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Cancer therapy melanoma

Fishman P, Bar-Yehuda S, Barer F, Madi L, Multani AF, Pathak S (2001) The A3 adenosine receptor as a new target for cancer therapy and chemoprotection. Exp Cell Res 269(2) 230-236 Fishman P, Madi L, Bar-Yehuda S, Barer F, Del Valle L, Khalili K (2002a) Evidence for involvement of Wnt signaling pathway in IB-MECA mediated suppression of melanoma cells. Oncogene 21(25) 4060-4064... [Pg.314]

IL-2 has been approved for the heatment of renal cell carcinoma and also has shown good activity in malignant melanoma. Both of these tumors are refractory to chemotherapy. IL-2 has also been used invesdgationally, both alone and in combinadon with LAK cells, with chemotherapy and with other biological response modifier s (BRM s) to d eat a variety of different cancers (e.g., head and neck carcinoma, colorectal cancer, cend al nervous system cancer etc). In addidon to cancer therapy, IL-2 has been used to d eat padents infected with human immunodeficiency virus and it has been used ex vivo to generate antiviral T cells which were reinfused into padents (Lewko and Oldham, 2003 Dorr, 1993). [Pg.557]

Chronic PUVA therapy accelerates photoaging and the development of actinic keratoses, nonmelanoma skin cancer, and melanoma. Squamous cell carcinomas occur at 10 times the expected frequency. In patients receiving 250 or more treatments, there is an increased risk of melanoma. Careful monitoring of patients for cutaneous carcinoma therefore is essential. [Pg.429]

Metal-based drugs have probably had most impact in the area of cancer therapy, with cisplatin still used to treat approximately 70% of all cancer patients. Cisplatin is particularly useful for treatment of testicular, ovarian, oropharyngeal, bronchogenic, cervical, and bladder carcinomas, lymphoma, osteosarcoma, melanoma, and neuroblastoma. Metallocene-type compounds were the first organometallic compounds to be evaluated in cancer therapy, and until recently, Ti(77 -C5H5)2Cl2 was undergoing clinical trials (see above). Despite this setback to the field,... [Pg.445]

Kingston TP, Lowe NJ, Winston J, Heckenlively J (1986) Visual and cutaneous toxicity which occurs during N-(4-hydroxyphenyl)retinamide therapy for psoriasis. Clin Exp Dermatol 11 624-627 Modiano MR, Dalton WS, Lippman SM, Joffe L, Booth AR, Meyskens FL Jr (1990) Phase II study of fenretinide (N-[4-hydroxyphenyl]retinamide) in advanced breast cancer and melanoma. Invest New Drugs 8 317-319... [Pg.249]

Polyamine analogs for cancer therapy often induce apoptosis, but so far the mechanisms have not been satisfactorily defined. Elevated levels of H2O2 as a byproduct of the catabolism of polyamines by spermine/spermidine acetyl-transferase (SSAT) are assumed to induce apoptosis by oxidative stress. In a recent study, Chen et al. demonstrated that a suppression of SSAT prevented the depletion of polyamine pools by polyamine analog-induced apoptosis in human melanoma cells [101]. The observation that this phenomenon is mainly related to the polyamine analogs opens a new route for the development of novel analogs inhibiting the SSAT induction that could lead to the disruption of the tumor, but not generally of normal tissues. [Pg.152]


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See also in sourсe #XX -- [ Pg.263 ]




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Cancer melanoma

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