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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 | Expression of L amino acid transport system 1 and analysis of iodine-123-methyltyrosine tumor uptake in a pancreatic xenotransplantation model using fused high-resolution-micro-SPECT-MRI显示文摘BACKGROUND:The specificity in discriminating pancreatitis is limited in the positron emission tomography(PET)using Fluorine-18-fluorodeoxyglucose.Furthermore,PET is not widely available compared to the single photon emission computed tomography(SPECT).Since amino acids play a minor role in metabolism of inflammatory cells,the potential of the SPECT tracer,3-[ 123 I]iodo-L-α-methyltyrosine(123I-IMT),for detecting pancreatic cancer was examined in xenotransplantation models of human pancreatic carcinoma in mice. METHODS: 123 I-IMT was injected to eight mice inoculated with subcutaneous or orthotopic pancreatic tumors.Fused high-resolution-micro-SPECT(Hi-SPECT)and magnetic resonance imaging were performed.The gene expression level of L amino acid transport-system 1(LAT1)was analyzed and correlated with tumor uptake of 123 I-IMT. RESULTS:A high uptake of 123 I-IMT was detected in all tumor-bearing mice.The median tumor-to-background ratio (T/B)was 12.1(2.0-13.2)for orthotopic and 8.4(1.8-11.1)for subcutaneous xenotransplantation,respectively.Accordingly, the LAT1 expression in transplanted Colo357 cells was increased compared to non-malignant controls.CONCLUSIONS:Our mouse model could show a high 123 I-IMT uptake in pancreatic cancer.Fused MRI scans facilitate precise evaluation of uptake in the specific regions of interest.Further studies are required to confirm these findings in tumors derived from other human pancreatic cancer cells.Since amino acids play a minor role in the metabolism of inflammatory cells,the potential for application of 123 I-IMT to distinguish pancreatic tumor from inflammatory pancreatitis warrants further investigation. | Corinna von Forstner Maaz Zuhayra Ole Ammerpohl Sanjay Tiwari Olav Jansen Holger Kalthoff Eberhard Henze Jan-Hendrik Egberts | 2011 | Hepatobiliary & Pancreatic Diseases International2011，10，1： | 1 |
| 12 | Expression of Lymphangiogenic Factors and Evidence of Intratumoral Lymphangiogenesis in Pancreatic Endocrine Tumors显示文摘 | Bence Sipos Wolfram Klapper Marie-Luise Kruse Holger Kalthoff Dontscho Kerjaschki Günter Kl?ppel | 2004 | The American Journal of Pathology2004，，4： | 1 |
| 13 | Genetic profile of 22 pancreatic carcinoma cell lines显示文摘 | Patrick S. Moore Bence Sipos Simonetta Orlandini Claudio Sorio Francisco X. Real Nicholas R. Lemoine Thomas Gress Claudio Bassi Günter Kl?ppel Holger Kalthoff Hendrik Ungefroren Matthias L?hr Aldo Scarpa | 2001 | Virchows Archiv2001，，6： | 1 |
| 14 | Disseminated tumour cells显示文摘 | Ilka Vogel Holger Kalthoff | 2001 | Virchows Archiv2001，，2： | 1 |
| 15 | 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： | 1 |
| 16 | Gene Expression Patterns and Tumor Uptake of ^sup 18^F-FDG, ^sup 18^F-FLT, and ^sup 18^F-FEC in PET/MRI of an Orthotopic Mouse Xenotransplantation Model of Pancreatic Cancer显示文摘 | von Forstner Corinna Egberts Jan-Hendrik Ammerpohl Ole Niedzielska Dagmara Buchert Ralph Mikecz Pal Schumacher Udo Peldschus Kersten Adam Gerhard Pilarsky Christian Grutzmann Robert Kalthoff Holger Henze Eberhard Brenner Winfried | 2008 | The Journal of Nuclear Medicine2008，，8： | 1 |
| 17 | 绿色荧光蛋白在人大肠癌HT-29c细胞的表达显示文摘目的 观察增强型绿色荧光蛋白 (enhancedgreenfluorescentprotein ,EGFP)在人大肠癌细胞的表达情况。 方法 构建逆转录病毒载体质粒prkatEGFP/neo ,用磷酸钙沉淀法转导 2 93T细胞 ,4 8h获得高滴度病毒颗粒上清液并转染人大肠癌HT 2 9c细胞。荧光显微镜及流式细胞仪观察转染的EGFP基因在人大肠癌HT 2 9c细胞体内外的表达。 结果 携带EGFP的逆转录病毒载体能有效地转染人大肠癌细胞 ,HT 2 9c细胞能稳定、高效和持久地表达EGFP ,与未转染细胞比较 ,他们的生物学特性未改变 (F =0 6 2 ,P >0 0 5 )。在裸大鼠皮下肿瘤中 ,EGFP也能稳定、高效的表达。 结论 外源性EGFP能在人大肠癌HT 2 9c细胞内进行有效的复制、转录和翻译 ,在体内外可持续、稳定、高效的表达。它能作为一种新的实验方法应用于肿瘤细胞生长。 | 王敏 Boenicke Lars Howard D.Bradley Vogel Ilka Kalthoff Holger | 2002 | 中华外科杂志2002，40，5： | 1 |
| 18 | Efficient dose-dependent and time-dependent protein transduction of pancreatic carcinoma cells in vitro and in vivo using purified VP22-EGFP fusion protein显示文摘 | Lars Boenicke Kang Chu Regina Pauls Claudia Tams Marie-Luise Kruse Roland Kurdow Bodo Schniewind Arnd B?hle Bernd Kremer Holger Kalthoff | 2003 | Journal of Molecular Medicine2003，，3： | 1 |
| 19 | Isolated Tumor Cells Are Frequently Detectable in the Peritoneal Cavity of Gastric and Colorectal Cancer Patients and Serve as a New Prognostic Marker显示文摘 | Astrid Schott Ilka Vogel Uwe Krueger Holger Kalthoff Hans-Wilhelm Schreiber Wolff Schmiegel Doris Henne-Bruns Bernd Kremer Hartmut Juhl | 1998 | Annals of Surgery1998，，3： | 1 |
| 20 | How open is the therapeutic horizon for pancreatic cancer patients?显示文摘In the nineties of the last century,it was typical for an article about pancreatic cancer to start with an introductory remark,that this malignancy is a very desperate one and that surgery is the only curative option.But it was also obvious that surgery was not really curative and most importantly,not feasible in the majority of cases.In the last two decades,we observed a dramatic increase in research on pancreatic cancer(e.g.more than 65000 articles mentioning pancreatic cancer in PubMed only in the last decade),and clearly,there is scientific progress. | Holger Kalthoff | 2022 | Hepatobiliary & Pancreatic Diseases International2022，21，1： | 0 |
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