Evidence map›Paper›PMID 20418918›Full record

ReviewOncogene2010

Genetic determinants at the interface of cancer and neurodegenerative disease.

L G T Morris, S Veeriah, T A Chan

Open access · greenAbstract readReview
In one paragraph

Review in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
7.1field-weighted citation impact, top 3% 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

57 citing papers in PubMed, 98 citations in OpenAlex.

  1. Brain communications · 2025
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Molecular crosstalk between cancer and neurodegenerative diseases.Cellular and molecular life sciences : CMLS · 2020
    Review
  14. International journal of molecular sciences · 2020
    Article
  15. Article
  16. Modeling Neurodegenerative Disorders inInternational journal of molecular sciences · 2020
    Review
  17. Article
  18. Review
  19. Targeting mitochondria in cancer: current concepts and immunotherapy approaches.Translational research : the journal of laboratory and clinical medicine · 2018
    Review
  20. Article
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

3 authors at 1 institution in 1 country.

L G T MorrisHuman Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.
S Veeriah
T A Chan
Memorial Sloan Kettering Cancer Center · US

Funding

HEAD AND NECK TRAINING PROGRAM SURGICAL ONCOLOGYT32CA009685 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI FAGIN, JAMES A, WONG, RICHARD J · 1992 to 2022
$3.6M
Role of Parkinson's disease gene PARK2 in GBM oncogenesis and genomic instabilityR01NS086875 · NINDS · SLOAN-KETTERING INST CAN RESEARCH · PI CHAN, TIMOTHY AN-THY · 2013 to 2015
$1.2M
NCI NIH HHS T32 CA009685NINDS NIH HHS R01 NS086875
6 · The paper itself

Abstract

It has been hypothesized that oncogenesis and neurodegeneration may share common mechanistic foundations. Recent evidence now reveals a number of genes in which alteration leads to either carcinogenesis or neurodegeneration, depending on cellular context. Pathways that have emerged as having critical roles in both cancer and neurodegenerative disease include those involving genes such as PARK2, ATM, PTEN, PTPRD, and mTOR. A number of mechanisms have been implicated, and commonly affected cellular processes include cell cycle regulation, DNA repair, and response to oxidative stress. For example, we have recently shown that the E3 ubiquitin ligase PARK2 is mutated or deleted in many different human malignancies and helps drive loss on chromosome 6q25.2-27, a genomic region frequently deleted in cancers. Mutation in PARK2 is also the most common cause of juvenile Parkinson's disease. Mutations in PARK2 result in an upregulation of its substrate cyclin E, resulting in dysregulated entry into the cell cycle. In neurons, this process results in cell death, but in cycling cells, the result is a growth advantage. Thus, depending on whether the cell affected is a dividing cell or a post-mitotic neuron, responses to these alterations may differ, ultimately leading to varying disease phenotypes. Here, we review the substantial data implicating specific genes in both cancer and neurodegenerative disease.

Indexed as

AnimalsAutophagyCell CycleDNA RepairHumansMitochondriaNeoplasmsNeurodegenerative Diseases

Identifiers

PMID20418918
PMCPMC3005561
OpenAlexW2010359358

What OpenQuestion holds

Textmetadata
LicenceTDM
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.