Evidence map›Paper›PMID 24397609›Full record

ArticleCancer science2014

Nuclear export signal within CALM is necessary for CALM-AF10-induced leukemia.

Mai Suzuki, Kazutsune Yamagata, Mika Shino, Yukiko Aikawa, Koichi Akashi, Toshio Watanabe, Issay Kitabayashi

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Mai SuzukiDivision of Hematological Malignancy, National Cancer Center Research Institute, Tokyo, Japan.
Kazutsune Yamagata
Mika Shino
Yukiko Aikawa
Koichi Akashi
Toshio Watanabe
Issay Kitabayashi
Kyushu University · JPNara Women's University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The CALM-AF10 fusion gene, which results from a t(10;11) translocation, is found in a variety of hematopoietic malignancies. Certain HOXA cluster genes and MEIS1 genes are upregulated in patients and mouse models that express CALM-AF10. Wild-type clathrin assembly lymphoid myeloid leukemia protein (CALM) primarily localizes in a diffuse pattern within the cytoplasm, whereas AF10 localizes in the nucleus; however, it is not clear where CALM-AF10 acts to induce leukemia. To investigate the influence of localization on leukemogenesis involving CALM-AF10, we determined the nuclear export signal (NES) within CALM that is necessary and sufficient for cytoplasmic localization of CALM-AF10. Mutations in the NES eliminated the capacity of CALM-AF10 to immortalize murine bone-marrow cells in vitro and to promote development of acute myeloid leukemia in mouse models. Furthermore, a fusion of AF10 with the minimal NES can immortalize bone-marrow cells and induce leukemia in mice. These results suggest that during leukemogenesis, CALM-AF10 plays its critical roles in the cytoplasm.

Indexed as

Amino Acid SequenceAnimalsCarcinogenesisChlorocebus aethiopsCOS CellsFemaleLeukemiaMiceMice, Inbred C57BLMolecular Sequence DataMonomeric Clathrin Assembly ProteinsNeoplasm TransplantationNuclear Export SignalsOncogene Proteins, FusionTranscription FactorsTumor Cells, CulturedMllt10 protein, mouseMonomeric Clathrin Assembly ProteinsNuclear Export SignalsOncogene Proteins, FusionPICALM protein, mouseTranscription FactorsAF10chromosome translocationhistone modificationleukemianuclear export signal

Identifiers

PMID24397609
PMCPMC4317939
OpenAlexW2162366456

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.