Evidence map›Paper›PMID 35583594›Full record

ReviewBreast cancer (Tokyo, Japan)2022

The potential role of nicotine in breast cancer initiation, development, angiogenesis, invasion, metastasis, and resistance to therapy.

Zhila Khodabandeh, Mohammad Valilo, Kobra Velaei, Abbas Pirpour Tazehkand

Abstract readReview
PubMed Publisher
In one paragraph

Review in Breast cancer (Tokyo, Japan), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.4field-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

18 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Review
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  6. Cell signaling and epigenetic regulation of nicotine-induced carcinogenesis.Environmental pollution (Barking, Essex : 1987) · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Nicotine: From Discovery to Biological Effects.International journal of molecular sciences · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. Review
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

4 authors at 2 institutions in 1 country.

Zhila KhodabandehDepartment of Biology, Faculty of Science, Urmia University, Urmia, Iran.
Mohammad ValiloDepartment of Clinical Biochemistry and Medical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Kobra VelaeiDepartment of Anatomical Sciences, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. kobravelaei@gmail.com.
Abbas Pirpour TazehkandDepartment of Clinical Biochemistry and Medical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. abbaspirpour94@gmail.com.ORCID http://orcid.org/0000-0002-9094-9134
Tabriz University of Medical Sciences · IRUrmia University · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A large body of research studying the relationship between tobacco and cancer has led to the knowledge that smoking cigarettes adversely affects cancer treatment while contributing to the development of various tobacco-related cancers. Nicotine is the main addictive component of tobacco smoke and promotes angiogenesis, proliferation, and epithelial-mesenchymal transition (EMT) while promoting growth and metastasis of tumors. Nicotine generally acts through the induction of the nicotinic acetylcholine receptors (nAChRs), although the contribution of other receptor subunits has also been reported. Nicotine contributes to the pathogenesis of a wide range of cancers including breast cancer through its carcinogens such as (4-methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and N-nitrosonornicotine (NNN). Current study aims to review the mechanistic function of nicotine in the initiation, development, angiogenesis, invasion, metastasis, and apoptosis of breast cancer with the main focus on nicotine acetylcholine receptors (nAChRs) and nAChR-mediated signaling pathways as well as on its potential for the development of an effective treatment against breast cancer. Moreover, we will try to demonstrate how nicotine leads to poor treatment response in breast cancer by enhancing the population, proliferation, and self-renewal of cancer stem cells (CSCs) through the activation of α7-nAChR receptors.

Indexed as

Breast NeoplasmsNicotineReceptors, NicotinicCarcinogensCigarette SmokingFemaleHumansNeovascularization, PathologicCarcinogensNicotineReceptors, NicotinicBreast cancerCancer stem cells (CSCs)NicotineNicotine acetylcholine receptor

Identifiers

PMID35583594
OpenAlexW4280537227

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.