1) The tumour burden. Cancers occur with vastly different frequencies in different human populations. The risks of cancers often seem to be increased by assignable influences including lifestyle.
2) Genetic alterations in cancer cells. Chromosome alterations. Mutations causing cancer occur in both the germ-line and the soma. The karyotype of cancer cells is often changed through alterations in chromosome structure and number.
3) The Nature of Cancer. Tumours arise from many specialized cell types throughout the body and are complex tissues. Tumours are monoclonal growths and develop progressively. Chemical and physical carcinogens act as mutagens and epimutagens, which may be responsible for some human cancers.
4) Tumour viruses. RNA and DNA viruses can both induce cancer. Tumour viruses genomes persist in virus-transformed cells by becoming part of host cell DNA and induce multiple changes in cell phenotype including acquisition of tumourigenicity.
5) Cellular oncogenes and tumour suppressors. Oncogenes discovered in human tumour cell lines are related to those carried by transforming retroviruses. Proto-oncogenes can be activated by genetic and epigenetic changes affecting either protein expression or structure. The cancer phenotype is recessive and loss-of-heterozygosity events can be used to find tumour suppressor genes. Examples of tumour suppressor genes.
6) Growth factors and their receptors. Examples of growth factors and receptors as oncogenes, such as Src, Ras, EGF receptors, sis. Signalling circuitry programs from the cell surface to the nucleus are important traits of cancer and control various cellular processes, from differentiation, proliferation, metabolism, apoptosis to cell survival.
7) Control of the Cell Cycle Clock. Role of external signals for the cell cycle and downstream effects. Cyclin-CdK complexes and their inhibitors. pRb-E2F complexes.
8) Cell Immortalization and Tumorigenesis. Cell immortalization during tumorigenesis. p53 and Apoptosis: master guardian and executioner. Independent p53 apoptotic processes.
9) Cancer Stem cells, a hierarchy-based model for tumour generation and progression. The ability of Cancer stem cells (CSCs) to self-renew, to give rise to differentiated tumour cells and are their role for the overall organization of a tumour.
10) Maintenance of genomic integrity and the development of cancer. DNA repair and cancer. Epigenetics and cancer.
11) Angiogenesis and cancer. The angiogenic switch and cancer.
12) The role of the micro-environment in cancer development. Inflammation hyphen dependent tumour promotion operates through defined signaling pathways. Chronic inflammation can promote tumour progression. The role of stromal cells, macrophages, lymphocytes and fibroblasts.
13) Multistep tumorigenesis. Transformation usually requires collaboration between two or more mutant genes. The stem cell model for cancer.
14) Invasion and Metastasis. Travel of cancer cells from a primary tumour to a site of potential metastasis depends on a series of complex biological steps. Colonization represents the most complex and challenging step of the invasion-metastasis cascade. The epithelial-mesenchymal transition, induced by stromal signals, and associated loss of E-cadherin expression enables carcinoma cells to become invasive.