Evidence map›Paper›PMID 30417470›Full record

ArticleCancer science2019

Identification of TRA-1-60-positive cells as a potent refractory population in follicular lymphomas.

Katsuyoshi Takata, Ken Saito, Satoshi Maruyama, Tomoko Miyata-Takata, Hidekazu Iioka, Shujiro Okuda, Yiwei Ling, Kennosuke Karube, Yukari Miki, Yoshinobu Maeda and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Selective ablation of TRA-1-60Theranostics · 2023
    Article
  3. Article
  4. Article
  5. 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

13 authors at 8 institutions in 2 countries.

Katsuyoshi TakataDepartment of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.ORCID http://orcid.org/0000-0001-6890-1276
Ken SaitoDivision of Molecular and Cellular Pathology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Satoshi MaruyamaOral Pathology Section, Department of Surgical Pathology, Niigata University Hospital, Niigata, Japan.
Tomoko Miyata-TakataDepartment of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Hidekazu IiokaDivision of Molecular and Cellular Pathology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Shujiro OkudaBioinformatics Laboratory, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Yiwei LingBioinformatics Laboratory, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Kennosuke KarubeDepartments of Pathology and Cell Biology, Graduate School of Medicine, University of the Ryukyus, Nishihara, Japan.
Yukari MikiDepartment of Medical Hygiene, Medical Technology Course, Kochi Gakuen Junior College, Kochi, Japan.
Yoshinobu MaedaDepartment of Hematology and Oncology, Okayama University Hospital, Okayama, Japan.
Tadashi YoshinoDepartment of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Christian SteidlDepartment of Lymphoid Cancer Research, Centre for Lymphoid Cancer, British Columbia Cancer, Vancouver, Canada.
Eisaku KondoDivision of Molecular and Cellular Pathology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Niigata University · JPOkayama University · JPNiigata University Medical and Dental Hospital · JPKochi Gakuen College · JPNiigata University of Rehabilitation · JPOkayama University Hospital · JPUniversity of British Columbia · CAUniversity of the Ryukyus · JP

Funding

Japan Society for the Promotion of Science 16K15245Japan Society for the Promotion of Science 24790350
6 · The paper itself

Abstract

Despite receiving rituximab-combined chemotherapy, follicular lymphoma (FL) patients often suffer tumor recurrence and understand that the cause of relapse in FL would thus significantly ameliorate the tumor therapeutics. In the present study, we show that TRA-1-60-expressing cells are a unique population in FL, converge to the conventional stem cell marker Oct3/4 and ALDH1-positive population, and resist current B-lymphoma agents. TRA-1-60 expression was observed in scattered lymphoma cells in FL tissues only as well as in resting B-lymphocytes inside germinal centers. Retrospective comparison between recurrent and cognate primary tissues showed that the number of TRA-1-60-positive cells from rituximab, cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone (R-CHOP)-treated FL had increased relative to primary tissue, a finding corroborated by assays on different rituximab-treated FL cell lines, FL-18 and DOHH2, wherein TRA-positive cell numbers increased over 10-fold compared to the untreated sample. Concordantly, scanty TRA-1-60-positive FL-18 cells implanted s.c. into mice evinced potent tumor-initiating capacity in vivo, where tumors were 12-fold larger in volume (P = 0.0021 < 0.005) and 13-fold heavier in weight (P = 0.0015 < 0.005) compared to those xenografted from TRA-negative cells. To explain these results, gene expression profiling and qPCR analysis indicated that TRA-1-60-positive cells defined a distinct population from that of TRA-negative cells, with upregulation of multiple drug transporters and therapeutic resistance genes. Hence, TRA-1-60-expressing cells in FL are considered to be vigorously intractable against conventional therapeutic agents, which may explain its refractory recurrence.

Indexed as

AdultAgedAged, 80 and overAnimalsAntigens, SurfaceAntineoplastic Combined Chemotherapy ProtocolsCell Line, TumorDrug Resistance, NeoplasmFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansLymphoma, FollicularMaleMice, Inbred NODMice, SCIDAntigens, SurfaceProteoglycansTRA-1-60 antigen, humandrug resistancefollicular lymphomarituximabTRA-1-60tumor recurrence

Identifiers

PMID30417470
PMCPMC6317956
OpenAlexW2900582772

What OpenQuestion holds

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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.