Evidence map›Paper›PMID 41064357›Full record

ArticleFrontiers in endocrinology2025

Prolactin and DNA damage trigger an anti-breast cancer cell immune response.

Ödül Karayazi Atici, Nayantara Govindrajan, Isbel Lopetegui-González, Constance A M Finney, Carrie S Shemanko

Abstract read
In one paragraph

Article in Frontiers in endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

5 authors.

Ödül Karayazi AticiDepartment of Biological Sciences, University of Calgary, Calgary, AB, Canada.
Nayantara GovindrajanDepartment of Biological Sciences, University of Calgary, Calgary, AB, Canada.
Isbel Lopetegui-GonzálezDepartment of Biological Sciences, University of Calgary, Calgary, AB, Canada.
Constance A M FinneyDepartment of Biological Sciences, University of Calgary, Calgary, AB, Canada.
Carrie S ShemankoDepartment of Biological Sciences, University of Calgary, Calgary, AB, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: The role of prolactin (PRL) in breast cancer and its role within the context of the tumor microenvironment are not well understood. In our previous study, we demonstrated a cross-talk between the ataxia telangiectasia-mutated (ATM) DNA damage response pathway and the PRL-Janus-kinase-2 (JAK2)-signal transducer and activator of transcription-5 (STAT5)-heat shock protein-90 (HSP90) pathway. Here we investigated the role of PRL in tumor initiation and the effect of DNA damage. Methods: We used an Results: Doxorubicin and PRL combination increased the tumor latency, although PRL secretion alone did not change the tumor latency compared to the controls. Depletion of glycolipid asialo ganglioside-GM1-positive immune cells using anti-asialo GM1 antibody resulted in faster tumor formation only in the PRL-secreting breast cancer cells that were pre-treated with doxorubicin. Additionally, doxorubicin plus the PRL treatment of breast cancer cells was shown Discussion: These results demonstrate that combined breast cancer cell DNA damage and PRL exposure results in the anti-tumor cell activity of asialo-GM1-positive immune cells.

Indexed as

Breast NeoplasmsDNA DamageProlactinAnimalsCell Line, TumorDoxorubicinFemaleHumansMiceMice, SCIDTumor MicroenvironmentXenograft Model Antitumor AssaysDoxorubicinProlactinbreast cancerDNA damage responsenatural killer cellsprolactinxenograft

Identifiers

PMID41064357
PMCPMC12500456

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Registered trials

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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.