Evidence map›Paper›PMID 18318112›Full record

ReviewMolekuliarnaia biologiia

[The use of p53 as a tool for human cancer therapy].

V P Almazov, D V Kochetkov, P M Chumakov

Open access · greenAbstract readEnglish AbstractReview
In one paragraph

Review in Molekuliarnaia biologiia. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–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

7 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. 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

3 authors.

V P Almazov
D V Kochetkov
P M Chumakov

Funding

Potentials of reactivated mutant p53R01CA104903 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI CHUMAKOV, PETER M · 2004 to 2008
$1.5M
Role of sestrin family genes in antioxidant defenseR01AG025278 · NIA · CLEVELAND CLINIC LERNER COM-CWRU · PI CHUMAKOV, PETER M · 2005 to 2009
$1.5M
NCI NIH HHS R01 CA104903NIA NIH HHS R01 AG025278
6 · The paper itself

Abstract

The p53 tumor suppressor is a central component of a system that reinforces genetic stability of somatic cells in animals and humans. Inactivation of this gene occurs virtually in every cancer case, which eliminates results in further rapid accumulation of additional mutations leading to progression of a cancer cell toward more malignant phenotype. The mechanisms of p53 inhibition in cancer include point mutations leading to accumulation of inactive protein, deletion of the whole gene, or its portion, alteration in the genes involved in regulation of activity of p53, and defects in the genes controlled by p53. In addition, oncogenic viruses encode specialized proteins that are entitled to modify p53 functions in order to provide optimal condition for replication of viral genome. These viral proteins play central role in viral carcinogenesis, including 95% of cases of cervical carcinoma in women. The approacheas to restoration of p53 activity depend on particular type of alteration within the p53 pathway. In some cases an effective mean would be introduction of exogenous p53, particularly with the use of adenoviral vectors. There are also approaches in development that target reactivation of mutant proteins, or suppress natural inhibitors of p53. The review summarizes various schemes for therapy and prevention of cancer that are based on our knowledge of the p53 gene functions. Potential usefulness of the approaches for practical applications is discussed.

Indexed as

Cell Transformation, NeoplasticFemaleHumansMutationTumor Suppressor Protein p53Uterine Cervical NeoplasmsTumor Suppressor Protein p53

Identifiers

PMID18318112
PMCPMC2634859
OpenAlexW2616116563

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.