Impacts of Activation of the Mitogen-Activated Protein Kinase Pathway in Pancreatic Cancer
Open accessAbstract
Pancreatic cancer is characterized by constitutive activation of the mitogen-activated protein kinase (MAPK) pathway. Mutations of KRAS or BRAF and epigenetic abrogation of DUSP6 contribute synergistically to the constitutive activation of MAPK. Active MAPK induces the expression of a variety of genes that are thought to play roles in malignant phenotypes of pancreatic cancer. By blocking the functions of such induced genes, it is possible to attenuate the malignant phenotypes. The development of drugs targeting genes downstream of MAPK may provide a novel therapeutic option for pancreatic cancer.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Aurora kinase A is commonly overexpressed in pancreatic cancers and contributes to chromosomal instability and tumor progression.
“The encoded protein Aurora kinase A is commonly overexpressed in pancreatic cancers, and contributes to both chromosomal instability through destabilization of the mitotic spindle assembly and towards tumor progression via phosphorylation of substrate proteins19,20.”
From Occult polyclonality of preclinical pancreatic cancer models drives in vitro evolution (2022) · cites this paper as [19]
PDOs have emerged as a promising preclinical model for therapeutic prediction and functional studies across multiple cancer types, including in PDAC.
“PDOs have emerged as a promising preclinical model for therapeutic prediction and functional studies across multiple cancer types, including in PDAC18,19,48–50.”
From Occult polyclonality of preclinical pancreatic cancer models drives in vitro evolution (2022) · cites this paper as [19]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 48 · Cited by 70
- Authors
- Furukawa, T.
- Affiliations
- Tokyo Women's Medical University (JP)
- Corresponding author
- Furukawa, Toru
- ORCID
- Furukawa, Toru
- Venue
- Frontiers in Oncology
- Publisher
- Frontiers Media SA
- Published
- 2015-02-04
- Volume
- 5
- Pages
- 23-23
- ISSN
- 2234-943X (ISSN-L)
- PMC
- PMC4316689
- OpenAlex
- W2091843466
- Cited by
- 70
- References
- 48
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 5 · 2023: 4 · 2022: 11 · 2021: 8 · 2020: 15 · 2019: 2 · 2018: 3 · 2017: 5 · 2016: 4 · 2015: 4
- FWCI
- 0.57
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Oncology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Japan Society for the Promotion of Science (24659167)
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Keywords
- pancreatic cancer, MAPK signaling, KRAS mutation, BRAF mutation, DUSP6, epigenetic silencing, malignant phenotype, targeted therapy
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
