Evidence map›Paper›PMID 25019218›Full record

ArticlePloS one2014

Antileukemic activity of sulforaphane in primary blasts from patients affected by myelo- and lympho-proliferative disorders and in hypoxic conditions.

Carmela Fimognari, Eleonora Turrini, Piero Sestili, Cinzia Calcabrini, Giovanni Carulli, Giulia Fontanelli, Martina Rousseau, Giorgio Cantelli-Forti, Patrizia Hrelia

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Integrative Hematology: State of the Art.International journal of molecular sciences · 2023
    Review
  4. Review
  5. Article
  6. Article
  7. Sulforaphane Modulates AQP8-Linked Redox Signalling in Leukemia Cells.Oxidative medicine and cellular longevity · 2018
    Article
  8. Article
  9. Review
  10. Review
  11. 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

9 authors at 3 institutions in 1 country.

Carmela FimognariDepartment for Life Quality Studies, Alma Mater Studiorum-University of Bologna, Rimini, Italy.
Eleonora TurriniDepartment for Life Quality Studies, Alma Mater Studiorum-University of Bologna, Rimini, Italy.
Piero SestiliDepartment of Biomolecular Sciences, University of Urbino "Carlo Bo", Urbino, Italy.
Cinzia CalcabriniDepartment of Biomolecular Sciences, University of Urbino "Carlo Bo", Urbino, Italy.
Giovanni CarulliDivision of Hematology, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Giulia FontanelliDivision of Hematology, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Martina RousseauDivision of Hematology, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Giorgio Cantelli-FortiDepartment for Life Quality Studies, Alma Mater Studiorum-University of Bologna, Rimini, Italy.
Patrizia HreliaDepartment of Pharmacy and BioTechnology, Alma Mater Studiorum-University of Bologna, Bologna, Italy.
University of Bologna · ITUniversity of Pisa · ITUniversity of Urbino · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sulforaphane is a dietary isothiocyanate found in cruciferous vegetables showing antileukemic activity. With the purpose of extending the potential clinical impact of sulforaphane in the oncological field, we investigated the antileukemic effect of sulforaphane on blasts from patients affected by different types of leukemia and, taking into account the intrinsically hypoxic nature of bone marrow, on a leukemia cell line (REH) maintained in hypoxic conditions. In particular, we tested sulforaphane on patients with chronic lymphocytic leukemia, acute myeloid leukemia, T-cell acute lymphoblastic leukemia, B-cell acute lymphoblastic leukemia, and blastic NK cell leukemia. Sulforaphane caused a dose-dependent induction of apoptosis in blasts from patients diagnosed with acute lymphoblastic or myeloid leukemia. Moreover, it was able to cause apoptosis and to inhibit proliferation in hypoxic conditions on REH cells. As to its cytotoxic mechanism, we found that sulforaphane creates an oxidative cellular environment that induces DNA damage and Bax and p53 gene activation, which in turn helps trigger apoptosis. On the whole, our results raise hopes that sulforaphane might set the stage for a novel therapeutic principle complementing our growing armature against malignancies and advocate the exploration of sulforaphane in a broader population of leukemic patients.

Indexed as

AnaerobiosisAnalysis of VarianceAnticarcinogenic AgentsApoptosisCell Line, TumorCell ProliferationCells, CulturedCellular MicroenvironmentDose-Response Relationship, DrugFlow CytometryHumansIsothiocyanatesLymphoproliferative DisordersMyeloproliferative DisordersReactive Oxygen SpeciesSulfoxidesAnticarcinogenic AgentsIsothiocyanatesReactive Oxygen SpeciessulforaphaneSulfoxides

Identifiers

PMID25019218
PMCPMC4096754
OpenAlexW2008655407

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.