Cancer Biology 2007/8
TRIAL EXAMINATION
Give reasons for why data from epidemiological cancer cohorts is not always conceivable with what can be expected from the number of carcinogenic constituents found in edible plant, food stuff including those that are formed in cooking? (3)
What is an Oncogene?
Give an example of a mammalian oncogene and its corresponding oncoprotein. (2p)
Which of the following was used to detect oncogenes in the DNA of cancer cells
(a)Translation
(b)Transcription
(c)Transfection
Briefly describe how this method was initally used in cancer research. (4p)
What are the cell surface receptors called that sense the cell contact with the Extra Cellular Matrix (ECM)? (2p)
Cancer cells are characterized by hyperactive signalling. Give three examples of how a cancer cell can obtain hyperactive signalling caused by processes that involve growth factors and growth factor receptors.
Assume that the Ras proteins in a cell have a mutation that’s make them constantly active. How would that influence the cell cycle? (2p)
a) It will stop retinoblastoma protein (pRb) phosphorylation and thereby start cell differentiation.
b) It will lead to cyclin D accumulation and thereby entering of the cell cycle.
c) Cyclin B will be down regulated and the cell will thereby stop in G2.
d) It will lead to an enhanced signal from the TGF-B receptor that will favour cell proliferation.
P53 is an important tumour suppressor gene. Describe in detail the molecular mechanisms how p53 function to prevent cancer outgrowth. (6p)
What is the meaning of the ALT-mechanism and how does it work? (3p)
Give an example of two strategies used to protect normal stem cells from transformation. (2p) Which different types of genotoxic damage can be found at high frequencies in tumour cells and what type of DNA lesions might have caused the damage? (2)。