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High mobility group A (HMGA) proteins alter chromatin structure and therefore affect the transcription of large sets of genes. This can contribute to both benign and malignant disease in several ways.
Centrosomes have a crucial role in the formation of bipolar mitotic spindles, which are essential for accurate chromosome segregation. Certain oncogenic and tumour-suppressor proteins control centrosome duplication and function. How does their mutation result in numeral and functional centrosome abnormalities?
CHK2, an important player in the DNA-damage response signalling pathway, is a candidate multiorgan tumour susceptibility gene. Will the targeted modulation of this kinase or exploitation of its loss in tumours prove to be an effective anti-cancer strategy?
Mutations inBRCA1 and BRCA2are associated with cancer risk. However, it is important to understand the differences between populations, as both the prevalence of the mutations and the nature of their effects can differ between groups.
Cells with defects in the autophagic pathway are sensitized to apoptosis in response to metabolic stress, but, paradoxically, autophagy defects are associated with increased tumorigenesis. How can this paradox be resolved?
The ability to fuse cells is shared by many viruses. Does cell fusion, by inducing chromosomal instability, for example, link more viruses to cancer development? How can such hypotheses be tested?
