Evidence map›Paper›PMID 33275808›Full record

ArticleCancer science2021

Intestinal phenotype is maintained by Atoh1 in the cancer region of intraductal papillary mucinous neoplasm.

Nobuhiro Katsukura, Sho Watanabe, Tomoaki Shirasaki, Shuji Hibiya, Yoshihito Kano, Keiichi Akahoshi, Minoru Tanabe, Susumu Kirimura, Takumi Akashi, Masanobu Kitagawa and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. 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 1 institution in 1 country.

Nobuhiro KatsukuraDepartment of Gastroenterology and Hepatology, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan.
Sho WatanabeDepartment of Gastroenterology and Hepatology, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan.
Tomoaki ShirasakiDepartment of Gastroenterology and Hepatology, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan.
Shuji HibiyaDepartment of Gastroenterology and Hepatology, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan.
Yoshihito KanoDepartment of Clinical Oncology, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan.
Keiichi AkahoshiDepartment of Hepato-Biliary-Pancreatic Surgery, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan.
Minoru TanabeDepartment of Hepato-Biliary-Pancreatic Surgery, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan.
Susumu KirimuraDepartment of Surgical Pathology, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan.
Takumi AkashiDepartment of Surgical Pathology, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan.
Masanobu KitagawaDepartment of Comprehensive Pathology, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan.
Ryuichi OkamotoDepartment of Gastroenterology and Hepatology, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan.ORCID https://orcid.org/0000-0002-7047-571X
Mamoru WatanabeDepartment of Gastroenterology and Hepatology, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan.
Kiichiro TsuchiyaDepartment of Gastroenterology and Hepatology, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan.ORCID https://orcid.org/0000-0002-1977-8707
Tokyo Medical and Dental University · JP

Funding

Japan Foundation for Applied Enzymology; the Health and Labor Sciences Research Grant from the Japanese Ministry of Health, Labor and Welfare (MHLW) 14526073Research Grant of the Princess Takamatsu Cancer Research Fundscientific Research, from the Japanese Ministry of Education, Culture, Sports, Science and Technology 17H06654scientific Research, from the Japanese Ministry of Education, Culture, Sports, Science and Technology 17K15930scientific Research, from the Japanese Ministry of Education, Culture, Sports, Science and Technology 17K159301scientific Research, from the Japanese Ministry of Education, Culture, Sports, Science and Technology 17K19513scientific Research, from the Japanese Ministry of Education, Culture, Sports, Science and Technology 18H02791The Practical Research for Innovative Cancer Control, Rare/Intractable Diseases from Japan Agency for Medical Research and Development (AMED) 15Ack0106017h0002The Practical Research for Innovative Cancer Control, Rare/Intractable Diseases from Japan Agency for Medical Research and Development (AMED) 16ck0106017h0003
6 · The paper itself

Abstract

Intraductal papillary mucinous neoplasm (IPMN) is a precancerous lesion of pancreatic cancer. Although there are 4 types of IPMN, among which intestinal-type IPMN is likely to progress into invasive cancer known as colloid carcinoma, no information regarding the involvement of the intestinal phenotype in the carcinogenesis of IPMN exists. The present study was conducted to explore how the intestinal differentiation system is maintained during the tumor progression of intestinal-type IPMN using surgical resection specimens. Results showed that Atoh1, a critical transcriptional factor for intestinal differentiation toward the secretory lineages of intestinal epithelial cells, was expressed in an invasive-grade IPMN. To determine the function of Atoh1 in pancreatic cancer, we generated a pancreatic ductal adenocarcinoma (PDAC) cell line overexpressing Atoh1. In a xenograft model, we successfully induced an IPMN phenotype in PDAC cells via Atoh1 induction. Finally, for the first time, we discovered that GPA33 is expressed in intestinal-type IPMN, thereby suggesting a novel target for cancer therapy. In conclusion, the intestinal differentiation system might be maintained during tumor progression of intestinal-type IPMN. Further analysis of the function of Atoh1 in IPMN might be useful for understanding the molecular mechanism underlying the malignant potential during the tumor progression of IPMN.

Indexed as

AgedAged, 80 and overAnimalsBasic Helix-Loop-Helix ProteinsCell DifferentiationCell Line, TumorFemaleHeterograftsHumansIntestinesMaleMembrane GlycoproteinsMiceMiddle AgedPancreatic Intraductal NeoplasmsPhenotypeATOH1 protein, humanBasic Helix-Loop-Helix ProteinsGPA33 protein, humanMembrane GlycoproteinsAtoh1differentiationGPA33intestinal typeintraductal papillary mucinous neoplasm

Identifiers

PMID33275808
PMCPMC7894004
OpenAlexW3106560378

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.