Evidence map›Paper›PMID 33446256›Full record

ArticleClinical epigenetics2021

Different methylation signatures at diagnosis in patients with high-risk myelodysplastic syndromes and secondary acute myeloid leukemia predict azacitidine response and longer survival.

M Cabezón, R Malinverni, J Bargay, B Xicoy, S Marcé, A Garrido, M Tormo, L Arenillas, R Coll, J Borras and 11 more

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 46 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

21 authors at 11 institutions in 1 country.

M Cabezón *Hematology Laboratory Service, ICO Badalona-Hospital Germans Trias I Pujol, Myeloid Neoplasms Group, Josep Carreras Leukemia Research Institute (IJC), Badalona, Spain.
R Malinverni *Cancer and Leukemia Epigenetics and Biology Program, Josep Carreras Leukemia Research Institute (IJC), Campus ICO-GTP-UAB, Badalona, Spain.
J BargayHematology Service, Hospital Son Llàtzer, Palma de Mallorca, Spain.
B XicoyHematology Laboratory Service, ICO Badalona-Hospital Germans Trias I Pujol, Myeloid Neoplasms Group, Josep Carreras Leukemia Research Institute (IJC), Badalona, Spain.
S MarcéHematology Laboratory Service, ICO Badalona-Hospital Germans Trias I Pujol, Myeloid Neoplasms Group, Josep Carreras Leukemia Research Institute (IJC), Badalona, Spain.
A GarridoHematology Service, Hospital de Sant Pau, Barcelona, Spain.
M TormoHematology Service, Hospital Clínico de Valencia, Valencia, Spain.
L ArenillasHematology Service, Hospital del Mar, Barcelona, Spain.
R CollHematology Service, ICO Girona - Hospital Josep Trueta, Girona, Spain.
J BorrasHematology Service, Hospital Son Llàtzer, Palma de Mallorca, Spain.
M J JiménezHematology Laboratory Service, ICO Badalona-Hospital Germans Trias I Pujol, Myeloid Neoplasms Group, Josep Carreras Leukemia Research Institute (IJC), Badalona, Spain.
M HoyosHematology Service, Hospital de Sant Pau, Barcelona, Spain.
D ValcárcelHematology Service, Hospital Vall D'Hebron, Barcelona, Spain.
L EscodaHematology Service, Hospital Joan XXIII, Tarragona, Spain.
F Vall-LloveraHematology Service, Hospital Mútua de Terrassa, Terrassa, Spain.
A GarciaHematology Service, Hospital Arnau de Vilanova, Lleida, Spain.
L L FontHematology Service, Hospital Verge de La Cinta, Tortosa, Spain.
E RámilaHematology Service, Hospital Parc Taulí, Sabadell, Spain.
M BuschbeckCancer and Leukemia Epigenetics and Biology Program, Josep Carreras Leukemia Research Institute (IJC), Campus ICO-GTP-UAB, Badalona, Spain.
L ZamoraHematology Laboratory Service, ICO Badalona-Hospital Germans Trias I Pujol, Myeloid Neoplasms Group, Josep Carreras Leukemia Research Institute (IJC), Badalona, Spain. lzamora@iconcologia.net.ORCID 0000-0003-1713-7110
CETLAM group
Hospital de Sant Pau · ESHospital Son Llatzer · ESJosep Carreras Leukaemia Research Institute · ESUniversitat Autònoma de Barcelona · ESUniversity Hospital Mútua de Terrassa · ESHospital Arnau de Vilanova · ESHospital Clínico Universitario de Valencia · ESHospital Del Mar · ESHospital Universitari de Tortosa Verge de la Cinta · ESInstitute of Predictive and Personalized Medicine of Cancer · ESVall d'Hebron Hospital Universitari · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpigenetic therapy, using hypomethylating agents (HMA), is known to be effective in the treatment of high-risk myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) patients who are not suitable for intensive chemotherapy and/or allogeneic stem cell transplantation. However, response rates to HMA are low and there is an unmet need in finding prognostic and predictive biomarkers of treatment response and overall survival. We performed global methylation analysis of 75 patients with high-risk MDS and secondary AML who were included in CETLAM SMD-09 protocol, in which patients received HMA or intensive treatment according to age, comorbidities and cytogenetic.

resultsUnsupervised analysis of global methylation pattern at diagnosis did not allow patients to be differentiated according to the cytological subtype, cytogenetic groups, treatment response or patient outcome. However, after a supervised analysis we found a methylation signature defined by 200 probes, which allowed differentiating between patients responding and non-responding to azacitidine (AZA) treatment and a different methylation pattern also defined by 200 probes that allowed to differentiate patients according to their survival. On studying follow-up samples, we confirmed that AZA decreases global DNA methylation, but in our cohort the degree of methylation decrease did not correlate with the type of response. The methylation signature detected at diagnosis was not useful in treated samples to distinguish patients who were going to relapse or progress.

conclusionsOur findings suggest that in a subset of specific CpGs, altered DNA methylation patterns at diagnosis may be useful as a biomarker for predicting AZA response and survival.

Indexed as

DNA MethylationAdultAgedAged, 80 and overAntimetabolites, AntineoplasticAzacitidineFemaleHumansLeukemia, Myeloid, AcuteMaleMiddle AgedMyelodysplastic SyndromesRisk AssessmentSpainAntimetabolites, AntineoplasticAzacitidineAzacitidineDNA methylationEpigenetic drugsHypomethylating agentsMyelodysplastic syndromesPrognostic factorsSecondary acute myeloid leukemia

Identifiers

PMID33446256
PMCPMC7809812
OpenAlexW3124427154

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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.