NC.
Thomas F TedderDepartment of Immunology, Duke University Medical Center, Durham, NC.
Duke Medical Center · US

Funding

TRANSFUSION MEDICINE AND RELATED AREAST32HL007057 · NHLBI · DUKE UNIVERSITY · PI Gowthami M Arepally · 1985 to 2026
$10.6M
Basic Immunology Training ProgramT32AI052077 · NIAID · DUKE UNIVERSITY · PI KRANGEL, MICHAEL S · 2002 to 2024
$4.2M
NHLBI NIH HHS T32 HL007057NIAID NIH HHS T32 AI052077
6 · The paper itself

Abstract

Non-Hodgkin lymphoma (NHL) is the most commonly diagnosed hematologic cancer of adults in the United States, with the vast majority of NHLs deriving from malignant B lymphocytes that express cell surface CD20. CD20 immunotherapy (rituximab) is widely used to treat NHL, even though the initial effectiveness of rituximab varies widely among patients and typically wanes over time. The mechanisms through which lymphomas initially resist or gain resistance to immunotherapy are not well established. To address this, a preclinical mouse model system was developed to comprehensively identify lymphoma transcriptomic changes that confer resistance to CD20 immunotherapy. The generation of spontaneous primary and familial lymphomas revealed that sensitivity to CD20 immunotherapy was not regulated by differences in CD20 expression, prior exposure to CD20 immunotherapy, or serial in vivo passage. An unbiased forward exome screen of these primary lymphomas was used to validate the utility of this expansive lymphoma cohort, which revealed that increased lymphoma galectin-1 (Gal-1) expression strongly correlated with resistance to immunotherapy. Genetically induced lymphoma Gal-1 expression ablated antibody-dependent lymphoma phagocytosis in vitro and lymphoma sensitivity to CD20 immunotherapy in vivo. Human NHLs also express elevated Gal-1 compared with nonmalignant lymphocytes, demonstrating the ability of this preclinical model system to identify molecular targets that could be relevant to human therapy. This study therefore established a powerful preclinical model system that permits the comprehensive identification of the dynamic lymphoma molecular network that drives resistance to immunotherapy.

Indexed as

Drug Resistance, NeoplasmAnimalsAntigens, CD20Antineoplastic AgentsDisease Models, AnimalGalectin 1Green Fluorescent ProteinsHemizygoteHumansImmunotherapyLymphoma, B-CellMacrophagesMiceMice, Inbred C57BLMicroscopy, FluorescencePhagocytosisAntigens, CD20Antineoplastic AgentsGalectin 1Green Fluorescent ProteinsRituximab

Identifiers

PMID26888257
PMCPMC4832507
OpenAlexW2286233039

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.