Deadline: 15th August 2012
Job description
Tumors often display
altered metabolic characteristics that are exclusive to the cancer cells
and thus, can be targeted for efficient treatment.
The zebrafish is emerging as a valid model to study processes underlying cancer and provides an ideal setting to conduct chemical genetic screens for synthetic lethal interactions in the intact organism.
The tumor suppressor LKB1 is mutated in a familial cancer-predisposition syndrome and in over 30% of lung adenocarcinomas, one of the most common human tumors with a very poor prognosis. LKB1 is a serine-threonine kinase that phosphorylates the AMP-activated protein kinase (AMPK), a key energy checkpoint in the cell. AMPK activation leads to growth suppression through several pathways including inhibition of the mTOR pathway. Human tumors with LKB1 mutations exhibit fast metabolic rate, increased invasiveness and poor prognosis. We have recently shown that Lkb1 is critical to maintain energy homeostasis in zebrafish. lkb1 zebrafish mutants are embryonic-viable (in contrast to mice), exhibit deregulated metabolism and fast metabolic rate, a characteristic of tumors cells.
We will use our lkb1 zebrafish model as a discovery platform in chemical genetic synthetic-lethal screens and to resolve the LKB1 network in control of metabolism.
The zebrafish is emerging as a valid model to study processes underlying cancer and provides an ideal setting to conduct chemical genetic screens for synthetic lethal interactions in the intact organism.
The tumor suppressor LKB1 is mutated in a familial cancer-predisposition syndrome and in over 30% of lung adenocarcinomas, one of the most common human tumors with a very poor prognosis. LKB1 is a serine-threonine kinase that phosphorylates the AMP-activated protein kinase (AMPK), a key energy checkpoint in the cell. AMPK activation leads to growth suppression through several pathways including inhibition of the mTOR pathway. Human tumors with LKB1 mutations exhibit fast metabolic rate, increased invasiveness and poor prognosis. We have recently shown that Lkb1 is critical to maintain energy homeostasis in zebrafish. lkb1 zebrafish mutants are embryonic-viable (in contrast to mice), exhibit deregulated metabolism and fast metabolic rate, a characteristic of tumors cells.
We will use our lkb1 zebrafish model as a discovery platform in chemical genetic synthetic-lethal screens and to resolve the LKB1 network in control of metabolism.
Requirements
You
must be a motivated enthusiastic researcher with a degree (drs./MSc) in
the domain of Biomedical Sciences and/or related subject and have a
strong interest in the fields of Developmental biology, cancer biology,
molecular genetics. You have demonstrated a strong interest in an
academic career through your publication record and prior engagement in
collaborative research and teaching. Furthermore you have excellent
communication skills in English, both written and verbal and are
expected to master the Dutch language sufficiently.
Faculty of Science
To the attention of:
Mrs. S. Wijfjes-Chang
e-mail s.t.s.wijfjes-chang@biology.leidenuniv.nl
Application procedure information
Do you identify with the profile above and do you aspire to have a career in research? Please apply by sending your written application before 15/08/2012, using the vacancy number, including full Curriculum Vitae and the names and phone numbers of two references to:Faculty of Science
To the attention of:
Mrs. S. Wijfjes-Chang
e-mail s.t.s.wijfjes-chang@biology.leidenuniv.nl
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