Evidence map›Paper›PMID 31407254›Full record

ArticleInternational journal of hematology2019

FF-10501 induces caspase-8-mediated apoptotic and endoplasmic reticulum stress-mediated necrotic cell death in hematological malignant cells.

Taichi Matsumoto, Shiro Jimi, Keisuke Migita, Kazuki Terada, Masayoshi Mori, Yasushi Takamatsu, Junji Suzumiya, Shuuji Hara

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Article in International journal of hematology, 2019. 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
–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

3 citing papers in PubMed.

  1. Review
  2. Review
  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

8 authors.

Taichi MatsumotoDepartment of Drug Informatics, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1, Nanakuma, Jounan, Fukuoka, 814-0180, Japan. tmatsumoto@fukuoka-u.ac.jp.ORCID http://orcid.org/0000-0001-5301-1481
Shiro JimiCentral Laboratory of Pathology and Morphology, Department of Medicine, Fukuoka University, Fukuoka, Japan.
Keisuke MigitaDepartment of Drug Informatics, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1, Nanakuma, Jounan, Fukuoka, 814-0180, Japan.
Kazuki TeradaLaboratory of Drug Design and Drug Delivery, Faculty of Pharmaceutical Sciences, Fukuoka University, Fukuoka, Japan.
Masayoshi MoriDepartment of Pharmacotherapeutics, Faculty of Pharmaceutical Sciences, Fukuoka University, Fukuoka, Japan.
Yasushi TakamatsuDivision of Medical Oncology, Hematology, and Infectious Diseases, Department of Medicine, Fukuoka University, Fukuoka, Japan.
Junji SuzumiyaDepartment of Oncology/Hematology, Shimane University Hospital, Shimane, Japan.
Shuuji HaraDepartment of Drug Informatics, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1, Nanakuma, Jounan, Fukuoka, 814-0180, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

FF-10501 is a novel inhibitor of inosine monophosphate dehydrogenase (IMPDH). Clinical trials of FF-10501 for myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) are currently being conducted in the United States. Although it has been shown that FF-10501 induces apoptosis in hematological malignant cells, the intracellular mechanisms of this effect have not been characterized. We conducted an in vitro study to elucidate the mechanisms of FF-10501-induced cell death using 12 hematological malignant cell lines derived from myeloid and lymphoid malignancies. FF-10501 suppressed the growth of each cell line in a dose-dependent manner. However, the clinically relevant dose (40 μM) of FF-10501 induced cell death in three cell lines (MOLM-13, OCI-AML3, and MOLT-3). Investigation of the cell death mechanism suggested that FF-10501 induces both apoptotic and necrotic cell death. FF-10501-induced apoptosis was mediated by caspase-8 activation followed by activation of the mitochondrial pathway in MOLM-13 and MOLT-3 cells. FF-10501 induced necrotic cell death via endoplasmic reticulum stress in OCI-AML3 cells. The present study is the first to identify intracellular pathways involved in FF-10501-induced cell death.

Indexed as

ApoptosisCaspase 8Cell DeathCell Line, TumorEndoplasmic Reticulum StressEnzyme InhibitorsHematologic NeoplasmsHumansIMP DehydrogenaseMitochondriaNecrosisCaspase 8Enzyme InhibitorsIMP DehydrogenaseApoptosisCaspase-8Endoplasmic reticulum stressFF-10501Necrosis

Identifiers

PMID31407254

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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.