Evidence map›Paper›PMID 39095874›Full record

ReviewMolecular cancer2024

Cancer, metastasis, and the epigenome.

Saurav Kiri, Tyrone Ryba

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Molecular cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed, 2 pooled it
–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

128 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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  19. ADCY7 dictates N-cadherin stability to inhibit HCC metastasis.JHEP reports : innovation in hepatology · 2026
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68 more citing papers are in PubMed but not listed here.

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.

Saurav KiriCollege of Medicine, University of Central Florida, 6850 Lake Nona Blvd., Orlando, 32827, Florida, USA. sa939682@ucf.edu.
Tyrone RybaDepartment of Natural Sciences, New College of Florida, 5800 Bay Shore Rd., Sarasota, 34243, Florida, USA. tryba@ncf.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer is the second leading cause of death worldwide and disease burden is expected to increase globally throughout the next several decades, with the majority of cancer-related deaths occurring in metastatic disease. Cancers exhibit known hallmarks that endow them with increased survival and proliferative capacities, frequently as a result of de-stabilizing mutations. However, the genomic features that resolve metastatic clones from primary tumors are not yet well-characterized, as no mutational landscape has been identified as predictive of metastasis. Further, many cancers exhibit no known mutation signature. This suggests a larger role for non-mutational genome re-organization in promoting cancer evolution and dissemination. In this review, we highlight current critical needs for understanding cell state transitions and clonal selection advantages for metastatic cancer cells. We examine links between epigenetic states, genome structure, and misregulation of tumor suppressors and oncogenes, and discuss how recent technologies for understanding domain-scale regulation have been leveraged for a more complete picture of oncogenic and metastatic potential.

Indexed as

Epigenesis, GeneticEpigenomeNeoplasm MetastasisNeoplasmsAnimalsGene Expression Regulation, NeoplasticHumansMutationChromatin stateEMTEpigeneticMetastasisTopologyTranscription

Identifiers

PMID39095874
PMCPMC11295362

What OpenQuestion holds

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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.