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| 1 | Detection of tumor stem cell markers in pancreatic carcinoma cell lines显示文摘BACKGROUND: Cancer of the pancreas is the fourth leading cause of cancer death in industrialized countries. In malignancy, actively proliferating cells may be effectively targeted and killed by anti-cancer therapies, but stem cells may survive and support re-growth of the tumor. Thus, new strategies for the treatment of cancer clearly will also have to target cancer stem cells. The goal of the present study was to determine whether pancreatic carcinoma cell growth may be driven by a subpopulation of cancer stem cells. Because previous data implicated ABCG2 and CD133 as stem cell markers in hematopoietic and neural stem/progenitor cells, we analyzed the expression of these two proteins in pancreatic carcinoma cell lines. METHODS: Five established pancreatic adenocarcinoma cell lines were analyzed. Total RNA was isolated and real- time RT-PCR was performed to determine the expression of ABCG2 and CD133. Surface expression of ABCG2 and CD133 was analyzed by flow cytometric analysis. RESULTS: All pancreatic carcinoma cell lines tested expressed significantly higher levels of ABCG2 than non-malignant fibroblasts or two other malignant non- pancreatic cell lines, i.e., SaOS2 osteosarcoma and SKOV3 ovarian cancer. Elevated CD133 expression was found in two out of five pancreatic carcinoma cell lines tested. Using flow cytometric analysis we confirmed surface expression of ABCG2 in all five lines. Yet, CD133 surface expression was detectable in the two cell lines, A818-6 and PancTu1, which exhibited higher mRNA levels.CONCLUSIONS: Two stem cell markers, ABCG2 and CD133 are expressed in pancreatic carcinoma cell lines. ABCG2 and/or CD133 positive cells may represent subpopulation of putative cancer stem cells also in this malignancy. Because cancer stem cells are thought to be responsible for tumor initiation and its recurrence after an initial response to chemotherapy, they may be a very promising target for new drug developments. | Monika Olempska Patricia Alice Eisenach Ole Ammerpohl Hendrik Ungefroren Fred Fandrich Holger Kalthoff | 2007 | Hepatobiliary & Pancreatic Diseases International2007，6，1： | 69 |
| 2 | Orthotopic transplantation model of human gastrointestinal cancer and detection of micrometastases显示文摘AIM To establish a relevant animal model ofhuman gastrointestinal cancer, which can beused for repetitive investigations, so as toimprove our understanding and management ofcarcinogenesis and cancer metastasis.METHODS Intact tissues of human colorectaland pancreatic cancers were transplanted innude mice. The biological characteristics of theoriginal and the corresponding transplantedtumors were investigated by HE staining, PASstaining and immunostaining. The metastases inthe livers and lungs of nude mice wereinvestigated by immunostaining withbiotinylated mab KL-1 and by RT-PCR using CK20specific primers.RESULTS There were totally 9 of 16 surgicalspecimens growing in nude mice subcutaneouslyand/.or orthotopically (4 of 6 colorectal and 5 of10 pancreatic cancer). Tumor cell content of thespecimens and freezing of tissue specimens areimportant factors influencing the growth oftransplanted tumor. In the group of fresh tumortissues with greater than 50% tumor cellcontent, the success rate of the transplantationwas 100% (3 cases of pancreatic cancer and 3cases of colorectal cancer). The orthotopicallytransplanted tumors resemble the original tumormorphologically and biologically, including TAAexpression such as CEA byimmunohistochemistry, and CEA level in theserum of mice. Ki-67 labeling index and theexpression of TAA especially K-ras, 17-lA andRA-96, are associated with the potential of tumorgrowth in nude mice. Micrometastases in thelungs and livers of tumor bearing mice can bedetected by immunostaining with biotinylatedmab KL-1 and CK20-specific RT-PCR.CONCLUSION An orthotopic transplantationmodel for human colon and pancreatic cancer innude mice has been set up. We have alsoestablished sensitive detection methods withCK-immunohistochemistry and CK20-RT-PCR tostudy xenotransplanted human cancer and itsmetastatic cancer cells in the liver and lung ofnude mice. This study may be helpful inunderstanding the mechanism of cancermetastasis and in developing new diagnosticmethods and therapeutic strategies formetastases including micrometastases. | Jun Hui Cui~1 Uwe Krueger~2 Doris Henne-Bruns~2 Bemd Kremer~2 Holger Kalthoff~2 ~1Department of General Surgery,First Affiliated Hospital,College of Medicine,Zhejiang University,Hangzhou 310003,Zhejiang Province,China ~2Department of General Surgery,Christian-Albrechts-University,Kiel,GermanyDr.Jun Hui Cui graduated from Zhejiang Medical University in 1984,earned master degree in 1990,studied in the Surgical Department of Kiel University and worked in the Lab of Molecular Oncology of Kiel University from 1994-1997achieved M.D.from Kiel University.Germany,now associate professor of surgery,specialized in colorectal oncology.Adviser of graduated student for master degree,having 20 publications published in key Chinese or English journals. | 2001 | World Journal of Gastroenterology2001，7，3： | 19 |
| 3 | Interleukin-6: a villain in the drama of pancreatic cancer development and progression显示文摘BACKGROUND: Pancreatic ductal adenocarcinoma(PDAC)is a devastating malignancy with a poor prognosis and little treatment options. The development and progression of the disease is fostered by inflammatory cells and cytokines. One of these cytokines is interleukin-6(IL-6), which plays an important role in a wide range of biologic activities.DATA SOURCES: A systematic search of PubMed was performed to identify relevant studies using key words such as interleukin-6,inflammatory cytokines, inflammation and pancreatic cancer or PDAC. Articles related to IL-6 and pancreatic cancer were systematically reviewed.RESULTS: IL-6 is elevated in the serum of pancreatic cancer patients and correlates with cachexia, advanced tumor stage and poor survival. Its expression is enhanced by hypoxia and proteins involved in pancreatic cancer development like Kras,mesothelin or ZIP4. IL-6 in turn contributes to the generation of a pro-tumorigenic microenvironment and is probably involved in angiogenesis and metastasis. In experimental mouse models of PDAC, IL-6 was important for the development and progression of precursor lesions.CONCLUSION: IL-6 emerges as a key player in pancreatic cancer development and progression, and hence should be considered as a new therapeutic target. | Reinhild Holmer Freya A Goumas Georg H Waetzig Stefan Rose-John Holger Kalthoff | 2014 | Hepatobiliary & Pancreatic Diseases International2014，13，4： | 16 |
| 4 | The potential molecular mechanism of overexpression of uPA, IL-8, MMP-7 and MMP-9 induced by TRAIL in pancreatic cancer cell显示文摘BACKGROUND:TNF-related apoptosis-inducing ligand (TRAIL) is a death ligand of the TNF-superfamily that has been implicated in inducing apoptosis in some tumor cells. The purpose of this study was to find out if TRAIL could induce the expression of uPA, IL-8, MMP-7 and MMP-9. and to explore the corresponding potential signaling transduction pathway in pancreatic cancer cells. METHODS:Colo357wt, Panc89 and PancTuⅠ cell lines were stimulated by TRAIL (100 ng/ml). Crystal violet cell vitality assay was used to check the sensitivity to TRAIL-induced apoptosis. Real-time RT-PCR tested the expression of uPA, IL-8, MMP-7 and MMP-9. RESULTS:TRAIL can stimulate the expression of uPA, IL-8, MMP-7 and MMP-9 in pancreatic cancer cell lines, especially in Colo357wt. The members of caspases, MEK1/2, PKC, and NF-κB are involved in TRAIL-induced expression of uPA, IL-8, MMP-7 and MMP-9. Furthermore, caspases play a different role in Colo357wt, Panc89 and PancTuⅠ. CONCLUSIONS:TRAIL-treatment may result in the enhancement of invasion involving the signaling pathways of caspases, MEK1/2, PKC and NF-κB, in pancreatic cancer cells. It points to the necessity to carefully evaluate in vivo side effects of TRAIL. | Anna Trauzold Christian Rder Holger Kalthoff | 2008 | Hepatobiliary & Pancreatic Diseases International2008，7，2： | 6 |
| 5 | TRAIL-induced expression of uPA and IL-8 strongly enhanced by overexpression of TRAF2 and Bcl-xL in pancreatic ductal adenocarcinoma cells显示文摘BACKGROUND:The death ligand,tumor necrosis factor(TNF)related apoptosis-inducing ligand(TRAIL),induces apoptosis and non-apoptotic signaling in some tumor cells.The purpose of this study was to investigate the roles of the pro-apoptotic TRAIL receptors,TRAIL-R1 and TRAIL-R2,as well as Bcl-xL and TRAF2 in TRAIL-induced expression of the pro-inflammatory cytokine IL-8 and the invasion-promoting protein urokinase(uPA) in pancreatic ductal adenocarcinoma(PDAC) cells.METHODS:Colo357wt,Colo357/TRAF2,Colo357/Bcl-xL,Panc89 and PancTuI cells were stimulated with TRAIL and uPA and IL-8 expression was detected using real-time PCR.Antagonistic,receptor-specific antibodies were used to investigate the effects of TRAIL-R1 or TRAIL-R2 inhibition.RESULTS:Dose-dependent increases in uPA and IL-8 expression were detected following TRAIL stimulation in PDAC cells.These effects were inhibited when TRAIL-R1 but not TRAIL-R2 was blocked.Overexpression of TRAF2 or Bcl-xL strongly increased TRAIL-mediated upregulation of uPA and IL-8.CONCLUSIONS:In PDAC cells,TRAIL strongly induced uPA and IL-8 via TRAIL-R1.This response was further enhanced in cells overexpressing TRAF2 and Bcl-xL.Therefore,inhibition of the non-apoptotic 'side-effects' of TRAIL treatments by inactivation of TRAF2 and Bcl-xL might represent additional relevant strategies for the treatment of pancreatic cancer. | Dong-Hui Zhou Li-Na Yang Christian Rder Holger Kalthoff Anna Trauzold | 2013 | Hepatobiliary & Pancreatic Diseases International2013，12，1： | 5 |
| 6 | A comprehensive characterization of pancreatic ductal carcinoma cell lines: towards the establishment of an in vitro research platform显示文摘 | Bence Sipos Simone M?ser Holger Kalthoff Virag T?r?k Matthias L?hr Günter Kl?ppel | 2003 | Virchows Archiv2003，，5： | 4 |
| 7 | The diversity between pancreatic head and body/tail cancers:clinical parameters and in vitro models显示文摘BACKGROUND:Pancreatic ductal adenocarcinoma(PDAC) can be divided into head,body and tail cancers according to the anatomy.Distinctions in tissue composition,vascularization and innervations have been clearly identified between the head and body/tail of the pancreas both in embryological development and in histopathology.To understand the postulated genotype difference,we present comprehensive information on two PDAC cell lines as typical representatives originating from pancreatic head and body/tail cancers,respectively.DATA SOURCE:In the present review,we compare the difference between pancreatic head and body/tail cancers regarding clinical parameters and introducing an in vitro model.RESULTS:Increasing evidence has shown that tumors at different locations(head vs body/tail) display different clinical presentation(e.g.incidence,symptom),treatment efficiency(e.g.surgery,chemotherapy) and thus patient prognosis.However,the genetic or molecular diversity(e.g.mutations,microRNA) between the two subtypes of PDAC has not been elucidated so far.They present different chemo-and/or radio-resistance,extracellular matrix adhesion and invasiveness,as well as genetic profiles.CONCLUSION:Genetic and tumor biological diversity exists in PDAC according to the tumor localization. | Qi Ling Xiao Xu Shu-Sen Zheng Holger Kalthoff | 2013 | Hepatobiliary & Pancreatic Diseases International2013，12，5： | 3 |
| 8 | Topology impacts TRAIL therapy: Differences in primary cancer growth and liver metastasis between orthotopic and subcutaneous xenotransplants of pancreatic ductal adenocarcinoma cells显示文摘Background: To study novel treatment modalities for pancreatic ductal adenocarcinoma(PDAC), we need to transfer the knowledge from in vitro to in vivo. It is important to mirror the clinical characteristics of the typically local invasive growth of pancreatic cancer and the distant spread resulting in liver metastasis. Notably, for xenotransplant studies using human specimen, two models, i.e. subcutaneous(s.c.) and orthotopic(o.t.) transplantation are widely used. Methods: The subcutaneously and orthotopically inoculated Colo357 Bcl-x L cell-derived tumors were directly compared with and without TNF-related apoptosis inducing ligand(TRAIL) treatment. The size of primary tumors, number of liver metastasis and the histologic markers Ki67, M30, TNF-α and CD31 were assessed. Results: Upon TRAIL treatment, the primary tumors did not change their size, neither in the s.c. nor in the o.t. approaches. But when s.c. was compared to o.t., the size of the s.c. tumors was more than twofold bigger than that of the o.t. tumors( P<0.01). However, mice with orthotopically inoculated PDAC cells developed liver metastasis upon TRAIL treatment much more frequently( n=13/17) than mice with subcutaneously inoculated PDAC cells( n=1/11)( P<0.01). As a likely driving force for this increased metastasis, a higher TNF-α staining intensity in the o.t. tumors was observed by immunohistochemistry. Conclusions: These data from a direct side-by-side comparison underline the importance of the proper inoculation site of the PDAC cells. Local invasion and liver metastases are a hallmark of PDAC in the clinic;the o.t. model is clearly superior in reflecting this setting. Moreover, a serious side-effect of a possible new therapeutic compound became obvious only in the o.t. model. | Bastian Kettler Anna Trauzold Christian Röder Jan-Hendrik Egberts Holger Kalthoff | 2021 | Hepatobiliary & Pancreatic Diseases International2021，20，3： | 3 |
| 9 | 大肠癌HT-29细胞亚系与母系转移能力和相关因子的比较显示文摘目的 :探讨大肠癌细胞转移能力与肿瘤相关因素的关系。方法 :用结肠癌 HT- 2 9亚系 HT- 2 9c和 HT- 2 9d细胞在裸大鼠体内建立转移模型 ,比较其与母系的转移能力。用 ELISA法测定 3个大肠癌细胞系的尿激酶型纤溶酶原激活因子 (u PA)及纤溶酶原抑制剂 - 1(PAI- 1)含量 ;用免疫组化技术检测癌胚抗原和 3-磷酸肌醇激酶(PI3- Kinase)在体内外的表达 ;用流式细胞仪测定癌胚抗原表达。结果 :在裸鼠体内 HT- 2 9d细胞的肝转移率明显高于母系 HT- 2 9细胞 ,转移累及的脏器增多。在体外培养中 ,HT- 2 9d细胞的 u PA及 PAI- 1含量明显高于 HT- 2 9和 Wi Dr细胞。在裸鼠体内 ,HT- 2 9d细胞的 PI3- Kinase表达明显高于 HT- 2 9和 Wi Dr细胞。结论 :经裸鼠体内筛选的大肠癌 HT- 2 9细胞亚系表现出增强的肿瘤转移能力。UPA、PAI- 1的含量及 PI3- Kinase的表达与肿瘤转移能力有关。 | 王敏 VOGEL Ilka KALTHOFF Holger | 2002 | 浙江大学学报(医学版)2002，31，5： | 2 |
| 10 | Combined evaluation of a panel of protein and miRNA serum‐exosome biomarkers for pancreatic cancer diagnosis increases sensitivity and specificity显示文摘 | Bindhu Madhavan Shijing Yue Uwe Galli Sanyukta Rana Wolfgang Gross Miryam Müller Nathalia A. Giese Holger Kalthoff Thomas Becker Markus W Büchler Margot Z?ller | 2015 | Int. J. Cancer2015，，11： | 2 |
| 11 | Skin-derived aeroallergen-specific T-cell clones of Th2 phenotype in patients with atopic dermatitis显示文摘 | Bruijnzeel-Koomen CA Kalthoff FS | 1992 | J Allergy Clin Immunol1992，90，： | 1 |
| 12 | The different courses of early- and late-onset idiopathic and alcoholic chronic pancreatitis显示文摘 | Yamamoto H Kalthoff L | 1994 | Gastroenterology1994，107，： | 1 |
| 13 | Specific detection of carci-noembryonic antigen2 expressing tumor cells in bone marrow aspirates by polymerase chain reaction显示文摘 | Gerhard M Juhl H Kalthoff H | 1994 | J Clin Onco11994，12，4： | 1 |
| 14 | Apoptosis:targets in pancreatic cancer显示文摘 | Kalthoff H | 2003 | Mol Cancer2003，2，1： | 1 |
| 15 | Specific detection of carcinoembryonic antigenexpressing tumor cells in bone marrow aspirates by polymerase chain reaction 显示文摘 | Gerhard M Juhl H Kalthoff H | 1994 | J Clin Oncol1994，12，4： | 1 |
| 16 | Specific detection of carcinoembryonic antigen-expressing tumor cells in bone marrow aspirates by polymerase chain reaction显示文摘 | Juhi H Kalthoff H | 1994 | J Clin Oncol1994，12，4： | 1 |
| 17 | Specific detection of carcinoembryonic antigen- expressing tumor cells in bone marrow aspirates by polymerase chain reaction显示文摘 | Juhl H Kalthoff H | 1994 | J Clin Oncol1994，12，4： | 1 |
| 18 | Rapid Allelic Discrimination by TaqMan PCR for the Detection of the Gilbert’s Syndrome Marker UGT1A1*28显示文摘 | Ursula Ehmer Tim O. Lankisch Thomas J. Erichsen Sandra Kalthoff Nicole Freiberg Michael Wehmeier Michael P. Manns Christian P. Strassburg | 2008 | The Journal of Molecular Diagnostics2008，，6： | 1 |
| 19 | Highly Pathogenic Avian Influenza Subtype H5N1 escaping neutralization: more than HA variation显示文摘 | Htiper D Kalthoff D Hoffmann B | 2012 | J Virot2012，86，3： | 1 |
| 20 | Apoptosis: targets in pancreatic cancer显示文摘 | Westphal S Kalthoff H | 2003 | Mol Cancer2003，2，： | 1 |
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