hrvatski

Aktivacija signalnih molekula u karcinogenezi

In the last decade, basic cancer research has produced remarkable advances in our understanding of cancer biology and cancer genetics. Among the most important of these advances is the realization that programmed cell death (apoptosis) and the genes that control it have a profound effect on the malignant phenotype. Apoptosis is a natural process for removing unwanted cells such as those with potentially harmful mutations or alterations in cell-cycle control. Deregulation of apoptosis can disrupt the delicate balance between cell proliferation and cell death and can lead to diseases such as cancer. In many cancers pro-apoptotic proteins have inactivating mutations or the expression of anti-apoptotic proteins is up-regulated, leading to the unchecked growth of the tumour and the inability to respond to cellular stress, harmful mutations and DNA damage. The evasion of programmed cell death has been recognized today as one of the six essential alterations in cell physiology that dictate malignant growth and is a hallmark of most, and maybe all, types of cancer. An intense research effort is uncovering the underlying mechanisms of apoptosis in order to discover new biochemical markers that could be used for early diagnosis of cancer, and to produce new therapies that are less toxic and mutagenic than current treatment regimens. Apoptosis targets that are currently being explored for cancer diagnostics and drug discovery include death receptors triggering apoptosis from the cell surface, Bcl-2 proteins as the gatekeepers of the mitochondrial pathway, caspases as the executioner enzymes or endogenous caspase inhibitors. Some of these potentially promising signalling molecules in cancer diagnostics and treatment will be discussed.

karcinogeneza; signalne molekule; apoptoza

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