Evidence map›Paper›PMID 18026859›Full record

ArticleEndocrine pathology2007

P53 gene mutations in pituitary carcinomas.

Yoshinori Tanizaki, Long Jin, Bernd W Scheithauer, Kalman Kovacs, Federico Roncaroli, Ricard V Lloyd

Abstract read
PubMed Publisher
In one paragraph

Article in Endocrine pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Grading and staging for pituitary neuroendocrine tumors.Brain pathology (Zurich, Switzerland) · 2025
    Review
  5. Review
  6. Article
  7. Review
  8. Aggressive Pituitary Tumors and Pituitary Carcinomas: From Pathology to Treatment.The Journal of clinical endocrinology and metabolism · 2023
    Article
  9. Review
  10. Article
  11. Aggressive corticotroph tumors and carcinomas.Journal of neuroendocrinology · 2022
    Review
  12. Genetic Basis of ACTH-Secreting Adenomas.International journal of molecular sciences · 2022
    Review
  13. [Update on mechanisms of pituitary tumorigenesis.]Revista de la Facultad de Ciencias Medicas (Cordoba, Argentina) · 2021
    Review
  14. Article
  15. Article
  16. Corticotroph Aggressive Pituitary Tumors and Carcinomas Frequently Harbor ATRX Mutations.The Journal of clinical endocrinology and metabolism · 2021
    Article
  17. Review
  18. Review
  19. 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

6 authors at 3 institutions in 3 countries.

Yoshinori TanizakiDepartment of Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.
Long Jin
Bernd W Scheithauer
Kalman Kovacs
Federico Roncaroli
Ricard V Lloyd
Mayo Clinic · USImperial College London · GBSt. Michael's Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although p53 overexpression detected by immunohistochemistry has been reported in pituitary adenomas and carcinomas, genetic mutations in the p53 gene have not been previously detected in these tumors. We analyzed a series of eight pituitary adenomas and six pituitary carcinomas by immunohistochemistry, polymerase chain reaction amplification, and sequencing of p53 exon 5 through exon 8 for genetic mutations. Three carcinomas showed more than 20% expression of p53 protein in the tumor cells. One of these tumors with 60% overexpression of p53 protein had a mutation in codon 248, a common "hot spot" for p53 mutation, while the other carcinoma with 90% overexpression of p53 protein had a mutation in codon 135. All adenomas were negative for p53 mutations and had 15% of the cells expressing the p53 protein. Analysis of control tumors including four lung carcinomas with proven p53 mutations also had greater than 85% of the tumor cells overexpressing p53 protein. Two breast carcinoma cell lines with known p53 mutations, MBA-MD 231 and MBA-MD-486, also showed greater than 85% of the tumor cells overexpressing p53. These results show that p53 mutations are present in a subset of pituitary carcinomas and are usually associated with a high percentage of tumor cells overexpressing the p53 protein.

Indexed as

AdenomaAdultAgedBase SequenceCarcinomaDNA Mutational AnalysisFemaleGenes, p53HumansImmunohistochemistryMaleMiddle AgedMutationPituitary NeoplasmsReverse Transcriptase Polymerase Chain ReactionTumor Suppressor Protein p53Tumor Suppressor Protein p53

Identifiers

PMID18026859
OpenAlexW2060900142

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.