Evidence map›Paper›PMID 26486787›Full record

ArticleBlood2015

Identification of the Ki-1 antigen (CD30) as a novel therapeutic target in systemic mastocytosis.

Katharina Blatt, Sabine Cerny-Reiterer, Juliana Schwaab, Karl Sotlar, Gregor Eisenwort, Gabriele Stefanzl, Gregor Hoermann, Matthias Mayerhofer, Mathias Schneeweiss, Sylvia Knapp and 8 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
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  9. Mastocytosis.Nature reviews. Disease primers · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 8 institutions in 3 countries.

Katharina BlattDepartment of Internal Medicine I, Division of Hematology and Hemostaseology and.
Sabine Cerny-ReitererDepartment of Internal Medicine I, Division of Hematology and Hemostaseology and Ludwig Boltzmann Cluster Oncology, Medical University of Vienna, Vienna, Austria;
Juliana SchwaabDepartment of Hematology and Oncology, University Hospital Mannheim, Mannheim, Germany;
Karl SotlarInstitute of Pathology, Ludwig-Maximilians-University, Munich, Germany;
Gregor EisenwortLudwig Boltzmann Cluster Oncology, Medical University of Vienna, Vienna, Austria;
Gabriele StefanzlDepartment of Internal Medicine I, Division of Hematology and Hemostaseology and.
Gregor HoermannDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria;
Matthias MayerhoferDepartment of Laboratory Medicine, Hanusch Hospital, Vienna, Austria;
Mathias SchneeweissDepartment of Internal Medicine I, Division of Hematology and Hemostaseology and Department of Internal Medicine I, Laboratory of Infection Biology, Medical University of Vienna, Vienna, Austria;
Sylvia KnappDepartment of Internal Medicine I, Laboratory of Infection Biology, Medical University of Vienna, Vienna, Austria; Research Center for Molecular Medicine (CeMM) of the Austrian Academy of Sciences, Vienna, Austria; and.
Thomas RülickeInstitute of Laboratory Animal Science and.
Emir HadzijusufovicDepartment of Internal Medicine I, Division of Hematology and Hemostaseology and Ludwig Boltzmann Cluster Oncology, Medical University of Vienna, Vienna, Austria; Department/Clinic for Companion Animals and Horses, Clinic for Small Animals, Clinical Unit of Internal Medicine, University of Veterinary Medicine, Vienna, Austria.
Karin BauerDepartment of Internal Medicine I, Division of Hematology and Hemostaseology and.
Dubravka SmiljkovicDepartment of Internal Medicine I, Division of Hematology and Hemostaseology and.
Michael WillmannDepartment/Clinic for Companion Animals and Horses, Clinic for Small Animals, Clinical Unit of Internal Medicine, University of Veterinary Medicine, Vienna, Austria.
Andreas ReiterDepartment of Hematology and Oncology, University Hospital Mannheim, Mannheim, Germany;
Hans-Peter HornyInstitute of Pathology, Ludwig-Maximilians-University, Munich, Germany;
Peter ValentDepartment of Internal Medicine I, Division of Hematology and Hemostaseology and Ludwig Boltzmann Cluster Oncology, Medical University of Vienna, Vienna, Austria;
Medical University of Vienna · ATLudwig-Maximilians-Universität München · DEHanusch Hospital · ATHeidelberg University · DEInstitute of Laboratory Animal Science · CNLudwig Boltzmann Cluster for Cardiovascular Research · ATUniversity Medical Centre Mannheim · DEUniversity of Veterinary Medicine Vienna · AT

Funding

Austrian Science Fund FWF F 4611Austrian Science Fund FWF F 4704Austrian Science Fund FWF P 25937
6 · The paper itself

Abstract

The Ki-1 antigen (CD30) is an established therapeutic target in patients with Hodgkin lymphoma and anaplastic large-cell lymphoma. We have recently shown that CD30 is expressed abundantly in the cytoplasm of neoplastic mast cells (MCs) in patients with advanced systemic mastocytosis (SM). In the current study, we asked whether CD30 is expressed on the surface of neoplastic MCs in advanced SM, and whether this surface structure may serve as therapeutic target in SM. As assessed by flow cytometry, CD30 was found to be expressed on the surface of neoplastic MCs in 3 of 25 patients (12%) with indolent SM, 4 of 7 patients (57%) with aggressive SM, and 4 of 7 patients (57%) with MC leukemia. The immature RAS-transformed human MC line MCPV-1.1 also expressed cell surface CD30, whereas the KIT-transformed MC line HMC-1.2 expressed no detectable CD30. The CD30-targeting antibody-conjugate brentuximab-vedotin inhibited proliferation in neoplastic MCs, with lower IC50 values obtained in CD30(+) MCPV-1.1 cells (10 µg/mL) compared with CD30(-) HMC-1.2 cells (>50 µg/mL). In addition, brentuximab-vedotin suppressed the engraftment of MCPV-1.1 cells in NSG mice. Moreover, brentuximab-vedotin produced apoptosis in all CD30(+) MC lines tested as well as in primary neoplastic MCs in patients with CD30(+) SM, but did not induce apoptosis in neoplastic MCs in patients with CD30(-) SM. Furthermore, brentuximab-vedotin was found to downregulate anti-IgE-induced histamine release in CD30(+) MCs. Finally, brentuximab-vedotin and the KIT D816V-targeting drug PKC412 produced synergistic growth-inhibitory effects in MCPV-1.1 cells. Together, CD30 is a promising new drug target for patients with CD30(+) advanced SM.

Indexed as

AnimalsApoptosisBrentuximab VedotinCell ProliferationEnzyme-Linked Immunosorbent AssayFlow CytometryHeterograftsHumansImmunoconjugatesImmunohistochemistryKi-1 AntigenMast CellsMastocytosis, SystemicMiceMice, Inbred NODMice, SCIDBrentuximab VedotinImmunoconjugatesKi-1 Antigen

Identifiers

PMID26486787
PMCPMC4692143
OpenAlexW2179483502

What OpenQuestion holds

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Registered trials

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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.