Evidence map›Paper›PMID 37046108›Full record

ReviewMolecular biology reports2023

The dynamic tumor-stromal crosstalk: implications of 'stromal-hot' tumors in the process of epithelial-mesenchymal transition in breast cancer.

Apoorva D Mavatkar, Chandrakala M Naidu, Jyothi S Prabhu, Madhumathy G Nair

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular biology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 21% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

4 authors at 1 institution in 1 country.

Apoorva D Mavatkar *Division of Molecular Medicine, St. John's Research Institute, St. John's Medical College, Bangalore, Karnataka, India.
Chandrakala M Naidu *Division of Molecular Medicine, St. John's Research Institute, St. John's Medical College, Bangalore, Karnataka, India.
Jyothi S PrabhuDivision of Molecular Medicine, St. John's Research Institute, St. John's Medical College, Bangalore, Karnataka, India.
Madhumathy G NairDivision of Molecular Medicine, St. John's Research Institute, St. John's Medical College, Bangalore, Karnataka, India. madhumathy@sjri.res.in.ORCID http://orcid.org/0000-0002-8119-4876
St.John's Medical College Hospital · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBreast cancer metastatic programming involves an intricate process by which the tumor cell coevolves with the surrounding extracellular niche. The supporting cells from the local host stroma get transformed into cancer-associated stromal cells. This complex crosstalk leads to extracellular matrix remodeling, invasion, and eventually distant metastasis.

methodsIn this review, we examine the protein-miRNA secretome that is crucial for this crosstalk. We also provide evidence from the literature for the pivotal role played by the various stromal cells like fibroblasts, adipocytes, and immune cells in promoting the process of EMT in breast cancer. Through in-silico analysis, we have also attempted to establish that stromal presence is integral to the process of EMT. RESULTS AND

conclusionThe in-silico analysis delineates the persuasive role of the stroma in mediating epithelial-to-mesenchymal transition. This review elucidates the importance of examining the role of the stromal niche that can yield promising diagnostic markers and pave avenues for formulating tailored anti-cancer therapy. Process of EMT as driven by 'stroma-hot' tumors: The process of EMT is driven by the stromal cells. The stromal cells in the form of  fibroblasts, adipocytes, endothelial cells, mesenchymal stromal cells and tissue associated macrophages secrete the miRNA-protein secretome that modulates the stromal niche and the tumor cells to be become 'tumor associated'. This drives tumor progression and invasion. The 'stromal-hot' tumors eventually get the benefit of the surplus nurturing from the stroma that facilitates EMT leading to distant organ seeding and metastasis.

Indexed as

Breast NeoplasmsMicroRNAsEndothelial CellsEpithelial-Mesenchymal TransitionFemaleHumansStromal CellsMicroRNAsBreast cancerEpithelial–mesenchymal transitionMetastasisMicroRNAsTumor–stromal crosstalk

Identifiers

PMID37046108
OpenAlexW4365141286

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.