Telomeres are formed by specific DNA sequences at the ends of the chromosomes and their shortening during cell division plays an important role in limiting proliferation. Recently, it has become apparent that telomere signaling can also be induced in cancer cells delayed in mitosis, leading to activation of the ATM kinase and subsequent activation of the p53 tumor suppressor (Hayashi et al, 2012). This response can be induced by drugs such as taxol (paclitaxel) that inhibit progression through mitosis.
Breast cancer patients who are treated with chemotherapy show a huge variability in their response. Chemotherapy often results in undesirable side effects that can reduce quality of life and lead to life threating complications. Therefore, identifying patients who will benefit from chemotherapy remains a major research challenge. The p53 tumour suppressor plays a key role in the response to chemotherapy and is frequently mutated in many cancers.
Background : The RNA helicase p68 is an important transcriptional coactivator of several proteins that play key roles in cancer development. p68 is aberrantly expressed/modified in several cancers, suggesting that alteration in p68 expression/function may be key events in tumour development.
It is now well established that atherosclerosis is an inflammatory disease with a broad array of inflammatory cells and pathways implicated at every stage of the disease . Acute and chronic inflammation are key factors in the development of endothelial damage [2,3]. As endothelial dysfunction is a validated biomarker for future cardiovascular events, closer study of the role of inflammation in early-stage endothelial dysfunction should be undertaken, particularly in high risk populations.
Background: Cyclin subunits, in combination with their Cyclin-dependent kinase (Cdk) domains, regulate many aspects of cell cycle progression, including DNA replication (Cyclin A2) and cell division (Cyclin B1). Cyclin A2 and Cyclin B1 share the same catalytic subunits, Cdk1 and Cdk2, therefore it is difficult to separate their functions because Cdk1 or Cdk2 inhibitors affect multiple Cyclin/Cdk complexes at once. For example, Cyclin B/Cdk1 is known to stimulate mitotic entry but Cyclin A2/Cdk1 could well play an important undiscovered role.
Wnt signalling was first discovered in tumour models and has been recognized as a key regulator in cancer for several decades. This has prompted a number of researchers and pharmaceutical companies to develop Wnt-modulating drugs for cancer treatment. However, we are still learning about the complex and often context-dependent effects of WNT signalling in differing tumour types, so it is important to understand the role of Wnt signalling in individual cancers before Wnt-modulating therapeutics can be used to treat patients.