Evidence map›Paper›PMID 30813354›Full record

ReviewCancers2019

Emerging Therapies for Acute Myelogenus Leukemia Patients Targeting Apoptosis and Mitochondrial Metabolism.

Germana Castelli, Elvira Pelosi, Ugo Testa

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Expression of Enhancer of Zeste Homolog 2 (EZH2) Gene in Acute Myeloid Leukemia.Asian Pacific journal of cancer prevention : APJCP · 2023
    Article
  5. Article
  6. Article
  7. Article
  8. Drug Repurposing by Tumor Tissue Editing.Frontiers in oncology · 2022
    Review
  9. Review
  10. Review
  11. Extinguishing the Embers: Targeting AML Metabolism.Trends in molecular medicine · 2021
    Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. 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

3 authors at 1 institution in 1 country.

Germana CastelliDepartment of Oncology, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy. germana.castelli@iss.it.
Elvira PelosiDepartment of Oncology, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy. elvira.pelosi@iss.it.
Ugo TestaDepartment of Oncology, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy. ugo.testa@iss.it.ORCID 0000-0001-7900-8942
Istituto Superiore di Sanità · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute Myelogenous Leukemia (AML) is a malignant disease of the hematopoietic cells, characterized by impaired differentiation and uncontrolled clonal expansion of myeloid progenitors/precursors, resulting in bone marrow failure and impaired normal hematopoiesis. AML comprises a heterogeneous group of malignancies, characterized by a combination of different somatic genetic abnormalities, some of which act as events driving leukemic development. Studies carried out in the last years have shown that AML cells invariably have abnormalities in one or more apoptotic pathways and have identified some components of the apoptotic pathway that can be targeted by specific drugs. Clinical results deriving from studies using B-cell lymphoma 2 (BCL-2) inhibitors in combination with standard AML agents, such as azacytidine, decitabine, low-dose cytarabine, provided promising results and strongly support the use of these agents in the treatment of AML patients, particularly of elderly patients. TNF-related apoptosis-inducing ligand (TRAIL) and its receptors are frequently deregulated in AML patients and their targeting may represent a promising strategy for development of new treatments. Altered mitochondrial metabolism is a common feature of AML cells, as supported through the discovery of mutations in the isocitrate dehydrogenase gene and in mitochondrial electron transport chain and of numerous abnormalities of oxidative metabolism existing in AML subgroups. Overall, these observations strongly support the view that the targeting of mitochondrial apoptotic or metabolic machinery is an appealing new therapeutic perspective in AML.

Indexed as

acute myeloid leukemiaapoptosisBCL-2leukemiaMCL-1TRAIL

Identifiers

PMID30813354
PMCPMC6406361
OpenAlexW2915293258

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.