Cancer therapies

The progestin doses necessary for effective cancer therapy are very high, reaching 1000-2000 mg/d. These high concentrations of progestins may... 

Modem cancer therapy has been primarily dependent upon surgery, radiotherapy, chemotherapy, and hormonal therapy (72) (see Chemotherapeutics,anticancer Hormones Radiopharmaceuticals). Chemotherapeutic agents maybe able to retard the rate of growth, but are unable to eradicate the entire population of neoplastic cells without significant destmction of normal host tissue. This serious side effect limits general use. More recentiy, the immunotherapeutic approach to cancer has involved modification and exploitation of the cellular and molecular mechanisms in host defense, regulation of tissue proliferation, tissue differentiation, and tissue survival. The results have been more than encouraging. 

In 1971, levamisole, an anthelmintic compound widely used in catde and swine, was shown to improve the effects of an experimental Brucella abortus vaccine in mice. Since that time, the veterinarians and physicians have explored the effects of levamisole in such diverse areas as arthritis, lupus erythematosis, cancer therapy, respiratory diseases, Newcastle disease, foot-and-mouth disease, mastitis, and vaccine potentiation. Although the exact mechanism of action has as yet not been deterrnined there is substantial evidence that, under defined circumstances, levamisole can augment the animal s natural immune response (9). New immunostimulants include Staph Ijysate acemannon, NLAB-31. 

R. H. Shoemaker and co-workers, in Prediction ofKesponse to Cancer Therapy Alan B. Liss, New York, 1988, pp. 265—286. 

Radium occurs only in association with uranium (Chapter 31) the observed ratio Ra/U is 1 mg per 3 kg, leading to a terrestrial abundance for Ra of 10 ppm. As uranium ores normally contain only a few hundred ppm of U, it follows that about 10 tonnes of ore must be processed for 1 mg Ra. The total amount of Ra available worldwide is of the order of a few kilograms, but its use in cancer therapy has been superseded by the use of other isotopes, and the... 

Naphthalocyanins, phthalocyanins, and porphyrins as sensitizers in photodynamic cancer therapy 98IZV836. 

Cobalt-60 cancer therapy. Gamma rays from the rotating radiation source are concentrated at the location of the diseased tissue. 

Water-soluble ruthenium phthalocyanines show promise as photodynamic cancer therapy agents [129b],... 

Besides direct apoptosis effectors, there are a number of other diugs which influence the above explained apoptosis pathways more indirectly. This class of diugs includes molecules which inhibit survival pathways like e.g. the Ras/Raf kinase pathway, the NF-kB pathway and many others. Also inhibitors of survival cytokines which are sometimes produced by cancer cells in an autocrine fashion can render cells susceptible to apoptosis and, hence, effective cancer therapy. These include, but are not limited to, ligands for dependence receptors and cytokines like e.g. interleukin-4. 

Dixon MJ (2006) Aromatase inhibitors in early beast cancer therapy a variety of treatment strategies. Expert Opin 7 (18)2465-2479... 

Targeted Cancer Therapy P450 Mono-Oxygenase System... 

Cytokines and biological response modifiers represent a broad class of therapeutic agents that modify the hosts response to cancer or cancer therapies. The enormous body information about their clinical uses and their side effects is beyond the scope of this essay that can only give illustrative examples. For an up-to-date information the reader can resort to reference [5]. As many as 33 different interleukins are known and the list continues to grow IL-2 used in the treatment of kidney cancer is one example. Interferon alpha is used for chronic myelogenous leukeia, hairy cell leukaemia and Kaposi s sarcoma. Interferons are also used in the treatment of chronic infections such as viral hepatitis. Tumor necrosis factor (alpha), G/GM/M-CSF, and several other cellular factors are used in treatment of various cancers. Many of these cytokines produce serious side effects that limit their use. 

A substantial amount of indirect evidence supports the contention that the induction of apoptosis in tumor cells is critical to successful therapy. Cancer therapy might therefore be viewed as an attempt to induce apoptosis in a population of cells that have undergone selection for apoptotic defects. If correct, this hypothesis would suggest why cancer therapy is in many cases unsuccessful. However, recent studies indicate that this fundamental problem can be circumvented. Progress in the identification of molecules key to the cell death pathways has led to a growing understanding of how apoptosis occurs [3]. It has become clear that pathways to apoptosis are numerous and often interconnected. A solution to the clinical problem of therapeutic resistance, then, may lie in the fact that there appears to be multiple ways that a cell death program can be implemented. 

Bunz F (2001) Cell death and cancer therapy. Curr Opin Pharmacol 1 337-341... 

Blagden S, de Bono J (2005) Drugging cell cycle kinases in cancer therapy. Curr Drug Targets 6 325-335... 

Catlett-Falcone R, Dalton WS, Jove R (1999) STAT proteins as novel targets for cancer therapy. Curr Opin Oncol 11 490-496... 

Kohno M, Pouyssegur J (2006) Targeting the ERK signaling pathway in cancer therapy. Ann Med 38 200-211... 

Mikalsen T, Gerits N, Moens U (2006) Inhibitors of signal transduction protein kinases as targets for cancer therapy. Biotechnol Annu Rev 16 153-223... 

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