Evidence map›Paper›PMID 31799787›Full record

ArticleCancer science2020

Pathogenesis of multiple pancreatic cancers involves multicentric carcinogenesis and intrapancreatic metastasis.

Yusuke Fujita, Sachiko Matsuda, Yasushi Sasaki, Yohei Masugi, Minoru Kitago, Hiroshi Yagi, Yuta Abe, Masahiro Shinoda, Takashi Tokino, Michiie Sakamoto and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 15 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

11 authors at 2 institutions in 2 countries.

Yusuke FujitaDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Sachiko MatsudaEndowed Research Chair in Molecular Targeted Therapy of Gastrointestinal Cancer, Keio University School of Medicine, Tokyo, Japan.
Yasushi SasakiDepartment of Medical Genome Sciences, Research Institute for Frontier Medicine, Sapporo Medical University, Sapporo, Japan.ORCID https://orcid.org/0000-0002-3500-8059
Yohei MasugiDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.ORCID https://orcid.org/0000-0002-6952-4043
Minoru KitagoDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Hiroshi YagiDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Yuta AbeDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Masahiro ShinodaDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Takashi TokinoDepartment of Medical Genome Sciences, Research Institute for Frontier Medicine, Sapporo Medical University, Sapporo, Japan.ORCID https://orcid.org/0000-0001-9428-9543
Michiie SakamotoDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Yuko KitagawaDepartment of Surgery, Keio University School of Medicine, Tokyo, Japan.
Keio University · JPSapporo Medical University · JP

Funding

Chugai Pharmaceutical Co., LtdJapan Society for the Promotion of Science 16H06279Japan Society for the Promotion of Science 18K15094Keio UniversitySchool of Medicine
6 · The paper itself

Abstract

There are increased opportunities in oncology clinics to identify multiple pancreatic ductal adenocarcinomas (PDAC) that co-occur simultaneously or arise metachronously in the pancreatic parenchyma, yet their pathogenesis remains elusive. We hypothesized that two potential pathways, multicentric carcinogenesis and intrapancreatic metastasis, might contribute to forming multiple PDAC. Among 241 resected cases, we identified 20 cancer nodules from nine patients with multiple PDAC (six with synchronous PDAC, one with metachronous PDAC, and two with both synchronous and metachronous PDAC). Integrated clinical, pathological, and mutational analyses, using TP53 and SMAD4 immunostaining and targeted next-generation sequencing of 50 cancer-related genes, were conducted to examine the intertumor relationships. Four of the nine patients were assessed as having undergone multicentric carcinogenesis because of heterogeneity of immunohistochemical and/or mutation characteristics. In contrast, tumors in the other five patients showed intertumor molecular relatedness. Two of these five patients, available for matched sequencing data, showed two or more shared mutations. Moreover, all the smaller nodules in these five patients showed identical TP53 and SMAD4 expression patterns to the corresponding main tumors. Consequently, these five patients were considered to have undergone intrapancreatic metastasis. None of the five smaller nodules arising from intrapancreatic metastasis was accompanied by pancreatic intraepithelial neoplasia, and three of them were tiny (≤1mm). Patients whose tumors resulted from intrapancreatic metastasis appeared to have higher disease stages and worse outcome than those with tumors from multicentric carcinogenesis. Our results provide insight into pancreatic carcinogenesis, showing that the development of multiple PDAC involves distinct evolutionary paths that potentially affect patient prognosis.

Indexed as

Biomarkers, TumorCarcinoma, Pancreatic DuctalCell Line, TumorDNA Mutational AnalysisFemaleHigh-Throughput Nucleotide SequencingHumansMaleNeoplasms, Multiple PrimaryNeoplasms, Second PrimaryNeoplasm StagingPancreatectomyPancreatic NeoplasmsProto-Oncogene Proteins p21(ras)Sequence Analysis, DNASmad4 ProteinBiomarkers, TumorKRAS protein, humanProto-Oncogene Proteins p21(ras)Smad4 ProteinSMAD4 protein, humanTP53 protein, humanTumor Suppressor Protein p53multicentric occurrencemultiple pancreatic cancersnext-generation sequencepancreatic carcinogenesispancreatic intraepithelial neoplasia

Identifiers

PMID31799787
PMCPMC7004534
OpenAlexW2993964280

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.