Evidence map›Paper›PMID 42639977›Full record

ReviewMolecular oncology2026

Unraveling the epigenetic code in cancer cell-tumor microenvironment crosstalk.

Ji Hoon Park, Mi-Young Kim

Abstract readReview
In one paragraph

Review in Molecular oncology, 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

2 authors.

Ji Hoon ParkDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea.
Mi-Young KimDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea.ORCID https://orcid.org/0000-0002-1386-5164

Funding

KAIST Grand Challenge 30 Project (KC30) N11240024National Research Foundation of Korea RS-2024-00337733National Research Foundation of Korea RS-2025-14383304
6 · The paper itself

Abstract

Epigenetics plays a central role in cancer development and progression by governing the expression of genes involved in these processes. Accumulating evidence strongly indicates that these mechanisms not only alter cancer cell-intrinsic properties but also mediate reciprocal interactions between cancer cells and the tumor microenvironment (TME). In the context of cancer cell-intrinsic changes, epigenetic alterations contribute to cancer cell plasticity by regulating stemness, cell state transitions, and therapy resistance. In addition, epigenetic changes are a key driver of the establishment of a tumor-supportive environment by modifying the states of TME components, including fibroblasts, macrophages, and myeloid-derived suppressor cells. Epigenetic reprogramming in cancer cells and TME components is often induced by factors such as hypoxia and the secretion of exosomal long noncoding RNAs (lncRNAs), cytokines, and metabolites. In this review, we discuss various epigenetic mechanisms controlling cancer cell-intrinsic states, cancer cell-TME crosstalk, current epigenetic therapies, and future research directions that may lead to the discovery of new biomarkers and the development of effective epigenetic anticancer therapeutics.

Indexed as

cancer epigeneticschromatin modificationsepigenetic drugsepitranscriptomicstumor microenvironment

Identifiers

PMID42639977
PMCPMC13505161

What OpenQuestion holds

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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.