The paper describes the influence of selected genes on neogenesis, including their expression, RNA transformation, translation and transcription. The role of adhesive molecules, extracellular matrix, cytoskeleton and signal conduction in neoplastic induction is described. External stimuli, internal factors and disturbances in DNA repair can cause cell mutations (fig. 1). An accumulation of various factors in different gene classes, together with their amplification, leads to tumour formation. Neoplastic cells undergo a dominant mutation, thereby gaining a new function, or cumulate recessive mutations which cause the loss of a function. This is particularly true in genetic anomalies associated with the cadherin system, e.g. the loss of E-cadherin expression in mammary cancer. The loss of E-cadherin or catenin expression causes the loss of cell connections, which facilitates metastasizing. Cells in metastases often show genetic disorders, a more malignant phenotype and increased drug resistance, which worsens clinical prognosis. The search for new anti-neoplastic drugs for humans is based on molecular studies and mice experimental models. The animals in these models show a phenotype corresponding with specific human diseases, e.g. Pax gene mutation in sarcomas and carcinomas, antisense DNA therapy (in Burkitt’s lymphoma or chronic leukaemia) or induction of retroviral vectors (thymidine kinase gene) in herpes virus (HS-th) in proliferating cells in multiform glioblastoma.
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