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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.
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?
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.
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?
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?
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?
Several recent papers have shown that the miR-34 family of microRNAs is directly involved in mediating the effects of p53, indicating that non-coding RNAs have an important role in tumorigenesis. This Progress article discusses these papers and their implications.
Tumour-induced expansion of regulatory T (TReg) cells is an obstacle to successful cancer immunotherapy. Does it make more sense to suppress the function of these cells rather than deplete them to improve the efficacy of cancer immunotherapy?
How do DNA damage response pathways respond to low levels of DNA damage? Understanding this is essential when assessing environmental cancer risk. This Perspective considers the impact of a negligent G2/M checkpoint on genomic stability and cancer risk.
Cancer dormancy is a very important yet poorly understood phenomenon in cancer progression. What do we know about the mechanisms of cancer dormancy and can it be targeted therapeutically?
Fox proteins are transcriptional regulators of many biological processes. The authors discuss how these proteins are deregulated in cancer and the roles they have in both tumorigenesis and cancer progression.
Gene-directed enzyme–prodrug therapy (GDEPT) aims to improve the therapeutic ratio by increasing tumour cell kill and decreasing systemic toxicity. How is this achieved and how close is this therapy to entering the clinic?
Mixed lineage leukaemia (MLL) has histone methyltransferase activity and regulates the expression of genes such as Hox genes. This activity is lost in MLL fusion proteins resulting from inter-chromosomal translocations, which are leukemogenic. How do MLL fusions function and what is their role in leukaemia stem cells?
Glioblastoma stem cells might be dependent on cues from aberrant vascular niches that mimic the normal neural stem cell niche. What are the implications of these findings for treatment of this disease?
Studying metastasis has been difficult because until recently only the end result (metastases) could be observed. Advances in imaging technology have enabled us to begin to unravel the steps of metastasisin vivo.
Fatty acid synthase (FASN) catalyses the synthesis of fatty acids, and this synthetic pathway is upregulated in many tumours. How might FASN and increased lipogenesis be involved in cancer, and is FASN a valid therapeutic target?
Approximately 25% of lung cancer cases worldwide are not attributable to smoking, accounting for over 300,000 deaths each year. What do we know about this unique but poorly characterized disease?
Mantle cell lymphoma, characterized by proliferation of mature B lymphocytes, is one of the most aggressive lymphomas. What molecular pathways are involved in its pathogenesis, and how can these be exploited to predict patient prognosis and design new therapies?
