Evidence map›Paper›PMID 32201436›Full record

ReviewActa histochemica et cytochemica2020

Codependency of Metabolism and Epigenetics Drives Cancer Progression: A Review.

Kenta Masui, Mio Harachi, Webster K Cavenee, Paul S Mischel, Noriyuki Shibata

Open access · diamondAbstract readReview
In one paragraph

Review in Acta histochemica et cytochemica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Histochemistry, Cytochemistry and Epigenetics.Acta histochemica et cytochemica · 2022
    Review
  10. Metabolic Rewiring in Glioblastoma Cancer:Frontiers in oncology · 2022
    Review
  11. Article
  12. Review
  13. Article
  14. 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 at 2 institutions in 2 countries.

Kenta MasuiDepartment of Pathology, Division of Pathological Neuroscience, Tokyo Women's Medical University, Tokyo 162-8666, Japan.
Mio HarachiDepartment of Pathology, Division of Pathological Neuroscience, Tokyo Women's Medical University, Tokyo 162-8666, Japan.
Webster K CaveneeLudwig Institute for Cancer Research, University of California San Diego, La Jolla, CA 92093, USA.
Paul S MischelLudwig Institute for Cancer Research, University of California San Diego, La Jolla, CA 92093, USA.
Noriyuki ShibataDepartment of Pathology, Division of Pathological Neuroscience, Tokyo Women's Medical University, Tokyo 162-8666, Japan.
Tokyo Women's Medical University · JPLudwig Cancer Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer is widely considered to be a set of genetic diseases that are currently classified by tissue and cell type of origin and, increasingly, by its molecular characteristics. This latter aspect is based primarily upon oncogene gains, tumor suppressor losses, and associated transcriptional profiles. However, cancers are also characterized by profound alterations in cellular metabolism and epigenetic landscape. It is particularly noteworthy that cancer-causing genomic defects not only activate cell cycle progression, but regulate the opportunistic uptake and utilization of nutrients, effectively enabling tumors to maximize growth and drug resistance in changing tissue and systemic microenvironments. Shifts in chromatin architecture are central to this dynamic behavior. Further, changes in nutrient uptake and utilization directly affect chromatin structure. In this review, we describe a set of recent discoveries of metabolic and epigenetic reprogramming in cancer, and especially focus on the genomically well-characterized brain tumor, glioblastoma. Further, we discuss a new mode of metabolic regulation driven by epigenetic mechanisms, that enables cancer cells to autonomously activate iron metabolism for their survival. Together, these underscore the integration of genetic mutations with metabolic reprogramming and epigenetic shifts in cancer, suggesting a new means to identifying patient subsets suitable for specific precision therapeutics.

Indexed as

cancer metabolismepigeneticsglioblastomahistone acetylationiron metabolism

Identifiers

PMID32201436
PMCPMC7076272
OpenAlexW3007063270

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.