Evidence map›Paper›PMID 31534006›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2019

Cutting Edge: ROR1/CD19 Receptor Complex Promotes Growth of Mantle Cell Lymphoma Cells Independently of the B Cell Receptor-BTK Signaling Pathway.

Qian Zhang, Hong Y Wang, Xiaobin Liu, Selene Nunez-Cruz, Mowafaq Jillab, Olga Melnikov, Kavindra Nath, Jerry Glickson, Mariusz A Wasik

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.0field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 40 citations in OpenAlex.

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  9. Phase I Study of ROR1-Specific CAR-T Cells in Advanced Hematopoietic and Epithelial Malignancies.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
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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

9 authors at 2 institutions in 1 country.

Qian ZhangDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104; Mariusz.Wasik@fccc.edu qian2@pennmedicine.upenn.edu.
Hong Y WangDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104.ORCID 0000-0001-5194-7462
Xiaobin LiuDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104.
Selene Nunez-CruzDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104.
Mowafaq JillabFox Chase Cancer Center, Philadelphia, PA 19111.ORCID 0000-0002-8090-4143
Olga MelnikovFox Chase Cancer Center, Philadelphia, PA 19111.
Kavindra NathDepartment of Radiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104; and.ORCID 0000-0002-3197-5703
Jerry GlicksonDepartment of Radiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104; and.
Mariusz A WasikDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104; Mariusz.Wasik@fccc.edu qian2@pennmedicine.upenn.edu.
University of Pennsylvania · USFox Chase Cancer Center · US

Funding

UNIVERSITY OF PENNSYLVANIA CAN CTR SUPPORT GRANTP30CA016520 · NCI · UNIVERSITY OF PENNSYLVANIA · PI SHELLEY L BERGER · 1985 to 2026
$222.3M
NCI NIH HHS P30 CA016520
6 · The paper itself

Abstract

Inhibitors of Bruton tyrosine kinase (BTK), a kinase downstream of BCR, display remarkable activity in a subset of mantle cell lymphoma (MCL) patients, but the drug resistance remains a considerable challenge. In this study, we demonstrate that aberrant expression of ROR1 (receptor tyrosine kinase-like orphan receptor 1), seen in a large subset of MCL, results in BCR/BTK-independent signaling and growth of MCL cells. ROR1 forms a functional complex with CD19 to persistently activate the key cell signaling pathways PI3K-AKT and MEK-ERK in the BCR/BTK-independent manner. This study demonstrates that ROR1/CD19 complex effectively substitutes for BCR-BTK signaling to promote activation and growth of MCL cells. Therefore, ROR1 expression and activation may represent a novel mechanism of resistance to inhibition of BCR/BTK signaling in MCL. Our results provide a rationale to screen MCL patients for ROR1 expression and to consider new therapies targeting ROR1 and/or CD19 or their downstream signaling pathways for MCL-expressing ROR1.

Indexed as

Signal TransductionAdenineAgammaglobulinaemia Tyrosine KinaseCell Line, TumorCell ProliferationDose-Response Relationship, DrugHumansLymphoma, Mantle-CellPiperidinesProtein Kinase InhibitorsPyrazolesPyrimidinesReceptors, Antigen, B-CellReceptors, Antigen, T-CellReceptor Tyrosine Kinase-like Orphan ReceptorsStructure-Activity RelationshipAdenineAgammaglobulinaemia Tyrosine KinaseBTK protein, humanCD19-specific chimeric antigen receptoribrutinibPiperidinesProtein Kinase InhibitorsPyrazolesPyrimidinesReceptors, Antigen, B-CellReceptors, Antigen, T-CellReceptor Tyrosine Kinase-like Orphan ReceptorsROR1 protein, human

Identifiers

PMID31534006
PMCPMC10013414
OpenAlexW2974369408

What OpenQuestion holds

Textmetadata
LicenceTDM
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.