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Metabolic disturbance was observed in cancer cells. For example, excess glucose
and glutamine uptake by cancer cells. But the functional consequence of these
observation could not be linked to the autonomous growth potential of cancer
cells. The mitochondrial functionality was thought to be disturbed as was
hypothesised by Warburg. But this observation remained controversial as the
oxygen uptake of cancer cells did not show significant variation in cancer cells as
compared to normal cells. Therefore, there was a general consensus against the
metabolic theory of cancer. It was generally believed that cancer cannot be
considered as a metabolic disease while diabetes is a metabolic diseases. Only in
the last 15 years or so the metabolic basis of cancer has come to the forefront.
The focus of this course is to look at the genetic and metabolic basis of the rapid
proliferative property of the cancer cells. The theme is to learn the
aetiology/biology of cancer as much as to learn to do science objectively. Can
we understand the basis of cancer by looking at other organisms such as
microbes. Is the underlying basis of cells undergoing rapid proliferative process
fundamental biological design? Can we address this using other model systems?
The answer is yes. Yeast metabolism and genetics provides a great opportunity
to understand the metabolic basis of cancer.
First assignament
Paper presentation:
After midsem- each student has to make 1 hr present of a paper. (15%)
Take a paper, preferably published after 2000.
Have approximately a maximum of fifteen slides. That is 4 minutes/slide
Do not clutter the slides with text.
Give sufficient background. At least two to three slides
Experiments-give sufficient details/interpretations
Second assignment
Not more than three pages. 550 words/ page. Gives an idea of the content.
Questions to be addressed.
References and figures any, to be given at the end. This is not included in
three page limit. References should be not less than 10. Figures 2 to 3.
Third assignment: