title: [Pharmacokinetic aspects of tumor tissue impairment by cancerostatics. Ways for the intensification of the induced attack in the multiple step cancer therapy. CMT-Selectine].
abstract: After discussion of the causes of natural selectivity of cancerostatics it is pointed out that, thanks to recent advances in cell kinetics (cycle-adequate selection of cancerostatics) combined with microtopography of substrate supply in the intercapillary region of cancer tissue, chemotherapeutic treatment of cancer is developing into a theoretically founded and modifiable therapy. Within the nexus of closely related problems it is especially the studies on pharmacokinetics of cancerostatics that still are in arreals. The discussed course of such an investigation basis oe the carticularly of cancer tissue, i.e., the often inadequate vascularization parameters that deteriorate even further with growing tumor size. -- The given valance equation for a change in the concentration of a cancerostatic in tumor tissue has been evaluated using, for an example, a substance from the alkylating group whose mass number approximately coindices with that of cyclophosphamide in its active form. As far as the better vascularized cancer tissue farther from the capillaries are concerned (e.g. early stages of tumors and metastases) the effective dose only drops from 1 to about 0.7. In poorly vacularized cancer tissue, on the other hand, the respective effective dose is reduced from 1 to approx. 0.25. Unfortunately, however, this drop in effective dose takes place exactly in a location where the most resistant fractions of tumor cells are to be found. A feasible way out this crucial dilemma inherent in the chemotherapy of cancer is to combine a substance of low mass numer that causes a pronounced long-term stimulation of body own defence (e.g. our BA 1, and N-(2-cyanoethylene)-urea) with a cancerostatic like CMT-selectine that -- in optimally hyperacidified cancer tissues -- reaches its active form only at a reduced pH so that (contrary to normal cancerostatics) stimulation of the body-own defence caused by the first mentioned substance is not impaired.
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000378:metabolism* / Q000494:pharmacology / Q000627:therapeutic use; D002196:Capillaries / Q000503:physiopathology; D002455:Cell Division; D004305:Dose-Response Relationship, Drug; D004359:Drug Therapy, Combination; D004361:Drug Tolerance; D005947:Glucose / Q000378:metabolism; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007700:Kinetics; D008433:Mathematics; D009369:Neoplasms / Q000098:blood supply / Q000188:drug therapy / Q000378:metabolism*; D010100:Oxygen / Q000502:physiology; D011817:Rabbits
chemical_list: D000970:Antineoplastic Agents; D005947:Glucose; D010100:Oxygen
vernacular_title: Pharmakokinetische Aspekte zur Krebsgewebeschädigung durch Kanzerostatika. Wege zur Intensivierung der auslösenden Attacke bei der Krebs-Mehrschritt-Therapie. CMT-Selectine