BIOL 314 (Fall)

Molecular Biology of Oncogenes

D. Dankort (Coordinator)
Bellini 264
(514) 398-2307
L. Majewska
Glen Campus
(514) 412-4400 ext. 23279
K. Christensen Glen Campus
S. Del Rincon
Lady Davis Institute
3 credits (3-0-6)
BIOL 200, BIOL 201 or ANAT 212 / BIOC 212; or BIOL 219 (or permission of instructor)
Successive accumulation of mutations of normal genes in a single cell results in the alteration of several physiological pathways/events/molecules, which collectively contribute to the genesis of cancer.   Genetic damage found in cancer cells is of two types: 1. One is dominant and in this process the genes are termed proto-oncogenes. A proto-oncogene is a normal gene whose protein product has the capacity to induce cellular transformation given it sustains some genetic insult. An oncogene is the gene that has sustained some genetic damage and, therefore, produces an abnormal protein capable of cellular transformation and cancer. 2. The other is recessive and the genes involved in this process are variously termed as tumor suppressors, growth suppressors, recessive oncogenes or anti-oncogenes. Events known to promote the formation of oncogenes, the biochemical properties of the proteins encoded by these mutated genes, and their functions will be analyzed in an attempt to understand the molecular basis of human cancers.  We will also examine current molecular targets for cancer therapy and the concepts and consequences of inheriting mutations in genes that predispose to cancer.

The Aim of this course is to:
Evaluate the relationship between oncogenes and cancer;                        
Analyze the key physiological changes in cancer cells and oncogenes involved in the induction of such changes
Compare the major requirements for cancer
Analyze these requirements during normal development
Critically analyze research papers in cancer
Propose hypothetical new molecular targets for cancer therapy

I. Evaluate the relationship between oncogenes and cancer
  1. Indentify and Define and structure cellular components from gene to proteins
  2. Define cellular homeostasis and apply the concept to a concrete example
  3. Provide a comprehensive classification of proto-oncogenes
  4. Identify some common facts about cancer
  5. Compare and identify the common activation mechanisms of normal genes to activate oncogenes
  6. Define concepts of cancer predisposition in the context of heritable mutations in cancer associated genes
II. Characterize the role of growth factor receptors and major signal transduction pathways in cancer 
  1. Growth factor receptors as oncoproteins and the role of tyrosine phosphorylation in cancer. (Provide example of GFR and means of abnormal activation)
  2. Intra-cellular signaling: describe major oncogenes and signaling pathways involved in cancer including src, ras and Akt; integrate molecular events from the cell surface to the nucleus.
  3. The contribution of aberrant signal transduction to cancer cell using specific examples for cell surface, intracellular and nuclear events. Provide specific examples of known cancers that thrive on aberrant signaling events and how different oncogenic signals can be integrated in the same cell.
III. Cell cycle, inflammation and apoptosis in cancer
  1. Review the cell cycle and describe the two major cell cycle pathways p53 and Rb.
  2. Describe the mechanisms of cell death and inflammation
  3. Explain how evasion of apoptosis can lead to cancer (Oncogenes bcl/bax; p53)
  4. Define the Limitless replicative potential (immortalization)-Telomere, telomerase and immortalization (oncogene hEST2/hTERT/hTRT)
  5. Describe the one carbon metabolism pathway and its relationship to cancer.
  6. Justify the need for Genomic instability - Loss of genes involved in sensing and repairing DNA damage or chromosomal segregation during mitosis (example: MSH2 family of genes, hSecurin gene)
IV. Angiogenesis, epithelial mesenchymal transition and cancer models
  1. Define Sustained angiogenesis and explain its role in cancer - Production of angiogenesis inducing factors  (VEGF)
  2. Analyze the need for cancer cells to invade tissues and to metastasize -Functional elimination of genes that suppress the cell’s ability to invade tissues and to metastasize (example: E-cadherin gene, CDH1 gene
  3. Compare the role of EMT in development with cancer – does E-cadherin and stromal genes play similar roles?
  4. Compare in vivo versus in vitro models of cancer
V. Translating molecular events to cancer therapy: How a precise molecular understanding of cancer can directly affect cancer therapy.
  1. An overview of molecules designed or selected to target major oncogenes and are currently used in cancer therapy: Farnesyl transferase inhibitors, receptor tyrosine kinase inhibitors, angiogenesis inhibitors, mTor inhibitors.
  2. What cancers can be molecularly targeted? Example of Chronic Myelogenous Leukemia, Gastro-intestinal stromal tumours, breast, lung and brain cancers.
  3. The role of gene therapy in cancer. Other perspectives currently under investigation in cancer therapy.
  4. Immunotherapy and cancer (hairy cell leukemia, BCG inoculations, stem cell transplantation).
  5. Through the example of one highly aggressive cancer the review of major oncogenes, oncogenic pathways and available molecular targets for adjuvant treatments will be performed.


The lectures and notes will be based on primary literature (reviews or papers that will be assigned by each professor). Students are strongly encouraged to attend lectures and use, as a reference, The Biology of Cancer  by Robert Weinberg. Garland Science, 2006.
Three hours of lectures per week

Mid-terms, written assignments, final examination. Exams will be based on materials presented and discussed in class and on assigned readings

McGill University values academic integrity. Therefore all students must understand the meaning and consequences of cheating, plagiarism and other academic offences under the Code of Student Conduct and Disciplinary Procedures (see for more information).

Last update: March 22, 2019