Evidence map›Paper›PMID 25565868›Full record

ArticleOncoTargets and therapy2015

Decreased expression of APAF-1 and increased expression of cathepsin B in invasive pituitary adenoma.

Cristiana Tanase, Radu Albulescu, Elena Codrici, Bogdan Calenic, Ionela Daniela Popescu, Simona Mihai, Laura Necula, Maria Linda Cruceru, Mihail Eugen Hinescu

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Review
  3. Architects of Pituitary Tumour Growth.Frontiers in endocrinology · 2022
    Review
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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

9 authors at 1 institution in 1 country.

Cristiana Tanase"Victor Babes" National Institute of Pathology, Biochemistry-Proteomics Department, Bucharest, Romania.
Radu Albulescu"Victor Babes" National Institute of Pathology, Biochemistry-Proteomics Department, Bucharest, Romania ; National Institute for Chemical Pharmaceutical R&D, Department of Biochemistry, Bucharest, Romania.
Elena Codrici"Victor Babes" National Institute of Pathology, Biochemistry-Proteomics Department, Bucharest, Romania.
Bogdan Calenic"Victor Babes" National Institute of Pathology, Biochemistry-Proteomics Department, Bucharest, Romania ; "Carol Davila" University of Medicine and Pharmacy, Department of Biochemistry, Bucharest, Romania.
Ionela Daniela Popescu"Victor Babes" National Institute of Pathology, Biochemistry-Proteomics Department, Bucharest, Romania.
Simona Mihai"Victor Babes" National Institute of Pathology, Biochemistry-Proteomics Department, Bucharest, Romania.
Laura Necula"Victor Babes" National Institute of Pathology, Biochemistry-Proteomics Department, Bucharest, Romania ; Stefan S. Nicolau Institute of Virology, Cellular and Molecular Pathology, Cellular and Molecular Medicine Department, Bucharest, Romania.
Maria Linda Cruceru"Carol Davila" University of Medicine and Pharmacy, Cellular and Molecular Medicine Department, Bucharest, Romania.
Mihail Eugen Hinescu"Victor Babes" National Institute of Pathology, Biochemistry-Proteomics Department, Bucharest, Romania ; "Carol Davila" University of Medicine and Pharmacy, Cellular and Molecular Medicine Department, Bucharest, Romania.
Institutul National Victor Babes · RO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeApoptotic protease-activating factor-1 (APAF-1) and cathepsin B are important functional proteins in apoptosis; the former is involved in the intrinsic (mitochondrial) pathway, while the latter is associated with both intrinsic and extrinsic pathways. Changes in the expression of apoptosome-related proteins could be useful indicators of tumor development since a priori defects in the mitochondrial pathway might facilitate the inception and progression of human neoplasms. Our aim was to evaluate the profiles of APAF-1 and cathepsin B in relation with other molecules involved in apoptosis/proliferation and to correlate them with the aggressive behavior of invasive pituitary adenomas. MATERIALS AND

methodsAPAF-1 and cathepsin B were assessed in tissue samples from 30 patients with pituitary adenomas, of which 16 were functional adenomas and 22 were invasive adenomas.

resultsA positive relationship between high proliferation and invasiveness was observed in invasive pituitary adenomas when compared to their noninvasive counterparts (Ki-67 labeling index - 4.72% versus 1.75%). Decreased expression of APAF-1 was recorded in most of the invasive adenomas with a high proliferation index, while the cathepsin B level was elevated in this group. We have noticed a negative correlation between the low level of APAF-1 and invasiveness (63.63%; P<0.01); at the same time, a positive correlation between cathepsin B expression and invasiveness (59.09%; P<0.01) was found. In all, 81.25% out of the total APAF-1-positive samples were cathepsin B negative (P<0.01); 76.92% out of the total cathepsin B-positive samples were APAF-1-negative (P<0.01). These results were reinforced by an apoptosis protein array examination, which showed inhibition of the extrinsic apoptotic pathway in an invasive pituitary adenoma.

conclusionA bidirectional-inverted relationship between APAF-1 and cathepsin B expressions was noticed. One might hypothesize that shifting the balance between mediators of cell death could result in changes in tumor behavior.

Indexed as

APAF-1apoptosiscathepsin BKi-67p53pituitary adenoma

Identifiers

PMID25565868
PMCPMC4278787
OpenAlexW2004779945

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.