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The molecular and cellular pathogenesis of tumor growth and development

Zdenko Kovač


Puni tekst: hrvatski pdf 8.776 Kb

str. 13-32

preuzimanja: 2.903

citiraj

Puni tekst: engleski pdf 8.776 Kb

str. 13-32

preuzimanja: 318

citiraj


Sažetak

Molecular and cellular basis of pathophysiological mechanisms of tumor growth have been discussed in the paper. Long before clinical tumor appearance cells undergo various molecular alterations, some of which might have a pathogenic role in the tumor development. Genome in stability is the first prequisite step in the development of tumor. Due to physical chemical and biological enironmental in fluences, as well as endogenous disorders, such as in creased oxidative stress and inherited errors of repair mechanisms, somatic cell migh acquire a tumor cell phenotipe. Activation of protooncogens, inhibition of apoptosis and loss of antioncogene function are potential molecular mechanisms of cell immortalisation. In addition, some viral proteins interfere with the cellular regulatory processes, producing there with the malign antalternation of the host cell. Tumor cell survival is faced with genomic, immune defence and energy barriers in the host. An extensive cellular loss contributes to slow growth kinetics of the tumor. Those host barriers are a strong selective presure, due to which tumor cells survival and expansion depends on the activation of multiple, very often parallel, pathogenic molecular mechanisms. The synthesis of selective proteolytic enzymes, expression of tisue homing receptors, as well as the expression of certain enzyme in hibitory molecules, seem to be the critical molecular evants which contribute to the metastatic potential of tumor cells. Molecular aspects of tumor in heritance as well as some molecular differences of benign and malignant neoplasms are discussed in the paper.

Ključne riječi

pathophysiology; tumor growth

Hrčak ID:

192485

URI

https://hrcak.srce.hr/192485

Datum izdavanja:

1.12.1996.

Podaci na drugim jezicima: hrvatski

Posjeta: 3.920 *