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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Der Onkologe 5 (1999), S. 468-475 
    ISSN: 1433-0415
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Themen des internationalen Symposiums waren Epidemiologie, Biologie, Genetik und Pathologie der malignen Keimzelltumoren sowie die Behandlung von seminomatösen und nichtseminomatösen Keimzelltumoren in niedrigen und fortgeschrittenen Krankheitsstadien.
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Der Onkologe 5 (1999), S. 824-825 
    ISSN: 1433-0415
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Das metastasierte Nierenzellkarzinom gilt als weitgehend Chemotherapie-resistent. Die mediane Überlebenszeit bei patienten mit metastasierter Erkrankung liegt nur zwischen 2–12 Monaten. Mit Interferon- α2a (INF-α2a) als auch Interleukin-2 (IL-2), als Monosubstanz oder in Kombination, wurden Ansprechraten zwischen 5%–40% berichtet. Dies spricht für eine potentialle Aktivität dieser Substanzen in der Behandlung des metastasierten Nierenzellkarzinoms. Dennoch bleiben nach wie vor viele Fragen offen. In der aktuellen Arbeit aus Frankreich wird gezeigt, daß bei Krankheitsprogreß der Wechsel von einem Zytokin auf das andere nicht effektiv ist.
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Der Onkologe 6 (2000), S. 587-589 
    ISSN: 1433-0415
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Osseäre Metastasen stellen ein häufiges Problem für Patientinnen mit metastasiertem Mammakarzinom dar, das auf Grund der oftmals ausgeprägten Schmerzsymptomatik und der potentiellen Frakturgefahr die Lebensqualität dieser Patientinnen deutlich beeinträchtigt. Durch den Einsatz des Bisphosphonates Pamidronat konnte in zwei randomisierten Studien die Zahl der Komplikationen durch osseäre Filiae signifikant reduziert werden. Die Kosten einer Langzeittherapie mit Bisphosphonaten sind erheblich, so dass Fragen bezüglich der Kosteneffektivität dieser neuen, nicht lebensverlängernden Therapieoption nicht nur für die Behandlung von Malignomen sondern auch für die Behandlung von Nicht-Malignomen zunehmend wichtiger werden.
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  • 4
    ISSN: 1433-0563
    Keywords: Key words Testicular cancer • Late toxicity • Chemotherapy • Radiotherapy • Leukemia • Cisplatin • Neurotoxicity • Ototoxicity • Vascular toxicity • Renal toxicity ; Schlüsselwörter Hodentumoren • Spättoxizität • Chemotherapie • Strahlentherapie • Leukämie • Cisplatin • Neurotoxizität • Ototoxizität • Gefäßtoxizität • Nephrotoxizität
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Verbesserung der Überlebensraten bei der Behandlung von Patienten mit Hodentumoren wird von der Sorge um mögliche Langzeitnebenwirkungen der eingesetzten Therapieformen begleitet. Eine sekundäre Neoplasie ist eine gefürchtete Langzeitnebenwirkung, die die ansonsten exzellente Prognose kurativ behandelter Patienten erheblich beeinträchtigt. Patienten mit Hodentumoren haben ein etwa 2fach erhöhtes Risiko, 25–30 Jahre nach Diagnosestellung an einer malignen Zweitneoplasie erkrankt zu sein, das entspricht einer kumulativen Inzidenz von 16–23 %. Das Risiko für sekundäre solide Tumoren ist vorwiegend mit der Strahlentherapie verbunden und scheint mit zunehmender Beobachtungsdauer anzusteigen. Für folgende Tumoren ist ein statistisch signifikant erhöhtes relatives Risiko belegt: Magenkarzinome, Pankreaskarzinome, Blasenkarzinome, kolorektale Karzinome, Prostatakarzinome, Nierenzellkarzinome, Schilddrüsenkarzinome, Melanome, Sarkome und Non-Hodgkin-Lymphome. Nach alleiniger Chemotherapie ist das Risiko für sekundäre solide Tumoren nicht signifikant erhöht. Das Risiko für sekundäre Leukämien ist auch mit der Strahlentherapie aber vorwiegend mit dem Einsatz von Chemotherapie assoziiert. Neuere klinische Analysen der Daten von Patienten mit Hodentumoren haben nach Durchführung einer Chemotherapie ein 10- bis 300faches Risiko für eine Sekundärleukämie gezeigt. Das erhöhte Risiko bezieht sich nur auf die ersten zwei Jahrzehnte nach der Diagnosestellung, danach besteht kein Unterschied zur Normalbevölkerung. Etoposid scheint leukämogen zu sein, insbesondere nach kumulativen Dosen über 2 g/m2. Die genauen Zusammenhänge mit der Dosis, der Applikationsweise, den anderen Zytostatika und der Radiotherapie sind allerdings noch nicht vollständig geklärt. Auf dem Boden der derzeit verfügbaren Daten von Patienten mit Hodentumoren ist festzustellen, daß nach einer chemotherapeutischen Behandlung ein signifikant erhöhtes Risiko für eine Sekundärleukämie besteht. Bei gleichzeitiger Abwägung der hohen Heilungsrate ist das Risiko für den individuellen Patienten gering, aber nicht vollständig zu vernachlässigen. Das sekundäre Raynaud-Syndrom stellt die wesentliche vaskuläre Spättoxizität dar und betrifft etwa ein Drittel der Patienten nach kurativer Chemotherapie des Hodentumors. Bei einem fünftel der Patienten tritt eine arterielle Hypertonie auf. Es ist allerdings zu erwarten, daß die Häufigkeit dieser Nebenwirkungen durch Einsatz des PEB-Regimes (im Vergleich zum PVB-Regime) in Zukunft sinken werden. Schwere vaskuläre Komplikationen scheinen nur sehr selten aufzutreten. Weitere häufige Toxizitäten sind Ototoxizität und periphere Neuropathie. Einer der wichtigsten Risikofaktoren für das Auftreten dieser Toxizitäten ist die kumulativ applizierte Cisplatindosis. Bei mehr als der Hälfte der jungen Patientenpopulation ließen sich, nach erfolgreicher cisplatin-basierten Kombinationschemotherapie, persistierende Veränderungen der Gonadotropinspiegel und eine Leydigzellinsuffizienz nachweisen. Etwa ein viertel der Patienten wiesen erniedrigte Magnesium- oder Phosphatwerte auf, oder hatten einen erhöhten Kreatininwert im Serum. Diese Toxizitäten führen selten zu klinischen Symptomen. Zusammengefaßt läßt sich derzeit feststellen, daß 3-4 Serien einer Therapie mit Bleomycin, Cisplatin und Etoposid bei Patienten mit Hodentumoren nur selten zu symptomatischen Störungen der Organfunktionen und zu einer Beeinträchtigung der Lebensqualität führen. Die vorliegende Übersicht zeigt, daß das „Modell Hodentumor“ nicht nur die Therapieentwicklung, bei der es ja entscheidend zur Definition der Rolle von Cisplatin, Etoposid und in neuerer Zeit von Ifosfamid in der klinischen Onkologie beigetragen hat, sondern auch für die Untersuchung der Langzeitfolgen dieser eingesetzten Therapien von breiter klinischer Relevanz ist. Somit könnte der maligne Hodentumor nicht nur „a model for a curable neoplasm“ (LH. Einhorn) sondern auch „a model for the study of late sequelae of modern oncological therapies“ darstellen.
    Notes: Summary Improved survival in testicular cancer has been accompanied by concern about long-term side effects of chemotherapy or radiotherapy. Secondary malignant neoplasia represents one of the worst possible long-term complications, leading to death in patients cured of their primary malignancy. Patients with testicular germ cell tumors appear to have a 2-fold increased risk of developing any second cancer 25–30 years after the diagnosis, resulting in a cumulative incidence of 16–23 % at that time. The risk for secondary solid tumors can be mainly attributed to radiotherapy. There is strong evidence of an increasing risk for secondary solid tumors with time since treatment. Tumor-specific analysis of the risk for second cancers revealed statistically significant excesses for stomach, pancreas, bladder, rectum, prostate, and kidney cancer, as well as for cancer of the thyroid, melanoma, sarcomas, and non-Hodgkin's lymphoma. No significantly elevated risk for secondary solid tumors was observed after treatment with chemotherapy alone. The risk of secondary leukemia was associated with both radiotherapy and in particular with chemotherapy. In recent clinical surveys of patients with testicular cancer, estimates of the risk of leukemia after chemotherapy have ranged from 10- to 300-fold. An elevated risk was observed within the first two decades after diagnosis, later the risk was as expected in the normal population. Etoposide seems to be leukemogenic, especially at cumulative doses higher than 2 g/m2, although the effects of dose and schedule as well as the effects of other cytotoxic agents and radiotherapy remain to be finally clarified. Based on currently available data in patients with testicular cancer, it can be concluded that a significant elevated risk for the development of secondary leukemia exits after chemotherapy. However this risk does by far not outweigh the therapeutic benefit of etoposid-based therapy in patients with germ cell tumors. Secondary Raynaud's phenomenon is the main late vascular toxicity affecting about one third of patients after curative chemotherapy for testicular cancer. Hypertension will occur in one fifths of the patients. The incidence of vascular toxicity appears to be lower following PEB-therapy compared to PVB-therapy and major vascular events seem to be rare. Other frequent symptomatic toxicities are ototoxicity and peripheral neuropathy. A major risk factor for the development of toxicity is the cumulative dose of cisplatin given. Alterations of gonadotropin levels and Leydig cell insufficiency persist in more than half of young patients cured from testicular cancer by cisplatin-based combination chemotherapy. Approximately one fourth of patients have low serum magnesium or phosphat levels, or elevated creatinine levels. These toxicities seldomly result in clinical symptoms. We conclude that 3–4 courses with bleomycin, cisplatin and etoposide in testicular cancer patients will only rarely lead to symptomatic impairment of organ functions and a decrease of quality of life. Germ cell cancers have served as a valuable model for the development of new treatment strategies contributing largely to defining the role of cisplatinum, etoposide and recently ifosfamide in medical oncology. However, germ cell cancer may also be a useful model for investigating the long term side effects of the oncological therapies. Thus, germ cell cancer is not only a “model for a curable neoplasm” (L. H. Einhorn) but can also be seen as a “model for the study of late sequelae of modern oncological therapies”.
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  • 5
    ISSN: 1433-8726
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Paclitaxel, a natural anticancer drug, has gained widespread acceptance as an active broad-spectrum antitumor agent, including its use in urological malignancies, particularly urothelial tract cancer and testicular cancer. The mechanism of action, based on the premature stabilization of the microtubule assembly with disruption of the cytoskeletal framework, is completely different from those of DNA-damaging agents, e.g., cisplatin and ifosfamide. As a single agent, paclitaxel is one of the most active drugs in metastatic bladder cancer, with an overall response rate of 40–50% being obtained in previously untreated patients. These promising single-agent results have prompted the use of combination regimens including, in particular, cisplatin and paclitaxel. A high degree of activity for the cisplatin-paclitaxel combination as reflected by responses in 50–80% of patients, including a substantial number of complete responses (〉30%), has been identified. The role of other agents such as vinorelbine, methotrexate, 5-fluorouracil, or ifosfamide as additions to this two-drug combination currently remains open. The combination of paclitaxel plus ifosfamide or vinorelbine in the absence of a platinum derivative has yielded rather disappointing results. Of particular interest may be the combination of paclitaxel and carboplatin. Both drugs can be given to patients with impaired renal function. Overall response rates of 45–60% have been reported in phase II studies. The so-called platelet-sparing effect of paclitaxel given in combination with carboplatin has resulted in a surprisingly low frequency of myelotoxicity, particularly thrombocytopenia. The combination of paclitaxel with carboplatin is being compared in an ongoing trial against the current standard MVAC regimen (methotrexate/vinblastine/Adriamycin/cisplatin) in patients with metastatic disease. Furthermore, the activity of paclitaxel-based combinations is currently being explored in the neoadjuvant setting in phase II studies, and the potential for the combination with the other new promising agent – gemcitabine – will be evalutated in a phase I setting. In prostate cancer, estramustine phosphate is widely used as palliative treatment for patients with hormone-refractory disease. In vitro synergistic activity has been observed between estramustine and paclitaxel in prostate-cancer cell lines, although paclitaxel has not demonstrated single-agent activity in patients with hormone-refractory prostate cancer. In clinical trials the combination of the two agents was associated with increased gastrointestinal toxicity. The addition of etoposide as a third drug has yielded prostate-specific antigen (PSA)-response rates of 〉50%, but data on quality of life and survival time have not been reported for these combinations. A true clinical role for paclitaxel in prostate cancer has therefore not been established. Paclitaxel has finally demonstrated single-agent activity in relapsed and/or cisplatin-refractory testicular cancer in recent phase II trials, indicating different mechanisms of resistance to cisplatin and paclitaxel. These results have formed the rationale for the introduction of paclitaxel as part of combination chemotherapy regimens in patients with relapsed but chemosensitive testicular cancer. Preliminary results demonstrate that paclitaxel can be safely included into these conventional-dose combination regimens. When it is used prior to high-dose chemotherapy, sufficient numbers of peripheral blood stem cells (PBSCs) for high-dose therapy can be collected. The final role of paclitaxel in risk-adapted chemotherapeutic strategies in testicular cancer is not defined, but it appears that paclitaxel-based combinations can achieve a substantial response rate in patients with relapsed disease.
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  • 6
    ISSN: 1433-8726
    Keywords: Key words Testicular cancer ; Metastatic disease ; Conventional chemotherapy ; High dose chemotherapy ; New drugs ; Toxicity of chemotherapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The current aims of chemotherapy in metastatic testicular cancer are to reduce treatment-related toxicity in patients with “good-prognosis” metastatic disease without compromising the efficacy and to improve treatment results in “poor-prognosis” patients according to the IGCCCG classification by the use of more dose-intensive regimens. Three cycles of PEB chemotherapy, consisting of cisplatin, etoposide, and bleomycin, remain the standard treatment for good-prognosis patients despite a number of randomized studies trying to avoid the toxicity of bleomycin or to abandon cisplatin-associated side effects by substitution with the less toxic analogue carboplatin. In patients with intermediate- and poor-prognosis criteria, four cycles of PEB given at 3-weekly intervals are considered routine treatment. The role of high-dose chemotherapy with peripheral blood stem-cell (PBSC) transplantation (HDCT) is currently being investigated for patients who initially present with poor-prognosis metastatic disease and for patients with relapse after previous chemotherapy. Favorable results with long-term survival rates of approximately 75% have been achieved with up-front sequential HDCT in a phase I–II trial of the German Testicular Cancer Study Group (GTCSG) in such patients. A randomized phase III trial comparing conventional dose chemotherapy (4× PEB) with HDCT (2× PEB + 2× HD-CEC) was initiated as a United States intergroup trial in 1996. In patients with relapsed disease, conventional salvage chemotherapy results in only an approximately 20% long-term survival rate. Particularly, primary mediastinal disease and chemotherapy refractoriness represent variables associated with a very poor outcome. HDCT is also employed in relapsed patients to improve the long-term outcome. Long-term toxicity of treatment has become an important issue due to the large group of patients with metastatic disease now being cured with modern treatment strategies. The cumulative dose of cisplatin applied has been identified as a major risk factor for the development of many types of late toxicity. Despite the major advances made in the last 20 years, evaluation of the role of HDCT in both first-line and salvage treatment, investi- gation of new cytotoxic agents in refractory patients, and assessment of the long-term toxicities are major tasks that remain to be addressed in controlled clinical trials.
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  • 7
    ISSN: 1432-1335
    Keywords: Key words Secondary leukemia ; High-dose chemotherapy ; Autologous bone marrow transplantation ; Peripheral stem cell transplantation ; Etoposide ; Etoposide-related leukemia ; Secondary myelodysplastic syndrome ; Allogenic bone-marrow transplantation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Secondary acute myeloid leukemia (s-AML) and secondary myelodysplastic syndrome (s-MDS) probably represent the worst possible long-term complications of cancer therapy in patients originally cured of their primary malignancy. The frequency and type of s-AML and s-MDS are reviewed for patients treated with standard and/or high-dose chemotherapy for Hodgkin's disease, non-Hodgkin's lymphoma (NHL), and breast or testicular cancer. Patients treated for Hodgkin's disease, have a 20- to 40-fold increased risk of developing s-AML, this risk increasing with the number of mechlorethamine-containing cycles given as well as following splenectomy and in patients more than 40–50 years of age. Generally, patients with NHL, breast or testicular cancer experience a lower, 2- to 15-fold, risk of developing s-AML. Epipodophyllotoxins appear to be the most important factor for s-AML in patients treated for testicular cancer. Doses of 2g/m2 or more are associated with an increased risk of s-AML and, with these high doses, a cumulative incidence of 2%–3% at 5 years is observed. Adjuvant cyclophosphomide, methobrexate, 5-Fu therapy in breast cancer patients does not appear to increase risk significantly as compared to the general population. The extent of the leukemogenic potential of anthracyclines remains to be defined. NHL patients receiving mechlorethamine, prednimustine or long-term maintenance therapy are also at an increased risk of s-AML. A considerably increased risk of developing AML, with a cumulative incidence of approximately 9% at 5 years, has been observed following allogenic bone marrow transplantation (ABMT) or peripheral stem cell transplantation (PBSCT) in patients with NHL. It is likely that the increased risk of s-AML/s-MDS following high-dose chemotherapy with ABMT or PBSCT is related to prior treatment rather than to high-dose chemotherapy itself. However, this issue remains to be conclusively addressed. s-AML or s-MDS rarely develops after allogenic bone marrow transplantation. s-AML and s-MDS increasingly represent a problem in modern cancer therapy because of better treatment strategies, which result in improved cure rates. Patients who receive chemotherapy must be informed about the potential risk of developing s-AML or s-MDS. Future studies should include a follow-up long enough to record the occurrence of all s-AML/s-MDS and all potential influencing factors reliably. These data would enable risk factors to be defined and risk/benefit analyses to be carried out, allowing the correct assessment of current and future therapy strategies.
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  • 8
    ISSN: 1569-8041
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
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  • 9
    ISSN: 1569-8041
    Keywords: brain metastases ; germ-cell cancer ; high-dose chemotherapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Purpose:To examine the feasibility and efficacy of first-linehigh-dose chemotherapy (HD-CTX) in patients with advanced metastatic germ-celltumors (GCT) and brain metastases. Patients and methods:Twenty-two patients with brain metastasesat initial diagnosis were identified within a cohort of two hundred thirty-oneconsecutive patients with advanced metastatic disease, entered on a Germanmulticenter trial between January 1993 and July 1998. All patients receivedfirst-line HD-CTX with cisplatin–etoposide–ifosfamide (HD-VIP)followed by autologous stem-cell transplantation. Brain irradiation (BRT) with30–50 Gy ± 10 Gy boost was applied in patients with symptomaticCNS disease or as consolidation in case of residual CNS lesions after HD-CTX. Results:A median number of 4 HD-CTX cycles (range 2–5) wereapplied to the 22 patients. Ten patients received HD-CTX alone and twelvepatients were treated with HD-CTX plus BRT. Median duration of WHO grade 4granulocytopenia and thrombocytopenia was seven and five days after eachcycle, respectively. Non-hematologic toxicity consisted mainly ofmucositis/enteritis (WHO grade 3–4 32%). Two early deathsoccurred in twenty-two patients (one CNS-bleeding/one sepsis). Fourteen oftwenty patients achieved a CR/PRm− status. Twenty patients (91%)responded in the brain (55% CR/36% PR). Two-yearprogression-free and overall survival rates were 72% and 81%,respectively. These survival rates are substantially higher compared to theavailable data in the literature. Conclusions:High-dose chemotherapy with autologous stem-cellsupport ± BRT appears to be feasible without increased therapy-relatedmortality in patients with advanced metastatic GCT and brain metastases. Theresults achieved emphasize the high chemosensitivity of CNS metastases fromGCT and suggest a potential role for dose intensification. The dose of BRT inaddition to HD-CTX may be tailored to the presence of clinical symptoms andthe response of CNS metastases to chemotherapy.
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  • 10
    ISSN: 1569-8041
    Keywords: germ-cell cancer ; poor prognosis ; prognostic subgroups
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objectives:The IGCCCG classification has identified threeprognostic groups of patients with metastatic germ-cell tumors. `Poorprognosis' is based on primary tumor localization, the presence of visceralmetastases, and/or high tumor-marker levels. The overall survival rate ofthese patients is about 45%–55%. The present analysisattempts to identify subsets of patients with a more or less favorable outcomeamong the `poor-prognosis' group. Patients and methods:We retrospectively explored prognosticsubgroups in 332 patients with `IGCCCG' poor-risk GCT using theclassification-and-regression-tree model (CART). The following variables wereincluded: primary tumor localization, presence of visceral or lung metastases,presence of an abdominal tumor, number of metastatic sites, serum levels ofβ-HCG, AFP and LDH. All patients had been treated withcisplatin–etoposide-based chemotherapy within controlled clinical trialsbetween 1984 and 1997. Results:Patient characteristics: gonadal/retroperitoneal (G/R)primary tumor 260 patients (78%), mediastinal primary tumor 72 patients(22%), visceral metastases 205 patients (62%) including 33patients with CNS metastases, lung metastases 247 patients (74%),abdominal tumor 241 patients (72%), elevated AFP, β-HCG or LDHlevels 235 (71%), 253 (76%) and 275 (83%) of patients,respectively. Patients with primary mediastinal disease plus lung metastasesexhibited the worst two-year PFS (28%), whereas patients with a primaryG/R tumor and without visceral metastases showed the highest chance oftwo-year PFS (75%). The latter group of patients without visceralmetastases and with a primary G/R tumor also had the most favourable two-yearOS (84%). In contrast, patients with a primary mediastinal tumor andvisceral metastases displayed the worst two-year OS (49%). Conclusions:Different prognostic subsets of patients can beidentified among the group of `poor-prognosis' GCT patients. The CART analysismodel results in a hierarchy of prognostic factors which may allow to moreprecisely estimate the individual patient's prognosis. Identifying subgroupsof `very poor-prognosis' among `poor-prognosis' patients may allow to test fornew treatment strategies in selected subgroups.
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