Evidence map›Paper›PMID 42638906›Full record

ReviewFrontiers in immunology2026

Deciphering the malignant synergy: metabolic reprogramming, epigenetic circuitry, and niche remodeling in osteosarcoma-macrophage crosstalk.

Zhi Zheng

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

1 author.

Zhi ZhengDepartment of Orthopedics, Chengdu Integrated TCM & Western Medicine Hospital, Chengdu, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteosarcoma (OS) prognosis remains stagnant due to the complex tumor microenvironment. This review deconstructs the "malignant synergy" between OS cells and tumor-associated macrophages (TAMs). Beyond the traditional M1/M2 dichotomy, we highlight the functional heterogeneity of TAMs, tracking their evolution from resident defenders to pro-metastatic accomplices. We elucidate three critical mechanisms driving this domestication: (1) Metabolic Reprogramming, where OS cells enforce immunosuppression via amino acid and lipid hijacking; (2) Epigenetic Circuitry, involving m6A modifications and ceRNA networks that create self-reinforcing malignant loops; and (3) Niche Remodeling, where exosomal fusion proteins remotely condition the lung for metastasis. By synthesizing these mechanisms, we identify key vulnerabilities in immune evasion and chemoresistance, providing a rationale for therapies targeting this critical interaction.

Indexed as

Bone NeoplasmsEpigenesis, GeneticMacrophagesOsteosarcomaTumor-Associated MacrophagesTumor MicroenvironmentAnimalsHumansMetabolic Reprogrammingepigenetic circuitrymetabolic reprogrammingosteosarcomapre-metastatic nichetumor-associated macrophages

Identifiers

PMID42638906
PMCPMC13501079

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.