Evidence map›Paper›PMID 35008235›Full record

ReviewCancers2021

Genetic Mutations of Pancreatic Cancer and Genetically Engineered Mouse Models.

Yuriko Saiki, Can Jiang, Masaki Ohmuraya, Toru Furukawa

Abstract 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 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–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

29 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Targeting the MAPK Pathway in Cancer.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Review
  7. Review
  8. Precision immune regulation in KRAS-mutated cancers: the final piece of the puzzle?Journal of experimental & clinical cancer research : CR · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Inflammation, microbiota, and pancreatic cancer.Cancer cell international · 2025
    Review
  13. Review
  14. Article
  15. Molecular Imaging of p53 in Mouse Models of Cancer Using a Radiolabeled Antibody TAT Conjugate with SPECT.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2024
    Article
  16. TGFβ in Pancreas and Colorectal Cancer: Opportunities to Overcome Therapeutic Resistance.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Review
  17. Review
  18. Article
  19. Review
  20. 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.

Yuriko SaikiDepartment of Investigative Pathology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.
Can JiangDepartment of Investigative Pathology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.
Masaki OhmurayaDepartment of Genetics, Hyogo College of Medicine, Hyogo 663-8501, Japan.
Toru FurukawaDepartment of Investigative Pathology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.ORCID 0000-0002-1083-2324

Funding

Japan Society for the Promotion of Science 20K07386
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy, and the seventh leading cause of cancer-related deaths worldwide. An improved understanding of tumor biology and novel therapeutic discoveries are needed to improve overall survival. Recent multi-gene analysis approaches such as next-generation sequencing have provided useful information on the molecular characterization of pancreatic tumors. Different types of pancreatic cancer and precursor lesions are characterized by specific molecular alterations. Genetically engineered mouse models (GEMMs) of PDAC are useful to understand the roles of altered genes. Most GEMMs are driven by oncogenic Kras, and can recapitulate the histological and molecular hallmarks of human PDAC and comparable precursor lesions. Advanced GEMMs permit the temporally and spatially controlled manipulation of multiple target genes using a dual-recombinase system or CRISPR/Cas9 gene editing. GEMMs that express fluorescent proteins allow cell lineage tracing to follow tumor growth and metastasis to understand the contribution of different cell types in cancer progression. GEMMs are widely used for therapeutic optimization. In this review, we summarize the main molecular alterations found in pancreatic neoplasms, developed GEMMs, and the contribution of GEMMs to the current understanding of PDAC pathobiology. Furthermore, we attempted to modify the categorization of altered driver genes according to the most updated findings.

Indexed as

GEMMKRASPDAC

Identifiers

PMID35008235
PMCPMC8750056

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.