Evidence map›Paper›PMID 39110298›Full record

ReviewCell biochemistry and biophysics2024

Multi-Drug Resistance and Breast Cancer Progression via Toll-Like Receptors (TLRs) Signaling.

Harikumar Pallathadka, Abdulrahman Qais Khaleel, Ahmed Hussein Zwamel, H Malathi, Snehlata Sharma, Jasur Alimdjanovich Rizaev, Yasser Fakri Mustafa, Atreyi Pramanik, Mahmood Hasen Shuhata Alubiady, Mohammed Abed Jawad

Abstract readReview
PubMed Publisher
In one paragraph

Review in Cell biochemistry and biophysics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Article
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.

Harikumar PallathadkaManipur International University, Imphal, Manipur, India. Pallathadkaharikumar1402@gmail.com.
Abdulrahman Qais KhaleelDepartment of Medical Instruments Engineering, Al-Maarif University College, Al Anbar, 31001, Iraq. abdulrahman.qais@uoa.edu.iq.
Ahmed Hussein ZwamelMedical laboratory technique college, the Islamic University, Najaf, Iraq.
H MalathiDepartment of Biotechnology and Genetics, School of Sciences, JAIN (Deemed to be University), Bangalore, Karnataka, India.
Snehlata SharmaChandigarh Pharmacy College, Chandigarh Group of Colleges, Jhanjheri, Mohali, 140307, Punjab, India.
Jasur Alimdjanovich RizaevDepartment of Public health and Healthcare management, Rector, Samarkand State Medical University, 18, Amir Temur Street, Samarkand, Uzbekistan.
Yasser Fakri MustafaDepartment of Pharmaceutical Chemistry, College of Pharmacy, University of Mosul, Mosul, 41001, Iraq.
Atreyi PramanikSchool of Applied and Life Sciences, Division of Research and Innovation, Uttaranchal University, Dehradun, Uttarakhand, India.
Mahmood Hasen Shuhata AlubiadyMahmood Hasen Shuhata alubiady, Al-Hadi University College, Baghdad, 10011, Iraq.
Mohammed Abed JawadDepartment of Medical Laboratories Technology, Al-Nisour University College, Baghdad, Iraq.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toll-like receptors (TLRs) are essential receptors involved in inflammation and innate immunity. Various types of cancer cells, as well as innate immune cells, express TLRs. There is mounting proof that TLRs are critical to the development and spread of cancer as well as metabolism. In breast cancer, up-regulated levels of TLRs have been linked to the aggressiveness of the diseases, worse treatment outcomes, and the emergence of therapeutic resistance. Patients with advanced non-resectable, recurring, and metastatic breast cancer currently have few available treatment choices. An intriguing new strategy is an innate immunity-mediated anticancer immunotherapy, either used alone or in conjunction with existing treatments. In fact, several TLR agonists and antagonists have been used in clinical studies for anti-cancer immunotherapy. Consequently, TLRs serve as critical targets for controlling the course of breast cancer and treatment resistance in addition to being implicated in immune responses against pathogen infection and cancer immunology. In this review, we deliver an overview of the most current findings on TLR involvement in the development of breast cancer and treatment resistance.

Indexed as

Breast NeoplasmsDrug Resistance, NeoplasmSignal TransductionToll-Like ReceptorsDisease ProgressionDrug Resistance, MultipleFemaleHumansImmunity, InnateToll-Like ReceptorsBreast cancerDrug resistancePathogenesisProgressionToll-like receptors (TLRs)

Identifiers

PMID39110298

What Socratic 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 Socratic graph.