Evidence map›Paper›PMID 34992627›Full record

ReviewFrontiers in genetics2021

The Role of Janus Kinase/STAT3 Pathway in Hematologic Malignancies With an Emphasis on Epigenetics.

Elham Zeinalzadeh, Alexey Valerievich Yumashev, Heshu Sulaiman Rahman, Faroogh Marofi, Navid Shomali, Hossein Samadi Kafil, Saeed Solali, Mehdi Sajjadi-Dokht, Sajjad Vakili-Samiani, Mostafa Jarahian and 1 more

RetractedOpen access · goldAbstract readReviewRetracted Publication
In one paragraph

Review in Frontiers in genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Review
  6. JMJD3 PromotesDNA and cell biology · 2022
    Article
  7. Review
  8. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 4 countries.

Elham ZeinalzadehStudent Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran.
Alexey Valerievich YumashevDepartment of Prosthetic Dentistry, Sechenov First Moscow State Medical University, Moscow, Russia.
Heshu Sulaiman RahmanCollege of Medicine, University of Sulaimani, Sulaimaniyah, Iraq.
Faroogh MarofiDepartment of Immunology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Navid ShomaliDepartment of Immunology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Hossein Samadi KafilGerman Cancer Research Center, Toxicology and Chemotherapy Unit (G401), Heidelberg, Germany.
Saeed SolaliHematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Mehdi Sajjadi-DokhtHematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Sajjad Vakili-SamianiHematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Mostafa JarahianGerman Cancer Research Center, Toxicology and Chemotherapy Unit (G401), Heidelberg, Germany.
Majid Farshdousti HaghHematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Tabriz University of Medical Sciences · IRHeidelberg University · DESechenov University · RUUniversity of Sulaimani · IQ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway has been known to be involved in cell growth, cellular differentiation processes development, immune cell survival, and hematopoietic system development. As an important member of the STAT family, STAT3 participates as a major regulator of cellular development and differentiation-associated genes. Prolonged and persistent STAT3 activation has been reported to be associated with tumor cell survival, proliferation, and invasion. Therefore, the JAK-STAT pathway can be a potential target for drug development to treat human cancers, e.g., hematological malignancies. Although STAT3 upregulation has been reported in hematopoietic cancers, protein-level STAT3 mutations have also been reported in invasive leukemias/lymphomas. The principal role of STAT3 in tumor cell growth clarifies the importance of approaches that downregulate this molecule. Epigenetic modifications are a major regulatory mechanism controlling the activity and function of STAT3. So far, several compounds have been developed to target epigenetic regulatory enzymes in blood malignancies. Here, we discuss the current knowledge about STAT3 abnormalities and carcinogenic functions in hematopoietic cancers, novel STAT3 inhibitors, the role of epigenetic mechanisms in STAT3 regulation, and targeted therapies, by focusing on STAT3-related epigenetic modifications.

Indexed as

epigeneticsJanus kinaseleukemiamethylationSTAT3

Identifiers

PMID34992627
PMCPMC8725977
OpenAlexW4200074112

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.