Evidence map›Paper›PMID 22623890›Full record

ArticleTheScientificWorldJournal2012

PTEN gene: a model for genetic diseases in dermatology.

Corrado Romano, Carmelo Schepis

Open access · goldAbstract read
In one paragraph

Article in TheScientificWorldJournal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

  1. Benign Cutaneous Neoplasms with Syndromic Associations.Dermatopathology (Basel, Switzerland) · 2025
    Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Focus on PTEN Regulation.Frontiers in oncology · 2015
    Review
  11. Review
  12. The role of microRNAs in skin fibrosis.Archives of dermatological research · 2013
    Review
  13. Thyroid involvement in two patients with Bannayan-Riley-Ruvalcaba syndrome.Journal of clinical research in pediatric endocrinology · 2013
    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

2 authors at 1 institution in 1 country.

Corrado RomanoUnit of Pediatrics and Medical Genetics, I.R.C.C.S. Associazione Oasi Maria Santissima, Troina, Italy.
Carmelo Schepis
I.R.C.C.S. Oasi Maria SS · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PTEN gene is considered one of the most mutated tumor suppressor genes in human cancer, and it's likely to become the first one in the near future. Since 1997, its involvement in tumor suppression has smoothly increased, up to the current importance. Germline mutations of PTEN cause the PTEN hamartoma tumor syndrome (PHTS), which include the past-called Cowden, Bannayan-Riley-Ruvalcaba, Proteus, Proteus-like, and Lhermitte-Duclos syndromes. Somatic mutations of PTEN have been observed in glioblastoma, prostate cancer, and brest cancer cell lines, quoting only the first tissues where the involvement has been proven. The negative regulation of cell interactions with the extracellular matrix could be the way PTEN phosphatase acts as a tumor suppressor. PTEN gene plays an essential role in human development. A recent model sees PTEN function as a stepwise gradation, which can be impaired not only by heterozygous mutations and homozygous losses, but also by other molecular mechanisms, such as transcriptional regression, epigenetic silencing, regulation by microRNAs, posttranslational modification, and aberrant localization. The involvement of PTEN function in melanoma and multistage skin carcinogenesis, with its implication in cancer treatment, and the role of front office in diagnosing PHTS are the main reasons why the dermatologist should know about PTEN.

Indexed as

Genes, Tumor SuppressorHamartoma Syndrome, MultipleHumansMelanomaProteus SyndromePTEN PhosphohydrolaseSkin NeoplasmsTumor Suppressor ProteinsPTEN PhosphohydrolasePTEN protein, humanTumor Suppressor Proteins

Identifiers

PMID22623890
PMCPMC3353286
OpenAlexW1976229198

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.