OF HEALTH AND DISEASE
THEME 1: MOLECULAR REGULATION OF ENERGY AND NUTRIENT
METABOLISM
Learning outcome Theme 1: Compare the results of homeostatic shift in cancer cells and normal cells with
regard to the energy and nutrient metabolism and infer how this translates to nutritional and
pharmaceutical anti-cancer intervention
INTRODUCTION TO CANCER
Cancer is the disease with the highest number of deaths.
Tumour – neoplasm
Cancer – malignant neoplasm a group of cells displays uncontrolled growth and invasion that intrudes upon
and destroys adjacent tissues (as long as nutrition is provided). These cells are immortal and lead to increased loss
of functions and chromosomal aberrations. Sometimes also metastasis takes place, or spreading to other locations
in the body via lymph or blood. These malignant properties of cancers differentiate them from benign tumours,
which do not invade or metastasize.
Tumour and cancer cells display cell proliferation and rapid growth. Cell proliferation is required for :
- Embryogenesis
- Growth
- Proper function of several adult tissues (in particular immune cells)
- Tumorigenesis
Metabolism in proliferating cells differs from metabolism in quiescent cells by:
1. High rates of glycolysis
2. Lactate production
3. Increased biosynthesis of lipids and other macromolecules
Making energy and biomass by cell metabolism is essential for cell proliferation.
Cancer cells are not fundamentally different from normal cells, but they are re-programmed such that optimal
growth of the individual cell is facilitated at the expense of the organism to which the cancer cell belongs.
Reprogramming results in improved fitness to provide a selective advantage during tumorigenesis. The
reprogrammed activities related to metabolism are the following :
- Altered bioenergetics
- Enhanced biosynthesis
- Optimized redox balance
The 8 Hallmarks of Cancer by Weinberg 8 biological capabilities that cancer cells acquire when they
progress into tumorigenic malignant neoplastic states
1. Sustaining proliferative signalling
o Abnormal receptors (always activated)
o Display lower growth factor requirements ( only a low concentration of serum which contains
growth factors is required)
o Produce their own activation signals
o Activation of downstream signalling events
2. Evading growth suppressors
o Tumor suppressors block cell proliferation when cells are damaged (p53, Rb), but these are often
mutated in cancers.
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