Beneficial Effects of 5-Fluorouracil and Heparin-Based Portal Infusion Chemotherapy Combined with Mitomycin C and Cisplatin after Curative Resection of Pancreatic Cancer

Aiura, Koichi; Takahashi, Shin; Matsui, Junichi; Ueda, Mitsuharu; Kitagawa, Yuko

doi:10.1159/000244265

Cited by 16 publications

(18 citation statements)

References 25 publications

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“…There was no connection to the main lesion, and we diagnosed this small lesion as intrapancreatic micrometastasis of PDAC. The patient was administered 5-fluorouracil and heparin-based infusion chemotherapy combined with cisplatin and mitomycin C (PI4W) as perioperative chemotherapy[4], and was discharged without any complications. He was administered S-1 (tegafur, gimeracil, and oteracil potassium combination) for 6 mo as adjuvant chemotherapy.…”

Section: Case Reportmentioning

confidence: 99%

“…There was no continuity between this small lesion and the main tumor or carcinoma in situ , and we diagnosed the small lesion as an intrapancreatic micrometastasis of PDAC. We administered PI4W as perioperative chemotherapy[4] and discharged the patient without any complications. She was administered gemcitabine for 6 mo as adjuvant chemotherapy.…”

Section: Case Reportmentioning

confidence: 99%

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Two cases of pancreatic ductal adenocarcinoma with intrapancreatic metastasis

Fujita

Kitago

Masugi

et al. 2016

WJG

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There are no standardized diagnostic criteria for intrapancreatic metastasis of pancreatic ductal adenocarcinoma (PDAC). Here, we report two cases of patients with PDAC who were pathologically diagnosed as harboring intrapancreatic metastasis. In both cases, the main lesions were located in the pancreatic body, and no other lesion was detected preoperatively. The patients were diagnosed with pancreatic body cancers and distal pancreatectomy was performed. Pathological findings revealed microscopic cancer nests, which had connections to neither the main lesion nor the premalignant lesion in the pancreatic tail parenchyma. In both cases, the histological type of the daughter lesion was quite similar to that of the main lesion. Hence, we diagnosed the daughter lesions as metastatic foci in the pancreas. Although intrapancreatic metastasis of PDAC has been regarded as a poor prognostic factor, few reports of intrapancreatic metastasis are available. This article reports two such cases and provides a review of the literature.

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Section: Case Reportmentioning

confidence: 99%

Section: Case Reportmentioning

confidence: 99%

Two cases of pancreatic ductal adenocarcinoma with intrapancreatic metastasis

Fujita

Kitago

Masugi

et al. 2016

WJG

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“…The translational aspect of our research is emphasized by many types of cancers that are being characterized by an increase in glucose metabolism, which can be visualized by positron emission tomography (PET) using Fluorine-18 labeled [F18] fluorodeoxyglucose (FDG). 16, 17, 18, 19, 20, 21, 22 FDG-PET has gained a significant clinical importance for diagnosis and treatment monitoring of cancer patients over the past decade. Tumor glucose metabolism provides important information about cell viability and early treatment effects and FDG-PET has the potential to serve as a surrogate marker of treatment response to new targeted treatments.…”

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confidence: 99%

Resistance to the tyrosine kinase inhibitor axitinib is associated with increased glucose metabolism in pancreatic adenocarcinoma

et al. 2014

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Alterations in energy (glucose) metabolism are key events in the development and progression of cancer. In pancreatic adenocarcinoma (PDAC) cells, we investigated changes in glucose metabolism induced by resistance to the receptor tyrosine kinase inhibitor (RTKI) axitinib. Here, we show that human cell lines and mouse PDAC cell lines obtained from the spontaneous pancreatic cancer mouse model (KrasG12DPdx1-cre) were sensitive to axitinib. The anti-proliferative effect was due to a G2/M block resulting in loss of 70–75% cell viability in the most sensitive PDAC cell line. However, a surviving sub-population showed a 2- to 3-fold increase in [C-14]deoxyglucose ([C-14]DG) uptake. This was sustained in axitinib-resistant cell lines, which were derived from parental PDAC. In addition to the axitinib-induced increase in [C-14]DG uptake, we observed a translocation of glucose transporter-1 (Glut-1) transporters from cytosolic pools to the cell surface membrane and a 2-fold increase in glycolysis rates measured by the extracellular acidification rate (ECAR). We demonstrated an axitinib-induced increase in phosphorylated Protein Kinase B (pAkt) and by blocking pAkt with a phosphatidylinositol-3 kinase (PI3K) inhibitor we reversed the Glut-1 translocation and restored sensitivity to axitinib treatment. Combination treatment with both axitinib and Akt inhibitor in parental pancreatic cell line resulted in a decrease in cell viability beyond that conferred by single therapy alone. Our study shows that PDAC resistance to axitinib results in increased glucose metabolism mediated by activated Akt. Combining axitinib and an Akt inhibitor may improve treatment in PDAC.

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“…18 Many other institutions, including our facility, have also used fluorouracilbased NACRT. [23][24][25] Continuous intravenous infusion of fluorouracil has become standard, and, to get better results, some institutions have reported co-use of MMC and CDDP to be effective. 25,26 pCR to NACRT is rare in pancreatic cancer, which is thought to be chemoradioresistant relative to other gastrointestinal malignancies.…”

Section: Discussionmentioning

confidence: 99%

“…[23][24][25] Continuous intravenous infusion of fluorouracil has become standard, and, to get better results, some institutions have reported co-use of MMC and CDDP to be effective. 25,26 pCR to NACRT is rare in pancreatic cancer, which is thought to be chemoradioresistant relative to other gastrointestinal malignancies. 8 In our institution, 25 patients with locally invasive PDA without distant metastasis underwent fluorouracil-based NACRT (5-FU+MMC+CDDP+radiation 40 Gy) between 2003 and 2011.…”

Section: Discussionmentioning

confidence: 99%

Two Cases of Pathological Complete Response to Neoadjuvant Chemoradiation Therapy in Pancreatic Cancer

et al. 2015

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Neoadjuvant chemoradiation therapy (NACRT) is increasingly used in patients with a potentially or borderline resectable pancreatic ductal adenocarcinoma (PDA) and it has been shown to improve survival and reduce locoregional metastatic disease. It is rare for patients with PDA to have a pathological complete response (pCR) to NACRT, but such patients reportedly have a good prognosis. We report the clinicopathological findings of two cases of pCR to NACRT in PDA. Both patients underwent pancreatectomy after NACRT (5-fluorouracil, mitomycin C, cisplatin, and radiation). Neither had residual invasive carcinoma and both showed extensive fibrotic regions with several ducts regarded as having pancreatic intraepithelial neoplasia 3/carcinoma in situ in their post-therapy specimens. It is noteworthy that both patients had a history of a second primary cancer. They both had comparatively good outcomes: one lived for 9 years after the initial pancreatectomy and the other is still alive without recurrence after 2 years.

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Beneficial Effects of 5-Fluorouracil and Heparin-Based Portal Infusion Chemotherapy Combined with Mitomycin C and Cisplatin after Curative Resection of Pancreatic Cancer

Cited by 16 publications

References 25 publications

Two cases of pancreatic ductal adenocarcinoma with intrapancreatic metastasis

Two cases of pancreatic ductal adenocarcinoma with intrapancreatic metastasis

Resistance to the tyrosine kinase inhibitor axitinib is associated with increased glucose metabolism in pancreatic adenocarcinoma

Two Cases of Pathological Complete Response to Neoadjuvant Chemoradiation Therapy in Pancreatic Cancer

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