Evidence map›Paper›PMID 28776573›Full record

ArticleModern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc2017

Pancreatic intraductal tubulopapillary neoplasm is genetically distinct from intraductal papillary mucinous neoplasm and ductal adenocarcinoma.

Olca Basturk, Michael F Berger, Hiroshi Yamaguchi, Volkan Adsay, Gokce Askan, Umesh K Bhanot, Ahmet Zehir, Fatima Carneiro, Seung-Mo Hong, Giuseppe Zamboni and 18 more

Abstract read
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In one paragraph

Article in Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

  1. Pooled it
  2. SWI/SNF Complex-Deficient Undifferentiated Carcinoma of the Pancreas: Clinicopathologic and Genomic Analysis.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2024
    Trial
  3. Review
  4. Article
  5. Article
  6. When BRG1 Turns Off: Chromatin Remodeling and YAP Signaling Drive ITPN Progression.Cellular and molecular gastroenterology and hepatology · 2026
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Fusion genes in pancreatic tumors.Trends in cancer · 2024
    Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. The Dual Role of Necroptosis in Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2023
    Review
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

28 authors at 9 institutions in 5 countries.

Olca BasturkDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Michael F BergerDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Hiroshi YamaguchiDepartment of Pathology, Tokyo Medical University, Tokyo, Japan.
Volkan AdsayDepartment of Pathology, Emory University, Atlanta, GA, USA.
Gokce AskanDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Umesh K BhanotDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Ahmet ZehirDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Fatima CarneiroDepartment of Pathology, Centro Hospitalar São João/Faculty of Medicine of Porto University and Institute for Research and Innovation in Health/Institute of Molecular Pathology and Immunology of the University of Porto (Ipatimup), Porto, Portugal.
Seung-Mo HongDepartment of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Giuseppe ZamboniDepartment of Pathology, University of Verona, Ospedale S.C.-Don Calabria-Negrar, Verona, Italy.
Esra DikogluNew York Genome Center, Molecular Diagnostics, New York, NY, USA.
Vaidehi JobanputraNew York Genome Center, Molecular Diagnostics, New York, NY, USA.
Kazimierz O WrzeszczynskiNew York Genome Center, Molecular Diagnostics, New York, NY, USA.
Serdar BalciDepartment of Pathology, Emory University, Atlanta, GA, USA.
Peter AllenDepartment of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Naoki IkariInstitute for Integrated Medical Sciences, Tokyo Women's Medical University, Tokyo, Japan.
Shoko TakeuchiInstitute for Integrated Medical Sciences, Tokyo Women's Medical University, Tokyo, Japan.
Hiroyuki AkagawaInstitute for Integrated Medical Sciences, Tokyo Women's Medical University, Tokyo, Japan.
Atsushi KannoDepartment of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Tooru ShimosegawaDepartment of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Takanori MorikawaDepartment of Surgery, Tohoku University Graduate School of Medicine, Sendai, Japan.
Fuyuhiko MotoiDepartment of Surgery, Tohoku University Graduate School of Medicine, Sendai, Japan.
Michiaki UnnoDepartment of Surgery, Tohoku University Graduate School of Medicine, Sendai, Japan.
Ryota HiguchiDepartment of Surgery, Tokyo Women's Medical University, Tokyo, Japan.
Masakazu YamamotoDepartment of Surgery, Tokyo Women's Medical University, Tokyo, Japan.
Kyoko ShimizuDepartment of Gastroenterology, Tokyo Women's Medical University, Tokyo, Japan.
Toru FurukawaDepartment of Pathology, Tokyo Women's Medical University, Tokyo, Japan.
David S KlimstraDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Memorial Sloan Kettering Cancer Center · USTokyo Women's Medical University · JPTohoku University · JPNew York Genome Center · USEmory University · USTokyo Medical University · JPUlsan College · KRUniversidade do Porto · PTUniversity of Verona · IT

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
6 · The paper itself

Abstract

Intraductal tubulopapillary neoplasm is a relatively recently described member of the pancreatic intraductal neoplasm family. The more common member of this family, intraductal papillary mucinous neoplasm, often carries genetic alterations typical of pancreatic infiltrating ductal adenocarcinoma (KRAS, TP53, and CDKN2A) but additionally has mutations in GNAS and RNF43 genes. However, the genetic characteristics of intraductal tubulopapillary neoplasm have not been well characterized. Twenty-two intraductal tubulopapillary neoplasms were analyzed by either targeted next-generation sequencing, which enabled the identification of sequence mutations, copy number alterations, and selected structural rearrangements involving all targeted (≥300) genes, or whole-exome sequencing. Three of these intraductal tubulopapillary neoplasms were also subjected to whole-genome sequencing. All intraductal tubulopapillary neoplasms revealed the characteristic histologic (cellular intraductal nodules of back-to-back tubular glands lined by predominantly cuboidal cells with atypical nuclei and no obvious intracellular mucin) and immunohistochemical (immunolabeled with MUC1 and MUC6 but were negative for MUC2 and MUC5AC) features. By genomic analyses, there was loss of CDKN2A in 5/20 (25%) of these cases. However, the majority of the previously reported intraductal papillary mucinous neoplasm-related alterations were absent. Moreover, in contrast to most ductal neoplasms of the pancreas, MAP-kinase pathway was not involved. In fact, 2/22 (9%) of intraductal tubulopapillary neoplasms did not reveal any mutations in the tested genes. However, certain chromatin remodeling genes (MLL1, MLL2, MLL3, BAP1, PBRM1, EED, and ATRX) were found to be mutated in 7/22 (32%) of intraductal tubulopapillary neoplasms and 27% harbored phosphatidylinositol 3-kinase (PI3K) pathway (PIK3CA, PIK3CB, INPP4A, and PTEN) mutations. In addition, 4/18 (18%) of intraductal tubulopapillary neoplasms had FGFR2 fusions (FGFR2-CEP55, FGFR2-SASS6, DISP1-FGFR2, FGFR2-TXLNA, and FGFR2-VCL) and 1/18 (5.5%) had STRN-ALK fusion. Intraductal tubulopapillary neoplasm is a distinct clinicopathologic entity in the pancreas. Although its intraductal nature and some clinicopathologic features resemble those of intraductal papillary mucinous neoplasm, our results suggest that intraductal tubulopapillary neoplasm has distinguishing genetic characteristics. Some of these mutated genes are potentially targetable. Future functional studies will be needed to determine the consequences of these gene alterations.

Indexed as

Adenocarcinoma, MucinousAdenocarcinoma, PapillaryAdultAgedBiomarkers, TumorCarcinoma, Pancreatic DuctalDNA Mutational AnalysisFemaleHumansMaleMiddle AgedPancreatic NeoplasmsYoung AdultBiomarkers, Tumor

Identifiers

PMID28776573
OpenAlexW2742970081

What OpenQuestion holds

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Read underepoch 390

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.