Evidence map›Paper›PMID 37138421›Full record

ReviewCurrent medicinal chemistry2024

The Function of Autophagy in the Initiation, and Development of Breast Cancer.

Elmira Aboutalebi Vand Beilankouhi, Mohammad Valilo, Narges Dastmalchi, Shahram Teimourian, Reza Safaralizadeh

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current medicinal chemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. The cross-talk between NRF2 and apoptosis in cancer.Medical molecular morphology · 2025
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Autophagy Regulators in Cancer.International journal of molecular sciences · 2023
    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

5 authors at 4 institutions in 1 country.

Elmira Aboutalebi Vand BeilankouhiDepartment of Animal Biology, Faculty of Natural Sciences, University of Tabriz, Tabriz, Iran.
Mohammad ValiloDepartment of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran.
Narges DastmalchiDepartment of Biology, University College of Nabi Akram, Tabriz, Iran.
Shahram TeimourianDepartment of Medical Genetics, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Reza SafaralizadehDepartment of Animal Biology, Faculty of Natural Sciences, University of Tabriz, Tabriz, Iran.
University of Tabriz · IRIran University of Medical Sciences · IRUniversity College of Nabi Akram · IRUrmia University of Medical Sciences

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a significant catabolic procedure that increases in stressful conditions. This mechanism is mostly triggered after damage to the organelles, the presence of unnatural proteins, and nutrient recycling in reaction to these stresses. One of the key points in this article is that cleaning and preserving damaged organelles and accumulated molecules through autophagy in normal cells helps prevent cancer. Since dysfunction of autophagy is associated with various diseases, including cancer, it has a dual function in tumor suppression and expansion. It has newly become clear that the regulation of autophagy can be used for the treatment of breast cancer, which has a promising effect of increasing the efficiency of anticancer treatment in a tissue- and cell-type-specific manner by affecting the fundamental molecular mechanisms. Regulation of autophagy and its function in tumorigenesis is a vital part of modern anticancer techniques. This study discusses the current advances related to the mechanisms that describe essential modulators of autophagy involved in the metastasis of cancers and the development of new breast cancer treatments.

Indexed as

AutophagyBreast NeoplasmsAnimalsAntineoplastic AgentsFemaleHumansAntineoplastic Agentsanticancer techniquesAutophagybreast cancercancer therapydamaged.metastasis

Identifiers

PMID37138421
OpenAlexW4368355828

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.