In 2007 I had the opportunity to work in the Wallenberg Laboratory, Department of Medicine, Sahlgrenska University Hospital, Gothenburg University, Sweden with Professor Martin Bergo, now in the Cancer Center. The group’s goal is to define the biochemical and medical importance of the posttranslational processing of CAAX proteins—including K-RAS as therapeutic targets for the treatment of cancer and other diseases. Ras proteins regulate cell fates by cycling between an active GTP-bound state and an inactive GDP-bound state in response to extra-cellular stimuli. Mutations activate some Ras protein forms, especially the K and N Ras isoforms which are implicated in the pathogenesis of haematological malignancies such as Acute Myeloid Leukaemia (AML) – Juvenile Myelomonocytic Leukaemia (JMML) in children and Chronic (CMML) in adults. Myeloproliferative Disorders (MPDs) can result from over-expression of K-Ras (oncogenic isoform) or inactivation of Neurofibromatosis Type 1-NF1 (tumour suppressor). The title of my in this hematology/oncology project was ‘Determination of the NF1 Knock-out Efficiency in NMK and RMN Mice, in vivo’ using Cre-loxP mouse models where the switched-on/expressed ‘Cre’ causes the excision of the loxP sites, leading to activation of K-Ras. NF1 is knocked-out in the NMK mice and similarly, Rce1 in the RMN mice.
I enjoyed working in oncology, a subject I am also interested in. I used familiar techniques such as PCRs but I improved my knowledge on them as I learnt gene sequencing and primer design.