Evidence map›Paper›PMID 27475430›Full record

ReviewCurrent hematologic malignancy reports2016

What Is the Optimal Induction Therapy for Younger Fit Patients With AML?

Hugo F Fernandez

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current hematologic malignancy reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 39% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. 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

1 author at 1 institution in 1 country.

Hugo F FernandezDepartment of Blood and Marrow Transplantation, Moffitt Cancer Center and Research Institute, 12902 Magnolia Drive, FOB3, Tampa, FL, 337612, USA. hugo.fernandez@moffitt.org.
Moffitt Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a complex clonal disorder. The disease is characterized by chromosomal and molecular abnormalities that propagate and expand the abnormal clone(s). The main goal of therapy is to achieve and ultimately maintain a complete remission. In the younger AML patient (less than 60 years of age), there has been a standardization of the initial therapy with the 3 + 7 regimen, consisting of an anthracycline and cytarabine combination. Recent intensification of the anthracycline has led to improved remission and survival outcomes in these patients. Prognosis and therapy in this disease is driven by cytogenetic studies and the additional molecular information that is gathered at the time of diagnosis. With the finding of potential targetable lesions within these molecular aberrancies, new treatments are emerging to deepen remissions and ultimately improve survival.

Indexed as

AnthracyclinesAntimetabolites, AntineoplasticCytarabineDrug Therapy, Combinationfms-Like Tyrosine Kinase 3HumansLeukemia, Myeloid, AcuteMolecular Targeted TherapyPrognosisRemission InductionSurvival RateAnthracyclinesAntimetabolites, AntineoplasticCytarabineFLT3 protein, humanfms-Like Tyrosine Kinase 3Acute myeloid leukemiaInduction therapyTargeted AML therapy

Identifiers

PMID27475430
OpenAlexW2478863565

What OpenQuestion holds

Textmetadata
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.