Evidence map›Paper›PMID 24413064›Full record

ArticleBlood cancer journal2014

Dual epigenetic targeting with panobinostat and azacitidine in acute myeloid leukemia and high-risk myelodysplastic syndrome.

P Tan, A Wei, S Mithraprabhu, N Cummings, H B Liu, M Perugini, K Reed, S Avery, S Patil, P Walker and 5 more

Abstract read
In one paragraph

Article in Blood cancer journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
–field-weighted citation impact
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

54 citing papers in PubMed.

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  5. Molecularly targeted therapy and immunotherapy in leukemias.Journal of hematology & oncology · 2026
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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

15 authors.

P TanDepartment of Clinical Haematology, Alfred Hospital, Australian Centre for Blood Diseases, Monash University, Melbourne, Victoria, Australia.
A WeiDepartment of Clinical Haematology, Alfred Hospital, Australian Centre for Blood Diseases, Monash University, Melbourne, Victoria, Australia.
S MithraprabhuDepartment of Clinical Haematology, Alfred Hospital, Australian Centre for Blood Diseases, Monash University, Melbourne, Victoria, Australia.
N CummingsDepartment of Clinical Haematology, Alfred Hospital, Australian Centre for Blood Diseases, Monash University, Melbourne, Victoria, Australia.
H B LiuAustralian Centre for Blood Diseases, Biotechnology Division, Eastern Clinical Research Unit, Monash University, Melbourne, Victoria, Australia.
M PeruginiInstitute of Medical and Veterinary Science, Department of Haematology and Centre for Cancer Biology, Adelaide, South Australia, Australia.
K ReedDepartment of Clinical Haematology, Alfred Hospital, Australian Centre for Blood Diseases, Monash University, Melbourne, Victoria, Australia.
S AveryDepartment of Clinical Haematology, Alfred Hospital, Australian Centre for Blood Diseases, Monash University, Melbourne, Victoria, Australia.
S PatilDepartment of Clinical Haematology, Alfred Hospital, Australian Centre for Blood Diseases, Monash University, Melbourne, Victoria, Australia.
P WalkerDepartment of Clinical Haematology, Alfred Hospital, Australian Centre for Blood Diseases, Monash University, Melbourne, Victoria, Australia.
P MolleeDivision of Cancer Services, Princess Alexandra Hospital, Brisbane, Queensland, Australia.
A GriggDepartment of Haematology, Austin Hospital, Melbourne, Victoria, Australia.
R D'AndreaInstitute of Medical and Veterinary Science, Department of Haematology and Centre for Cancer Biology, Adelaide, South Australia, Australia.
A DearAustralian Centre for Blood Diseases, Biotechnology Division, Eastern Clinical Research Unit, Monash University, Melbourne, Victoria, Australia.
A SpencerDepartment of Clinical Haematology, Alfred Hospital, Australian Centre for Blood Diseases, Monash University, Melbourne, Victoria, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Therapeutic options are limited for elderly patients with acute myeloid leukemia (AML). A phase Ib/II study was undertaken to evaluate the maximum-tolerated dose (MTD) and preliminary efficacy of the pan-histone deacetylase inhibitor panobinostat (LBH589) in combination with azacitidine in patients with AML or high-risk myelodysplastic syndrome (MDS) naïve to intensive chemotherapy. Thirty-nine patients (AML=29, MDS=10) received azacitidine 75 mg/m(2) subcutaneously (days 1-5) and oral panobinostat (starting on day 5, thrice weekly for seven doses) in 28-day cycles until toxicity or disease progression. Dose-limiting toxicities during the phase Ib stage were observed in 0/4 patients receiving 10 mg panobinostat, in 1/7 patients (fatigue) receiving 20 mg, in 1/6 patients (fatigue) receiving 30 mg and in 4/5 patients (fatigue, syncope, hyponatremia and somnolence) receiving 40 mg. In phase II, an additional 17 patients received panobinostat at a MTD of 30 mg. The overall response rate (ORR=CR+CRi+PR) in patients with AML was 31% (9/29) and that in patients with MDS was 50% (5/10). After a median follow-up of 13 months, the median overall survival was 8 and 16 months in patients with AML and MDS, respectively. Increased histone H3 and H4 acetylation was a useful early biomarker of clinical response. Combining panobinostat with azacitidine was tolerable and clinically active in high-risk MDS/AML patients, warranting further exploration.

Identifiers

PMID24413064
PMCPMC3913937

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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.