Evidence map›Paper›PMID 38238319›Full record

ReviewBlood cancer journal2024

The constitutive activation of STAT3 gene and its mutations are at the crossroad between LGL leukemia and autoimmune disorders.

Gianpietro Semenzato, Giulia Calabretto, Antonella Teramo, Vanessa Rebecca Gasparini, Elisa Rampazzo, Gregorio Barilà, Renato Zambello

Open access · goldAbstract readReview
In one paragraph

Review in Blood cancer journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 4% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

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  15. Non-Malignant Granulocyte and Monocyte Disorders: An Update.British journal of biomedical science · 2025
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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

7 authors at 1 institution in 1 country.

Gianpietro SemenzatoUniversity of Padova, Department of Medicine, Hematology Unit, Padova, Italy. g.semenzato@unipd.it.ORCID 0000-0002-6061-4595
Giulia CalabrettoUniversity of Padova, Department of Medicine, Hematology Unit, Padova, Italy.
Antonella TeramoUniversity of Padova, Department of Medicine, Hematology Unit, Padova, Italy.ORCID 0000-0002-2754-699X
Vanessa Rebecca GaspariniUniversity of Padova, Department of Medicine, Hematology Unit, Padova, Italy.ORCID 0000-0001-8689-3759
Elisa RampazzoUniversity of Padova, Department of Medicine, Hematology Unit, Padova, Italy.
Gregorio BarilàUniversity of Padova, Department of Medicine, Hematology Unit, Padova, Italy.ORCID 0000-0003-3430-6115
Renato ZambelloUniversity of Padova, Department of Medicine, Hematology Unit, Padova, Italy.ORCID 0000-0002-8799-5324
University of Padua · IT

Funding

Associazione Italiana per la Ricerca sul Cancro (Italian Association for Cancer Research) IG-20216
6 · The paper itself

Abstract

Type T Large Granular Lymphocyte Leukemia (T-LGLL) is a chronic disorder characterized by the abnormal proliferation of clonal cytotoxic T cells. The intriguing association of T-LGLL with autoimmune and inflammatory diseases, the most prominent example being rheumatoid arthritis, raises questions about the underlying pathophysiologic relationships between these disorders which share several biological and clinical features, most notably neutropenia, which is considered as a clinical hallmark. Recent progress in molecular genetics has contributed to a better understanding of pathogenetic mechanisms, thus moving our knowledge in the field of LGL leukemias forward. Focusing on the constitutive activation of STAT3 pathway and the well-established role of STAT3 mutations in T-LGLL, we herein discuss whether the T cell clones occurring in comorbid conditions are the cause or the consequence of the immune-inflammatory associated events. Overall, this review sheds light on the intricate relationships between inflammation and cancer, emphasizing the importance of the STAT3 gene and its activation in the pathophysiology of these conditions. Gaining a deeper understanding of these underlying mechanisms seeks to pave the way for the development of novel targeted therapies for patients affected by inflammation-related cancers.

Indexed as

Arthritis, RheumatoidLeukemia, Large Granular LymphocyticHumansInflammationMutationSTAT3 Transcription FactorT-Lymphocytes, CytotoxicSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID38238319
PMCPMC10796758
OpenAlexW4390976724

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.