Evidence map›Paper›PMID 35000018›Full record

ArticleBrain tumor pathology2022

Role of proliferative marker index and KBTBD4 mutation in the pathological diagnosis of pineal parenchymal tumors.

Eita Uchida, Atsushi Sasaki, Mitsuaki Shirahata, Tomonari Suzuki, Jun-Ichi Adachi, Kazuhiko Mishima, Masanori Yasuda, Takamitsu Fujimaki, Koichi Ichimura, Ryo Nishikawa

Abstract read
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In one paragraph

Article in Brain tumor pathology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

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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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. 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

10 authors at 2 institutions in 1 country.

Eita UchidaDepartment of Neuro-Oncology/Neurosurgery, Saitama Medical University International Medical Center, Hidaka, Saitama, Japan. eita1985@saitama-med.ac.jp.
Atsushi SasakiDepartment of Pathology, Saitama Medical University, Moroyama-machi, Saitama, Japan.
Mitsuaki ShirahataDepartment of Neuro-Oncology/Neurosurgery, Saitama Medical University International Medical Center, Hidaka, Saitama, Japan.
Tomonari SuzukiDepartment of Neuro-Oncology/Neurosurgery, Saitama Medical University International Medical Center, Hidaka, Saitama, Japan.
Jun-Ichi AdachiDepartment of Neuro-Oncology/Neurosurgery, Saitama Medical University International Medical Center, Hidaka, Saitama, Japan.
Kazuhiko MishimaDepartment of Neuro-Oncology/Neurosurgery, Saitama Medical University International Medical Center, Hidaka, Saitama, Japan.
Masanori YasudaDepartment of Pathology, Saitama Medical University International Medical Center, Hidaka, Saitama, Japan.
Takamitsu FujimakiDepartment of Neurosurgery, Saitama Medical University, Moroyama-machi, Saitama, Japan.
Koichi IchimuraDivision of Brain Tumor Translational Research, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan.
Ryo NishikawaDepartment of Neuro-Oncology/Neurosurgery, Saitama Medical University International Medical Center, Hidaka, Saitama, Japan.
Saitama Medical University · JPJuntendo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pineal parenchymal tumors (PPTs) are clinically rare and a biopsy is often required for a definitive diagnosis. To improve the accuracy of histological assessment of PPTs, we examined the proliferative capacity of PPT cells and investigated DICER1 expression and KBTBD4 mutations. This study included 19 cases of PPTs [3 pineocytomas (PCs), 10 PPTs of intermediate differentiation (PPTID), and 6 pineoblastomas (PBs)]. Immunohistochemistry for Ki-67, PHH3, and DICER1, as well as Sanger sequencing analysis for KBTBD4 mutations, was performed using formalin-fixed paraffin-embedded tissue specimens that were resected during surgery. Tumor cell proliferation was quantified using an image analysis software. For the PHH3 and MIB-1 indices, a significant difference was observed between the PPTIDs and PBs (P < 0.05). Loss of DICER1 was not specific for PB; 0/3 PCs (0.0%), 2/9 PPTIDs (22.2%), and 2/4 PBs (50.0%). KBTBD4 mutations were detected in 1/3 PCs (33.3%), 6/9 PPTIDs (66.7%), and 0/4 PBs (0.0%). Thus, combined application of the proliferative marker index and KBTBD4 mutation analysis may be useful for the differential diagnosis of PPTs. Furthermore, detection of KBTBD4 mutations using Sanger sequencing analysis may support the diagnosis of PPTID.

Indexed as

Brain NeoplasmsCarrier ProteinsDEAD-box RNA HelicasesMutationPineal GlandRibonuclease IIICell ProliferationHumansImmunohistochemistryCarrier ProteinsDEAD-box RNA HelicasesDICER1 protein, humanKBTBD4 protein, humanRibonuclease IIIDifferential diagnosisKBTBD4 mutationMIB-1PHH3Pineal parenchymal tumor

Identifiers

PMID35000018
OpenAlexW4206020619

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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.