Evidence map›Paper›PMID 34771461›Full record

ReviewCancers2021

Intraductal Papillary Mucinous Neoplasms of the Pancreas: A Review of Their Genetic Characteristics and Mouse Models.

Jin Li, Tao Wei, Jian Zhang, Tingbo Liang

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 28% 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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Transgenic mouse model of congenital choledochal cyst.Pediatric surgery international · 2026
    Article
  3. Article
  4. Dual Role of NRF2 in Pancreatic Precursor Lesions.Cancer research communications · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Modern aspects of the management of pancreatic intraductal papillary mucinous neoplasms: a narrative review.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
    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

4 authors at 1 institution in 1 country.

Jin LiDepartment of Hepatobiliary and Pancreatic Surgery, School of Medicine, The First Affiliated Hospital of Zhejiang University, 79 Qingchun Road, Hangzhou 310003, China.ORCID 0000-0002-4538-4285
Tao WeiDepartment of Hepatobiliary and Pancreatic Surgery, School of Medicine, The First Affiliated Hospital of Zhejiang University, 79 Qingchun Road, Hangzhou 310003, China.
Jian ZhangDepartment of Hepatobiliary and Pancreatic Surgery, School of Medicine, The First Affiliated Hospital of Zhejiang University, 79 Qingchun Road, Hangzhou 310003, China.
Tingbo LiangDepartment of Hepatobiliary and Pancreatic Surgery, School of Medicine, The First Affiliated Hospital of Zhejiang University, 79 Qingchun Road, Hangzhou 310003, China.
National Center for Chronic and Noncommunicable Disease Control and Prevention · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The intraductal papillary mucinous neoplasm (IPMN) is attracting research attention because of its increasing incidence and proven potential to progress into invasive pancreatic ductal adenocarcinoma (PDAC). In this review, we summarized the key signaling pathways or protein complexes (GPCR, TGF, SWI/SNF, WNT, and PI3K) that appear to be involved in IPMN pathogenesis. In addition, we collected information regarding all the genetic mouse models that mimic the human IPMN phenotype with specific immunohistochemistry techniques. The mouse models enable us to gain insight into the complex mechanism of the origin of IPMN, revealing that it can be developed from both acinar cells and duct cells according to different models. Furthermore, recent genomic studies describe the potential mechanism by which heterogeneous IPMN gives rise to malignant carcinoma through sequential, branch-off, or de novo approaches. The most intractable problem is that the risk of malignancy persists to some extent even if the primary IPMN is excised with a perfect margin, calling for the re-evaluation and improvement of diagnostic, pre-emptive, and therapeutic measures.

Indexed as

genetic mouse modelsIPMNmolecular signaturepancreatic cancerpathogenesis

Identifiers

PMID34771461
PMCPMC8582516
OpenAlexW3209215048

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.