Evidence map›Paper›PMID 41294803›Full record

ReviewCells2025

Exosome-Mediated Crosstalk Between Cancer Cells and Tumor Microenvironment.

Sara H Saad, Alex Kashanchi, Mohammad Asad Zadeh, Anastasia Williams, Elena V Batrakova

Abstract readReview
In one paragraph

Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Article
  2. Extracellular vesicles and epigenetic aging clocks in tissue aging: an exosome-focused conceptual framework with a focus on skin.The journals of gerontology. Series A, Biological sciences and medical sciences · 2026
    Review
  3. Tumor-Associated Macrophage Exosomal miR-142-5p Drives Prostate Cancer Neuroendocrine Differentiation via RERG/Ras/ERK Axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. 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.

Sara H SaadLaboratory of Molecular Virology, School of Systems Biology, George Mason University, Discovery Hall Room 182, 10900 University Blvd, Manassas, VA 20110, USA.
Alex KashanchiLaboratory of Molecular Virology, School of Systems Biology, George Mason University, Discovery Hall Room 182, 10900 University Blvd, Manassas, VA 20110, USA.
Mohammad Asad ZadehLaboratory of Molecular Virology, School of Systems Biology, George Mason University, Discovery Hall Room 182, 10900 University Blvd, Manassas, VA 20110, USA.
Anastasia WilliamsLaboratory of Molecular Virology, School of Systems Biology, George Mason University, Discovery Hall Room 182, 10900 University Blvd, Manassas, VA 20110, USA.ORCID 0009-0002-9049-2530
Elena V BatrakovaLaboratory of Molecular Virology, School of Systems Biology, George Mason University, Discovery Hall Room 182, 10900 University Blvd, Manassas, VA 20110, USA.

Funding

HIV1 INHIBITION USING TAT PEPTIDE DERIVATIVESR01AI043894 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI KASHANCHI, FATAH · 1999 to 2015
$4.4M
Cell-derived extracellular vesicle mediated epigenetic silencing of HIV in the brainR01MH134389 · NIMH · GEORGE MASON UNIVERSITY · PI Fatah Kashanchi · 2023 to 2026
$2.0M
HIV neuropathogenesis related to exosomes containing HIV non-coding RNAsR01NS099029 · NINDS · GEORGE MASON UNIVERSITY · PI KASHANCHI, FATAH · 2016 to 2020
$1.9M
Effect of chromatin remodelers/modifiers on HIV-1 Tat activated transcriptionR21AI074410 · NIAID · GEORGE WASHINGTON UNIVERSITY · PI KASHANCHI, FATAH · 2009 to 2010
$432k
A radiation-induced cellular stress activates HIV and induces killing of infected cellsR21AI127351 · NIAID · GEORGE MASON UNIVERSITY · PI KASHANCHI, FATAH · 2016 to 2017
$418k
HIV-1 TAR derived miRNA: Implications for Latency and PathogenesisR21AI078859 · NIAID · GEORGE WASHINGTON UNIVERSITY · PI KASHANCHI, FATAH · 2009 to 2010
$400k
NIAID NIH HHS R01 AI043894NIAID NIH HHS R21 AI074410NIAID NIH HHS R21 AI078859NIAID NIH HHS R21 AI127351NIH HHS 1R01MH134389-25NIMH NIH HHS R01 MH134389NINDS NIH HHS R01 NS099029
6 · The paper itself

Abstract

Exosomes are extracellular vesicles that play a central role in mediating intercellular communication within the tumor microenvironment (TME). Cancer-derived exosomes carry proteins, nucleic acids, and lipids that reshape the phenotype and function of surrounding stromal and immune cells, thereby promoting tumor progression, angiogenesis, metastasis, and resistance to therapy. At the same time, exosomes derived from TME components, including macrophages, dendritic cells, B cells, T cells, fibroblasts, neutrophils, and NK cells, reciprocally influence tumor growth and immune evasion. These bidirectional interactions highlight exosomes as both drivers of tumor progression and regulators of antitumor immunity. In this review, we synthesize current evidence on the diverse mechanisms by which exosomes reprogram immune and stromal cells, with a focus on their dual roles in cancer biology. We also discuss emerging therapeutic strategies to inhibit exosome biogenesis, release, and function, underscoring their translational potential as novel targets for cancer diagnosis and treatment.

Indexed as

Cell CommunicationExosomesNeoplasmsTumor MicroenvironmentAnimalsHumansB cellscancer progressiondendritic cellsexosomesextracellular vesicles (EVs)immune modulationtumor-associated macrophages (TAMs)tumor microenvironment (TME)

Identifiers

PMID41294803
PMCPMC12651011

What Socratic 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 Socratic graph.