Evidence map›Paper›PMID 34190440›Full record

ReviewJournal of breast cancer2021

The Role of STAT1 in T Helper Cell Differentiation during Breast Cancer Progression.

Sayantan Banik, Sudeshna Rakshit, Koustav Sarkar

Open access · goldAbstract readReview
In one paragraph

Review in Journal of breast cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 29 citations in OpenAlex.

  1. Targeting BCL9/BCL9L enhances CD4Acta pharmacologica Sinica · 2026
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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

3 authors at 1 institution in 1 country.

Sayantan BanikDepartment of Biotechnology, SRM Institute of Science and Technology, Kattankulathur, India.ORCID https://orcid.org/0000-0002-8070-6390
Sudeshna RakshitDepartment of Biotechnology, SRM Institute of Science and Technology, Kattankulathur, India.ORCID https://orcid.org/0000-0002-7496-3155
Koustav SarkarDepartment of Biotechnology, SRM Institute of Science and Technology, Kattankulathur, India. koustavsarkar@gmail.com.ORCID https://orcid.org/0000-0002-0696-6688
SRM Institute of Science and Technology · IN

Funding

Science and Engineering Research Board ECR/2016/000965
6 · The paper itself

Abstract

Members of the signal transducer and activator of transcription (STAT) protein family are intracellular transcription factors that facilitate several facets of cellular immunity, proliferation, apoptosis, and differentiation. They are principally stimulated by membrane receptor-associated Janus kinases. Dysregulation of this pathway is often detected in primary tumors and hints at augmented angiogenesis, which enriches tumors persistence and immunosuppression. STAT proteins play indispensable roles in cytokine signaling and T helper (Th) cell differentiation. Among STAT proteins, STAT1 plays a vital role in interferon signaling, which initiates the expression of genes encoding proteins with antitumor and apoptotic roles. STAT1 signaling is essential for Th1 cell differentiation. Several studies have also shown the role of STAT1 as a tumor suppressor in breast cancer, which is the most common intrusive malignancy and the second most common cause of cancer death in women. Herein, we review the intricate STAT1-mediated molecular mechanisms associated with Th cell differentiation and anti-tumor function in breast cancer.

Indexed as

Breast neoplasmsInterferonSTATTh cell

Identifiers

PMID34190440
PMCPMC8250105
OpenAlexW3175465509

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.