Evidence map›Paper›PMID 36316776›Full record

ReviewCell communication and signaling : CCS2022

Potential role of autophagy induced by FLT3-ITD and acid ceramidase in acute myeloid leukemia chemo-resistance: new insights.

Hamidreza Zalpoor, Maryam Bakhtiyari, Abdullatif Akbari, Fatemeh Aziziyan, Hooriyeh Shapourian, Mahsa Liaghat, Zahra Zare-Badie, Sheida Yahyazadeh, Vahideh Tarhriz, Mazdak Ganjalikhani-Hakemi

Open access · goldAbstract readVideo-Audio MediaReview
In one paragraph

Review in Cell communication and signaling : CCS, 2022. 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
3.7field-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, 25 citations in OpenAlex.

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  14. The role of mCell death discovery · 2023
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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

10 authors at 5 institutions in 1 country.

Hamidreza ZalpoorShiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. hamidreza.zlpr1998@gmail.com.ORCID 0000-0002-8057-2804
Maryam BakhtiyariNetwork of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Tehran, Iran.
Abdullatif AkbariShiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Fatemeh AziziyanNetwork of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Tehran, Iran.
Hooriyeh ShapourianDepartment of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Mahsa LiaghatNetwork of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Tehran, Iran.
Zahra Zare-BadieDiagnostic Laboratory Sciences and Technology Research Center, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran.
Sheida YahyazadehDepartment of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Vahideh TarhrizMolecular Medicine Research Center, Biomedicine Institute, Tabriz University of Medical Sciences, Tabriz, Iran. tarhrizv@tbzmed.ac.ir.
Mazdak Ganjalikhani-HakemiDepartment of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. mghakemi@med.mui.ac.ir.
Isfahan University of Medical Sciences · IRShiraz University of Medical Sciences · IRUniversal Scientific Education and Research Network · IRTabriz University of Medical Sciences · IRTarbiat Modares University · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a type of leukemia with a poor prognosis and survival characterized by abnormal cell proliferation and differentiation. Despite advances in treatment, AML still has a low complete remission rate, particularly in elderly patients, and recurrences are frequently seen even after complete remissions. The major challenge in treating AML is the resistance of leukemia cells to chemotherapy drugs. Thus, to overcome this issue, it can be crucial to conduct new investigations to explore the mechanisms of chemo-resistance in AML and target them. In this review, the potential role of autophagy induced by FLT3-ITD and acid ceramidase in chemo-resistance in AML patients are analyzed. With regard to the high prevalence of FLT3-ITD mutation (about 25% of AML cases) and high level of acid ceramidase in these patients, we hypothesized that both of these factors could lead to chemo-resistance by inducing autophagy. Therefore, pharmacological targeting of autophagy, FLT3-ITD, and acid ceramidase production could be a promising therapeutic approach for such AML patients to overcome chemo-resistance. Video abstract.

Indexed as

Acid CeramidaseLeukemia, Myeloid, AcuteAgedAutophagyfms-Like Tyrosine Kinase 3HumansMutationAcid CeramidaseFLT3 protein, humanfms-Like Tyrosine Kinase 3Acid ceramidaseAcute myeloid leukemiaAutophagyChemo-resistanceFLT3-ITDSphingosine

Identifiers

PMID36316776
PMCPMC9620650
OpenAlexW4307885324

What OpenQuestion holds

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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.