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Libri sul tema "Cyclophosphamide"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 9 giugno 2025

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1

Boche, Gernot. Cyclopropane derived reactive intermediates. Chichester: Wiley, 1990.

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2

R, Nowrousian M., ed. Ifosfamide in cancer therapy: A comparison with cyclophosphamide. Jena: Universitätsverlag, 1993.

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3

Asli-Yalfani, Esmael. Cellular and molecular studies of the immunopharmacology of cyclophosphamide. Manchester: University of Manchester, 1995.

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4

Azria, M. (Moïse). Calcitonins: Physiological and pharmacological aspects. Berlin: Springer Verlag, 1989.

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5

Lewtas, Joellen. Final report on the evaluation of four toxic chemicals in an In Vivo/In Vitro toxicological screen--acrylamide, chlordecone, cyclophosphamide, and diethylstilbestrol. Research Triangle Park, N.C: U.S. Environmental Protection Agency, Health Effects Research Laboratory, 1986.

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6

Lundbeck, Finn. The normal mouse urinary bladder reservoir function evaluated by repeated cystometries: Early and late changes after irradiation alone and irradiation combined with cis-diaminedichloroplatinum (II) or cyclophosphamide. Oslo: Distributed by Scandinavian University Press, 1994.

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7

Gutenberg-Universität, Johannes, ed. Untersuchungen zur posttranslationalen Modifikation von Cytochrom P450 2B1 und deren Konsequenzen für die Aktivierung von Cyclophosphamid. [s.l.]: [s.n.], 1998.

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8

Renk-Gees, Annemarie. Untersuchungen über den Gehalt an Adeninribonukleotiden und die Zellzahl von Mäuseembryonen in der Präimplantationsphase nach Behandlung mit Cyclophosphamid (Endoxan R). [S.l.]: [s.n.], 1986.

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9

Karakas, Tunca. Therapie hochmaligner Non-Hodgkin-Lymphome: Eine Phase-II-Studie mit Vincristin, Adriamycin, Cyclophosphamid, Prednison und Etoposid (VACPE) sowie randomisiert rhGM-CSF. [s.l.]: [s.n.], 1995.

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10

Blokdijk, G. J. Cyclophosphamide; The Ultimate Step-By-Step Guide. CreateSpace Independent Publishing Platform, 2018.

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11

Cyclophosphamide: Clinical Pharmacology, Uses and Potential Adverse Effects. Nova Science Publishers, Incorporated, 2015.

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12

Publications, ICON Health. Cyclophosphamide - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

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13

Progress in Clinical Biochemistry and Medicine. Springer Verlag, 1989.

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14

Chen, Chu-liang. Identification of an inguinal adipocyte-specific protein using monoclonal antibody selected by cyclophosphamide. 1992.

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15

Foster, Helen, and Paul A. Brogan, eds. British Society of Paediatric and Adolescent Rheumatology clinical guidelines and protocols. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199592630.003.0009.

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BSPAR Standards of Care for children and young people with JIA 410BSPAR drug information leaflets for parents and families 412BSPAR guidelines for treatments used in paediatric rheumatology 415Non-steroidal anti-inflammatory drugs (NSAIDs) 416Disease-modifying anti-rheumatic drugs (DMARDs) 418Azathioprine 423Ciclosporin 425Intravenous cyclophosphamide ...
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16

Jayne, David. Treatment of ANCA-associated vasculitis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0132.

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The goals of treatment in anti-neutrophil cytoplasm antibody (ANCA) vasculitis are to stop vasculitic activity, to prevent vasculitis returning, and to address longer-term comorbidities caused by tissue damage, drug toxicity, and increased cardiovascular and malignancy risk. Cyclophosphamide and high-dose glucocorticoids remain the standard induction therapy with alternative immunosuppressives, such as methotrexate or azathioprine, to prevent relapse. Refractory disease resulting from a failure of induction or remission maintenance therapy requires alternative agents and rituximab has been particularly effective. Replacement of cyclophosphamide by rituximab for remission induction is supported by recent evidence. Additional therapy with intravenous methylprednisolone and plasma exchange is employed in severe presentations with failing vital organ function. Drug toxicity contributes to comorbidity and mortality and has led to newer regimens with reduced cyclophosphamide exposure. Glucocorticoid toxicity remains a major problem, with controversy over the rapidity with which glucocorticoids can be reduced or withdrawn. Disease relapse occurs in 50% and requires early detection at a stage when it will not adversely affect outcomes. Rates of cardiovascular disease and malignancy are higher than in control populations but strategies to reduce their risk, apart from cyclophosphamide-sparing regimens, have not been developed. Thromboembolic events occur in 10% and may be linked to the recently identified autoantibodies to plasminogen and tissue plasminogen activator. Outcomes of vasculitis depend heavily on the level of tissue damage at diagnosis, especially renal dysfunction, but are also influenced by patient age, ANCA subtype, disease extent, and response to therapy. Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)is treated along similar principles to granulomatosis with polyangiitis (GPA) and microscopic polyangiitis but the persistence of steroid-dependent asthma in over one-third and differences in pathogenesis has suggested alternative treatment approaches. Chronic morbidity results from tissue damage and is especially common in the upper and lower respiratory tract and kidneys. Tracheobronchial disease is a severe late complication of GPA, while deafness, nasal obstruction, and chronic sinusitis are sequelae of nasal and ear vasculitis. Chronic infection of damaged epithelial surfaces acts as a drive for vasculitic activity and adequate infection control is necessary for stable remission. Chronic kidney disease can stabilize for many years but the risks of endstage renal disease (ESRD) are increased by acute kidney injury at presentation or renal relapse. Renal transplantation is successful, with similar outcomes to other causes of ESRD.
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17

Harper, Lorraine, and David Jayne. The patient with vasculitis. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0160.

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The goals of treatment in renal vasculitis are to stop vasculitic activity and recover renal function. Subsequent strategies are required to prevent vasculitis returning and to address longer-term co-morbidities caused by tissue damage, drug toxicity, and increased cardiovascular and malignancy risk.Cyclophosphamide and high-dose glucocorticoids remain the standard induction therapy with alternative immunosuppressives, such as azathioprine, to prevent relapse. Plasma exchange improves renal recovery in severe presentations. Refractory disease resulting from a failure of induction or remission maintenance therapy requires alternative agents and rituximab has been particularly effective. Replacement of cyclophosphamide by rituximab for remission induction is supported by recent evidence. Methotrexate is effective in non-renal vasculitis but difficult to use in patients with renal impairment. Mycophenolate mofetil seems to be effective but there is less long-term evidence.Drug toxicity contributes to co-morbidity and mortality and has led to newer regimens with reduced cyclophosphamide exposure. Glucocorticoid toxicity remains a major problem with controversy over the rapidity with which glucocorticoids can be reduced or withdrawn.Disease relapse occurs in about 50% of patients. Early detection is less likely to lead to an adverse affect on outcomes. Rates of cardiovascular disease and malignancy are higher than in control populations but strategies to reduce their risk, apart from cyclophosphamide-sparing regimens, have not been developed. Thromboembolic events occur in 10% and may be linked to the recently identified autoantibodies to plasminogen and tissue plasminogen activator.Renal impairment at diagnosis is a strong predictor of patient survival and renal outcome. Other predictors include patient age, antineutrophil cytoplasmic antibody subtype, disease extent and response to therapy. Chronic kidney disease can stabilize for many years but the risks of end-stage renal disease are increased by acute kidney injury at presentation or renal relapse. Renal transplantation is successful with similar outcomes to other causes of end-stage renal disease.
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18

Hardy, Robert William. Analysis of cyclophosphamide and phosphoramide mustard, their pharmacokinetics and the relationship of serum drug concentrations to toxicity in patients undergoing cancer chemotherapy. 1988.

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19

Pagnoux, Christian, and Richard H. Swartz. Vasculitis of the Central Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0099.

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Central nervous system (CNS) vasculitis is an extremely challenging diagnostic and therapeutic disease. Multiple conditions, including reversible cerebral vasoconstrictive syndrome and intracranial atherosclerosis, can mimic it. Infections, systemic diseases, particularly systemic vasculitides, drug abuse, neoplasms, and some other disorders can cause secondary CNS vasculitis. Primary CNS vasculitis is extremely rare. A definite diagnosis requires a brain biopsy, which may show granulomatous inflammation, lymphocytic inflammation, and/or acute necrotizing vasculitis. The pathogeny remains unknown. The treatment of secondary CNS vasculitis relies on that of its cause, whereas treatment for primary CNS vasculitis is not codified but usually relies on high-dose glucocorticoids, combined, at least for the most severe forms, with an immunosuppressant, mainly cyclophosphamide.
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20

Wijdicks, Eelco F. M., and Sarah L. Clark. Immunosuppression and Immunotherapy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190684747.003.0010.

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Immune modulation in the neurosciences intensive care unit mostly involves high-dose corticosteroids, plasma exchange, and immunoglobulin. Corticosteroids are frequently used in patients with neurologic complications of cancer. Neurosurgeons typically use corticosteroids after performing a craniectomy to reduce cerebral edema. Corticosteroids are the established initial treatment modality of choice for patients with acute metastatic epidural spinal cord compression. Therapeutic apheresis or immunoglobulin is generally used as supportive therapy in patients with Guillain-Barré syndrome, myasthenia crisis, and autoimmune encephalitis. Immune modulation has been considered essential in autoimmune encephalitis despite lack of controlled clinical trials. In these now better characterized disorders, a combination of corticosteroids, intravenous immune globulin (IVIG), plasma exchange, rituximab, or cyclophosphamide are used. The use of acute immunotherapy and precautionary measures are discussed in this chapter.
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21

Sandstrom, Marie. Pharmacokinetics & Pharmacodynamics of Anti-Cancer Regimens: Emphasis on Busulphan and the Combination Therapies Epirubicin-Docetaxal and Fluorouracil-Epirubicin-Cyclophosphamide ... from the Faculty of Pharmacy, 265). Uppsala Universitet, 2002.

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22

Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0073_update_001.

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Cyclophosphamide and plasma exchange are the standard of care in rapidly progressive glomerulonephritis or lung haemorrhage caused by antiglomerular basement membrane (anti-GBM) disease, and it is unusual to encounter patients at earlier stages. Steroids are universally used in addition. There is some evidence that plasma exchange may not be a critical part of treatment at an earlier stage. There is no more than anecdotal evidence for other therapies. Slower-onset therapies such as antibodies to B cells are rarely appropriate. If untreated, patients with severe anti-GBM disease will not recover renal function and are at risk of pulmonary haemorrhage. Evidence for the pathogenicity of circulating anti-GBM antibodies provides rationale for removal of circulating antibodies as rapidly as possible, whilst simultaneously inhibiting their synthesis. This was behind the introduction of the combination of plasma exchange with immunosuppressive therapy in mid 1970s, which revolutionized outcomes. Plasmapheresis aims to remove circulating pathogenic antibodies against GBM and possibly other mediators; cyclophosphamide prevents further synthesis of autoantibodies; and steroids act as anti-inflammatory agents to attenuate the glomerular inflammatory response initiated by anti-GBM antibodies. It is clear from experimental models and occasional observations in man that the anti-cell mediated effects of current therapies are important too. Outcomes vary, but in general patient survival is now good, while renal survival remains poor, in many series less than 50% at 1 year. Treatment is toxic and after an early peak in deaths due to pulmonary haemorrhage, secondary infections are the next threat. It may therefore be best not to immunosuppress patients with a very poor renal prognosis who appear to be at low risk of pulmonary haemorrhage. Treatment can usually be curtailed after 3 months without recurrence. ANCA and anti-GBM antibodies occur together in some patients. This is typically an older group which often has features of vasculitis, and the anti-GBM response may often be secondary. Longer treatment as for small vessel vasculitis is usually indicated.
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23

Houssiau, Frédéric A. The patient with systemic lupus erythematosus. Edited by Giuseppe Remuzzi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0163_update_001.

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Major progress has been achieved in the field of lupus nephritis (LN) treatment over the last decade. Glucocorticoids and other immunosuppressants (including cyclophosphamide) are now used in a more patient-friendly way, minimizing their untoward effects. Mycophenolate mofetil is now an option, both for induction and maintenance immunosuppression. Ever increased standards for optimal global care have further contributed to lower end-stage renal disease rates.Better understanding of the mechanisms underlying lupus raises hopes for more targeted therapies with biologics. Thus, the anti-B-lymphocyte stimulator belimumab has been officially labelled for non-renal lupus by the medical agencies, which has not happened for more than 50 years, when cortisone and hydroxychloroquine were approved.These exciting developments should, however, not disguise the fact that LN still impacts survival of lupus patients and that no cure can be offered so far.
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24

Rahman, Anisur. Conventional treatments in systemic lupus erythematosus. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198739180.003.0006.

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A new diagnosis of SLE can be frightening for patients, and the importance of education and reassurance must be remembered—clinical nurse specialists can play a key role in this. Equally, lifestyle advice regarding sun-protection and smoking cessation should not be neglected. Many patients have a mild disease characterized by ongoing symptoms such as rash, hair loss, and joint or chest pain. Symptomatic treatment, topical corticosteroids, antimalarials, and non-steroidal anti-inflammatory drugs are generally sufficient to manage these cases, but acute symptomatic flares may require short-term oral or intramuscular corticosteroids. Lupus nephritis should be managed with a combination of corticosteroids and immunosuppressants. Oral mycophenolate, or the low-dose Euro-Lupus intravenous cyclophosphamide regimen, are used to induce remission. Low-dose corticosteroid plus azathioprine or mycophenolate is used to maintain remission. Corticosteroids are highly effective but have diverse side effects and should be used in the lowest dose compatible with maintaining control of disease activity.
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25

Wipprecht, Aline. Aktivierung Von Cyclophosphamid in Extrakten Aus Embryonalen Hühnerlebern. GRIN Verlag GmbH, 2013.

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26

Wells, Elizabeth M. Anti-N-Methyl-D-Aspartate Receptor Encephalitis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0091.

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Anti- N-methyl-D-aspartate receptor (NMDAR) encephalitis is a severe but treatable recently identified form of immune-mediated encephalitis associated with antibodies in serum and cerebrospinal fluid (CSF) against the GluN1 subunit of the NMDAR. Research has rapidly expanded the understanding of disease mechanisms and how the condition manifests in different populations (e.g., pediatrics vs. adult, cancer vs. noncancer, male vs. female). Immunocytochemical, physiological, and molecular studies of the effects of human CSF on the rodent and murine brain in vitro and in vivo indicate a noncytotoxic antibody-mediated mechanism of disease pathogenesis. Finding positive antibodies prompts a search for occult neoplasm, most likely ovarian teratoma in young women; other age groups and male patients are less likely to have tumor but need to be screened. Fifty percent of patients respond to first line steroids, IVIG, plasma exchange or a combination, and many others improve with addition of rituximab or cyclophosphamide. Cured patients may have cognitive or motor sequelae, and refractory disease and death may occur despite treatment. Knowledge about etiology and biomarkers of refractory disease are lacking. Additional work is needed to further elucidate the origin of the immune-mediated response, to determine optimal clinical management and develop effective therapies for refractory patients.
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27

Lai, Kar Neng, and Sydney C. W. Tang. Immunoglobulin A nephropathy. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0068_update_001.

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Immunoglobulin A nephropathy is characteristically slowly evolving, and studies from autopsies and kidney donors show that deposition of immunoglobulin A is quite common and not necessarily associated with overt disease. However, series of biopsy-diagnosed patients that extend to 20 or 30 years report rates of end-stage renal failure of up to 40–50%. A very approximate overall rate of end-stage renal disease of 1% per year has been suggested. Proteinuria, glomerular filtration rate (GFR), and possibly some features on renal biopsies enable risk stratification, but all patients need long-term monitoring. Treatment is based on the use of angiotensin converting-enzyme inhibitors for patients with proteinuria, and blood pressure control, and of course during most of the previous long-term studies patients would not have been treated with these agents or to modern blood pressure standards. For patients who show loss of GFR despite this, or other markers of high risk, the best evidence is for treatment with high-dose corticosteroids over a limited period of months. There is little convincing evidence for additional benefit from cytotoxic or other immunomodulatory agents, except possibly in the most aggressive disease, when there is weak evidence for cyclophosphamide. Some studies claim benefit from tonsillectomy, but this is not clear, and most nephrologists only recommend this for patients with recurrent tonsillitis.
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28

Bissell, Lesley-Anne, Dwomoa Adu, and Paul Emery. The patient with rheumatoid arthritis, mixed connective tissue disease, Sjögren syndrome, or polymyositis. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0166.

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Renal disease is a well-recognized cause of ill health and death in rheumatoid arthritis. Three broad categories of renal disease occur. The first—and by far the most common—arises from the nephrotoxicity of the drugs used in the treatment of arthritis, particularly with non-steroidal anti-inflammatory drugs. Disease-modifying antirheumatic drugs such as gold and D-penicillamine may lead to proteinuria and a glomerulonephritis in 10–30% of patients. Ciclosporin is associated with significant nephrotoxicity and hypertension. A second major but diminishing cause of renal disease in rheumatoid arthritis is amyloidosis. Thirdly, rheumatoid arthritis may be associated with the development of glomerulonephritis. The main types described are a mesangial proliferative glomerulonephritis with or without immunoglobulin A deposits, a membranous nephropathy, and a focal segmental necrotizing glomerulonephritis of the vasculitic type.Renal disease in mixed connective tissue disease and polymyositis is infrequent, but the former can be associated with a membranous and mesangial proliferative glomerulonephritis.Sjögren syndrome is rarely associated with clinically significant renal disease, but patients can present with proteinuria, acidosis, or hyperchloraemia. Interstitial nephritis and immune complex glomerulonephritis reflect the exocrinopathy and circulating immune complex disease pathognomonic of Sjögren syndrome. Evidence for effective treatment of the renal complications is lacking. Corticosteroids and cyclophosphamide are most commonly used, with newer biological drugs, such as rituximab, showing promise.
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29

Cattran, Daniel C., and Heather N. Reich. Membranous glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0062_update_001.

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A common rule of thumb in primary membranous glomerulonephritis (MGN) is that one-third of patients improve spontaneously, one-third progress, and one-third continue to have substantial proteinuria. The rate of spontaneous recovery may be near the truth, but MGN is usually an indolent condition and few studies have run long enough to give accurate outcomes for the remainder. However MGN is an important cause of end-stage renal failure. Treatment regimens that include cyclophosphamide or chlorambucil can improve the outcome of patients at greatest risk of deterioration, but their toxicity has limited their use in randomized studies to the highest risk patients. Steroids alone, and ciclosporin, do not improve long-term outcomes in these studies. Whether anti-B-cell antibodies offer additional benefits requires randomized studies. After confirming the diagnosis of primary MGN it is recommended to maximize supportive therapy and monitor for at least 6 months to give a clear picture of the long-term risk. For patients at lowest risk, supportive management and monitoring alone is recommended. Patients at medium risk (nephrotic range proteinuria but normal and stable glomerular filtration rate), or high risk (very heavy proteinuria, greater than 8 g/day or deterioration of glomerular filtration rate) may justify specific treatment directed at the immune response. For the medium-risk group it is not certain that it is required; for some in the high-risk group it may come too late. Overall outcomes in the high-risk group remain quite poor even with aggressive treatment.
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30

Krömann, Susanne. Experimenteller Antiinsulinserum-Diabetes bei NMRI-Mäusen unter dem Einfluss von Cyclophosphamid. 1987.

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31

Schmich, Uwe. Toxizität von Cyclophosphamid, Ifosfamid und deren Metaboliten in renalen epithelialen Zellkulturen. 1993.

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32

Zickert, Daniela. Embryotoxische Auswirkungen von Cyclophosphamid auf die frühe Entwicklung des kultivierten Wachtelembryos. 1990.

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33

Lassota, Antje. Zytotoxische Effekte von Cyclophosphamid und seinen Metaboliten in sensitiven und resistenten Zellkultursystemen. 1996.

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34

Hofmann, Petra. In-vivo-Untersuchungen zur Antiklastogenität von Gemüsen gegenüber Benzo(a)pyren und Cyclophosphamid. 1996.

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35

Laber, Peter. Die regionale Perfusion des tumortragenden Rattenbeins mit stabilisiertem, aktiviertem Cyclophosphamid (4-(S-aethanol)-sulfido-Cyclophosphamid): A. Entwicklung eines Perfusionsmodells und Uäberpruäfung der Eignung zur regionalen Tumortherapie an der hinteren Rattenextremitaät ; B. Regionale Perfusionen mit stabilisertem, aktiviertem Cyclophosphamid zur Therapie des Yoshida-Sarkoms an der hinteren Rattenextremitaät. 1985.

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36

Karcher, Kerstin. Über den Einfluss von Hochdosiertem Cyclophosphamid auf die Regulation einer Überempfindlichkeitsreaktion vom verzögerten Typ. 1992.

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37

Frangart-Schmidt, Jutta. Antiklastogene Effekte von Früchten und ausgewählten Inhaltsstoffen gegenüber Benzo(a)pyren und Cyclophosphamid im Mikrokerntest. 1997.

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38

Brandt, Dietrich. Therapeutischer Effekt der Alkylantien Cyclophosphamid und Ifosfamid im Autoimmunmodell der MRL/Ipr-Ipr (Lupus)-Maus. 1995.

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39

Gutenberg-Universität, Johannes, ed. Einfluss von 6-Merkaptopurin und Cyclophosphamid auf die humorale Immunantwort sowie auf das Differentialblutbild der Ratte. 1985.

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40

Hager, Marlin. Hemmeffekte von Obst und Gemüse auf die in vivo Klastogenität von Benzo(a)pyren und Cyclophosphamid. 1996.

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41

Gutenberg-Universität, Johannes, ed. In vivo Effekte von Interleukin-2 und Cyclophosphamid bei Patienten mit fortgeschrittenem malignen Melanom und Nierenzellkarzinom. 1989.

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42

Krausser, Stefan. Der Einfluss von Allopurinol, Cyclophosphamid und 6-Methylmercaptopurinribosid auf die Bildung und Ausscheidung von Purinkörpern beim Hühnerembryo. 1987.

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43

Kraatz, Ernst-Günter. Beeinflussung der B- und T-Zellreaktivität bei Mäusen durch eine Kombinationsbehandlung mit Cyclophosphamid oder Adriamycin und Allo-Antigen. 1991.

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44

Rudolf, Jörg. Über die Wirkungsweise von Cyclophosphamid und 6-Merkaptopurin auf das humorale Immunsystem und auf das weisse Blutbild beim Meerschweinchen. [s.l.], 1987.

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45

Brunnengräber, Rita. Zur Wirkung von Ampicillin und Doxycyclin auf das zelluläre und humorale Immunsystem der gesunden und der mit Cyclophosphamid immunsupprimierten Maus. 1989.

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46

Hibbe, Thomas. Immuntherapeutische Effekte von gamma-Interferon, Interleukin-2, Lipopolysacchariden, Cyclophosphamid und Thiamazol im Niedrigdosis-Streptozotocin-Modell und in der NOD-Maus. 1988.

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47

Gutenberg-Universität, Johannes, ed. Die in vitro-Chromatresistenz von Lymphozyten nach in vivo-Exposition gegenüber 1,1,1-Trichlorethan. Cyclophosphamid und Azathioprin - ein immuntoxikologisches ELISA-Verfahren. 2000.

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48

Küpper, Silke. Konzentrationen und molares Verhältnis aktiver cytostatischer Metabolite und protektiver Thiole im Plasma von Patienten unter der Therapie mit Ifosfamid / Cyclophosphamid und Mesna. 2001.

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49

Mrakawa, Diana. Induktion von DNA-Strangschäden in venösem Blut von Patientinnen mit Ovarial-Karzinom durch Chemotherapie mit Cyclophosphamid und Carboplatin in Relation zum Therapieerfolg. 1999.

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50

Kerkhoff, Guido. Einfluss von Ascorbinsäure, [beta]-Carotin, DL-alpha-Tocopherol, Vitamin A-aldehyd, Vitamin K undRiboflavin auf den durch Cyclophosphamid oder Trp-P-2 induzierten Schwesterchromatidaustausch in menschlichen Lymphozytenkulturen. 1995.

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