Evidence map›Paper›PMID 31310323›Full record

ArticleCancer2019

Sorafenib plus intensive chemotherapy improves survival in patients with newly diagnosed, FLT3-internal tandem duplication mutation-positive acute myeloid leukemia.

Koji Sasaki, Hagop M Kantarjian, Tapan Kadia, Keyur Patel, Sanam Loghavi, Guillermo Garcia-Manero, Elias J Jabbour, Courtney DiNardo, Naveen Pemmaraju, Naval Daver and 9 more

Abstract read
In one paragraph

Article in Cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Retinoic acid and proteotoxic stress induce AML cell death overcoming stromal cell protection.Journal of experimental & clinical cancer research : CR · 2023
    Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Therapeutic Advances in Immunotherapies for Hematological Malignancies.International journal of molecular sciences · 2022
    Review
  12. Article
  13. Which FLT3 Inhibitor for Treatment of AML?Current treatment options in oncology · 2022
    Review
  14. New Drugs Bringing New Challenges to AML: A Brief Review.Journal of personalized medicine · 2021
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

19 authors.

Koji SasakiDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID https://orcid.org/0000-0002-9140-0610
Hagop M KantarjianDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID https://orcid.org/0000-0002-1908-3307
Tapan KadiaDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID https://orcid.org/0000-0002-9892-9832
Keyur PatelDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Sanam LoghaviDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Guillermo Garcia-ManeroDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID https://orcid.org/0000-0002-3631-2482
Elias J JabbourDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID https://orcid.org/0000-0003-4465-6119
Courtney DiNardoDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID https://orcid.org/0000-0001-9003-0390
Naveen PemmarajuDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Naval DaverDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID https://orcid.org/0000-0001-7103-373X
Iman Abou DalleDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Nicholas ShortDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID https://orcid.org/0000-0002-2983-2738
Musa YilmazDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Prithviraj BoseDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Kiran NaqviDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID https://orcid.org/0000-0002-5511-6153
Sherry PierceDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Fevzi YalnizDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Jorge E CortesDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Farhad RavandiDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Leukemia TexasNCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

backgroundThe addition of midostaurin to induction chemotherapy improves survival in younger patients with newly diagnosed, FLT3-mutated acute myeloid leukemia (AML). Sorafenib is a potent multikinase inhibitor with efficacy when given as monotherapy. The authors investigated whether the addition of sorafenib to intensive induction chemotherapy improves outcomes in patients with FLT3-internal tandem duplication (ITD)-mutated AML.

methodsIn total, 183 patients who were newly diagnosed with FLT3-ITD-mutated AML between February 2001 and December 2017 were identified. Of these, 79 patients (43%) underwent intensive chemotherapy with the addition of sorafenib, and 104 (57%) received intensive chemotherapy alone. Propensity score matching identified 42 patients in each cohort.

resultsThe overall response rate was 98% in the sorafenib cohort and 83% in the intensive chemotherapy cohort (P = .057). The median follow-up was 54 months. The median event-free survival was 35 months in the sorafenib cohort and 8 months in the intensive chemotherapy cohort (P = .019), and the median overall survival was 42 and 13 months, respectively (P = .026). With censoring at the time of allogeneic stem cell transplantation, the median event-free survival was 31 and 8 months in the sorafenib and intensive therapy cohorts, respectively (P = .031), and the median overall survival was not reached and 10 months, respectively (P = .001). Multivariate Cox proportional hazards models confirmed that treatment with sorafenib was a favorable prognostic factor (P = .009; hazard ratio, 0.558; 95% CI, 0.360-0.865).

conclusionsThe addition of sorafenib improves survival in patients with FLT3-ITD-mutated AML regardless of whether they undergo allogeneic stem cell transplantation.

Indexed as

MutationAcute DiseaseAdultAntineoplastic Combined Chemotherapy ProtocolsCohort StudiesCombined Modality TherapyFemalefms-Like Tyrosine Kinase 3Hematopoietic Stem Cell TransplantationHumansInduction ChemotherapyKaplan-Meier EstimateLeukemia, MyeloidMaleMiddle AgedRemission InductionFLT3 protein, humanfms-Like Tyrosine Kinase 3midostaurinSorafenibStaurosporineacute myeloid leukemiaallogeneic stem cell transplantationFLT3-internal tandem duplication (FLT3-ITD)induction chemotherapysorafenib

Identifiers

PMID31310323
PMCPMC11849279

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Registered trials

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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.