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Jessica Doondeea
Jessica, a British native with familial roots on the tropical island of Mauritius, joined us in 2007. As our lab manager, she has since played a key role in keeping our operation running in general, but also in generating high quality tumour cell lysates from the large panel of HNC cell lines that we have gathered in our group in the last years. Building on this, she has recently started to screen for the abundance and activity of potentially cancer-driving proteins. From this, Src family kinases, enzymes that add phosphate groups onto tyrosine residues of specific target protein epitopes, have emerged as a very promising candidate for further exploration and potentially therapeutic targeting.
Oncogenic, i.e. cancer causing, Src was first found almost 100 years ago, as the key component of a virus that leads to tumour formation in infected chickens. Despite its very early emergence, it has only been recently recognised that Src and its relatives appear to play important roles in the survival and metastatic spread of cancer cells.
This delay is in part explained by the fact that Src and its siblings are rarely changed (mutated) in tumours. Instead their abundance and enzyme activity status becomes de-regulated in some tumours. In some major tumour types, for example, breast cancers, Src appears to drive primarily tumour metastasis, so knocking it out with drugs may prevent the formation of new tumours, but could have little effect on existing ones.
In contrast, our recently started work with HNC squamous carcinoma cells points towards a more vital role for Src family kinases in these tumour cells.
By following up this intriguing initial finding, we hope to gain insight into the actions of Src kinases in this tumour type, which may enable us to recommend that HNC patients are soon to be included into the different clinical trials currently starting or readily ongoing with novel Src family kinase inhibiting drugs.
This delay is in part explained by the fact that Src and its siblings are rarely changed (mutated) in tumours. Instead their abundance and enzyme activity status becomes de-
In contrast, our recently started work with HNC squamous carcinoma cells points towards a more vital role for Src family kinases in these tumour cells.
By following up this intriguing initial finding, we hope to gain insight into the actions of Src kinases in this tumour type, which may enable us to recommend that HNC patients are soon to be included into the different clinical trials currently starting or readily ongoing with novel Src family kinase inhibiting drugs.
Src family kinases in HNC