Evidence map›Paper›PMID 37264310›Full record

ArticleBMC cancer2023

The impact and outcomes of cancer-macrophage fusion.

Mengtao Li, John R Basile, Sanjay Mallya, Yi-Ling Lin

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Cell-cell fusion in cancer: The next cancer hallmark?The international journal of biochemistry & cell biology · 2024
    Review
  5. 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.

Mengtao LiDivision of Diagnostic and Surgical Sciences, School of Dentistry, University of California, CHS 23-068B. 10833 Le Conte Ave, Los Angeles, CA, 90095, USA.
John R BasileDepartment of Oncology and Diagnostic Sciences, University of Maryland Dental School, Baltimore, MD, USA.
Sanjay MallyaDivision of Diagnostic and Surgical Sciences, School of Dentistry, University of California, CHS 23-068B. 10833 Le Conte Ave, Los Angeles, CA, 90095, USA.
Yi-Ling LinDivision of Diagnostic and Surgical Sciences, School of Dentistry, University of California, CHS 23-068B. 10833 Le Conte Ave, Los Angeles, CA, 90095, USA. ylin@dentistry.ucla.edu.
University of California, Los Angeles · USUniversity of Maryland, Baltimore · US

Funding

UCLA Clinical Translational Science InstituteUL1TR001881 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARLEEN F. BROWN, ARASH NAEIM · 2016 to 2026
$118.1M
Clinical and Translational Science Institute, University of California, Los Angeles UL1TR001881NCATS NIH HHS UL1 TR001881UC Cancer Research Coordinating Committee CRR-18-525125
6 · The paper itself

Abstract

backgroundCancer's hallmark feature is its ability to evolve, leading to metastasis and recurrence. Although genetic mutations and epigenetic changes have been implicated, they don't fully explain the leukocytic traits that many cancers develop. Cell fusion between cancer and somatic cells, particularly macrophages, has been suggested as an alternative pathway for cancer cells to obtain new traits by acquiring exogenous genetic material.

methodsThis study aims to investigate the potential biological outcomes of tumor-myeloid cell fusion by generating tumor-macrophage hybrid cells. Two clones with markedly different tumorigenicity were selected, and RNA-seq was used to compare their RNA expressions with that of the control cells. Based on the results that the hybrid cells showed differential activation in several upstream regulator pathways that impact their biological behaviors, the hybrid cells' abilities to recruit stromal cells and establish angiogenesis as well as their cell cycle distributions were investigated through in vitro and in vivo studies.

resultsAlthough both hybrid clones demonstrated p53 activation and reduced growth rates, they exhibited distinct cell cycle distributions and ability to grow in vivo. Notably, while one clone was highly tumorigenic, the other showed little tumorigenicity. Despite these differences, both hybrid clones were potent environmental modifiers, exhibiting significant abilities to recruit stromal and immune cells and establish angiogenesis.

conclusionsThe study revealed that tumor-somatic cell fusion is a potent environmental modifier that can modulate tumor survival and evolution, despite its relatively low occurrence. These findings suggest that tumor-somatic cell fusion could be a promising target for developing new cancer therapies. Furthermore, this study provides an experimental animal platform to investigate cancer-myeloid fusion and highlights the potential role of tumor-somatic cell fusion in modulating the tumor environment.

Indexed as

NeoplasmsAnimalsCell CommunicationCell FusionHybrid CellsMacrophagesCancerCell fusionMacrophagesMyeloid cellsStromal cellsTumorigenicity

Identifiers

PMID37264310
PMCPMC10236829
OpenAlexW4379057098

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.