Home > IMMORTAL CELLS AN INTRODUCTION TO THE CELL CYCLE, MITOSIS & CANCER Lesson Overview This is a lesson to teach students about the life cy
IMMORTAL CELLS
AN INTRODUCTION
TO THE CELL CYCLE, MITOSIS & CANCER
Lesson Overview
This is a lesson to teach
students about the life cycle of a cell and cellular functions including
growth, division (mitosis), repair, and cell death (apoptosis).
It is intended for use in an introductory high school biology class.
The cell processes are taught through a disease theme, in this case,
exploring cancer.
Description of Activity
The lesson has 3 parts to
it. It begins with a writing prompt to engage students in a class
discussion about aging and death. From that the Hayflick limit
idea is introduced – that cells have a limited number of times they
can divide. This idea is compared to cancer cells which are essentially
immortal. Students then explore the Inside Cancer website to learn
about the Hallmarks of Cancer. Next, the students explore the
events of mitosis and the cell cycle by constructing a simple mitosis
puzzle and taking notes on the events happening at each stage.
Finally, students revisit the Inside Cancer site to find where disruption
of the normal life cycle occurs in cancer cells.
Background
Cell processes are the result of complex interactions between a cell’s genetic code (DNA) and its environment. Cells grow, divide, and die in response to cellular and extracellular signals. Sometimes cells are damaged beyond repair by environmental factors and undergo a programmed cell death - apoptosis. Some cells take advantage of apoptosis to die for the greater good of the organism.
Before a cell divides, it must make copies of its DNA and all the cellular organelles needed for the daughter cells. Each time DNA replication occurs, mutations occur. The cell has mechanisms for repairing both mistakes in DNA replication and other non-replication mutations that occur, but they are not foolproof. Even these mechanisms for repair are controlled by proteins that are produced from genes that are susceptible to mutations. If mutations occur in any of the key molecules along the repair pathways, cancer susceptibility increases as mutation rates accelerate.
In addition, with each cell division the non-coding ends of chromosomes (telomeres) get shorter and shorter. Eventually, these telomeres (junk DNA) will get so short that important information will no longer be copied leading to cell death. This, in part, placed a limit on the life of a cell. Telomere length alone does not account for the aging processes of cells or of an organism. Instead, the aging process is a complex interaction of intracellular events that are still not well understood. Cancer cells, however, have found a way around this limit. They have an enzyme called telomerase that extends the length of telomeres for unlimited cell divisions.
There are other noncancerous cells, however, that also produce telomerase –stem cells for example – so the characteristics of cancer cells must go beyond this. In fact, cancer is not as simple as inheriting one mutation in a single gene; it involves multiple mutations in multiple genes. There are checkpoints in a cells life cycle to make certain that the cell is on track for DNA replication and for cell division. Mutations in the proteins that regulate these check points are likely candidates for developing cancer.
The cell biology of aging. Hayflick L. Clin Geriatr Med. 1985 Feb;1(1):15-27.
Taken from: http://www.ncbi.nlm.nih.gov/pubmed/3913498?dopt=Abstract
It is only within the past ten
years that biogerontology has become attractive to a sufficient number
of biologists so that the field can be regarded as a seriously studied
discipline. Cytogerontology, or the study of aging at the cellular level,
had its genesis about 20 years ago when the dogma that maintained that
cultured normal cells could replicate forever was overturned.
Normal human and animal cells have a finite capacity to replicate and
function whether they are cultured in vitro or transplanted as grafts
in vivo. This phenomenon has been interpreted to be aging at the cellular
level. Only abnormal somatic cells are capable of immortality. In recent
years it has been found that the number of population doublings of which
cultured normal cells are capable is inversely proportional to donor
age. There is also good evidence that the number of population doublings
of cultured normal fibroblasts is directly proportional to the maximum
lifespan of ten species that have been studied. Cultures prepared from
patients with accelerated aging syndromes (progeria and Werner's syndrome)
undergo far fewer doublings than do those of age-matched controls. The
normal human fibroblast cell strain WI-38 was established in 1962 from
fetal lung, and several hundred ampules of these cells were frozen in
liquid nitrogen at that time. These ampules have been reconstituted
periodically and shown to be capable of replication. This represents
the longest period of time that a normal human cell has ever been frozen.
Normal human fetal cell strains such as WI-38 have the capacity to double
only about 50 times. If cultures are frozen at various population doublings,
the number of doublings remaining after reconstitution is equal to 50
minus the number of doublings that occurred prior to freezing. The memory
of the cells has been found to be accurate after 23 years of preservation
in liquid nitrogen. Normal human cells incur many physiologic decrements
that herald the approach of their failure to divide. Many of these functional
decrements are identical to decrements found in humans as they age.
Thus it is likely that these decrements are also the precursors of age
changes in vivo. The finite replicative capacity of normal cells is
never seen to occur in vivo because aging and death of the individual
occurs well before the doubling limit is reached.
The background information below describes the events at each of the stages of mitosis. There are many ways you can go from here to make sure your students receive the content you want them to have.
The information below is taken from: http://www.biology.arizona.edu/Cell_Bio/tutorials/cell_cycle/cells3.html
What is (and is not) mitosis?
Mitosis is nuclear division plus cytokinesis, and produces two identical daughter cells during prophase, prometaphase, metaphase, anaphase, and telophase. Interphase is often included in discussions of mitosis, but interphase is technically not part of mitosis, but rather encompasses stages G1, S, and G2 of the cell cycle. |
Interphase & Mitosis
Interphase |
The cell is engaged in metabolic activity and performing its prepare for mitosis (the next four phases that lead up to and include nuclear division). Chromosomes are not clearly discerned in the nucleus, although a dark spot called the nucleolus may be visible. The cell may contain a pair of centrioles (or microtubule organizing centers in plants) both of which are organizational sites for microtubules. |
Prophase |
Chromatin in the nucleus begins to condense and becomes visible in the light microscope as chromosomes. The nucleolus disappears. Centrioles begin moving to opposite ends of the cell and fibers extend from the centromeres. Some fibers cross the cell to form the mitotic spindle. |
Prometaphase |
The nuclear membrane dissolves, marking the beginning of prometaphase. Proteins attach to the centromeres creating the kinetochores. Microtubules attach at the kinetochores and the chromosomes begin moving. |
Metaphase |
Spindle fibers align the chromosomes along the middle of the cell nucleus. This line is referred to as the metaphase plate. This organization helps to ensure that in the next phase, when the chromosomes are separated, each new nucleus will receive one copy of each chromosome. |
Anaphase |
The paired chromosomes separate at the kinetochores and move to opposite sides of the cell. Motion results from a combination of kinetochore movement along the spindle microtubules and through the physical interaction of polar microtubules. |
Telophase |
Chromatids arrive at opposite poles of cell, and new membranes form around the daughter nuclei. The chromosomes disperse and are no longer visible under the light microscope. The spindle fibers disperse, and cytokinesis or the partitioning of the cell may also begin during this stage. |
Cytokinesis |
In animal cells, cytokinesis results when a fiber ring composed of a protein called actin around the center of the cell contracts pinching the cell into two daughter cells, each with one nucleus. In plant cells, the rigid wall requires that a cell plate be synthesized between the two daughter cells. |
Goals and Objectives
Students will be able to:
National Science Education Content Standards:
THE CELL:
THE MOLECULAR BASIS OF HEREDITY
Assumptions of Prior Knowledge
Common Misconceptions
Implementing the
Lesson
Time Allotment
Part 1. Hallmarks of
Cancer – approximately 80 minutes –some students may not finish
the Hallmarks of Cancer online activity. Decide how you want to
deal with that if your students do not all have access to the internet
at home. Some students may finish early, so consider a follow-up
activity for those that finish early.
Part 2. Mitosis–
approximately 80 minutes or less
Part 3. Mitosis and
Microscopes (1 class period – reduce assignment and combine with online
root tip activity if you have limited microscopes)
Part 4. Cell Cycle
and Cancer – approximately 50 minutes (65
with Nicotine Connection)
Before Class
During Class
DAY 1: Hallmarks of Cancer
What do you think: What does it mean to die of “natural causes” or to die of “old age?” And why does this happen?
(Free write for 4-5 minutes and then discuss)
Then orally pose the question… “Is there any living thing that doesn’t die, that can live forever?”
(Discuss ) Emryonic germ cells,
cell lines from tumors are capable of this but it doesn’t mean they
can’t die. Bacteria? Asexual organisms?
Table 1: The average number of cell doublings (or rounds of cell division) in human fetal cells in vitro. Source:
Normal Cells
20% Oxygen |
Normal Cells w/
3% Oxygen
(equal to internal environment of humans) |
Cancer cells |
|
Average Number of cell doublings | 50 |
70 |
No limit |
Place the table above on the board with a document camera (or write on the board).
Have students look briefly at the data and explain any unfamiliar vocabulary. Have them answer the following questions in their science journal or on a piece of paper:
The data shows that cells with more oxygen divide less than cells with less oxygen and cancer cells can divide unlimited in a petri dish(as long as they are moved to new dishes)
Oxygen kills cells. Cells have limits to the amount of times they can divide.
Isn’t oxygen a good thing? Why would it kill cells? Why can’t our cells divide forever? What would happen if you grew cells with no oxygen?
After about 5-7 minutes, discuss the answers to the questions as a class.
In order to understand how cancer
cells are able to evade death it is important to understand how normal
cells work and how cancer cells differ. Today we are going to
visit the Inside Cancer website to learn a little about normal
cell functions and abnormal cells that may become cancerous.
DAY 2: Mitosis
Tell students that to really understand why cells have limits, it is important to understand how cell division occurs, what those steps are, and how some cells (cancer cells) can escape death.
MITOSIS PUZZLE: Give them the handout for the mitosis puzzle. Read through the background together stopping to define the functions of the key players as a class.
Vocabulary Review:
When students are done with their puzzle they will take notes on the events happening at each stage of the cycle. You may want to allow a certain amount of time and then go over as a class. (Alternatively, you could start the next class period projecting a picture of one of the stages and ask students to say what stage it is in and what evidence in the picture led them to that conclusion. This is also assigned individually for Day 3.)
DAY 3: Stages of Mitosis & Microscopes
Considering reviewing how
to safely handle and use microscopes. Then have students search
for 3 different stages of Mitosis under the highest objective lens.
Have them draw the cells in their science notebook and label the major
structures visible including cell wall/cell membrane, chromosomes, spindle,
cell plate, nuclear membrane, nucleus, etc. Students should include
a sentence for each drawing stating what stage of mitosis the cell is
in and 2-3 observations/evidence to support this. It is recommended
that students get their first drawing signed off by their teacher to
make sure it meets standard for size, amount of detail, etc.
DAY 4: Cell Cycle and Cancer
(You may be able to start on this if you have time left over on day 2 or 3, or you could assign the online practice for homework.)
Go over the mitosis puzzles and stages as a class before moving on.
Then tell the students that they will have some time to practice identifying the stages of mitosis with an online tutorial. Then they will see how mitosis fits into the cell cycle and how disruptions in the cell cycle may result in cancer.
Hand out “Part 3. Cell Cycle and Cancer –Student Worksheet” and read directions together before releasing students to computers.
Go over material as a class
when finished either the same day or the next day.
Recommendations for Evaluation:
Suggestions for Extended Learning
Continue exploring the Inside Cancer website and have students look specifically for cell biology content.
Have students write a specific
question about cancer and have them look for it on the website.
Glossary
Apoptosis – programmed cell death
Mitosis – the process of cell division beginning with prophase and ending in cytokineses.
Protein Synthesis – the joining of amino acids to match mRNA that carries the DNA message of a particular gene
Telomerase – an enzyme responsible for extending the length of telomeres, present in cancer cells and embryonic stem cells
Telomere – the junk DNA
at the ends of chromosomes that does not get copied in DNA replication
and serves to protect the ends of chromosomes; telomeres get shorter
with each cell division and eventually so short that coding regions
of DNA may be lost
Resources
www.insidecancer.org
http://www.ncbi.nlm.nih.gov/pubmed/3913498?dopt=Abstract
http://www.biology.arizona.edu/Cell_BIO/activities/cell_cycle/activity_description.html
The following pages are Student Worksheets followed by Teacher Answer Keys:
INSIDE CANCER: Hallmarks of Cancer – Student Worksheet http://www.insidecancer.org/
Direction: Go to the website above and navigate through the Hallmarks of Cancer section to answer the following questions for each section.
OVERVIEW
Type of Mutation | Original DNA sequence | New DNA sequence |
Single Nucleotide
Change
(aka Point Mutation) |
CAGGCGCAT | |
Deletion | CAGGCGCAT | |
Duplication | CAGGCGCAT |
GROWING UNCONTROLLABLY
EVADING DEATH
PROCESSING NUTRIENTS
BECOMING IMMORTAL
INVADING TISSUES
AVOIDING DETECTION
PROMOTING MUTATIONS
Part 2. MITOSIS PUZZLE
Objective: To identify the stages and events of mitosis (cell division) in a multicellular organism.
Background: Human embryos are similar in size to a rat embryo. Why then do they end up being such different sized organisms? The size of an organism is determined mostly by its number of cells and partially by the sizes of those cells. Certain cells in a human might be smaller than certain cells in a mouse and vice versa. In addition, most cells have a limit to the size they can grow. On the other hand fat cells can grow larger when we stores excess calories as fat droplets inside those cells. The more droplets, the larger the cell becomes until it reaches a point in which the control center (nucleus) can no longer manage a cell of that size. At that point the cell must undergo cell division.
In order for a cell to divide, it needs to make copies of the genetic code, cell organelles and other molecules necessary for each of the daughter cells to survive. After this point, the cell is ready to divide. The process of cell division occurs in a series of observable steps that scientists have termed “mitosis.” Below are some key players (organelles) in mitosis. Review their functions before going on.
Directions: T rough observation
of the following stages of mitosis, one can figure out the most logical
sequence of events. You know you are starting with one cell and
ending with two. Use the information depicted in the pictures
to place them in the correct order. Once you have the correct
order (check with your teacher), cut each picture out and tape or glue
onto a clean page in your science notebook. Then use the vocabulary
words of the key players to write a complete caption for each picture
of what is going on in the cell at that time.
Pictures from: http://www.biology.arizona.edu/Cell_Bio/tutorials/cell_cycle/cells3.html
Name _________________________________________________________ Period _______ Date____________
Part 3: Cell Cycle and Cancer –Student Worksheet
Go to: http://www.biology.arizona.edu/Cell_BIO/activities/cell_cycle/activity_description.html
Directions: For review on the stages of mitosis, go through the activity to identify the state of the cell cycle for each of the cells sampled from the onion root tip.
The picture of the cell that you are trying to identify is small and is located here.
Remember that that the actual process of cell division does not begin until Prophase. So what exactly goes on during Interphase? The stages of Interphase can actually be broken down into three other stages: G1, S, and G2. To learn more about these stages and why they are important continue on to the Inside Cancer website.
Directions: Go to the Inside Cancer website (www.insidecancer.org). Navigate through the “Causes and Prevention” tab. Select “Smoking” and scroll to the “p53” link to answer the following questions:
CELL CYCLE
COMPARE THIS INFO TO THE CELL CYCLE OF THE ONION ROOT TIP.
FOR MORE ON CANCER CONTINUE
NAVIGATING THE “CAUSES AND PREVENTION” TAB &
“SMOKING”
Nicotine Connection
Prevention
Use the information Dr. Glorian
Sorenson presents as she discusses an anti-smoking campaign to answer
the following questions.
INSIDE CANCER: Hallmarks of Cancer – Student Worksheet TEACHER KEY http://www.insidecancer.org/
Direction: Go to the website above and navigate through the Hallmarks of Cancer section to answer the following questions for each section.
OVERVIEW
Type of Mutation | Original DNA sequence | New DNA sequence |
Single Nucleotide
Change
(aka Point Mutation) |
CAGGCGCAT | CAAGCGCAT (for example) |
Deletion | CAGGCGCAT | CAGCGCAT (for example) |
Duplication | CAGGCGCAT | CAGCAGGCGCAT (for example) |
It
is usually caused by more than one mutation and these mutations build
up over time.
GROWING UNCONTROLLABLY
-They grow in the absence of growth stimulatory signals from its environment.
-They grow even
in the presence of growth inhibitory signals.
EVADING DEATH
They degrade
the cell by breaking up DNA in the nucleus, breaking down proteins,
and causing the cell membrane to shrink.
They are engulfed
by neighboring cells.
For the common good – when there are too many cells it isn’t good for the organism.
PROCESSING NUTRIENTS
-Just like typical
cells they need a system to bring in nutrients and give up wastes.
-Oxygen, glucose,
amino acids
-Carbon dioxide,
urea, water
Leukemia and
other blood cancers because they are already bathed in nutrients in
the blood.
This concept
needs to be discusses and researched a bit more and the question tweaked
appropriately.
BECOMING IMMORTAL
-A specialized
DNA sequence found at the end of chromosomes; related to a cell’s
age; prevents end-to-end fusion of chromosomes
-They get shorter, eventually until they can’t protect chromosomal DNA anymore
-They start fusing
-This enzyme
elongates telomeres to extend the number of cell divisions that cell
is capable of.
-During embryonic development & in stem cells
INVADING TISSUES
-When cancer
cells spread and colonize other parts of the body
-They lose or inactivate the signals or controls that keep them in one place.
-Tissue function
is impaired.
AVOIDING DETECTION
-A cancer cell is different in shape and size.
-B cells make antibodies that bind and direct the elimination of abnormal cells
- T cells kill the cells these changed cells
-The immune system is stimulated with agents that make it hypersensitive to foreign cells.
PROMOTING MUTATIONS
-It unwinds the double helix.
-It is copied
backwards in pieces.
-Genes get distributed
unevenly
-Repair alterations or mistakes in DNA replication
-additional
mutations that could advance the progression to cancer
Part 3: Cell Cycle and Cancer –Student Worksheet
Go to: http://www.biology.arizona.edu/Cell_BIO/activities/cell_cycle/activity_description.html
Directions: For review on the stages of mitosis, go through the activity to identify the state of the cell cycle for each of the cells sampled from the onion root tip.
The picture of the cell that you are trying to identify is small and is located here.
~50% All others should be under 15%
Answers may vary slightly depending on their individual results but should match numbers above.
I’d expect to see more time in Interphase because those cells shouldn’t be growing as much as the tips.
Remember that that the actual process
of cell division does not begin until Prophase. So what exactly
goes on during Interphase? The stages of Interphase can actually
be broken down into three other stages: G1, S, and G2. To learn
more about these stages and why they are important continue on to the
Inside Cancer website.
Directions: Go to the Inside Cancer website (www.insidecancer.org). Navigate through the “Causes and Prevention” tab. Select “Smoking” and scroll to the “p53” link to answer the following questions:
p53
M – (mitosis) Cell divides into 2 daughter cells
CELL CYCLE*
*
G2 – cell synthesizes proteins and other cellular compounds needed for cell division
S – cell synthesizes DNA in preparation for cell division
G1 – cell grows and replenishes resources
Why?
Because the M check point is before division but the S check point comes before DNA replication so only spontaneous mutations have occurred at that point
Mutations and DNA damage accumulate
COMPARE THIS INFO TO THE CELL CYCLE OF THE ONION ROOT TIP.
It is shorter on the onion root tip diagram
Interphase
A mutation in a gene that controls the productionof centrioles
Nicotine Connection
Nicotinic acetylcholine
receptors
Cell cycle,
apoptosis, protein translation
Increases proliferation
and survival
Apoptosis
Prevention
Use the information Dr. Glorian Sorenson presents as she discusses an anti-smoking campaign to answer the following questions.
Blue-collar workers
They figured they were already exposed to other harmful chemicals in their work place so why bother?
Blue-collar
workers in the integrated group were twice as likely to quit smoking
as blue-collar workers in the group that got only the health promotion
piece.
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