Evidence map›Paper›PMID 31405039›Full record

ReviewInternational journal of molecular sciences2019

The SUMO Pathway in Hematomalignancies and Their Response to Therapies.

Mathias Boulanger, Rosa Paolillo, Marc Piechaczyk, Guillaume Bossis

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.7field-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

25 citing papers in PubMed, 42 citations in OpenAlex.

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  15. International journal of molecular sciences · 2021
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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

4 authors at 1 institution in 1 country.

Mathias BoulangerEquipe Labellisée Ligue Contre le Cancer, Institut de Génétique Moléculaire de Montpellier, University of Montpellier, CNRS, 34000 Montpellier, France.ORCID 0000-0002-2799-4047
Rosa PaolilloEquipe Labellisée Ligue Contre le Cancer, Institut de Génétique Moléculaire de Montpellier, University of Montpellier, CNRS, 34000 Montpellier, France.
Marc PiechaczykEquipe Labellisée Ligue Contre le Cancer, Institut de Génétique Moléculaire de Montpellier, University of Montpellier, CNRS, 34000 Montpellier, France.
Guillaume BossisEquipe Labellisée Ligue Contre le Cancer, Institut de Génétique Moléculaire de Montpellier, University of Montpellier, CNRS, 34000 Montpellier, France. guillaume.bossis@igmm.cnrs.fr.ORCID 0000-0002-3349-8250
Centre National de la Recherche Scientifique · FR

Funding

Association Laurette Fugain ALF-2017/02Fondation ARC pour la Recherche sur le Cancer 4eme année de thèseFondation Leucémie Espoir 2018Institut National Du Cancer PLBIO15-170Ligue Contre le Cancer equipe labellisée
6 · The paper itself

Abstract

SUMO (Small Ubiquitin-related MOdifier) is a post-translational modifier of the ubiquitin family controlling the function and fate of thousands of proteins. SUMOylation is deregulated in various hematological malignancies, where it participates in both tumorigenesis and cancer cell response to therapies. This is the case for Acute Promyelocytic Leukemias (APL) where SUMOylation, and subsequent destruction, of the PML-RARα fusion oncoprotein are triggered by arsenic trioxide, which is used as front-line therapy in combination with retinoic acid to cure APL patients. A similar arsenic-induced SUMO-dependent degradation was also documented for Tax, a human T-cell lymphotropic virus type I (HTLV1) viral protein implicated in Adult T-cell Leukemogenesis. SUMOylation also participates in Acute Myeloid Leukemia (AML) response to both chemo- and differentiation therapies, in particular through its ability to regulate gene expression. In Multiple Myeloma, many enzymes of the SUMO pathway are overexpressed and their high expression correlates with lower response to melphalan-based chemotherapies. B-cell lymphomas overexpressing the c-Myc oncogene also overexpress most components of the SUMO pathway and are highly sensitive to SUMOylation inhibition. Targeting the SUMO pathway with recently discovered pharmacological inhibitors, alone or in combination with current therapies, might therefore constitute a powerful strategy to improve the treatment of these cancers.

Indexed as

AnimalsAntineoplastic AgentsHematologic NeoplasmsHumansLeukemiaLymphomaMolecular Targeted TherapyMultiple MyelomaSignal TransductionSUMO-1 ProteinSumoylationAntineoplastic AgentsSUMO-1 ProteinhematomalignanciesleukemiaresistanceSUMOylation

Identifiers

PMID31405039
PMCPMC6721055
OpenAlexW2968436366

What OpenQuestion 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 OpenQuestion graph.