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Mendeley readers
Attention Score in Context
| Title |
Nrf2 promotes mutant K-ras/p53-driven pancreatic carcinogenesis
|
|---|---|
| Published in |
Carcinogenesis, May 2017
|
| DOI | 10.1093/carcin/bgx043 |
| Pubmed ID | |
| Authors |
Shin Hamada, Keiko Taguchi, Atsushi Masamune, Masayuki Yamamoto, Tooru Shimosegawa |
| Abstract |
The Keap1-Nrf2 system contributes to the maintenance of homeostasis by regulating oxidative stress responses in normal tissues and organs, and is exploited in various cancers for proliferation, survival and acquisition of therapy resistance. Pancreatic cancer remains one of the intractable cancers, despite the improved clinical outcomes of other types of cancer, due to its invasive and refractory nature to therapeutic intervention. The current study aimed to clarify the contribution of Nrf2 to pancreatic carcinogenesis using a pancreas-specific mutant K-ras and p53 (KPC) mouse model. Deletion of Nrf2 in KPC mice (KPCN) decreased the formation of precancerous lesions as well as the development of invasive pancreatic cancer. The pancreatic tumor-derived cancer cell lines from KPCN mouse showed decreased expression of glutathione S-transferases (GST), UDP glucuronosyltransferases (UGT) and ABC transporters. Along with these biochemical changes, cell lines from KPCN mice revealed increased sensitivity to oxidative stress and chemotherapeutic agent. The current study revealed that Nrf2 contributes to pancreatic carcinogenesis in a way distinct from the chemoresistance of lung and esophagus, and that Nrf2 could be a novel therapeutic target of pancreatic cancer. |
Mendeley readers
The data shown below were compiled from readership statistics for 42 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 42 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Ph. D. Student | 7 | 17% |
| Researcher | 7 | 17% |
| Student > Bachelor | 3 | 7% |
| Student > Postgraduate | 3 | 7% |
| Professor > Associate Professor | 3 | 7% |
| Other | 7 | 17% |
| Unknown | 12 | 29% |
| Readers by discipline | Count | As % |
|---|---|---|
| Biochemistry, Genetics and Molecular Biology | 20 | 48% |
| Medicine and Dentistry | 6 | 14% |
| Agricultural and Biological Sciences | 2 | 5% |
| Pharmacology, Toxicology and Pharmaceutical Science | 1 | 2% |
| Unknown | 13 | 31% |
Attention Score in Context
This research output has an Altmetric Attention Score of 3. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 07 March 2019.
All research outputs
#7,542,364
of 23,011,300 outputs
Outputs from Carcinogenesis
#1,664
of 4,760 outputs
Outputs of similar age
#119,451
of 310,821 outputs
Outputs of similar age from Carcinogenesis
#5
of 31 outputs
Altmetric has tracked 23,011,300 research outputs across all sources so far. This one is in the 44th percentile – i.e., 44% of other outputs scored the same or lower than it.
So far Altmetric has tracked 4,760 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.4. This one is in the 22nd percentile – i.e., 22% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 310,821 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 53% of its contemporaries.
We're also able to compare this research output to 31 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 80% of its contemporaries.