Tumors solid

The mitomycins do not react directly with DNA, but require prior activation by reduction of the quinone. This property of bioreductive activation has inspired the design and development of synthetic anticancer drugs that are also activated by reduction, as this is expected to confer a degree of tumor selectivity [45, 46]. Many solid tumors are short of oxygen relative to normal tissue, so reductive activation of the mitomycins and other bioreductive drugs can proceed in tumors, while it is inhibited by the oxidizing environments in normal tissues. 

Bendamustine is a useful antineoplastic drug for the treatment of non-Hodgkin s lymphomas, multiple myeloma and as a partner drug in the combination therapy of some solid tumors. The cross-resistance with other alkylating drugs is not complete. Myelosuppression and lymphocytopenia is its main dose-limiting toxicity. 

Cancer treatment is a multimodality treatment, i.e., surgery is combined with radiotherapy and antineoplastic chemotherapy. The latter treatment mode is used mainly for cancers which have disseminated. Different forms of cancer differ in their sensitivity to chemotherapy with antineoplastic agents. The most responsive include lymphomas, leukemias, choriocarcinoma and testicular carcinoma, while solid tumors such as colorectal, pancreatic and squamous cell bronchial carcinomas generally show a poor response. The clinical use of antineoplastic agents is characterized by the following principles. 

One commonly used agent is the antimetabolite 5-fluorouracil (5-FU), which is frequently used as an adjuvant therapy in conjunction with surgical excision in the treatment of solid tumors. p53 can directly trigger apoptosis in cells exposed to 5-FU in vitro [1]. In addition, there is a substantial amount of clinical... 

The presence of chromosomal translocations is a consistent feature of many leukemia s, lymphomas, and certain solid tumors. At the genetic level, these events can either deregulate an intact gene by disruption or removal and replacement of the adjacent controlling elements, or create a new fusion gene that express the N-terminus of one protein fused to the C-terminus of another protein. 

TNF was originally identified because of its cytotoxic activity against some tumor cell lines and its ability to induce hemorrhagic necrosis of solid tumors in various animal models. However, the clinical use of TNF as an anticancer drug has been so far limited by its severe cardiovascular side effects. Therefore, TNF treatment is limited to regional and local administration of high doses of TNF, often in combination with chemotherapy, as accomplished in isolated limb and isolated hepatic perfusion (ILP and IHP, respectively) [5]. In the case of ILP, typically metastases are treated, patients benefit from this procedure by salvage of limbs from a loss by amputation. 

FIGURE 9 Antitumor activity of liposome-encapsulated cDDP and free cDDP in solid IgM immunocytoma-bearing Lou/M rats. Tumorbearing rats were injected with 2 mg cDDP/kg body weight twice a week (arrow). Tumor diameter at the start of the experiment was 2-3 cm. Tumor growth during treatment is presented (mean SD of six animals unless otherwise indicated). Liposomes DPPC/DPPG/ chol (molar ratio 10 1 10) size about 0.7 pm. PC/PS/chol (molar... 

D. (1978). Effect of lipid vesicle (liposome) encapsulation of methotrexate on its chemotherapeutic efficacy in solid rodent tumors. Cancer Res., 38, 2848-2853. 

Storm, G., Roerdink, F. H., Steerenberg, P. A., De jong, W. H., and Crommelin, D. J. A. (1987). Influence of lipid composition on the antitumor activity exerted by doxorubicin-containing liposomes in a rat solid tumor model, Cancer Res., 47, 3366-3372. 

Figure 3.1 Time course of implanted tumor volume for one experimental subject (Control) and associated fitted model curves (solid line, exponential model dashed line, nonparametric kernel estimate).

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