CELLULAR AND MOLECULAR ONCOLOGY
- Scheda dell'insegnamento
- Obiettivi formativi
- Metodi didattici
- Verifica dell'apprendimento
The aim of the course is to introduce to the biological and molecular aspects of neoplastic transformation and to explore how these mechanisms are altered in different types of cancer. Emphasis will be given to the events that drive cancer initiation, cancer progression and metastatic dissemination. The role of the micro-environment will also be deeply investigated, now considered to be a key player in supporting all phases of the development of cancer.
This course will also provide the students with the opportunity to develop as adult learners and as effective contributors in a professional environment by:
1. Being responsible for their own learning and for the depth of their own study.
2. Using their own initiative to make use of all the available resources to complement lecture material, including academic staff resources.
3. Working in a team environment and contributing effectively to their own learning and to that of their peers by questioning each other and academic staff when uncertain.
4. Developing communication skills by effective interaction with peers and academic staff.
In order to follow the course, an adequate knowledge of cell and molecular biology, biochemistry and physiology is required.
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. Signaling 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) Maintenance of genomic integrity and the development of cancer. Stem cells and cancer. DNA repair and cancer. Epigenetics and cancer.
10) Angiogenesis and cancer. The angiogenic switch and cancer.
11) 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.
12) Multistep tumorigenesis. Transformation usually requires collaboration between two or more mutant genes. The stem cell model for cancer.
13) 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.
The course topics will be dealt with lectures-style instruction.
Oral exams. To pass the exam, the student will need to demonstrate sufficient knowledge of the topics covered during the lectures, and get a score of at least 18/30
The textbook is:
Authors: Robert Weinberg
Title: The biology of Cancer
Additional material will be provided during the course
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