Degree course: 
Corso di Second cycle degree in BIOMEDICAL SCIENCES
Academic year when starting the degree: 
Academic year in which the course will be held: 
Course type: 
Supplementary compulsory subjects
Second semester
Standard lectures hours: 
Detail of lecture’s hours: 
Lesson (48 hours)

In order to follow the course, an adequate knowledge of cell and molecular biology, biochemistry and physiology is required.

Final Examination: 

Oral exams. For the exam, the student will prepare a presentation on one of the topics discussed during the course. The students will be provided with a list of specific topics, among which they will chose one for the preparation of a presentation. Updated reviews and research articles for the presentation will be provided on each topic. The students will need to further search on PubMed for additional research articles on the topic of interest to personalise their presentation.
The presentation will be prepared on the basis of the material provided and of the further articles the students will have retrieved from PubMed and must not be longer than 40 min, 15 min of discussion will follow.
The students need to demonstrate:
 sufficient knowledge of the specific topic presented
 the ability to discuss cutting edge cellular and molecular aspect of oncology
 the correct use of scientific terms
 to be able to make connections between the topics covered during the course and those not included in the presentation

Voto Finale

The aim of the course is to introduce the students 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.
At the end of the course, the students will:
get to know the fundaments of molecular mechanism of cancer onset,
progression and metastasis
describe the reciprocal relationship between the microenvironment and
tumour cells
distinguish the role of cancer stem cells from the bulk tumour cells
return the complexity of the epigenetic processes involved in tumour
build conceptual maps for the explanation of the still unresolved aspects
of genetic and epigenetic hierarchy during tumour onset and progression
search PubMed for the relevant scientific articles for their exam
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
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.
The optional Cellular and Molecular Oncology course is part of the two
curricula (Basic and Applied Biomedical Sciences and Double Degree) of
the first year of the Master's Degree in Biomedical sciences, allowing the
student to study in depth cellular and molecular bases that govern
pathological processes in oncology

1) The tumour burden.
2) Genetic alterations in cancer cells.
3) The Nature of Cancer.
4) Tumour viruses.
5) Cellular oncogenes and tumour suppressors.
6) Growth factors and their receptors.
7) Control of the Cell Cycle Clock.
8) Cell Immortalization and Tumorigenesis.
9) Cancer Stem cells, a hierarchy-based model for tumour generation and progression.
10) Maintenance of genomic integrity and the development of cancer.
11) Angiogenesis and cancer.
12) The role of the micro-environment in cancer development.
13) Multistep tumorigenesis.
14) Invasion and Metastasis.

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.


The course topics will be dealt with lectures-style instruction with the use of electronic presentations.
Each lesson will be subdivided in three rounds of 50min each, two breaks of 10min and 15 minutes of discussion with the students on the topics covered, for a total of three hours.
Working groups will be organized on specific issues related to the course topics.

The teacher receives the students after each lesson and by appointment.