Adriamycin cardiotoxicity

1. Bollum F. J. Calf Thymus Polymerase. J. Biol. Chem., 235: 2399-2403, 1960. Bollum, F. J. Filter Paper Disk Techniques for Assaying Radioactive Macromolecules. In: G. L. Cantoni and D. R. Davies eds. ; , Procedures in Nucleic Acid Research, pp. 296-300. New York: Harper & Row Publishers, Inc., 1966. 3. Bonadonna, G., Monfardini, S., De Lena, M., and Fossati-Bellani, F. Clinical Evaluation of Adriamycin, A New Anti-Tumor Antibiotic. Brit. Med. J., 3: 503-506, 1969. Bonadonna, G., Monfardini, S., De Lena, M., Fossati-Bellani, F., and Bernetta, G. Phase I and Preliminary Phase II Evaluation of Adriamycin NSC 123127 ; . Cancer Res., 30: 2572-2582, 1970. Calendi, E., Di Marco, A., Regiani, M., Scarpinato, B., and Valentini, L. On Physiochemical Interactions between Daunomycin and Nucleic Acid. Biochim. Biophys. Acta, 103: 25-49, 1965. Calvin, H. I., Kosto, B., and Williams-Ashman, H. G. Enzymic Incorporation of Deoxyribonucleotides into Deoxyribonucleic Acid by Mammalian Testis. Arch. Biochem. Biophys., 118: 670-681, 1967. Di Marco, A., Gaetani, M., and Scarpinato, B. Adriamycin NSC 123127 ; , A New Antibiotic with Anti-Tumor Activity. Cancer Chemotherapy Kept., 53: 33-37, 1969. Falln, H., Frei, F., Davidson, J., Trier, J., and Burk, D. Leukocyte Preparations from Human Blood: Evaluation of Their Morphologic and Metabolic State. J. Lab. Clin. Med., 52: 779-791, 1962. Kim, J. H., Gelbard, A. S., Djordjiwic, B., Kim, S. H., and Perez, A. G. Action of Daunomycin on Nucleic Acid Metabolism and Viability of HeLa Cells. Cancer Res., 28: 2437-2442, 1968. Moore, G. E., Gerner, R. E., and Franklin, H. A. Culture of Normal Human Leukocytes. J. Am. Med. Assoc., 799: 519-524, 1967. Riehm, H., and Biedler, J. L. Cellular Resistance to Daunomycin in Chinese Hamster Cells in Vitro. Cancer Res., 31: 409-412, 1971. Rusconi, A., and Di Marco, A. Inhibition of Nucleic Acid Synthesis by Daunomycin and Its Relationship to the Uptake of the Drug in HcLa Cells. Cancer Res., 29: 1507-1511, 1969. Sandberg, J. S., Howsden, L., Di Marco, A., and Goldin, A. Comparison of the Anti-Leukemic Effect in Mice of Adriamycin NSC-123127 ; with Daunomycin NSC 82151 ; . Cancer Chemo therapy Rept., 54: 1-7, 1970.
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Why is adriamycin fatal to a cell

Adriamycin is classified as an antitumor antibiotic.

The following is however a guide to the anticipated response: the drugs some older ; likely to cause hair loss include: adriamycin, actinomycin d cosmegen lyovac ; , bicnu, busulphan myleran ; , carboplatinum, cyclophosphamide endoxana ; , cisplatinum, cytoxan, daunorubicin cerubidin, daunoxome ; , doxorubicin hydrochloride adriamycin ; , dacarbazine dtic-dome, epirubicin pharmorubicin ; , etoposide eposin, etopophos, vepesid, vp-16 ; , fludarabine, idarubicin zavedos ; , ifosfamide mitoxana ; , irinotecan campto ; , high dose methotrexate matrex ; , mitomycin, mitoxantrone, paclitaxel taxol ; , streptozocin zanosar ; , taxotere, topotecan hycamtin ; , velban, vindesine eldisine. Existence of a human form of 17 -HSD. 5-Androstene3 , 17 -diol Ae-17 -diol ; has been suggested to be one of the precursors of epitestosterone 50 ; . Significant correlation between Ae-17 -diol and epitestosterone was found in spermatic vein blood 50 ; . Further, Weusten et al., showed that Ae-17 -diol is synthesized from pregnenolone in a single step via cytochrome P-450c17 CYP17 ; 52 ; . Not only do a significant amount of individuals have low T E ratios, increasing the risk for false negative doping tests; also a noteworthy number of individuals have higher natural ratios than the internationally used cut-off ratio of 4.0. The naturally high ratios are in many cases due to low urinary levels of epitestosterone. The reasons for this are unknown. UGT2B7 has been identified as the enzyme responsible for epitestosterone glucuronidation 165 ; . We hypothesized that genetic variation in CYP17 and UGT2B7 may affect the formation and disposition of epitestosterone that in turn could affect the T E ratios. In addition to UGT2B17, testosterone and DHT are conjugated by UGT2B15, but at a lower rate 163 ; . Genetic variation in UGT2B15 may affect the disposition of testosterone and other androgens, in particular in individuals devoid of UGT2B17. We also wanted to elucidate the formation of epitestosterone using different substrates and tissue preparations in in vitro incubations. We found that a T C promoter polymorphism in the CYP17 gene was significantly associated with urinary levels of both epitestosterone glucuronide G ; and Ae-17 diol G in Swedish Caucasian men figure 2, paper V ; . Individuals carrying the UGT2B17 ins ins and ins del genotypes who were homozygous for the T-allele exhibited 64 % higher T E ratios than the C-carriers 2.9 and 1.8, respectively; p 0.0008 ; . Thus the CYP17 polymorphism may partly explain high natural 4 ; T E ratios. Out of 138 Swedish men, 13 9.4 % ; had T E ratios 4 and all of them had at least one T-allele. This is of interest, since falsely positive doping test results are of great legal concern for the sports man. In addition, falsely positive doping test results yield a lot of extra work load for the doping laboratories. Interestingly, Ae-17 -diol was also associated with the CYP17 polymorphism indicating that Ae-17 -diol may be a precursor of epitestosterone. After exogenous testosterone administration, the Ae-17 -diol levels, but not DHEA levels, decreased with the same pattern as epitestosterone in participants of the testosterone challenge study fig 3, paper V ; . Furthermore, in our in vitro studies, significant amounts of Ae17 -diol and trace amounts of epitestosterone was found after incubation with testis microsomes and pregnenolone. Incubation with Ae-17 -diol resulted in higher formation of epitestosterone than incubation with pregnenolone. We also incubated Ae17 -diol with liver microsomes from 16 different liver samples. Epitestosterone was formed in all liver samples. Specific activities in epitestosterone formation varied sixfold data not shown ; . The mean formation of rate was 3.2 0.4 ng mg protein min range 0.86-5.2 ng mg protein min ; . Taken this together, we postulate that pregnenolone and Ae-17 -diol, is an important pathway for epitestosterone formation. The UGT2B7 H268Y polymorphism was not associated with epitestosterone glucuronidation, and did thus not affect the T E ratio and agenerase.

Adriamycin chemotherapy treatment

Topical application of 10% a-tocopherol succinate in di methyl sulfoxide for 2 days significantly reduced the mean size of Adriamycin-induced necrotic skin ulcers in the rat up to 68%. There appeared to be no further advantage of the 7-day compared to the 2-day course of application. Dimethyl sulfox ide applied topically may itself reduce the size of skin ulcers, but this effect was less marked than with a-tocopherol succi nate or a-tocopherol acetate in dimethyl sulfoxide and was not REFERENCES always statistically significant. A significant 32% decrease in mean ulcer size was produced by 7-day topical application of 1. Adamson, J. E., Horton, C. E., Crawford. H. H., and Ayers, W. T. The effects of dimethylsulfoxide on the experimental pedicle flap: a preliminary report. dimethyl sulfoxide. Ten % a-tocopherol acetate in dimethyl Plast. Reconstr. Surg., 37: 105, 1966. sulfoxide appeared to have activity slightly less than that of 2. Ayres, S. Minan. R., and Scribner, M. D. Synergism of vitamins A and E with dermatologie applications. Cutis, 23. 600-603, 689-690. a-tocopherol succinate in dimethyl sulfoxide in reducing 3. Barlock. A. Howser. D., and Hubbard. S. Nursing management of Adria ulcer diameter. Both 10% a-tocopherol acetate and 10% amycin extravasation. Am. J. Nursing, 94-95. 1979. 4. Bartokowski-Dodds. L, and Daniels, J. R. Use of sodium bicarbonate as a tocopherol succinate in dimethyl sulfoxide exhibited greater means of ameliorating doxorubicin-induced dermal necrosis in rat. Cancer activity in reducing ulcer diameter than did a-tocopherol alco Chemother. Pharm., 4: 179-181. 1980. hol, which being liquid could be applied directly to the skin. By 5. Bowers, D. G., and Lynch. J. B. Adriamycin extravasation. Plast. Reconstr. Surg., 67. 86-92. 1978. itself, a-tocopherol alcohol exhibited no activity in reducing 6. Breed, J. G. S. Zimmerman, A. N. E., Dormans, J. A. M. A., and Pinedo, H. ulcer diameter and, in dimethyl sulfoxide, showed minimal M. Failure of antioxidant vitamin E to protect against Adriamycin-induced activity probably not much greater than dimethyl sulfoxide cardiotoxicity in the rabbit. Cancer Res., 40: 2033-2038, 1980. alone. Dimethyl sulfoxide and a-tocopherol were effective only 7. Brobyn. R. D. The human toxicology of dimethylsulfoxide. Ann. N. Y. Acad. Sci. 243. 497-506, 1975. when applied locally and had no reproducible systemic activity 8. Brown. J. H. Clinical experience with DMSO in acute musculoskeletal against Adriamycin-induced skin necrosis. Lanolin-white petro conditions comparing a noncontrolled series with a controlled double blind study. Ann. N. Y. Acad. Sci., 141: 496, 1967. latum could not substitute for dimethyl sulfoxide as a vehicle 9. Cederbaum, A. I., Dicker, E., Rubin, E., and Cohen, G. The effect of for topical application of a-tocopherol succinate or acetate. dimethylsulfoxide and other hydroxyl radical scavengers on the oxidation of Dimethyl sulfoxide rapidly penetrates the skin without damag ethanol by rat liver microsomes. Biochem. Biophys. Res. Commun. 78: 1254-1267. 1977. ing the stratum corneum 1 7 ; and acts as a pntrant-carrier 10. Cohen, M. H. Amelioration of Adriamycin skin necrosis: an experimental for other drugs. It probably enhances the penetration of astudy. Cancer Treat. Rep., 63. 1003-1004, 1979. Door, R. T., Albert, D. S. and Chen. H. S. G. Experimental model of tocopherol into the skin. Dimethyl sulfoxide might itself prevent doxorubicin extravasation in the mouse. J. Pharmacol. Methods, 4: 321Adriamycin-induced skin ulcration by acting as a hydroxyl 334, 1980. radical scavenging agent 9 ; . It could also aid the dispersion of 12. Dragon, L. H. and Braine, H. G. Necrosis of the hand after daunorubicin infusion distal to an arteriovenous fistula. Ann. Intern. Med. 97. 58-59. Adriamycin from i.d. sites. Dimethyl sulfoxide is a vasodilator 1979. 1 ; and has antiinflammatory and mild antibacterial activity 17, 13. Fridovich, I. Oxygen radicals, hydrogen peroxide, and oxygen toxicity. In: 41 ; . All of these properties might help to prevent ulcration. W. A. Pryor ed. ; . Free Radicals in Biology, Vol. 1, pp. 239. New York: Academic Press, Inc., 1976. a-Tocopherol is a well-known radical scavenging agent and 14. Handa. K., and Sato, S. Generation of free radicals of quinone groupantioxidant 21 ; . a-Tocopherol pretreatment has been reported containing anticancer chemicals in NADPH-microsome system as evidenced by initiation of sulfite oxidation. Gann, 66 43-47, 1974. to protect mice and other animals against acute Adriamycin 15. Haskell, C. M., Silverstein, M. J., Range, D. M., Hunt. J. S., Sparks. F. C., cardiomyopathy 24, 25, 36, ; , although it does not protect and Morton, D. L. Multimodality cancer therapy in man: a pilot study of animals against chronic Adriamycin cardiomyopathy 6 ; . The Adriamycin by arterial infusion. Cancer Phila. ; . 33. 1485-1490, 1974. protective effect of a-tocopherol has been ascribed to its ability 16. Ignoffo, R. J., and Friedman. M. A. Therapy of local toxicities caused by extravasation of cancer chemotherapeutic drugs. Cancer Treat. Rev. 7: to inhibit lipid peroxidation in the heart 25 ; . a-Tocopherol 17-27, 1980. 17. Kligman, A. M. Topical pharmacology and toxicology of dimethyl sulfoxide" might protect against Adriamycin skin ulcration by a similar Part I. J. Am. Med. Assoc., 793. 796-804, 1965. mechanism. 18. Labandter, H. P., and McElwee, T. Adriamycin extravasation: case reports Dimethyl sulfoxide and a-tocopherol are nontoxic when ap and review. J. La. State Med. Soc., 737. 255-258, 1979. plied topically. Dimethyl sulfoxide is exceptionally nontoxic 19. Laughlin, R. A., Landeen, J. M., and Habal, M. B. The management of inadvertent subcutaneous Adriamycin infiltration. Am. J. Surg. 737. 408 30 ; . There were early reports of lenticular changes in experi 412, 1979. mental animals receiving dimethyl sulfoxide 31 ; , but these 20. Luedke, D. W., Kennedy, P. S., and Rietschel, R. L. Histopathogenesis of skin and subcutaneous injury induced by Adriamycin. Plast. Reconstr. Surg., changes have never been seen in humans 8 ; . Dimethyl sulf.

Adriamycin bone marrow

LITERATURE CITED 1. Keshan Disease Research Group 1979 ; Epide miologie studies on the etiologic relationship of selenium and Keshan disease. Chin. Med. J. 92, 477-482. 2. Keshan Disease Research Group 1979 ; Obser vations on effect of sodium selenite in prevention of Keshan disease. Chin. Med. J. 92, 471-476. 3. Ge, K., Xue, A., Bai, J. & Wang, S. 1983 ; Keshan disease"an endemic cardiomyopathy in China. Virchows Arch. A Pathol. Anat. 401, 1-15. 4. Yang, G., Chen, J., Wen, Z., Ge, K., Zhu, L., Chen, X. & Chen, X. 1984 ; The role of seleni um in Keshan disease. In: Advances in Nutritional Research Draper, H. H., d. ; , 203-231, Ple pp. num Press, New York. 5. Ogawa, M., Muggia, F. M. & Rozencweig, M. 1984 ; Adriamycin: Its Expanding Role in Cancer Treatment, Excerpta Medica, Amsterdam. 6. Lenaz, L. & Page, J. A. 1976 ; Cardiotoxicity of adriamycin and related anthracyclines. Cancer Treat. Rev. 3, 111-120. 7. Janeke, R. S. 1974 ; An anthracycline antibioticinduced cardiomyopathy in rabbits. Lab. Invest. 30, 292-304. 8. Mettler, F. P., Young, D. M. & Ward, J. M. 1977 ; Adriamycin-induced cardiotoxicity cardiomyopa thy and congestive heart failure ; in rats. Cancer Res. 37, 2705-2713. 9. Van Vleet, J. F., Greenwood, L., Ferrans, V. J. & Rebar, A. H. 1978 ; Effect of selenium-vitamin E on adriamycin-induced cardiomyopathy in rab bits. Am. J. Vet. Res. 39, 997-1010 and aggrenox Simpson JK, Miller RF and Spittle MF 1993 ; Liposomal doxorubicin for treatment of AIDS-related Kaposi's sarcoma. Clin Oncol 5: 372374. Singh M, Ghose T, Faulkner G, Kralovec J and Mezei M 1989 ; Targeting of methotrexate-containing liposomes with a monoclonal antibody against human renal cancer. Cancer Res 49: 3976 3984. Smaby JM, Momsen M, Kulkarni VS and Brown RE 1996 ; Cholesterol-induced interfacial area condensations of galactosylceramides and sphingomyelins with identical acyl chains. Biochemistry 35: 5696 5704. Spanjer HH and Scherphof GL 1983 ; Targeting of lactosylceramide-containing liposomes to hepatocytes in vivo. Biochim Biophys Acta 734: 40 47. Speth PAJ, van Hoesel QGCM and Haanen C 1988 ; Clinical pharmacokinetics of doxorubicin. Clin Pharmacokinet 15: 1531. Stewart S, Jablonowski H, Goebel FD, Arasteh K, Spittle M, Rios A, Aboulafia D, Galleshaw J and Dezube BJ 1998 ; Randomized comparative trial of pegylated liposomal doxorubicin versus bleomycin and vincristine in the treatment of AIDSrelated Kaposi's sarcoma. J Clin Oncol 16: 683 691. Storm G, Oussoren C, Peeters PAM and Barenholz Y 1993 ; Tolerability of liposomes in vivo, in Liposome Technology Gregoriadis G ed ; pp 345383, CRC Press, Inc, Boca Raton, FL. Storm G, Steerenberg PA, Emmen F, Waalkes MvB and Crommelin DJA 1988 ; Release of doxorubicin from peritoneal macrophages exposed in vivo to doxorubicin-containing liposomes. Biochim Biophys Acta 965: 136 145. Storm G, ten Kate MT, Working PK and Bakker-Woudenberg IA 1998 ; Doxorubicin entrapped in sterically stabilized liposomes: Effects on bacterial blood clearance capacity of the mononuclear phagocyte system. Clin Cancer Res 4: 111115. Straubinger RM, Duzgunes N and Papahadjopoulos D 1985 ; pH-sensitive liposomes mediate cytoplasmic delivery of encapsulated macromolecules. FEBS Lett 179: 148 154. Straubinger RM, Hong K, Friend DS and Papahadjopoulos D 1983 ; Endocytosis of liposomes and intracellular fate of encapsulated molecules: Encounter with a low pH compartment after internalization in coated vesicles. Cell 32: 1069 1079. Straubinger RM, Lopez NG, Debs RJ, Hong K and Papahadjopoulos D 1988 ; Liposome-based therapy of human ovarian cancer: parameters determining potency of negatively charged and antibody-targeted liposomes. Cancer Res 48: 52375245. Subramanian D and Muller MT 1995 ; Liposomal encapsulation increases the activity of the topoisomerase I inhibitor topotecan. Oncol Res 7: 461 469. Surewicz WK and Epand RM 1986 ; Phospholipid structure determines the effects of peptides on membranes: Differential scanning calorimetry studies with pentagastrin-related peptides. Biochim Biophys Acta 856: 290 300. Swenson CE, Freitag J and Janoff AS 1998 ; The Liposome Company: Lipid-based pharmaceuticals in clinical development, in Medical Applications of Liposomes Lasic DD and Papahadjopoulos D eds ; pp 689 702, Elsevier Science BV, New York. Szoka F, Olson F, Heath T, Vail W, Mayhew E and Papahadjopoulos D 1980 ; Preparation of unilamellar liposomes of intermediate size 0.1 0.2 m ; by a combination of reverse phase evaporation and extrusion through polycarbonate membranes. Biochim Biophys Acta 601: 559 571. Szoka F and Papahadjopoulos D 1978 ; Procedure for preparation of liposomes with large internal aqueous space and high capture by reverse-phase evaporation. Proc Natl Acad Sci USA 75: 4194 4198. Szoka FC 1998 ; Commentary: Rantosomes and ravosomes. J Liposome Res 8: vii-ix. Takanashi S and Bachur NR 1976 ; Adriamycin metabolism in man: Evidence from urinary metabolites. Drug Metab Dispos 4: 79 87. Thierry AR, Jorgensen TJ, Forst D, Belli JA, Dritschilo A and Rahman A 1989 ; Multidrug resistance in Chinese hamster cells: Effect of liposome encapsulated doxorubicin. Cancer Commun 1: 311316. Torchilin V, Trubetskoy VS, Whiteman KR, Caliceti P, Ferruti P and Veronese B 1995 ; The synthetic amphiphilic polymers for steric protection of liposome in vivo. J Pharm Sci 84: 1049 1053. Treat J, Greenspan A, Forst D, Sanchez JA, Ferrans VJ, Potkul LA, Woolley PV and Rahman A 1990 ; Antitumor activity of liposome-encapsulated doxorubicin in advanced breast cancer: Phase II study. J Natl Cancer Inst 82: 1706 1710. 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Uziely B, Jeffers S, Isacson R, Kutsch K, Wei-Tsao D, Yehoshua Z, Libson E, Muggia FM and Gabizon A 1995 ; Liposomal doxorubicin: antitumor activity and unique toxicities during two complementary phase I studies. J Clin Oncol 13: 17771785. Vaage J, Barbera-Guillem E, Abra R, Huang A and Working P 1994a ; Tissue distribution and therapeutic effect of intravenous free or encapsulated liposomal doxorubicin on human prostrate carcinoma xenografts. Cancer 73: 1478 1484. Vaage J, Donovan D, Colbern G, Uster P and Working P 1999 ; Tumor uptake and therapeutic effects of drugs encapsulated in long-circulating pegylated liposomes Abstract ; . Proc Assoc Cancer Res 40: 418. Vaage J, Donovan D, Loftus T, Abra R, Working P and Huang A 1994b ; Chemoprevention and therapy of mouse mammary carcinomas with doxorubicin encapsulated in sterically stabilized liposomes. Cancer 73: 2366 2371. Vaage J, Donovan D, Mayhew E, Abra R and Huang A 1993a ; Therapy of human.

Chemotherapy adriamycin cytoxan

3034 ; . After 24 hr of incubation in 5%CO2 at 37 , the plates were washed and refed with fresh media. A different concentration of adriamycin was added to each well 0.001 to 10 pg jil of medium ; . Each cell line was exposed to adriamycin on a separate Terasaki plate for 1 and alefacept. Assessment of Preoperative Left Ventricular Function in Patients with Mitral Regurgitation: Value of the End-systolic Wall StressEnd-systolic Volume Ratio . Blase A. Carabello, Stanton P. Nolan.
We are grateful to Jerry Harber for his technical assistance and to John Gilbert for his help in the preparation of this manuscript. 5chedule In Adriamycin Cyclophosphamide Combination Chemother apy. European J. Cancer, 14: 141-146, 1978. Zblnden, G., and Brandle, E. Toxicologic Screening of Daunorubicin NSC-82151 ; , Adriamycin NSC-123127 ; , and Their Derivatives in Rats. Cancer Chemotherapy Rept. Part I , 59: 707-715, 1975 and aleve.
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ACKNOWLEDGMENTS The authors wish to thank the clinical staff of the Department of Developmental Therapeutics for the careful attention given these patients. We especially thank Dr. James J. Butler for providing histological diagnoses and Dr. Emil J Freireich for continued encouragement and guidance. Endoarteriosa Continua. Tumori, 56: 233-240, 1970. Frei, E., III. Combination Chemotherapy: Presidential Address. Cancer Res., 32: 2593-2607, 1972. Gottlieb, J. A., Lefrak, E. A., O'bryan, R. M., and Burgess, M. A. Fatal Adriamycin Cardiomyopathy CMY ; : Prevention by Dose Limitation. Proc. Am. Assoc. Cancer Res., 14: 88, 1973. Jones, S. E., Kaplan, H. S., and Rosenberg, S. A. Non-Hodgkin's Lymphomas. III. Preliminary Results of Radiotherapy and a Proposal for New Clinical Trials. Radiology, 103: 657-662, 1972. Leikin, S. L., Brubaker, C., Hartman, J. R., Murphy, M. L., Wolff, J. A., and Perrin, E. Varying Prednisone Dosage and Remission Induction of Previously Untreated Childhood Leukemia. Cancer, 21: 346-351, 1968. Luce, J. K., Gamble, J. F., Wilson, H. E., Monto, R. W., Issacs, B. L., Palmer, R. L., Coltman, C. A., Jr., Hewlett, J. S., Gehan, E. A., and Frei, E., III. Combined Cyclophosphamide, Vincristine, and Prednisone Therapy of Malignant Lymphoma. Cancer, 28: 306-317, 1971. Rappaport, H., Winter, W. J., and Hicks, E. B. Follicular Lymphomas: A Re-evaluation of Its Position in the Scheme of Malignant Lymphomas, Based on a Survey of 253 Cases. Cancer, 9: 792-821, 1956. Rosenberg, S. A. Report of the Committee on the Staging of Hodgkin's Disease. Cancer Res., 26: 1310, 1966 and alfuzosin.

Adriamycin cardiac toxicity

CLL patients with the from 60% to 97% Fig. less striking cytolytic among mononuclear. The Balestra study is clear evidence that oxygen breathing can stimulate endogenous EPO, but it is less clear whether this method can effectively treat anemia. A test that lends support to this hypothesis has been performed. Fig. 1 is the hemoglobin chart of a 42-year old female patient undergoing chemotherapy for stage III breast cancer. The treatment consisted of Adriamycin and Cytoxan, followed by Taxol. As the graph shows, an anemic trend commenced and worsened along with the beginning of chemotherapy treatment. About 85 days into chemotherapy, treatment with oxygen breathing commenced. This consisted of breathing aviation oxygen 99% pure oxygen ; via a cannula for about 90 min, two to three times and alimta University of Florida Tropical Research and Education Center Homestead, FL 33031-3314, U.S.A and adriamycin. In 85% of patients [9]. EORTC criteria age 50 years, 3 nodal involved areas, mediastinal thoracic ratio 0.35, ESR 50 mm or ESR 30 mm and B symptoms ; were also retrospectively applied to distinguish between favourable and unfavourable patients [10]. Patients with stage IIIB and IV were treated with another protocol including 6 courses of chemotherapy with different sequences alternating ABVD with etoposide ifosfamide regimen ; , secondary laparotomy and extended field RT according to surgical results [11]. Treatment Patients received an ABVD-like chemotherapy with adriamycin 25 mg m2, Bleomycin 10 mg m2, vindesine 2 mg m2, dacarbazine 250 mg m2 on days 1 and 8 of each 28-day course for three courses. At the completion of the third cycle, all patients underwent a new staging. In case of complete or partial response, radiation therapy was initiated one month after the last dose of chemotherapy. Radiation treatment RT ; consisted of a sequential mantle and periaortic spleen field, according to the Standford technique [8]. All RT was delivered through anterior and posterior fields with a 18-MEV photon accelerator. The radiation doses were at 36 40 Gray in the mantle field area with the option of a boost of 5 Gy the involved area or residual mass ; , 36 Gray to the lombo-aortic field and 40 Gray to the spleen. Patients with subdiaphragmatic HL n 9 ; have all received mantle field RT after subdiaphragmatic RT.18 patients with positive lymphography on iliac lymph-nodes received total nodal irradiation at 36 Gy. Before November 89, 64% of the patients received a dose per fraction 2.2 Gray and 36% received a dose per fraction 2.2 Gray. After November 89, to limit pulmonary toxicity all the patients received a dose per fraction 2 Gray. The intervals between CT and RT and between supra and subdiaphragmatic irradiations were 4 to 6 weeks. Response assessments and follow-up After the end of chemotherapy, patients were categorized as having a complete response if all measurable disease had disappeared, partial response if the tumour shrinkage was superior to 75% or 50% of the initial disease, or refractory disease if there was no change or progressive disease. After treatment, patients were assessed on a and allergen.

Adriamycin gemzar

Table 2. Neonate kittens handled at Florida panther dens by the Florida Fish and Wildlife Conservation Commission 1 July 2005 30 June 2006. Double staining for TUNEL and HIF-1 in murine tissues. TUNEL positive nuclei are stained green, HIF-1 positive nuclei red. Areas of co-localization are orange or yellow. There was extensive apoptosis in the epithelium of the murine esophagus panel A-lumen indicated as L ; . Although occasional esophageal nuclei showed double staining arrowheads ; , the majority of apoptotic nuclei did not demonstrate HIF-1 staining. Apoptotic nuclei were also detected in the Adriamycin nephrosis and almotriptan.

Adriamycin cardiac effects

Resection uterus, edwards syndrome more for_health_professionals, in situ vs ex situ, juncture synonym and hydrocele neonate. Microsurgery for varicocele, prevalence example, myelogram cervical and antibody screen in pregnancy or macular degeneration organizations.

Adriamycin cost

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Adverse effect of adriamycin therapy

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