Evidence map›Paper›PMID 33705488›Full record

ArticlePloS one2021

Ruxolitinib with resminostat exert synergistic antitumor effects in Cutaneous T-cell Lymphoma.

Fani Karagianni, Christina Piperi, Vassiliki Mpakou, Aris Spathis, Periklis G Foukas, Maria Dalamaga, Vasiliki Pappa, Evangelia Papadavid

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

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  13. Retinoids as anti-cancer agents and their mechanisms of action.American journal of cancer research · 2022
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  15. Malignant and Benign T Cells Constituting Cutaneous T-Cell Lymphoma.International journal of molecular sciences · 2021
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  16. Review
  17. Clinical Guidelines and New Molecular Targets for Cutaneous Lymphomas.International journal of molecular sciences · 2021
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  18. Review
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.

Fani Karagianni2nd Department of Dermatology and Venereal Diseases, NKUA, Athens, Greece.ORCID 0000-0001-9514-2199
Christina PiperiDepartment of Biological Chemistry, NKUA, Athens, Greece.
Vassiliki MpakouSecond Department of Internal Medicine and Research Institute, Attikon University General Hospital, NKUA, Athens, Greece.
Aris SpathisSecond Department of Pathology, National and Kapodistrian University of Athens, Athens, Greece.
Periklis G FoukasSecond Department of Pathology, National and Kapodistrian University of Athens, Athens, Greece.
Maria Dalamaga2nd Department of Dermatology and Venereal Diseases, NKUA, Athens, Greece.
Vasiliki PappaSecond Department of Internal Medicine and Research Institute, Attikon University General Hospital, NKUA, Athens, Greece.
Evangelia Papadavid2nd Department of Dermatology and Venereal Diseases, NKUA, Athens, Greece.
Hospital Venereal and Skin Diseases Thessaloniki · GRNational and Kapodistrian University of Athens · GRUniversity General Hospital Attikon · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe combination of JAK/STAT and HDAC inhibitors exerted beneficial effects in haematological malignancies, presenting promising therapeutic CTCL targets. We aim to investigate the efficacy of JAK1/2i ruxolitinib in combination with HDACi resminostat in CTCL in vitro. MATERIAL &

methodsNon-toxic concentrations of ruxolitinib and/or resminostat were administered to MyLa (MF) and SeAx (SS) cells for 24h. Cytotoxicity, cell proliferation and apoptosis were estimated through MTT, BrdU/7AAD and Annexin V/PI assay. Multi-pathway analysis was performed to investigate the effect of JAK1/2i and/or HDACi on JAK/STAT, Akt/mTOR and MAPK signalling pathways.

resultsBoth drugs and their combination were cytotoxic in MyLa (p<0.05) and in SeAx cell line (p<0.001), inhibited proliferation of MyLa (p<0.001) and SeAx (p<0.001) at 24h, compared to untreated cells. Moreover, combined drug treatment induced apoptosis after 24h (p<0.001) in MyLa, and SeAx (p<0.001). The combination of drugs had a strong synergistic effect with a CI<1. Importantly, the drugs' combination inhibited phosphorylation of STAT3 (p<0.001), Akt (p<0.05), ERK1/2 (p<0.001) and JNK (p<0.001) in MyLa, while it reduced activation of Akt (p<0.05) and JNK (p<0.001) in SeAx.

conclusionThe JAKi/HDACi combination exhibited substantial anti-tumor effects in CTCL cell lines, and may represent a promising novel therapeutic modality for CTCL patients.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsCell Line, TumorDrug SynergismHumansHydroxamic AcidsLymphoma, T-Cell, CutaneousMAP Kinase Signaling SystemNeoplasm ProteinsNitrilesPyrazolesPyrimidinesSulfonamidesHydroxamic AcidsNeoplasm ProteinsNitrilesPyrazolesPyrimidinesresminostatruxolitinibSulfonamides

Identifiers

PMID33705488
PMCPMC7951910
OpenAlexW3135108405

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.