Evidence map›Paper›PMID 36175687›Full record

ReviewMedical oncology (Northwood, London, England)2022

TNFR2 antagonist and agonist: a potential therapeutics in cancer immunotherapy.

Sameer Quazi

RetractedAbstract readReviewRetracted Publication
PubMed Publisher
In one paragraph

Review in Medical oncology (Northwood, London, England), 2022. 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 It has been retracted, and should not be counted.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 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Application of biosensors in cancers, an overview.Frontiers in bioengineering and biotechnology · 2023
    Review
  6. Telomerase gene therapy: a remission toward cancer.Medical oncology (Northwood, London, England) · 2022
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 2 countries.

Sameer QuaziGenLab Biosolutions Private Limited, Bangalore, 560043, Karnataka, India. Colonel.quazi@gmail.com.ORCID http://orcid.org/0000-0002-1258-4088
Manchester Academic Health Science Centre · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumour necrosis factor receptor 2 or TNFR2 is considered an appealing target protein due to its limited frequency to TREGs, which are highly immunosuppressive and present on human malignancies. Numerous studies have revealed that TNFR2 is primarily found on MDSCs (myeloid-derived suppressor cells) and CD + Foxp3 + regulatory T cells (TREGs). Therefore, it has great importance in the proliferation and functional activity of TREGs and MDSCs. TNFR2 suppression must be downregulated or upregulated as required to treat malignancies and diseases like autoimmune disorders. Therefore, at the molecular level, advances in the comprehension of TNFR2's complex structure and its binding to TNF have opened the door to structure-guided drug development. Two critical obstacles to cancer treatment are the dearth of TREG-specific inhibitors and the lack of widely applicable ways to target tumours via frequently expressed surface oncogenes directly. Many researchers have discovered potential antagonists and agonists of TNFR2, which were successful in inhibiting TREGs proliferation, reducing soluble TNFR2 secretion from normal cells, and expanding T effector cells. The data represented in the following review article elucidates the clinically administrated TNFR2 antagonist and agonist in treating cancers.

Indexed as

Myeloid-Derived Suppressor CellsNeoplasmsForkhead Transcription FactorsHumansImmunotherapyReceptors, Tumor Necrosis Factor, Type IIT-Lymphocytes, RegulatoryForkhead Transcription FactorsReceptors, Tumor Necrosis Factor, Type IIAgonistAntagonistCD + Foxp3 +MDSCsTREG

Identifiers

PMID36175687
OpenAlexW4297983491

What OpenQuestion holds

Textmetadata
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.