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This essay on prognosis in tumor diagnosis pathology resp. tumor etiology, cancerogenesis and molecular oncology is the authors personal opinion. Generally tumor diagnosis improves with progress in histo- and cytological methods for example in tumors of the APUD-system and precancerous lesions especially of the breast. Fundamental principle of developed tumor diagnosis is the knowledge of malignant transformation. Its profits favours the etiology in cancerogenesis and e.g. non Hodgkin lymphomas (Burkitt lymphoma, adult T-cell lymphoma) and to result from new methods in molecular biology and viral genetics (DNS-hybridizing, -recombination and gene technology). With the beginning century a stepwise fitted diagnosis of malignant lymphomas is evident up to monoclonal dedifferentiated lymphoid cells and their multifarious phenotypical markers. This concept may be of general significance in tumor diagnosis already indicated in prelymphomas. Finally the present prognosis of tumor diagnosis is evaluated by contents, tasks and strategies of its corresponding research lines in clinical and experimental tumor pathology resp. its organization.

Concentration-effectivity curves of Triton X-100 activity on ascitic cells of mouse leukemia 1210 and Zajdela-Hepatoma in rats have been plotted by electronic determination of cell numbers, indicating only one part of cytolysis which follows a sudden decrease of cell volumes. A better characterization of the whole cytolysis can be realised by volumetricall particle counter analysis. It first displays an increase in cell volumes for several concentrations in connection with microscopically observed increase in cells staining relatively weak by eosin. Staining and swelling nearly simultaneosly reach their maximum. Furthermore a sudden diminution of the cells follows with a shift of cell volumes distribution curves to the left, determined by particle counter depending on temperature, e. g. a strong delay at 0 degrees C.

In the recent century research in cancer metastasis has greatly improved; nowadays it is a superior topic in cancer literature. Most of its problems result from alternate assumptions: The functional seed and soil and the hemomechanic hypothesis, after all putting two questions on account of metastasis being either a permanent likewise passive or a cascade phenomenon. In regard of metastasizing bronchial-, breast- and prostate carcinomas or multifocal tumors and most of rodent neoplasms a passive tumor cell transport might be a single effect, but the characteristic feature rather a step by step metastasizing cascade, implicating special organ localizations, and the fact, that metastasis distribution correlates with tumor biology, localization of the first metastasis and in manifold metastasizing tumors with typical organ patterns. From introduction of recent in vitro and cloning-techniques the metastasizing potency of tumors now becoming able to be defined by function of its genetic heterogeneity, developing metastasizing phenotypes respective neoplastic evolution by mutation, gene amplification, and epigenetic factors. On the other side having an unique xenobiotic metabolism metastasizing tumor cells are in accordance with the conception of their inherent "commonality".