Evidence map›Paper›PMID 30055346›Full record

ArticleTranslational oncology2018

Variable Responses of MYC Translocation Positive Lymphoma Cell Lines To Different Combinations of Novel Agents: Impact of BCL2 Family Protein Expression.

Wenhan Deng, Alexandra Clipson, Hongxiang Liu, Yuanxue Huang, Rachel Dobson, Ming Wang, Peter Johnson, Ming-Qing Du

Open access · goldAbstract read
In one paragraph

Article in Translational oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

13 citing papers in PubMed, 28 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Wenhan DengDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge, UK.
Alexandra ClipsonDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge, UK.
Hongxiang LiuMolecular Malignancy Laboratory, Haematopathology and Oncology Diagnostic Service, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK.
Yuanxue HuangMolecular Malignancy Laboratory, Haematopathology and Oncology Diagnostic Service, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK.
Rachel DobsonDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge, UK.
Ming WangDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge, UK.
Peter JohnsonCancer Research UK Clinical Centre, University of Southampton, Southampton, United Kingdom.
Ming-Qing DuDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge, UK; Molecular Malignancy Laboratory, Haematopathology and Oncology Diagnostic Service, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK. Electronic address: mqd20@cam.ac.uk.
University of Cambridge · GBCambridge University Hospitals NHS Foundation Trust · GBCancer Research UK · GB

Funding

Cancer Research UK 12128
6 · The paper itself

Abstract

Several newly developed drugs including JQ1 (BET inhibitor), ABT199 (BCL2 inhibitor), and bortezomib (proteasome inhibitor) may offer novel therapeutic strategies for aggressive diffuse large B-cell lymphoma (DLBCL). We tested these drugs together with doxorubicin in a series of combinations in 16 DLBCL cell lines including 4 ABC-DLBCL (OCI-Ly3, OCI-Ly10, SUDHL2, RIVA) and 12 GCB-DLBCL lines (OCI-Ly4, OCI-Ly18, BJAB, SUDHL4, SUDHL6, SUDHL10, DB, PR1, VAL, SC1, Karpas-231, Karpas-422). Among these cell lines, ABT199 and doxorubicin, and to a lesser extent JQ1 and bortezomib, showed high variations in their ED50 values. Of the six cell lines showing high ABT199 ED50 values, four (SUDHL10, OCI-Ly4, SUDHL2, and BJAB) had no or little BCL2 expression, and SUDHL6 also displayed a low BCL2 expression. There was no association between the ED50 value of doxorubicin, JQ1 and bortezomib, and TP53/MYC/BCL2 genetic abnormalities or cell of origin subtype. A synergistic effect in all or the majority of drug combinations was seen in 11 cell lines, while an antagonistic effect in a high proportion of drug combinations was observed in the remaining 5 cell lines including the 3 (SUDHL10, OCI-Ly4, and SUDHL2) with little BCL2 expression, and additionally OCI-Ly18 and RIVA. Extensive Western blot analyses revealed high MCL1 expression in SUDHL10 and OCI-Ly4 but no apparent alterations in other cell lines. The molecular mechanism underlying the antagonistic effect of drug combinations in DLBCL is heterogeneous with the altered BCL2 family protein expression (absent BCL2, but high MCL1) in some cell lines.

Identifiers

PMID30055346
PMCPMC6077152
OpenAlexW2883362758

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.