Evidence map›Paper›PMID 33075166›Full record

Observational studyCancer science2021

FMS-like tyrosine kinase 3 (FLT3) amplification in patients with metastatic colorectal cancer.

Hiroko Hasegawa, Hiroya Taniguchi, Yoshiaki Nakamura, Takeshi Kato, Satoshi Fujii, Hiromichi Ebi, Manabu Shiozawa, Satoshi Yuki, Toshiki Masuishi, Ken Kato and 16 more

Abstract readMulticenter StudyObservational Study
In one paragraph

Observational study in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
–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

18 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Using cell-free DNA tumor methylation score to detect and monitor cholangiocarcinoma.HPB : the official journal of the International Hepato Pancreato Biliary Association · 2026
    Article
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  6. Targeting theBiomedicines · 2025
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  14. Molecular Modeling Studies ofInternational journal of molecular sciences · 2021
    Article
  15. Review
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  17. Observational
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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

26 authors.

Hiroko HasegawaDepartment of Gastroenterology and Hepatology, National Hospital Organization, Osaka National Hospital, Osaka, Japan.ORCID https://orcid.org/0000-0001-8330-5245
Hiroya TaniguchiDepartment of Gastroenterology and Gastrointestinal Oncology, National Cancer Center Hospital East, Kashiwa, Japan.ORCID https://orcid.org/0000-0003-1407-6682
Yoshiaki NakamuraDepartment of Gastroenterology and Gastrointestinal Oncology, National Cancer Center Hospital East, Kashiwa, Japan.
Takeshi KatoDepartment of Surgery, National Hospital Organization, Osaka National Hospital, Osaka, Japan.
Satoshi FujiiDivision of Pathology, Exploratory Oncology Research & Clinical Trial Center, National Cancer Center East, Kashiwa, Japan.ORCID https://orcid.org/0000-0001-7541-8469
Hiromichi EbiDivision of Molecular Therapeutics, Aichi Cancer Center Research Institute, Nagoya, Japan.ORCID https://orcid.org/0000-0003-3155-7576
Manabu ShiozawaDepartment of Gastrointestinal Surgery, Kanagawa Cancer Center, Kanagawa, Japan.
Satoshi YukiDepartment of Gastroenterology and Hepatology, Hokkaido University Hospital, Sapporo, Japan.
Toshiki MasuishiDepartment of Clinical Oncology, Aichi Cancer Center Hospital, Nagoya, Japan.
Ken KatoGastrointestinal Medical Oncology Division, National Cancer Center Hospital, Tokyo, Japan.
Naoki IzawaDivision of Clinical Oncology, St. Marianna University School of Medicine, Kawasaki, Japan.
Toshikazu MoriwakiDivision of Gastroenterology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Eiji OkiDepartment of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.ORCID https://orcid.org/0000-0002-9763-9366
Yoshinori KagawaDepartment of Surgery, Osaka Prefectural General Medical Center, Osaka, Japan.
Tadamichi DendaDivision of Gastroenterology, Chiba Cancer Center, Chiba, Japan.
Tomohiro NishinaDivision of Gastroenterology, National Hospital Organization, Shikoku Cancer Center, Matsuyama, Japan.
Akihito TsujiDepartment of Medical Oncology, Kagawa University Hospital, Kagawa, Japan.
Hiroki HaraDepartment of Gastroenterology, Saitama Cancer Center, Saitama, Japan.ORCID https://orcid.org/0000-0003-3881-9815
Taito EsakiDepartment of Gastrointestinal and Medical Oncology, National Hospital Organization Kyushu Cancer Center, Fukuoka, Japan.ORCID https://orcid.org/0000-0002-9169-8453
Tomohiro NishidaFrontier Science for Cancer and Chemotherapy, Osaka University, Osaka, Japan.
Hisato KawakamiDepartment of Medical Oncology, Kinki University, Osaka, Japan.ORCID https://orcid.org/0000-0002-3280-4850
Yasutoshi SakamotoTranslational Research Support Section, Clinical Research Support Department, National Cancer Center Hospital East, Kashiwa, Japan.
Izumi MikiTranslational Research Support Section, Clinical Research Support Department, National Cancer Center Hospital East, Kashiwa, Japan.
Wataru OkamotoTranslational Research Support Section, Clinical Research Support Department, National Cancer Center Hospital East, Kashiwa, Japan.
Kentaro YamazakiDivision of Gastrointestinal Oncology, Shizuoka Cancer Center, Shizuoka, Japan.ORCID https://orcid.org/0000-0001-6269-9345
Takayuki YoshinoDepartment of Gastroenterology and Gastrointestinal Oncology, National Cancer Center Hospital East, Kashiwa, Japan.

Funding

SCRUM-Japan funds
6 · The paper itself

Abstract

FMS-like tyrosine kinase 3 (FLT3) plays a key role in hematopoiesis. However, the oncogenic role of FLT3 amplification in patients with metastatic colorectal cancer (mCRC) remains unclear. Here, we aimed to evaluate the characteristics, prognosis, and treatment efficacy of an FLT3 inhibitor (regorafenib) in patients with mCRC with FLT3 amplifications. Tumor tissue samples from 2329 patients were sequenced using NGS in the Nationwide Cancer Genome Screening Project in Japan. The effects of clinicopathological features, co-altered genes, prognosis, and efficacy of regorafenib were investigated. Between April 2015 and June 2018, 85 patients with mCRC with FLT3 amplification were observed. There were no differences in baseline characteristics between patients with or without FLT3 amplification. The frequency of RAS or other gene co-alterations was inversely correlated with the copy number status. Median survival time in patients with FLT3 amplification was significantly shorter compared with those with non-FLT3 amplification. Further investigations of FLT3 amplification as a potential treatment target in mCRC are warranted.

Indexed as

AdenocarcinomaAdultAgedAged, 80 and overAntineoplastic AgentsColorectal NeoplasmsFemalefms-Like Tyrosine Kinase 3Gene AmplificationHumansMaleMiddle AgedPhenylurea CompoundsPyridinesRetrospective StudiesTreatment OutcomeAntineoplastic AgentsFLT3 protein, humanfms-Like Tyrosine Kinase 3Phenylurea CompoundsPyridinesregorafenibcolorectal cancercopy number statusFLT3 amplificationnext-generation sequencingprognosis

Identifiers

PMID33075166
PMCPMC7780005

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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.