Unit 2 used the analogy of cells as productive citizens in a community of organs and tissues. Unit 3 will now focus on the normal functions of a cell that get disrupted when it becomes cancerous. It examines the role of DNA mutations in cancer, and how cancer progression is a product of cellular evolution.
Lesson 1
Lesson 2
Lesson 3
Lesson 4
Lesson 5
Lesson 1
How is our DNA organized?
As an introduction to this unit, students will extend their understanding of molecular dogma to investigate how the genome is organized into gene and non-gene regions and how some of these different regions function to either produce proteins or regulate when and where genes are expressed. The lesson introduces a new concept -‘transposons’- which comprise repeating sequences of DNA that contain promoters and can jump around the genome. In small groups, students will use an online genome browser to investigate the genomic organization of certain genes that are commonly mutated in cancer.
Objectives
– Explain how the eukaryotic genome is organized. – Explain the function of introns and exons. – Explain how repeat-ing sequences in the genome called transposons can dynamically affect genome structure and dysregulate normal genes leading to hyperproliferation.
Activities
Examination of human genome using UCSC genome browser
Worksheet: Reading on how repeating DNA sequences are involved in cancer and answer questions.
Lesson 2
How do normal cells become cancer cells?
In this lesson, students will examine how DNA mutations of different kinds can alter the levels and functioning of proteins involved in cell growth regulation, thus leading to cancer. Students will perform group activities to examine how point mutations can affect protein sequence and structure. They will also use an online genome browser to explore the types of mutations that commonly occur in genes associated with cancer.
Objectives
– Explain how DNA mutations turn normal cells to cancer cells in a process called transformation. – Explain the difference between mutations that affect when a gene is transcribed and mutations that affect how a gene is translated. – Explain how mutations in proto-oncogenes and tumor suppressors lead to cancer.
Activities
– Examination of how SNPs can affect protein sequence and function, using a worksheet. -Jigsaw: Using UCSC genome browser, examine types of mutations that occur in genes associated with cancer.
Have the students read Student Workbook Lesson 3.2 and answer the questions.
Lesson 3
How can the immune system cause cancer?
In this lesson, students will discover that inflammation, while necessary under certain conditions, can be harmful if it becomes chronic. Students will examine how chronic inflammation exposes cells to molecules that can damage their DNA, and simultaneously produces signals that lead to hyperproliferation. Under these conditions normal cells have a greater likelihood of becoming cancerous. Students will work in small groups on an interrupted case study examining how chronic inflammation may be the explanation for how obesity leads to increased cancer risk.
Objectives
– Explain the difference between normal inflammation and chronic inflammation. – Explain the role of secondary factors in converting normal inflammation into chronic inflammation. – Explain how chronic inflammation can lead to cell proliferation and DNA damage.
Activities
Interrupted case study examining link between obesity, inflammation and tumor formation.
Worksheet: Reading on how aspirin may protect against cancer and answer questions.
Lesson 4
How does DNA damage allow cancer cells to cheat death?
Students will examine how telomere shortening acts as an internal ‘clock’ in cells to limit the number of times they can replicate, thereby preventing them from dividing indefinitely. They will discover how cancer cells can reset the clock to become ‘immortal’ by expressing telomerase. Students work in groups on an interrupted case study to investigate whether inhibiting telomerase could be a useful strategy in controlling the growth of tumors.
Objectives
– Explain what a telomere is and how it protects chromosomal DNA during mitosis. – Explain how telomere shortening limits how many times a cell can replicate. – Explain the function of telomerase, when it is normally expressed, and how its expression changes during cancer.
Activities
Interrupted case study examining inhibiting telomerase as a cancer treatment.
Worksheet: Reading on how telomerase and stem cells kept the world’s oldest woman alive and answer questions.
Lesson 5
How do cancer cells evolve?
In this lesson, students will explore how tumors evolve in response to selective pressure and will determine how evolution turns monoclonal tumors into polyclonal tumors. Students will perform an interrupted case study on how tumor heterogeneity affects our ability to treat tumors.
Objectives
– Understand the sequence of driver mutations required to transform a cell into a tumor. – Define the terms ‘monoclonal tumor’ and ‘polyclonal tumor’ and explain their relevance in cancer progression. – Interpret data showing that chemotherapy can select for drug resistant tumor cells.
Activities
Interrupted case study on how tumor heterogeneity affects our ability to treat tumors.
