Evidence map›Paper›PMID 32406600›Full record

ArticleCancer medicine2020

Higher methylation subtype of malignant melanoma and its correlation with thicker progression and worse prognosis.

Yosuke Yamamoto, Keisuke Matsusaka, Masaki Fukuyo, Bahityar Rahmutulla, Hiroyuki Matsue, Atsushi Kaneda

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

15 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. NAR cancer · 2023
    Article
  9. Epigenetics in the Diagnosis and Therapy of Malignant Melanoma.International journal of molecular sciences · 2022
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Targeted Therapy in Melanoma and Mechanisms of Resistance.International journal of molecular sciences · 2020
    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

6 authors at 1 institution in 1 country.

Yosuke YamamotoDepartment of Dermatology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Keisuke MatsusakaDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Masaki FukuyoDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Bahityar RahmutullaDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Hiroyuki MatsueDepartment of Dermatology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Atsushi KanedaDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0000-0002-6980-5515
Chiba University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant melanoma (MM) is the most life-threatening disease among all skin malignancies, and recent genome-wide studies reported BRAF, RAS, and NF1 as the most frequently mutated driver genes. While epigenetic aberrations are known to contribute to the oncogenic activity seen in various cancers, their role in MM has not been fully investigated. To investigate the role of epigenetic aberrations in MM, we performed genome-wide DNA methylation analysis of 51 clinical MM samples using Infinium 450k beadarray. Hierarchical clustering analysis stratified MM into two DNA methylation epigenotypes: high- and low-methylation subgroups. Tumor thickness was significantly greater in case of high-methylation tumors than low-methylation tumors (8.3 ± 5.3 mm vs 4.5 ± 2.9 mm, P = .003). Moreover, prognosis was significantly worse in high-methylation cases (P = .03). Twenty-seven genes were found to undergo significant and frequent hypermethylation in high-methylation subgroup, where TFPI2 was identified as the most frequently hypermethylated gene. MM cases with lower expression levels of TFPI2 showed significantly worse prognosis (P = .001). Knockdown of TFPI2 in two MM cell lines, CHL-1 and G361, resulted in significant increases of cell proliferation and invasion. These indicate that MM can be stratified into at least two different epigenetic subgroups, that the MM subgroup with higher DNA methylation shows a more progressive phenotype, and that methylation of TFPI2 may contribute to the tumor progression of MM.

Indexed as

DNA MethylationEpigenesis, GeneticAgedBiomarkers, TumorCell Line, TumorCell MovementCell ProliferationDisease ProgressionEpigenomicsFemaleGene Expression Regulation, NeoplasticGlycoproteinsGTP PhosphohydrolasesHumansMaleMelanomaBiomarkers, TumorBRAF protein, humanGlycoproteinsGTP PhosphohydrolasesMembrane ProteinsNRAS protein, humanProto-Oncogene Proteins B-raftissue-factor-pathway inhibitor 2DNA methylationepigenotypeinvasionmalignant melanomaskin neoplasm

Identifiers

PMID32406600
PMCPMC7541157
OpenAlexW3025795530

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.