Evidence map›Paper›PMID 32824846›Full record

ReviewInternational journal of molecular sciences2020

Role of Adipose Tissue-Derived Autotaxin, Lysophosphatidate Signaling, and Inflammation in the Progression and Treatment of Breast Cancer.

David N Brindley, Xiaoyun Tang, Guanmin Meng, Matthew G K Benesch

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05680311 (Is Autotaxin a Promising Biomarker for Breast Cancer), which is not on this map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.6field-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.

NCT05680311 nacompletednot on this map

Is Autotaxin a Promising Biomarker for Breast Cancer

TypeinterventionalSponsorAnkara Etlik City HospitalRan2019 to 2021Enrolled110ConditionsBreast CancerArmsmeasurement of serum autotaxin serum level
3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  18. Article
  19. International journal of molecular sciences · 2022
    Article
  20. Design and Development of Autotaxin Inhibitors.Pharmaceuticals (Basel, Switzerland) · 2021
    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.

David N BrindleyDepartment of Biochemistry, University of Alberta, Edmonton, AB T6G 2S2, Canada.ORCID 0000-0003-2227-0020
Xiaoyun TangDepartment of Biochemistry, University of Alberta, Edmonton, AB T6G 2S2, Canada.
Guanmin MengDepartment of Biochemistry, University of Alberta, Edmonton, AB T6G 2S2, Canada.
Matthew G K BeneschDepartment of Biochemistry, University of Alberta, Edmonton, AB T6G 2S2, Canada.ORCID 0000-0002-1326-684X
University of Alberta · CAMemorial University of Newfoundland · CA

Funding

Canadian Breast Cancer Foundation 300034Canadian Cancer Society Research Institute 703926CIHR PJT-169140
6 · The paper itself

Abstract

Autotaxin (ATX) is a secreted enzyme that produces lysophosphatidate (LPA), which signals through six G-protein coupled receptors, promoting tumor growth, metastasis, and survival from chemotherapy and radiotherapy. Many cancer cells produce ATX, but breast cancer cells express little ATX. In breast tumors, ATX is produced by tumor-associated stroma. Breast tumors are also surrounded by adipose tissue, which is a major bodily source of ATX. In mice, a high-fat diet increases adipocyte ATX production. ATX production in obesity is also increased because of low-level inflammation in the expanded adipose tissue. This increased ATX secretion and consequent LPA signaling is associated with decreased adiponectin production, which results in adverse metabolic profiles and glucose homeostasis. Increased ATX production by inflamed adipose tissue may explain the obesity-breast cancer association. Breast tumors produce inflammatory mediators that stimulate ATX transcription in tumor-adjacent adipose tissue. This drives a feedforward inflammatory cycle since increased LPA signaling increases production of more inflammatory mediators and cyclooxygenase-2. Inhibiting ATX activity, which has implications in breast cancer adjuvant treatments, attenuates this cycle. Targeting ATX activity and LPA signaling may potentially increase chemotherapy and radiotherapy efficacy, and decrease radiation-induced fibrosis morbidity independently of breast cancer type because most ATX is not derived from breast cancer cells.

Indexed as

Signal TransductionAdipose TissueAnimalsAntineoplastic Agents, HormonalBreast NeoplasmsDexamethasoneFemaleHumansLysophospholipase DLysophospholipidsPhosphoric Diester HydrolasesAntineoplastic Agents, HormonalDexamethasoneLysophospholipase DLysophospholipidsPhosphoric Diester Hydrolasesadiponectinchemokineschemotherapycytokinesfibrosismacrophagesradiotherapytumor microenvironment

Identifiers

PMID32824846
PMCPMC7460696
OpenAlexW3070149042

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.