Evidence map›Paper›PMID 28171800›Full record

ArticleLeukemia research2017

Epigenetic drug combination overcomes osteoblast-induced chemoprotection in pediatric acute lymphoid leukemia.

Anthony Quagliano, Anilkumar Gopalakrishnapillai, Sonali P Barwe

Abstract read
In one paragraph

Article in Leukemia research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Super-enhancers: a new frontier for epigenetic modifiers in cancer chemoresistance.Journal of experimental & clinical cancer research : CR · 2021
    Review
  5. Article
  6. Review
  7. Article
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

3 authors at 1 institution in 1 country.

Anthony QuaglianoNemours Center for Childhood Cancer Research, Alfred I. duPont Hospital for Children, Wilmington, DE 19803, United States; Department of Biological Sciences, University of Delaware, Wilmington, DE 19716, United States.
Anilkumar GopalakrishnapillaiNemours Center for Childhood Cancer Research, Alfred I. duPont Hospital for Children, Wilmington, DE 19803, United States. Electronic address: anil.g@nemours.org.
Sonali P BarweNemours Center for Childhood Cancer Research, Alfred I. duPont Hospital for Children, Wilmington, DE 19803, United States; Department of Biological Sciences, University of Delaware, Wilmington, DE 19716, United States. Electronic address: barwe@medsci.udel.edu.
Alfred I. duPont Hospital for Children · US

Funding

Predictive Modeling & Optimal Control Framework for Model-Based Epidemic Response in DelawareP20GM103446 · NIGMS · UNIVERSITY OF DELAWARE · PI MELINDA K DUNCAN · 2012 to 2026
$67.2M
Subproject Title: Clinical Research Education, Mentoring and Career Development CoreU54GM104941 · NIGMS · UNIVERSITY OF DELAWARE · PI Megan M Wenner · 2013 to 2026
$60.5M
Center for Pediatric ResearchP20GM103464 · NIGMS · NEMOURS CHILDREN'S HOSPITAL, DELAWARE · PI SHAFFER, THOMAS H · 2012 to 2014
$5.6M
NIGMS NIH HHS P20 GM103446NIGMS NIH HHS P20 GM103464NIGMS NIH HHS U54 GM104941
6 · The paper itself

Abstract

Although there has been much progress in the treatment of acute lymphoblastic leukemia (ALL), decreased sensitivity to chemotherapy remains a significant issue. Recent studies have shown how interactions with the bone marrow microenvironment can protect ALL cells from chemotherapy and allow for the persistence of the disease. Epigenetic drugs have been used for the treatment of ALL, but there are no reports on whether these drugs can overcome bone marrow-induced chemoprotection. Our study investigates the ability of the DNA methyltransferase inhibitor azacitidine and the histone deacetylase inhibitor panobinostat to overcome chemoprotective effects mediated by osteoblasts. We show that the combination of azacitidine and panobinostat has a synergistic killing effect and that this combination is more effective than cytarabine in inducing ALL cell death in co-culture with osteoblasts. We also show that this combination can be used to sensitize ALL cells to chemotherapeutics in the presence of osteoblasts. Finally, we demonstrate that these effects can be replicated ex vivo in a number of mouse passaged xenograft lines from both B-ALL and T-ALL patients with varying cytogenetics. Thus, our data provides evidence that azacitidine and panobinostat can successfully overcome osteoblast-induced chemoprotection in vitro and ex vivo in both B-ALL and T-ALL cells.

Indexed as

AnimalsAzacitidineCoculture TechniquesDNA Modification MethylasesDrug Resistance, NeoplasmEpigenesis, GeneticHeterograftsHistone Deacetylase InhibitorsHumansHydroxamic AcidsIndolesMiceOsteoblastsPanobinostatPrecursor B-Cell Lymphoblastic Leukemia-LymphomaPrecursor Cell Lymphoblastic Leukemia-LymphomaAzacitidineDNA Modification MethylasesHistone Deacetylase InhibitorsHydroxamic AcidsIndolesPanobinostatAcute lymphoid leukemiaAzacitidineChemoprotectionEpigeneticOsteoblastsPanobinostat

Identifiers

PMID28171800
PMCPMC5366080
OpenAlexW2580303125

What OpenQuestion holds

Textmetadata
LicenceTDM
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.