Evidence map›Paper›PMID 26341959›Full record

ArticleInternational journal of hematology2015

Overexpression of salivary-type amylase reduces the sensitivity to bortezomib in multiple myeloma cells.

Shohei Mizuno, Ichiro Hanamura, Akinobu Ota, Sivasundaram Karnan, Tomoko Narita, Masaki Ri, Motonori Mizutani, Mineaki Goto, Mayuko Gotou, Norikazu Tsunekawa and 7 more

Abstract read
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In one paragraph

Article in International journal of hematology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

4 citing papers in PubMed, 6 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

17 authors at 4 institutions in 1 country.

Shohei MizunoDivision of Hematology, Department of Internal Medicine, Aichi Medical University, 1, 1 Karimata, Yazako, Nagakute, Aichi, 480-1195, Japan.
Ichiro HanamuraDivision of Hematology, Department of Internal Medicine, Aichi Medical University, 1, 1 Karimata, Yazako, Nagakute, Aichi, 480-1195, Japan. hanamura@aichi-med-u.ac.jp.
Akinobu OtaDepartment of Biochemistry, Aichi Medical University, Nagakute, Aichi, Japan.
Sivasundaram KarnanDepartment of Biochemistry, Aichi Medical University, Nagakute, Aichi, Japan.
Tomoko NaritaDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi, Japan.
Masaki RiDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi, Japan.
Motonori MizutaniDivision of Hematology, Department of Internal Medicine, Aichi Medical University, 1, 1 Karimata, Yazako, Nagakute, Aichi, 480-1195, Japan.
Mineaki GotoDivision of Hematology, Department of Internal Medicine, Aichi Medical University, 1, 1 Karimata, Yazako, Nagakute, Aichi, 480-1195, Japan.
Mayuko GotouDivision of Hematology, Department of Internal Medicine, Aichi Medical University, 1, 1 Karimata, Yazako, Nagakute, Aichi, 480-1195, Japan.
Norikazu TsunekawaDivision of Hematology, Department of Internal Medicine, Aichi Medical University, 1, 1 Karimata, Yazako, Nagakute, Aichi, 480-1195, Japan.
Masato ShikamiDepartment of Hematology, Daiyukai General Hospital, Ichinomiya, Aichi, Japan.
Shinsuke IidaDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi, Japan.
Yoshitaka HosokawaDepartment of Biochemistry, Aichi Medical University, Nagakute, Aichi, Japan.
Hiroshi MiwaDepartment of Internal Medicine, Toyama Hospital, Tsu, Mie, Japan.
Ryuzo UedaDepartment of Tumor Immunology, Aichi Medical University, Nagakute, Aichi, Japan.
Masakazu NittaDivision of Hematology, Department of Internal Medicine, Aichi Medical University, 1, 1 Karimata, Yazako, Nagakute, Aichi, 480-1195, Japan.
Akiyoshi TakamiDivision of Hematology, Department of Internal Medicine, Aichi Medical University, 1, 1 Karimata, Yazako, Nagakute, Aichi, 480-1195, Japan.
Aichi Medical University · JPNagoya City University · JPDaiyūkaidaiichi Hospital · JPTsuyama Chuo Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amylase-producing myeloma exhibits refractoriness to chemotherapy and a dismal prognosis. In this study, we established a human myeloma cell line, 8226/AMY1, in which a lentivirally transfected AMY1 gene was stably expressed and explored its biological characteristics. 8226/AMY1 showed a survival advantage over mock control when treated with dexamethasone, bortezomib, and lenalidomide in vitro partly through inhibition of apoptosis induced by these reagents. In a xenograft murine model, 8226/AMY1 showed rapid tumor growth and reduced sensitivity to bortezomib compared with mock. A microarray gene expression analysis identified TCL1A, which functions as a coactivator of the cell survival kinase Akt, differentially up-regulated in 8226/AMY1. The expression of phosphorylated Akt was increased in the 8226/AMY1 cells following bortezomib treatment, but not in the mock cells. In addition, treatment with perifosine, an inhibitor of Akt phosphorylation, enhanced the anti-myeloma effect of bortezomib in the 8226/AMY1 cells. Our data suggest that amylase-producing myeloma reduced the sensitivity to bortezomib in vitro and in vivo, and the up-regulation of TCL1A may influence the drug susceptibility of 8226/AMY1 via the phosphorylation of Akt. These findings provide clues for developing treatment approaches for not only amylase-producing myeloma, but also relapsed and refractory myelomas.

Indexed as

Multiple MyelomaAmylasesAnimalsBortezomibCell Line, TumorDrug Resistance, NeoplasmGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticHumansMiceMice, Inbred NODMice, SCIDProto-Oncogene ProteinsProto-Oncogene Proteins c-aktXenograft Model Antitumor AssaysAmylasesBortezomibProto-Oncogene ProteinsProto-Oncogene Proteins c-aktTCL1A protein, humanAmylaseBortezomibLenalidomideMyelomaTransfectant

Identifiers

PMID26341959
OpenAlexW1260584024

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.