Evidence map›Paper›PMID 26601783›Full record

ReviewLeukemia2016

Interferon-alpha for the therapy of myeloproliferative neoplasms: targeting the malignant clone.

J-J Kiladjian, S Giraudier, B Cassinat

Abstract readReview
PubMed Publisher
In one paragraph

Review in Leukemia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
7.3field-weighted citation impact, top 2% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 128 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Review
  7. Review
  8. Article
  9. Pegylated interferon: the who, why, and how.Hematology. American Society of Hematology. Education Program · 2024
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Immunogenic Cell Death in Hematological Malignancy Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Review
  19. Polycythemia Vera: Barriers to and Strategies for Optimal Management.Blood and lymphatic cancer : targets and therapy · 2023
    Review
  20. Review

9 more citing papers are in PubMed but not listed here.

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.

J-J KiladjianCentre d'Investigations Cliniques, Hopital Saint-Louis, APHP, Paris, France.
S GiraudierINSERM UMR-S 1131, Institut Universitaire d'Hématologie, Université Paris Diderot, Paris, France.
B CassinatINSERM UMR-S 1131, Institut Universitaire d'Hématologie, Université Paris Diderot, Paris, France.ORCID http://orcid.org/0000-0002-6514-3905
Inserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interferon alpha (IFN-α) has been used for over 30 years to treat myeloproliferative neoplasms (MPNs). IFN-α was shown to induce clinical, hematological, molecular and histopathological responses in small clinical studies. Such combined efficacy has never been achieved with any other drug to date in such a significant proportion of patients. However, toxicity remains a limitation to its broader use despite the development of pegylated forms with better tolerance. Several on going phase 3 studies of peg- IFN-α versus hydroxyurea will help to define its exact place in MPN management. IFN-α efficacy is likely the consequence of a broad range of biological properties, including enhancement of immune response, direct effects on malignant cells and ability to cycle dormant malignant stem cells. However, comprehensive elucidation of its mechanism of action is still lacking. Sustained clinical, molecular and morphological responses after IFN-α discontinuation raised the hope that this drug could eradicate MPN. There is now consistent evidence showing that IFN-α is able to eliminate malignant clones harboring JAK2V617F or Calreticulin mutations. However, the molecular complexity of these diseases could hamper IFN-α efficacy, as the presence of additional non-driver mutations, like in the TET2 gene, could be associated with resistance to IFN-α. Therefore, combined therapy with another targeted agent could be required to eradicate MPN, and the best IFN-α companion for achieving this challenge remains to be determined.

Indexed as

Antiviral AgentsHumansInterferon-alphaMyeloproliferative DisordersAntiviral AgentsInterferon-alpha

Identifiers

PMID26601783
OpenAlexW2218840816

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.