ArticleNeoplasia (New York, N.Y.)2014
Chronic pancreatitis and systemic inflammatory response syndrome prevent impact of chemotherapy with gemcitabine in a genetically engineered mouse model of pancreatic cancer.
Article in Neoplasia (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Article
- Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance.Cancer research · 2019Article
- Prognostic value of γ-glutamyltransferase-to-albumin ratio in patients with pancreatic ductal adenocarcinoma following radical surgery.Cancer medicine · 2019Article
- The systemic inflammation response index predicts survival and recurrence in patients with resectable pancreatic ductal adenocarcinoma.Cancer management and research · 2019Article
- Histone deacetylase inhibitors provoke a tumor supportive phenotype in pancreatic cancer associated fibroblasts.Oncotarget · 2017Article
- Idiopathic pancreatitis in a patient with a STAT3 mutation.Allergy & rhinology (Providence, R.I.) · 2016Article
- Dynamic aberrant NF-κB spurs tumorigenesis: a new model encompassing the microenvironment.Cytokine & growth factor reviews · 2015Review
- Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
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Abstract
BACKGROUND AND
aimsBACKGROUND AND AIMSGemcitabine is the standard therapy for patients with pancreatic cancer with metastatic disease. Patients with metastatic pancreatic cancer presenting with increased values of C-reactive protein do not respond to gemcitabine. So far, no studies have evaluated the correlation between chronic pancreatitis, systemic inflammatory response syndrome, and the loss of chemotherapeutic benefit.
methodsPdx-1-Cre;LSL-Kras(G12D/+);LSL-Trp53(R172H/+) mice were assigned into four groups: 1) Sixteen animals received a daily intraperitoneal injection of caerulein from their ninth week of life on. 2) Sixteen mice were additionally given gemcitabine. 3) Twelve animals received gemcitabine only. 4) Saline-treated control group. Furthermore, human Paca44 pancreatic ductal adenocarcinoma cells were seeded and cultured in 0.5% FBS containing growth medium plus/minus 1 μM gemcitabine plus/minus recombinant human interleukin (IL)-6.
resultsInduced systemic inflammatory response syndrome and a mild chronic pancreatitis diminished the beneficial effects of gemcitabine upon median overall survival. In median, the monogemcitabine group survived 191 days, whereas the caerulein-mono group survived 114, the control group 121, and the caerulein gemcitabine group 127 days (P < .05). In vitro, the induction of STAT3 phosphorylation by recombinant human IL-6 promoted pancreatic ductal adenocarcinoma cell survival during gemcitabine treatment.
conclusionWe could demonstrate for the first time that an improvement in median overall survival with gemcitabine is significantly abolished by a persistent mild chronic pancreatitis and a systemic inflammatory response syndrome. In particular, the inflammation biomarkers C-reactive protein, IL-6, and IL-1α could indicate the prognostic benefit of gemcitabine chemotherapy and should now be tested in prospective patient-controlled trials.
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