Evidence map›Paper›PMID 28862699›Full record

ArticleBlood cancer journal2017

CXorf48 is a potential therapeutic target for achieving treatment-free remission in CML patients.

M Matsushita, K Ozawa, T Suzuki, M Nakamura, N Nakano, S Kanchi, D Ichikawa, E Matsuki, M Sakurai, D Karigane and 8 more

Open access · goldAbstract read
In one paragraph

Article in Blood cancer journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Road to treatment-free remission in chronic myeloid leukemia.International journal of hematology · 2026
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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

18 authors at 1 institution in 1 country.

M MatsushitaDivision of Clinical Physiology and Therapeutics, Keio University, Faculty of Pharmacy, Shiabakoen, Minato-ku, Tokyo, Japan.
K OzawaDivision of Clinical Physiology and Therapeutics, Keio University, Faculty of Pharmacy, Shiabakoen, Minato-ku, Tokyo, Japan.
T SuzukiDivision of Clinical Physiology and Therapeutics, Keio University, Faculty of Pharmacy, Shiabakoen, Minato-ku, Tokyo, Japan.
M NakamuraDivision of Clinical Physiology and Therapeutics, Keio University, Faculty of Pharmacy, Shiabakoen, Minato-ku, Tokyo, Japan.
N NakanoDivision of Clinical Physiology and Therapeutics, Keio University, Faculty of Pharmacy, Shiabakoen, Minato-ku, Tokyo, Japan.
S KanchiDivision of Clinical Physiology and Therapeutics, Keio University, Faculty of Pharmacy, Shiabakoen, Minato-ku, Tokyo, Japan.
D IchikawaDivision of Clinical Physiology and Therapeutics, Keio University, Faculty of Pharmacy, Shiabakoen, Minato-ku, Tokyo, Japan.
E MatsukiDivision of Hematology, Department of Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
M SakuraiDivision of Hematology, Department of Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
D KariganeDivision of Hematology, Department of Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
H KasaharaDivision of Hematology, Department of Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
N TsukamotoDivision of Cellular Signaling, Institute for Advanced Medical Research, Keio University, School of Medicine, Shinjuku-ku, Tokyo, Japan.
T ShimizuDivision of Hematology, Department of Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
T MoriDivision of Hematology, Department of Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
H NakajimaDivision of Hematology, Department of Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
S OkamotoDivision of Hematology, Department of Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Y KawakamiDivision of Cellular Signaling, Institute for Advanced Medical Research, Keio University, School of Medicine, Shinjuku-ku, Tokyo, Japan.
Y HattoriDivision of Clinical Physiology and Therapeutics, Keio University, Faculty of Pharmacy, Shiabakoen, Minato-ku, Tokyo, Japan.
Keio University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although the introduction of tyrosine kinase inhibitors (TKIs) has improved overall survival of patients with chronic myeloid leukemia (CML), about half of the patients eventually relapse after cessation of TKIs. In contrast, the remainder of the patients maintain molecular remission without TKIs, indicating that the patients' immune system could control proliferation of TKI-resistant leukemic stem cells (LSCs). However, the precise mechanism of immunity against CML-LSCs is not fully understood. We have identified a novel immune target, CXorf48, expressed in LSCs of CML patients. Cytotoxic T cells (CTLs) induced by the epitope peptide derived from CXorf48 recognized CD34

Indexed as

Bone Marrow CellsCD8-Positive T-LymphocytesFemaleGene Expression Regulation, LeukemicHumansK562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleNeoplasm ProteinsNeoplastic Stem CellsTHP-1 CellsNeoplasm Proteins

Identifiers

PMID28862699
PMCPMC5709753
OpenAlexW2752675000

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.