Evidence map›Paper›PMID 30161160›Full record

ArticlePloS one2018

A genome-wide association study identifies three novel genetic markers for response to tamoxifen: A prospective multicenter study.

Hiroshi Onishi, Chihiro Udagawa, Michiaki Kubo, Seigo Nakamura, Sadako Akashi-Tanaka, Takashi Kuwayama, Chie Watanabe, Tomoko Takamaru, Hiroyuki Takei, Takashi Ishikawa and 24 more

Abstract readMulticenter Study
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Rsu1-dependent control of PTEN expression is regulated via ATF2 and cJun.Journal of cell communication and signaling · 2019
    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

34 authors.

Hiroshi OnishiDivision of Genetics, National Cancer Center Research Institute, Tokyo, Japan.
Chihiro UdagawaDivision of Genetics, National Cancer Center Research Institute, Tokyo, Japan.ORCID 0000-0002-3430-2555
Michiaki KuboRIKEN, Center for Integrative Medical Sciences, Yokohama, Japan.
Seigo NakamuraDivision of Breast Surgical Oncology, Department of Surgery, Showa University School of Medicine, Tokyo, Japan.
Sadako Akashi-TanakaDivision of Breast Surgical Oncology, Department of Surgery, Showa University School of Medicine, Tokyo, Japan.
Takashi KuwayamaDivision of Breast Surgical Oncology, Department of Surgery, Showa University School of Medicine, Tokyo, Japan.
Chie WatanabeDivision of Breast Surgical Oncology, Department of Surgery, Showa University School of Medicine, Tokyo, Japan.
Tomoko TakamaruDivision of Breast Surgical Oncology, Department of Surgery, Showa University School of Medicine, Tokyo, Japan.
Hiroyuki TakeiDepartment of Breast Surgery, Nippon Medical School, Tokyo, Japan.
Takashi IshikawaDepartment of Breast Surgery, Tokyo Medical University, Tokyo, Japan.
Kana MiyaharaDepartment of Breast Surgery, Tokyo Medical University, Tokyo, Japan.
Hiroshi MatsumotoDepartment of Breast Surgery, Saitama Cancer Center, Saitama, Japan.
Yoshie HasegawaDepartment of Breast Surgery, Hirosaki Municipal Hospital, Hirosaki, Japan.
Yukihide MomozawaRIKEN, Center for Integrative Medical Sciences, Yokohama, Japan.
Siew-Kee LowRIKEN, Center for Integrative Medical Sciences, Yokohama, Japan.
Goro Kutomi1st Department of Surgery, Sapporo Medical University, Sapporo, Japan.
Hiroaki Shima1st Department of Surgery, Sapporo Medical University, Sapporo, Japan.
Fukino Satomi1st Department of Surgery, Sapporo Medical University, Sapporo, Japan.
Minoru OkazakiDepartment of Breast Surgery, Sapporo Breast Surgical Clinic, Sapporo, Japan.
Hisamitsu ZahaDepartment of Breast Surgery, Nakagami Hospital, Okinawa, Japan.
Mai OnomuraDepartment of Breast Surgery, Nakagami Hospital, Okinawa, Japan.
Ayami MatsukataDepartment of Breast Surgery, Sagara Hospital, Kagoshima, Japan.
Yasuaki SagaraDepartment of Breast Surgery, Sagara Hospital, Kagoshima, Japan.
Shinichi BabaDepartment of Breast Surgery, Sagara Hospital, Kagoshima, Japan.
Akimitsu YamadaDepartment of Breast and Thyroid Surgery, Yokohama City University Medical Center, Yokohama, Japan.
Kazuhiro ShimadaDepartment of Breast and Thyroid Surgery, Yokohama City University Medical Center, Yokohama, Japan.
Daisuke ShimizuDepartment of Breast Surgery, Yokohama Minato Red Cross Hospital, Yokohama, Japan.
Koichiro TsugawaDepartment of Breast and Endocrine Surgery, St. Marianna University School of Medicine Hospital, Kawasaki, Japan.
Arata ShimoDepartment of Breast and Endocrine Surgery, St. Marianna University School of Medicine Hospital, Kawasaki, Japan.
Mikael HartmanDepartment of Surgery, Yong Loo Lin School of Medicine, National University of Singapore and National University Health System, Singapore.
Ching-Wan ChanDepartment of Surgery, Yong Loo Lin School of Medicine, National University of Singapore and National University Health System, Singapore.
Soo Chin LeeDepartment of Hematology Oncology, National University Cancer Institute, National University Health System, Singapore.
Itaru EndoDepartment of Gastroenterological Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Hitoshi ZembutsuDivision of Genetics, National Cancer Center Research Institute, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeAlthough association studies of genetic variations with the clinical outcomes of breast cancer patients treated with tamoxifen have been reported, genetic factors which could determine individual response to tamoxifen are not fully clarified. We performed a genome-wide association study (GWAS) to identify novel genetic markers for response to tamoxifen. EXPERIMENTAL

designWe prospectively collected 347 blood samples from patients with hormone receptor-positive and human epidermal growth factor receptor 2-negative, invasive breast cancer receiving preoperative tamoxifen monotherapy for 14 to 28 days. We used Ki-67 response in breast cancer tissues after preoperative short-term tamoxifen therapy as a surrogate marker for response to tamoxifen. We performed GWAS and genotype imputation using 275 patients, and an independent set of 72 patients was used for replication study.

resultsThe combined result of GWAS and the replication study, and subsequent imputation analysis indicated possible association of three loci with Ki-67 response after tamoxifen therapy (rs17198973 on chromosome 4q34.3, rs4577773 on 6q12, and rs7087428 on 10p13, Pcombined = 5.69 x 10-6, 1.64 x 10-5, and 9.77 x 10-6, respectively). When patients were classified into three groups by the scoring system based on the genotypes of the three SNPs, patients with higher scores showed significantly higher after/before ratio of Ki-67 compared to those with lower scores (P = 1.8 x 10-12), suggesting the cumulative effect of the three SNPs.

conclusionWe identified three novel loci, which could be associated with clinical response to tamoxifen. These findings provide new insights into personalized hormonal therapy for the patients with breast cancer.

Indexed as

Genetic MarkersPolymorphism, Single NucleotideAdultAgedAged, 80 and overBreast NeoplasmsChromosomes, HumanErb-b2 Receptor Tyrosine KinasesFemaleGenome-Wide Association StudyHumansKi-67 AntigenMiddle AgedPreoperative CareProspective StudiesSequence Analysis, DNAERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesGenetic MarkersKi-67 AntigenMKI67 protein, humanTamoxifen

Identifiers

PMID30161160
PMCPMC6116947

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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.