Evidence map›Paper›PMID 30167087›Full record

ArticleOncotarget2018

Paradoxical counteraction by imatinib against cell death in myeloid progenitor 32D cells expressing p210BCR-ABL.

Morichika Takita, Fujiko Tsukahara, Taishi Mishima, Katsuaki Ieguchi, Masayuki Yamada, Hiroaki Honda, Yoshiro Maru

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Article
  3. 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

7 authors at 1 institution in 1 country.

Morichika Takita *Department of Pharmacology, Tokyo Women's Medical University, Tokyo, Japan.
Fujiko Tsukahara *Department of Pharmacology, Tokyo Women's Medical University, Tokyo, Japan.
Taishi MishimaDepartment of Pharmacology, Tokyo Women's Medical University, Tokyo, Japan.
Katsuaki IeguchiDepartment of Pharmacology, Tokyo Women's Medical University, Tokyo, Japan.
Masayuki YamadaDepartment of Pharmacology, Tokyo Women's Medical University, Tokyo, Japan.
Hiroaki HondaInstitute of Laboratory Animals, Tokyo Women's Medical University, Tokyo, Japan.
Yoshiro MaruDepartment of Pharmacology, Tokyo Women's Medical University, Tokyo, Japan.
Tokyo Women's Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic myeloid leukemia (CML) is believed to be caused by the tyrosine kinase p210BCR-ABL, which exhibits growth-promoting and anti-apoptotic activities. However, mechanisms that allow cell differentiation in CML still remain elusive. Here we established tetracycline (Tet)-regulatable p210BCR-ABL-expressing murine 32D myeloid progenitor (32D/TetOff-p210) cells to explore p210BCR-ABL-induced cell death and differentiation. Tet-regulatable overexpression of p210BCR-ABL induced cell death due to the activation of both caspase-1 and caspase-3, coincident with the differentiation from myeloid progenitors into CD11b

Indexed as

cell deathchronic myeloid leukemiadifferentiationImatinibp210BCR-ABL

Identifiers

PMID30167087
PMCPMC6114964
OpenAlexW2887424535

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.