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Pancreatic Neoplasms: HELP
Articles by Johan Permert
Based on 6 articles published since 2010
(Why 6 articles?)

Between 2010 and 2020, J. Permert wrote the following 6 articles about Pancreatic Neoplasms.
+ Citations + Abstracts
1 Review Pancreatic Exocrine Insufficiency in Pancreatic Cancer. 2017

Vujasinovic, Miroslav / Valente, Roberto / Del Chiaro, Marco / Permert, Johan / Löhr, J-Matthias. ·Center for Digestive Diseases, Karolinska University Hospital, Stockholm SE-141 86, Sweden. miroslav.vujasinovic@karolinska.se. · Center for Digestive Diseases, Karolinska University Hospital, Stockholm SE-141 86, Sweden. roberto.valente@karolinska.se. · Center for Digestive Diseases, Karolinska University Hospital, Stockholm SE-141 86, Sweden. marco.del-chiaro@ki.se. · Center for Digestive Diseases, Karolinska University Hospital, Stockholm SE-141 86, Sweden. johan.permert@karolinska.se. · Center for Digestive Diseases, Karolinska University Hospital, Stockholm SE-141 86, Sweden. matthias.lohr@ki.se. ·Nutrients · Pubmed #28241470.


2 Article Pancreatectomies for pancreatic neoplasms in pediatric and adolescent age: A single institution experience. 2018

Scandavini, Chiara / Valente, Roberto / Rangelova, Elena / Segersvärd, Ralf / Arnelo, Urban / Permert, Johan / Svensson, Pär-Johan / Stenman, Jakob / Del Chiaro, Marco. ·Pancreatic Surgery Unit, Division of Surgery (KLINTEC) - Karolinska Institutet at Center for Digestive Diseases Karolinska University Hospital, Stockholm, Sweden. · Pancreatic Surgery Unit, Division of Surgery (KLINTEC) - Karolinska Institutet at Center for Digestive Diseases Karolinska University Hospital, Stockholm, Sweden; Digestive and Liver Diseases Unit - Sapienza University of Rome, Italy. · Astrid Lindgren Children's Hospital, Karolinska University Hospital and Department for Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden. · Pancreatic Surgery Unit, Division of Surgery (KLINTEC) - Karolinska Institutet at Center for Digestive Diseases Karolinska University Hospital, Stockholm, Sweden. Electronic address: marco.del.chiaro@ki.se. ·Pancreatology · Pubmed #29277262.

ABSTRACT: BACKGROUND: There are very few data in the current literature regarding the short- and long-term outcome of surgery for pediatric pancreatic tumors (PPT). No data are available on the impact of pancreatic surgery on the children's growth. METHODS: This is a retrospective cohort study on a consecutive series of pediatric/adolescent patients who underwent pediatric surgery at Karolinska University Hospital from January 2005 to July 2017. RESULTS: Overall 14 pancreatic operations were performed in 13 patients. The median age was 11.4 years (range 3-15). Six pancreaticoduodenectomies (42.8%), 5 distal pancreatectomies (35.7%), and 3 enucleations (21.5%) were performed. The final histology revealed a solid pseudopapillary tumor in 9 cases (69.2%), neuroblastoma in 1 (7.7%), ganglioneuroma in 1 (7.7%), pancreatoblastoma in 1 (7.7%), and insulinoma in 1 (7.7%). Overall, 3 patients developed post-operative complications (23%). There was no peri-operative mortality. All patients are alive after a median follow-up time of 80 months. Exocrine insufficiency was detected post-operatively in 4 patients (30.7%) Endocrine insufficiency requiring insulin treatment developed in one patient (7.7%). No significant impact on growth was detected in any of the patients after pancreatic resection. CONCLUSIONS: In our series, surgery performed for PPTs seems to be safe and effective. The effect of pancreatic surgery on children's growth does not seem to be significant.

3 Article Bioinformatory-assisted analysis of next-generation sequencing data for precision medicine in pancreatic cancer. 2017

Malgerud, Linnéa / Lindberg, Johan / Wirta, Valtteri / Gustafsson-Liljefors, Maria / Karimi, Masoud / Moro, Carlos Fernández / Stecker, Katrin / Picker, Alexander / Huelsewig, Carolin / Stein, Martin / Bohnert, Regina / Del Chiaro, Marco / Haas, Stephan L / Heuchel, Rainer L / Permert, Johan / Maeurer, Markus J / Brock, Stephan / Verbeke, Caroline S / Engstrand, Lars / Jackson, David B / Grönberg, Henrik / Löhr, Johannes Matthias. ·Center for Digestive Diseases, Karolinska University Hospital, Stockholm, Sweden. · Department of Clinical Sciences, Intervention and Technology (CLINTEC), Karolinska Institutet, Stockholm, Sweden. · Department of Medical Epidemiology & Biostatistics (MEB), Karolinska Institutet, Stockholm, Sweden. · Science for Life Laboratory, Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institutet, Stockholm, Sweden. · Department of Oncology at Radiumhemmet, Karolinska University Hospital, Stockholm, Sweden. · Department of Pathology, Karolinska University Hospital, Stockholm, Sweden. · Molecular Health GmbH, Heidelberg, Germany. · Innovation Office, Karolinska University Hospital, Stockholm, Sweden. · Department of Laboratory Medicine (LABMED), Karolinska Institutet, Stockholm, Sweden. ·Mol Oncol · Pubmed #28675654.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is a tumor with an extremely poor prognosis, predominantly as a result of chemotherapy resistance and numerous somatic mutations. Consequently, PDAC is a prime candidate for the use of sequencing to identify causative mutations, facilitating subsequent administration of targeted therapy. In a feasibility study, we retrospectively assessed the therapeutic recommendations of a novel, evidence-based software that analyzes next-generation sequencing (NGS) data using a large panel of pharmacogenomic biomarkers for efficacy and toxicity. Tissue from 14 patients with PDAC was sequenced using NGS with a 620 gene panel. FASTQ files were fed into treatmentmap. The results were compared with chemotherapy in the patients, including all side effects. No changes in therapy were made. Known driver mutations for PDAC were confirmed (e.g. KRAS, TP53). Software analysis revealed positive biomarkers for predicted effective and ineffective treatments in all patients. At least one biomarker associated with increased toxicity could be detected in all patients. Patients had been receiving one of the currently approved chemotherapy agents. In two patients, toxicity could have been correctly predicted by the software analysis. The results suggest that NGS, in combination with an evidence-based software, could be conducted within a 2-week period, thus being feasible for clinical routine. Therapy recommendations were principally off-label use. Based on the predominant KRAS mutations, other drugs were predicted to be ineffective. The pharmacogenomic biomarkers indicative of increased toxicity could be retrospectively linked to reported negative side effects in the respective patients. Finally, the occurrence of somatic and germline mutations in cancer syndrome-associated genes is noteworthy, despite a high frequency of these particular variants in the background population. These results suggest software-analysis of NGS data provides evidence-based information on effective, ineffective and toxic drugs, potentially forming the basis for precision cancer medicine in PDAC.

4 Article Excess glucose induces hypoxia-inducible factor-1α in pancreatic cancer cells and stimulates glucose metabolism and cell migration. 2013

Liu, Zhiwen / Jia, Xiaohui / Duan, Yijie / Xiao, Huijie / Sundqvist, Karl-Gösta / Permert, Johan / Wang, Feng. ·Department of Clinical Immunology, Karolinska University Hospital, Huddinge, Sweden. ·Cancer Biol Ther · Pubmed #23377827.

ABSTRACT: Pancreatic cancer patients frequently show hyperglycemia, but it is uncertain whether hyperglycemia stimulates pancreatic cancer cells. We have investigated whether excess glucose induces hypoxia-inducible factor-1α (HIF-1α) and stimulates glucose metabolism and cell migration in pancreatic cancer cells. We studied wild-type (wt) MiaPaCa2 pancreatic cancer cells and a MiaPaCa2 subline (namely si-MiaPaCa2) that had HIF-1α-specific small interfering RNA. Wt-MiaPaCa2 cells are known to be HIF-1α-positive in hypoxia and HIF-1α-negative in normoxia, whereas si-MiaPaCa2 cells are devoid of HIF-1α in both normoxia and hypoxia. We incubated these cells with different amounts of glucose and determined HIF-1α mRNA and protein by real-time polymerase chain reaction and western blotting. We determined glucose consumption, lactate production and intracellular hexokinase-II and ATP to assess glucose metabolisms and determined pyruvate dehydrogenase kinase-1, reactive oxygen species and fumarate to assess mitochondrial activities. Further, we studied cell migration using a Boyden chamber. Excess glucose (16.7-22.2mM) increased HIF-1α in hypoxic wt-MiaPaCa2 cells. HIF-1α expression increased ATP contents and inhibited mitochondrial activities. Extracellular glucose and hypoxia stimulated glucose metabolisms independent of HIF-1α. Excess glucose stimulated the migration of wt- and si-MiaPaCa2 cells in both normoxia and hypoxia. Thus, glucose stimulated cell migration independent of HIF-1α. Nevertheless, hypoxic wt-MiaPaCa2 cells showed greater migrating ability than their si-MiaPaCa2 counterparts. We conclude that (1) excess glucose increases HIF-1α and ATP in hypoxic wt-MiaPaCa2 cells, (2) extracellular glucose and hypoxia regulate glucose metabolisms independent of HIF-1α and (3) glucose stimulates cell migration by mechanisms that are both dependent on HIF-1α and independent of it.

5 Article Pancreatic cancer cells expressing hypoxia-inducible factor-1α tend to be adjacent to intratumoral blood vessels. 2010

Cheng, B-Q / Segersvärd, R / Permert, J / Wang, F. ·Department of Surgery, Karolinska University Hospital, Huddinge, Sweden. ·Eur Surg Res · Pubmed #20924188.

ABSTRACT: We investigated whether cells expressing hypoxia-inducible factor-1α (HIF-1α) are specially related to blood vessels in human pancreatic tumors. HIF-1α and blood vessels were stained in 7 pancreatic ductal adenocarcinomas (PDAC) and 3 nonmalignant tumors. HIF-1α(+) cells accounted for 37 ± 5% of the total PDAC cells and increased to 52 ± 4% in perivascular PDAC cells and to 67 ± 4% in PDAC cells found in intratumoral blood vessels. In nonmalignant tumors, 12 ± 3% of the total tumoral cells examined were HIF-1α(+), and HIF-1α(+) cells decreased to 2 ± 0.3% in perivascular cells examined in the tumors. In conclusion, HIF-1α(+) cells in PDAC and nonmalignant pancreatic tumors differ not only in their amounts but also in their relation to intratumoral blood vessels. HIF-1α(+) cells usually are adjacent to intratumoral blood vessels in PDAC tumors, but are farther away from the vessels in nonmalignant pancreatic tumors.

6 Article PP56 improves energy homeostasis in a mouse model of pancreatic cancer. 2010

Wang, Feng / Larsson, Jörgen / Herrington, Margery K / Permert, Johan. ·Department of Clinical Science, Intervention and Technology, Division of Surgery, Karolinska University Hospital, Huddinge, Sweden. feng.wang@ki.se ·Tumour Biol · Pubmed #20422342.

ABSTRACT: In this study, we investigated whether the anti-inflammatory drug PP56 (alpha-trinositol) may improve cancer-induced metabolic disorders. We implanted human MiaPaCa2 pancreatic cancer cells in the pancreas of 14 athymic mice for 12 weeks, using six intact littermates as normal controls. During the 12 weeks, seven tumor-cell recipients were treated with PP56 by daily injection (PPT mice). The tumor-cell recipients that were otherwise untreated were used as tumor controls (TC mice). Impaired glucose tolerance and decreased body weight gain were seen in TC but not PPT mice. When an enzyme for fatty acid beta-oxidation namely medium-chain acyl-CoA dehydrogenase (MCAD) was determined in tumor grafts; tumors from PPT mice showed more MCAD than those from TC mice. This suggests that PP56 stimulated fatty acid beta-oxidation in MiaPaCa2 cells in vivo. In keeping with this notion, PPT mice had decreased plasma free fatty acids. In vitro, we demonstrated that MiaPaCa2 cells consumed more fatty acids in the presence of PP56. In another experiment, we infused PP56 or vehicle in normal mice and found that PP56 decreased circulating glucose in the animals. We also showed that PP56 increased glucose transport in L6 skeletal muscle cells in vitro. In conclusion, PP56 increases the turnover of circulating nutrients such as glucose and helps maintain energy homeostasis in mice with pancreatic cancer.