Chris Evans reveals his wife gave him a blood pressure monitor
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A gene commonly activated in aggressive cancer has also been implicated in heart failure and high blood pressure. The gene, called PBK, is upregulated in lung tissue leading to a thickening of the arteries linking the heart and lungs. This results in high blood pressure going through the heart and causing progressive and severe heart failure. The researchers have been awarded around £1.9 million to continue their research to hopefully provide information that could aid treatment.
The researchers think there could be similarity in the mechanisms of pulmonary hypertension and cancer.
Dr David Fulton says that the rapid cell division found in cancer is also present in pulmonary hypertension, where it causes the narrowing of arteries.
Dr Fulton said: “We were looking for genes involved in promoting smooth muscle proliferation that also are in cancer.
“It’s the uncontrolled proliferation that is the problem, and we are looking for targets that we could exploit to decrease it.”
Current treatments are broadly focused on the symptoms, looking to dilate the airways and increase the amount of oxygen absorbed.
The only currently effective cure is a lung transplant.
Dr Fulton said: “People need help and we think this offers one avenue toward helping.
“That is why we like it, we think it’s a good target.”
The PBK gene is found to be overexpressed in particularly bad cancers.
In bladder, lung, liver and brain tumours large amounts of PBK is associated with a worse prognosis.
The researchers note that PBK is not the only gene that regulates cell proliferation, but is often involved in the early development of pulmonary hypertension.
PBK is short for PDZ-Binding Kinase where the PDZ stands for “Post synaptic density protein, Drosophila disc large tumour suppressor, Zonula occludens-1 protein”.
PDZ is a structural region found in signalling proteins not only in animals but also in plants, fungi, bacteria and viruses.
Proteins containing PDZ are often involved in regulating cellular pathways.
Examining which pathways PBK is involved with could improve our understanding of the cancers that result from its overexpression.
One of the tests underway now involves attempting to “knock out” the gene, forcibly deactivating it in a rat to see what happens.
This is a common research approach to finding out how genes interact, as well as the implications it has on other bodily functions.
If the knockout of one gene causes change in other proteins, this can allow researchers to draw links between them and establish the chain of events that causes a specific outcome.
One linked protein is already known, YAP1 which stands for Yes Associated Protein 1.
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