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  • 1
    Keywords: CANCER ; CELLS ; EXPRESSION ; tumor ; BLOOD ; Germany ; SYSTEM ; GENE-EXPRESSION ; microarray ; TUMORS ; LINES ; PATIENT ; DNA ; MECHANISM ; prognosis ; CELL-LINES ; cytokines ; antibodies ; antibody ; immunohistochemistry ; DESIGN ; OBESITY ; LINE ; SKELETAL-MUSCLE ; adenocarcinoma ; MICROARRAY ANALYSIS ; OVEREXPRESSION ; PERIPHERAL-BLOOD ; cell lines ; pancreatic cancer ; THYROID-HORMONE ; SERUM ; ELISA ; PANCREATIC-CANCER ; CAPACITY ; DUCTAL ADENOCARCINOMA ; INTERLEUKIN-6 ; INFLAMMATORY CYTOKINES ; SCREEN ; ABILITY ; DNA-MICROARRAY ; ACUTE-PHASE RESPONSE ; ANOREXIA ; cachexia ; NEUROPEPTIDE-Y ; UNCOUPLING PROTEIN-3
    Abstract: Background and Purpose: The mechanism behind aggressive development of cachexia in patients suffering from pancreatic cancer is not well understood. In this study, we investigated which factors are associated with the cachectic status of the patients and evaluated cachexia-promoting capacity of cancer and inflammatory cells. Experimental Design: DNA microarray analysis and quantitative reverse transcription-PCR were used to screen for cachexia-associated factors in pancreatic specimens obtained from non-cachectic and cachetic patients diagnosed with pancreatic ductal adenocarcinoma. The expression pattern of the most prominently altered cachexia-associated factor, interleukin-6 (IL-6), was further analyzed in patients sera by ELISA, in pancreatic specimens by immunohistochemistry, and in a coculture system by quantitative reverse transcription-PCR using pancreatic cancer cell lines T3M4 (IL-6 positive) and Panc-1 (IL-6 negative) and peripheral blood mononuclear cells (PBMC) obtained from donors and noncachectic and cachectic patients. Results: Among numerous analyzed factors, IL-6 was significantly overexpressed in pancreatic specimens and elevated in serum of cachectic patients. The coculture system revealed that pancreatic cancer T3M4 cells but not Panc-1 cells were able to stimulate IL-6 exclusively in cachectic PBMC (by 14-fold) and this triggering was reduced by half in the presence of IL-6-neutralizing antibodies. Conclusion: IL-6 represents a prominent cachexia-associated factor in pancreatic cancer. IL-6 overexpression in cachectic patients is related to the ability of certain tumors to sensitize PBMC and induce cytokine expression in cachectic PBMC
    Type of Publication: Journal article published
    PubMed ID: 16115919
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  • 2
    Keywords: CANCER ; CELLS ; EXPRESSION ; SURVIVAL ; CELL ; Germany ; DISEASE ; liver ; PATIENT ; NF-KAPPA-B ; MACROPHAGES ; prognosis ; BODY-WEIGHT ; immunohistochemistry ; pancreatic cancer ; development ; INTERLEUKIN-6 ; KUPFFER CELLS ; ACUTE-PHASE RESPONSE ; cachexia ; macrophage ; MONOCYTES ; GROWTH-FACTORS ; grading ; NEUROPEPTIDES
    Abstract: Cachexia is a devastating process especially in pancreatic cancer patients and contributes to their poor survival. We attempted to clarify the pathological and molecular changes that occur in the liver during the development of cachexia. Using immunohistochemistry we investigated the infiltration of inflammatory mononuclear cells in liver biopsies of pancreatic cancer patients with or without cachexia, and the potential relevance of the cells for the nutritional and inflammatory status. Additionally, these findings were compared with the patients' clinical parameters. We found a significantly higher amount of CD68 immunoreactive macrophages in liver cross sections of patients with pancreatic cancer and cachexia. The number of CD68-positive macrophages was significantly inversely correlated with the nutritional status. Additionally, in these CD68-positive areas a significant increase in IL-6 and IL-1 immunoreactive cells was localized. Moreover, we found significantly increased areas of CD68-positive macrophages in liver biopsies of patients with a more dedifferentiated (aggressive) grading of the tumor. In conclusion, these results suggest that a crucial interaction between the tumor, PBMCs, and the liver may play a central role in the development and regulation of cachexia. Furthermore, pancreatic cancer may be able to alter systemic organ function even without obvious metastatic disease
    Type of Publication: Journal article published
    PubMed ID: 19148509
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