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  • 1
    Electronic Resource
    Electronic Resource
    Analysis of the MHC Class I Antigen Presentation Machinery in Human Embryonal Carcinomas: Evidence for Deficiencies in TAP, LMP and MHC Class I Expression and their Upregulation by IFN-γ (1997)
    Oxford, UK : Blackwell Science Ltd
    Scandinavian journal of immunology 46 (1997), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The expression of the major histocompatibility complex (MHC) class I antigens is suppressed in early post-implantation embryonic cells as well as in embryonal carcinoma (EC) cells, but could be upregulated by treatment with interferon (IFN)-γ or retinoic acid. In a number of human and murine tumours, defects in the expression of the different components of the MHC class I antigen processing machinery, such as the proteasomal subunits LMP-2 and LMP-7 and the peptide transporters TAP-1 and TAP-2, account for impaired MHC class I surface expression. Here, we analysed the constitutive and IFN-γ regulated mRNA and protein expression of the LMP, TAP and MHC class I molecules in the human EC line 577LM. In comparison to lymphoblastoid control cells, poor constitutive mRNA and protein expression of LMP-7, TAP-1, HLA class I, and β2-microglobulin, but not of TAP-2 and LMP-2, was detected in 577LM cells. The lack of MHC class I surface expression on 577LM cells could not be enhanced either by culturing cells at low temperature or by their incubation with exogenous MHC class I specific binding peptides: thus, the defective MHC class I surface expression was not only caused by impaired generation and processing of antigenic peptides. IFN-γ treatment of 577LM resulted in a significant increase of MHC class I surface expression which was preceded by an upregulation of TAP, LMP and MHC class I transcripts as well as of TAP-1 and TAP-2, but not of LMP-2 and LMP-7, protein expression. These data suggest that human EC cell lines show a stable expression of a MHC class I low/deficient phenotype. The deficiencies associated with this phenotype involve different levels of the MHC class I restricted antigen presentation machinery and could be modified by treatment with IFN-γ.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-3083.1997.d01-176.x
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  • 2
    Electronic Resource
    Electronic Resource
    Modulation of 5-fluorouracil with methotrexate and low-dose N-(phosphon-acetyl)-L-aspartate (PALA) is inactive in advanced pancreatic carcinoma (1997)
    Springer
    Annals of oncology 8 (1997), S. 917-918 
    Details
    ISSN: 1569-8041
    Keywords: biochemical modulation ; 5-fluorouracil ; methotrexate ; pancreatic cancer ; phosphonacetyl-L-aspartate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Purpose: To evaluate the effect of biochemical modulation by PALA and methotrexate on the therapeutic activity of 5-fluorouracil (5-FU) in patients with advanced pancreatic adenocarcinoma. Patients and methods: The treatment protocol consisted of phosphonacetyl-L-aspartate (PALA) 250 mg/m2 i.v. 15-minute infusion followed by methotrexate 200 mg/m2 i.v. 30-minute infusion on day 1 and 5-FU 600 mg/m2 i.v. push on day 2. Folinic acid was given at 15 mg/m2 p.o. every six hours for eight doses, starting 24 hours after methotrexate infusion. Cycles were repeated every two weeks. Results: Thirty patients with advanced chemotherapy-naive pancreatic cancer were included; 26 had measurable disease. Median age 56 years (27–72); median PS 1 (0–2). One PR (3.9%) was achieved; nine patients had stable disease. Median time to progression was 91 days. Median survival was 177 days and one year survival was 13.3% (4 of 30 patients). Treatment was well tolerated; diarrhea WHO grade 2 or 3 occurred in six patients; stomatitis WHO grade 2 and 3 in nine patients. Conclusions: Modulation of 5-FU by PALA and MTX given in this dose and schedule appears to be ineffective in patients with advanced pancreatic adenocarcinoma.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1008298102758
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  • 3
    Electronic Resource
    Electronic Resource
    Hematopoietic growth factors and treatment of testicular cancer: Biological interactions, routine use and dose-intensive chemotherapy (1996)
    Springer
    Annals of hematology 72 (1996), S. 1-9 
    Details
    ISSN: 1432-0584
    Keywords: Testicular cancer ; Germ cell tumors ; Hematopoietic growth factors ; G-CSF ; GM-CSF Stem cell factor (SCF) ; Peripheral blood stem cells (PBSC) ; Dose-intensive chemotherapy Neutropenia ; Infection ; Human testicular cancer cell lines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract With the use of aggressivecis-platinum-based combination chemotherapy the majority of patients with metastatic testicular cancer will be cured. Hematopoietic growth factors (HGFs), particularly G-and GM-CSF, have been investigated for the treatment of testicular cancer in order to (a) ameliorate chemotherapy-induced myelosuppression, (b) increase the dose intensity of treatment, or (c) generate peripheral blood stem cells (PBSC) as hematopoietic support for mega-dose chemotherapy. Results from in vitro and animal models have excluded a significant influence of both factors, G-CSF and GM-CSF, on tumor growth and response to cytotoxic treatment. For the group of ‘good-risk’ patients with metastatic testicular cancer, 85–90% of whom will reach long-term survival, the incidence of granulocytopenic infections after standard chemotherapy regimens appears to be lower than 20%. The prophylactic use of HGFs for these patients is not routinely recommended but may be considered in case of an increased risk for infections. For ‘risk’ patients, who will achieve a 50% survival following standard chemotherapy, different attempts of treatment intensification have been investigated. The use of aggressive multidrug regimens is associated with granulocytopenic infections in 20–70% of patients. A randomized trial has demonstrated that the prophylactic use of G-CSF significantly reduces granulocytopenia, the number of septic infections, and the infection-related death rate. For “poor-risk” patients the prophylactic use of HGFs, particularly G-CSF due to its favorable side effect profile, is recommended. The availability of G- and GM-CSF has made it possible to develop dose-intensified chemotherapy regimens. Demonstrated particularly for GM-CSF, a 1.5-fold dose increase can be achieved by the use of a myeloid growth factor alone, and thrombocytopenia and other organ toxicity will become dose limiting. Mobilization of PBSC, either after stimulation with HGFs alone or with HGFs, following chemotherapy has been successfully used in patients with testicular cancer. For the treatment of patients with relapsed disease PBSC support followed by HGFs has allowed the use of mega-dose therapy in multiple phase-II studies. This has prompted the investigation of high-dose therapy as first-line treatment for 'poor-risk' patients. In these patients sequential high-dose treatment withcis-platinum, etoposide, and ifosfamide for four consecutive cycles, each supported by G- or GM-CSF and PBSC, is currently being investigated by the German Testicular Cancer Study Group. HGFs have substantially reduced treatment-associated morbidity and mortality in patients receiving chemotherapy for testicular cancer. They make it possible for the first time to clinically explore the true value of dose-intensified chemotherapy regimens in testis cancer, serving as a model of a highly chemotherapy sensitive disease. Enrollment of patients in prospective clinical trials evaluating the role of high-dose therapy is strongly recommended.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00663009
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  • 4
    Electronic Resource
    Electronic Resource
    The role of insulin-like growth factor I and its receptor in cell growth, transformation, apoptosis, and chemoresistance in solid tumors (1999)
    Springer
    Journal of cancer research and clinical oncology 125 (1999), S. 166-173 
    Details
    ISSN: 1432-1335
    Keywords: Key wordsIGF ; Apoptosis ; Transformation ; Chemosensitivity ; Signaling
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Insulin-like growth factor I (IGF-I) exerts pleiotropic effects on mammalian cells via stimulation of its receptor (IGF-IR), a receptor tyrosine kinase. In vivo, IGF-I acts both as a local tissue growth factor and as a circulating hormone. In oncological research, IGF-I has received increased attention as the activated IGF-I/IGF-IR system displays mitogeneic, transforming, and anti-apoptotic properties in various cell types by stimulating distinct intracellular signaling pathways. Recent data suggest that the anti-apoptotic effect of IGF-I may mediate decreased sensitivity to chemotherapeutic drugs in vitro and in vivo. Thus, targeting the IGF-I/IGF-IR system could serve as an approach to overcome clinical drug resistance in certain tumors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004320050259
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  • 5
    Electronic Resource
    Electronic Resource
    Etoposid (VP 16-213) (1981)
    Springer
    Journal of molecular medicine 59 (1981), S. 1177-1188 
    Details
    ISSN: 1432-1440
    Keywords: Etoposide ; Mechanisms of action ; Pharmacoclinetics ; Toxicity ; Clinical activity ; Cancer ; Etoposid ; Wirkungsmechanismus ; Pharmakokinetik ; Toxizität ; Klinische Aktivität ; Krebs
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Etoposid ist ein halbsynthetisches Podophyllotoxinderivat mit einem breiten zytostatischen Wirkungsspektrum und relativ günstigem therapeutischen Index. Tierexperimentell zeigt diese Substanz einen Synergismus mitCis-Platin, Cyclophosphamid, BCNU und Cytosinarabinosid. Die Wirkmechanismen sind Hemmung des Nukleosidtransports in die Zelle, Störung der DNA- und RNA-Synthese, Einzelstrangbrüche, Störung der Proteinsynthese und Hemmung mikrotubulärer Proteine. In niedriger Konzentration wirkt Etoposid zellzyklusphasenspezifisch mit Akkumulation in der G2-Phase, in höherer Konzentration auch phasenunspezifisch. Am geeignetsten unter dem Aspekt von Wirkung und Toxizität ist die intravenöse oder orale Applikation in fraktionierten Dosen von 80–120 mg/m2 an 3–5 aufeinanderfolgenden Tagen und Wiederholung nach 21 [14–28] Tagen. Neben der dosislimitierenden Knochenmarkstoxizität sind weitere Nebenwirkungen Übelkeit, Erbrechen, Fieber, Kopfschmerz, Hypotension, Phlebitis, Mukositis, Neuropathie, Kardiotoxizität, Alopezie. Etoposid gehört zu den wirksamsten Substanzen beim kleinzelligen Bronchuskarzinom mit einer Ansprechrate von 37% (10% CR) und hat eine hohe Aktivität beim NHL (36%), Hodenkarzinom (37%), Chorion Karzinom der Frau (35%), beim Neuroblastom (29%) und bei der AMML (35%). Die Aktivität von Etoposid in Kombination mit anderen aktiven Substanzen bei diesen Tumoren wird in zur Zeit laufenden Studien untersucht; beim kleinzelligen Bronchuskarzinom sowie beim testikulären Karzinom und Non-Hodgkin-Lymphom wird Etoposid in Zukunft zu den Substanzen der ersten Wahl gehören können.
    Notes: Summary Etoposide is a semisynthetic podophyllotoxin derivative with a broad spectrum of antitumor activity and a relatively high therapeutic index. The synergism in animal withcis-platinum, cyclophosphamide, BCNU, and cytosinarabinoside is interesting for combination regimen. Mechanisms of action are inhibition of nucleoside transfer and of DNA and RNA synthesis, single stranded breaks, inhibition of protein synthesis and of microtubular assembly. While in lower concentrations etoposide is acting cell-cycle-dependent with accumulation of cells in the G2-phase it has, in high concentrations, also a cellcycle-phase-unspecific lethal effect. Most suitable is the oral and i.v. application of etoposide in fractionated doses of 80–120 mg/m2 on 3–5 consecutive days and repetition after 21 [14–28] days. Side effects are dose-limiting bone marrow toxicity, nausea, vomiting, fever, hypotension, phlebitis, mucositis, neuropathy, cardiotoxicity, alopecia. Etoposide is one of the most active single agents in small-cell bronchus carcinoma with a remission rate of 37% (10% CR), and is very active in NHL (36%), testicular carcinoma (37%), AMML (35%), choriocarcinoma (35%), and neuroblastoma (29%). The role of etoposide in combination with other active drugs in these tumors is currently investigated in bronchus and testicular carcinoma and NHL, where etoposide will belong to the drugs of the first choice in the future.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01721212
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  • 6
    Electronic Resource
    Electronic Resource
    Prognosefaktoren bei meta-stasierten seminomatösen und nichtseminomatösen Hodentumoren (1998)
    Springer
    Der Onkologe 4 (1998), S. 518-523 
    Details
    ISSN: 1433-0415
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Die differenzierte und stadienorientierte Therapie von seminomatösen und nichtseminomatösen Hodentumoren erfordert in zunehmendem Umfang die genaue Kenntnis von Prognosefaktoren, welche eine Abschätzung der individuellen Therapieaussichten eines Patienten erlauben. Nach dem derzeitigen Kenntnisstand stehen für einige Tumorstadien gleichwertige Therapieoptionen alternativ zur Verfügung, sodaß darüber hinaus individuelle Risiken und Präferenzen berücksichtigt werden müssen [2, 7]. Um Fehleinschätzungen zu minimieren, können jedoch für das Konzept einer risikoadaptierten Therapie nur Prognosefaktoren berücksichtigt werden, die an großen Patientenkollektiven retrospektiv gewonnen und idealerweise prospektiv validiert wurden. Nur wenige Prognosefaktoren erfüllen diese Voraussetzung. In der klinischen Praxis kommen Prognosefaktoren für die Wahl der Therapiestrategie vor allem in den niedrigen, auf den Hoden oder die paraaortalen Lymphknoten begrenzten Tumorstadien des Seminoms und des Nichtseminoms zum Einsatz, sowie bei den ausgedehnt metastasierten Tumorstadien.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007610050233
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  • 7
    Electronic Resource
    Electronic Resource
    Salvagetherapie rezidivierter und refraktärer Hodentumoren (1998)
    Springer
    Der Onkologe 4 (1998), S. 541-546 
    Details
    ISSN: 1433-0415
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Die Therapie der Patienten, die auf eine eine cisplatinhaltige Primärtherapie nicht oder nur inkomplett ansprechen oder bei denen ein Rezidiv auftritt, besteht in der „Salvage”- Therapie, unabhängig davon, ob diese bei primär refraktären Patienten oder bei Patienten im ersten oder nachfolgenden Rezidiv eingesetzt wird. Heilungen sind selbst bei dieser prognostisch ungünstigeren Patientengruppe möglich, erfordern jedoch den vollen Einsatz interdisziplinärer onkologischer Maßnahmen. In den vergangenen Jahren wurden große Anstrengungen unternommen, die Ergebnisse der Salvagechemotherapie zu verbessern und neben der Einführung neuerer Substanzen wird zunehmend die Hochdosischemotherapie untersucht.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007610050236
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  • 8
    Electronic Resource
    Electronic Resource
    Therapie des fortgeschrittenen nichtseminomatösen Keimzelltumors (1998)
    Springer
    Der Onkologe 4 (1998), S. 532-540 
    Details
    ISSN: 1433-0415
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Metastasierte Keimzelltumoren des Hodens sind mit der Entwicklung cisplatinbasierter Kombinationschemotherapien heute bei 70–80% aller Patienten heilbar geworden [3, 12]. Es besteht ein genereller Konsens, daß bei allen nicht-seminomatösen Keimzelltumoren des Hodens mit abdomineller Lymphknotenmetastasierung größer 5 cm oder Metastasen in anderen Lokalisationen eine primäre Chemotherapie nach der hohen inguinalen Orchiektomie das Standardvorgehen darstellt [1]. Der therapeutische Erfolg wird dabei anhand der häufig im Serum erhöht meßbaren Tumormarker Alpha-Fetoprotein (AFP) und Beta-Humanes-Chorion- Gonadotropin (β-HCG) sowie anhand des radiologischen Verlaufs beurteilt. Bei Ansprechen auf die durchgeführte Kombinationschemotherapie und Markernormalisierung, aber residuellen Tumorherden, schließt sich in der Regel eine chirurgische Entfernung dieser Residuen an [3, 8, 9, 16].
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007610050235
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  • 9
    Electronic Resource
    Electronic Resource
    Interdisziplinäre Konsensuskonferenz zur „Diagnostik und Therapie von Hodentumoren“ (1997)
    Springer
    Der Urologe 36 (1997), S. 362-368 
    Details
    ISSN: 1433-0563
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001200050113
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  • 10
    Electronic Resource
    Electronic Resource
    Hematopoietic growth factors and treatment of testicular cancer: Biological interactions, routine use and dose-intensive chemotherapy (1996)
    Springer
    Annals of hematology 72 (1996), S. 1-9 
    Details
    ISSN: 1432-0584
    Keywords: Key words Testicular cancer ; Germ cell tumors ; Hematopoietic growth factors ; G-CSF ; GM-CSF ; Stem cell factor (SCF) ; Peripheral blood stem cells ; (PBSC) ; Dose-intensive chemotherapy ; Neutropenia ; Infection ; Human testicular cancer ; cell lines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  With the use of aggressive cis–platinum-based combination chemotherapy the majority of patients with metastatic testicular cancer will be cured. Hematopoietic growth factors (HGFs), particularly G- and GM-CSF, have been investigated for the treatment of testicular cancer in order to (a) ameliorate chemotherapy-induced myelosuppression, (b) increase the dose intensity of treatment, or (c) generate peripheral blood stem cells (PBSC) as hematopoietic support for mega-dose chemotherapy. Results from in vitro and animal models have excluded a significant influence of both factors, G-CSF and GM-CSF, on tumor growth and response to cytotoxic treatment. For the group of 'good-risk' patients with metastatic testicular cancer, 85–90% of whom will reach long-term survival, the incidence of granulocytopenic infections after standard chemotherapy regimens appears to be lower than 20%. The prophylactic use of HGFs for these patients is not routinely recommended but may be considered in case of an increased risk for infections. For 'poor risk' patients, who will achieve a 50% survival following standard chemotherapy, different attempts of treatment intensification have been investigated. The use of aggressive multidrug regimens is associated with granulocytopenic infections in 20–70% of patients. A randomized trial has demonstrated that the prophylactic use of G-CSF significantly reduces granulocytopenia, the number of septic infections, and the infection-related death rate. For 'poor-risk' patients the prophylactic use of HGFs, particularly G-CSF due to its favorable side effect profile, is recommended. The availability of G- and GM-CSF has made it possible to develop dose-intensified chemotherapy regimens. Demonstrated particularly for GM-CSF, a 1.5-fold dose increase can be achieved by the use of a myeloid growth factor alone, and thrombocytopenia and other organ toxicity will become dose limiting. Mobilization of PBSC, either after stimulation with HGFs alone or with HGFs, following chemotherapy has been successfully used in patients with testicular cancer. For the treatment of patients with relapsed disease PBSC support followed by HGFs has allowed the use of mega-dose therapy in multiple phase-II studies. This has prompted the investigation of high-dose therapy as first-line treatment for 'poor-risk' patients. In these patients sequential high-dose treatment with cis–platinum, etoposide, and ifosfamide for four consecutive cycles, each supported by G- or GM-CSF and PBSC, is currently being investigated by the German Testicular Cancer Study Group. HGFs have substantially reduced treatment-associated morbidity and mortality in patients receiving chemotherapy for testicular cancer. They make it possible for the first time to clinically explore the true value of dose-intensified chemotherapy regimens in testis cancer, serving as a model of a highly chemotherapy sensitive disease. Enrollment of patients in prospective clinical trials evaluating the role of high-dose therapy is strongly recommended.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00663009
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