UBC9 inhibits myeloid differentiation in collaboration with AML1-MTG8.

Tomofusa Fukuyama, Toshio Kitamura, Tomoko Kozu

Abstract read

In one paragraph

Article in International journal of hematology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it

0cells of the map it votes in

0citing papers in PubMed

–field-weighted citation impact, top 98% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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

3 authors at 2 institutions in 2 countries.

Tomofusa FukuyamaDepartment of Cellular Therapy, The Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan. tfukuyam@ims.u-tokyo.ac.jp.ORCID http://orcid.org/0000-0002-0709-3188

Toshio KitamuraDepartment of Cellular Therapy, The Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan.

Tomoko KozuResearch Institute for Clinical Oncology, Saitama Cancer Center, 780 Ina, Saitama, 362-0806, Japan.

Saitama Cancer Center · JPInstitute for Advanced Medical Research · US

Funding

Japan Society for the Promotion of Science JP16K09841Japan Society for the Promotion of Science JP20K08706

6 · The paper itself

Abstract

The chimeric oncogene AML1-MTG8 (RUNX1-RUNX1T1) is generated in t(8;21) acute myeloid leukemia (AML). Here, we report a novel interaction of MTG8/RUNX1T1/ETO with UBC9/UBE2I. AML1-MTG8 protein also interacted with UBC9, suggesting a role in leukemogenesis. Overexpression of UBC9 in Kasumi-1 attenuated myeloid differentiation induced by all-trans retinoic acid, G-CSF, and GM-CSF (AGGM), which was judged by suppression of CD11b. In addition, the UBC9 inhibitor 2-D08 accelerated myeloid differentiation induced by AGGM in two t(8;21) AML cell lines, Kasumi-1 and SKNO-1. These data suggest that UBC9 may play a role in leukemogenesis in t(8;21) AML by working with AML1-MTG8 to suppress myeloid differentiation. Therefore, UBC9 may be a good target for new differentiation therapy against t(8;21) AML.

Indexed as

Leukemia, Myeloid, AcuteOncogene Proteins, FusionCell DifferentiationCell LineChromosomes, Human, Pair 21Chromosomes, Human, Pair 8Core Binding Factor Alpha 2 SubunitHumansRUNX1 Translocation Partner 1 ProteinTranslocation, GeneticCore Binding Factor Alpha 2 SubunitOncogene Proteins, FusionRUNX1 Translocation Partner 1 ProteinAML1ETOMTG8RUNX1UBC9

Identifiers

PMID35152350

DOI10.1007/s12185-022-03303-1

OpenAlexW4211146993

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.