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Outline What is cancer? How do people know they have cancer?

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1 Outline What is cancer? How do people know they have cancer?
How do tumors develop and cancer spread? Why are older people more likely to get cancer? What regulations do cells have that help prevent cancer? What are some of the causes of cancer? How can one’s environment affect their chances of getting cancer? How Can Chemicals Cause Cancer? How can viruses cause cancer? Why does one family have a history of cancer? What can you and your body do to help prevent getting cancer? What can you eat to help prevent you from getting cancer? Why do these foods help? How can my body fight cancer? How common is cancer? What are some of the common treatments for cancer and how do they work?

2 How do people find out if they have cancer?
What is cancer? Goal: To get students thinking on what cancer really is. Ask students what they already about what cancer is and how it is diagnosed. Ask what were they removing in Mr. Cole’s surgery? (in video of explore lesson) Many students may say something about tumors or lumps; thus there is a picture of a person with a tumor on his forehead. This is one of the only tumor photos that I could find that was not really gross. There is also the image of a metastasizing cancer cell on the left because it hopefully will help students make the connection between the lump and a cancer cell. The idea is to get students to understand that the metastasizing cell on the left is what makes up the tumor on the right. The picture on the left is of a man with the beginning stages of basal cell carcinoma. Left image: Right image: How do people find out if they have cancer?

3 Cancer Simplified Cells that have gone awry, because the genes that help cells “follow the rules” have mutated. Thus they can divide rapidly, start acting like other cells and move from where they are supposed to stay. Goal: For students to understand cancer in a simplified way. Cancer is cells that have gone awry, because the genes that help cells “follow the rules” have mutated. Thus they can divide rapidly, start acting like other cells and move from where they are supposed to stay. Image: Definition: Great Website for understanding cancer:

4 How do tumors develop and cancer spread?
Show animation of this process: Go to: Click on: Act 2 – Cell Cycle Animation 1 (6.5MB) This animation is 1:11 minutes long and talks about how tumors form and how cancer spreads. The image was chosen to show how tumors grow and also to show how it can spread into the blood stream and be transferred to other parts of the body in later stages of cancer. Background: Cancer begins when a cell breaks free from the normal restraints on cell division and begins to follow its own agenda for proliferation (Figure 3). All of the cells produced by division of this first, ancestral cell and its progeny also display inappropriate proliferation. A tumor, or mass of cells, formed of these abnormal cells may remain within the tissue in which it originated (a condition called in situ cancer), or it may begin to invade nearby tissues (a condition called invasive cancer). An invasive tumor is said to be malignant, and cells shed into the blood or lymph from a malignant tumor are likely to establish new tumors (metastases) throughout the body. Tumors threaten an individual's life when their growth disrupts the tissues and organs needed for survival. Image and info:

5 Differences between normal and cancerous cell
Goal: To show that cancerous cells have actually changed their structure and thus their function because of their mutations. Background: Additional research revealed that as a tumor develops, the cells of which it is composed become different from one another as they acquire new traits and form distinct subpopulations of cells within the tumor. These changes allow the cells that experience them to compete with increasing success against cells that lack the full set of changes. The development of cancer, then, occurs as a result of a series of clonal expansions from a single ancestral cell. A second critical understanding that emerged from studying the biology of cancer cells is that these cells show a wide range of important differences from normal cells. For example, cancer cells are genetically unstable and prone to rearrangements, duplications, and deletions of their chromosomes that cause their progeny to display unusual traits. Thus, although a tumor as a whole is monoclonal in origin, it may contain a large number of cells with diverse characteristics. Cancerous cells also look and act differently from normal cells. In most normal cells, the nucleus is only about one-fifth the size of the cell; in cancerous cells, the nucleus may occupy most of the cell's volume. Tumor cells also often lack the differentiated traits of the normal cell from which they arose. Whereas normal secretory cells produce and release mucus, cancers derived from these cells may have lost this characteristic. Likewise, epithelial cells usually contain large amounts of keratin, but the cells that make up skin cancer may no longer accumulate this protein in their cytoplasms. The key difference between normal and cancerous cells, however, is that cancer cells have lost the restraints on growth that characterize normal cells. Significantly, a large number of cells in a tumor are engaged in mitosis, whereas mitosis is a relatively rare event in most normal tissues. Cancer cells also demonstrate a variety of unusual characteristics when grown in culture; two such examples are a lack of contact inhibition and a reduced dependence on the presence of growth factors in the environment. In contrast to normal cells, cancer cells do not cooperate with other cells in their environment. They often proliferate indefinitely in tissue culture. The ability to divide for an apparently unlimited number of generations is another important characteristic of the cancerous state, allowing a tumor composed of such cells to grow without the constraints that normally limit cell growth. Image:

6 Why are older people more likely to get cancer?
Goal: For students to learn that cancer is not caused by a single event, but rather a multi-step event. Background: A central feature of today's molecular view of cancer is that cancer does not develop all at once, but across time, as a long and complex succession of genetic changes. Each change enables precancerous cells to acquire some of the traits that together create the malignant growth of cancer cells. Cancer, then, does not develop all at once as a massive shift in cellular functions that results from a mutation in one or two wayward genes. Instead, it develops step-by-step, across time, as an accumulation of many molecular changes, each contributing some of the characteristics that eventually produce the malignant state. The number of cell divisions that occur during this process can be astronomically large—human tumors often become apparent only after they have grown to a size of 10 billion to 100 billion cells. As you might expect, the time frame involved also is very long— it normally takes decades to accumulate enough mutations to reach a malignant state. Understanding cancer as a multistep process that occurs across long periods of time explains a number of long-standing observations. A key observation is the increase in incidence with age. Cancer is, for the most part, a disease of people who have lived long enough to have experienced a complex and extended succession of events. Because each change is a rare accident requiring years to occur, the whole process takes a very long time, and most of us die from other causes before it is complete. Understanding cancer in this way also explains the increase in cancer incidence in people who experience unusual exposure to carcinogens, as well as the increased cancer risk of people who inherit predisposing mutations. Exposure to carcinogens increases the likelihood that certain harmful changes will occur, greatly increasing the probability of developing cancer during a normal life span. Similarly, inheriting a cancer-susceptibility mutation means that instead of that mutation being a rare event, it already has occurred, and not just in one or two cells, but in all the body's cells. In other words, the process of tumor formation has leapfrogged over one of its early steps. Now the accumulation of changes required to reach the malignant state, which usually requires several decades to occur, may take place in one or two. Finally, understanding the development of cancer as a multistep process also explains the lag time that often separates exposure to a cancer-causing agent and the development of cancer. This explains, for example, the observation that severe sunburns in children can lead to the development of skin cancer decades later. It also explains the 20-to-25-year lag between the onset of widespread cigarette smoking among women after World War II and the massive increase in lung cancer that occurred among women in the 1970s. Images: Cancer develops step-by-step, across time, as an accumulation of many molecular changes, each contributing some of the characteristics that eventually produce cancer cells.

7 What regulations do cells have that help prevent Cancer?
There are built in ways in our body that prevent a cell from re 7

8 Cell Cycle Purpose of this slide: The purpose of this slide is to give the students a visual representation of the cell cycle. They are probably familiar with the mitotic phase, but need to be reminded that a cell undergoes other phases in its life. Here is a diagram of a cell cycle that shows the event of mitosis that students already know, but also adds the the terms G1, S, G2. G1 just means gap 1, g2 means gap 2, and S means synthesis. In Gap 1 the cell grows and makes the necessary enzymes for DNA replication that takes place in S phase. S Phase is when DNA replication occurs. The G2 phase is when the cell continues to grow in preparation for the cell division that will take place in mitosis. The transition to each of these phases is marked by checkpoints to ensure everything is in order and the process can continue. 8

9 Can anyone think of an Analogy for the Cell Cycle?
Purpose of this slide- The purpose of this slide is for the students to put the cell cycle in terms that they deal with everyday. They might continue to use the analogy as they learn more. A great example is: The cell is like a car, faults in the design or assembly of a car can lead to a defect that appears in every copy. The cell cycle is the program that a cell follows in duplicating itself. 9

10 Cells maintain strict control over Cell Division
We have genes in our DNA called tumor suppressor genes that code for proteins that interact with the molecules cyclin and CDK which are controlling the cell cycle at certain checkpoints to determine if the DNA is good enough shape to proceed to division. If the DNA is damaged in anyway it is either repaired or the cell undergoes programmed cell death. Purpose of this slide: The purpose of this slide is to show an example of a tumor suppressor genes. The idea is that our DNA contains genes the code for proteins that interact with other proteins during the cell cycle to determine if the cell is fit enough to divide. If not, the cell is killed. I chose this image because it shows DNA and then show a protein that it produces which should get the students thinking that if the DNA is damaged, then the protein will be messed up too. Cell division is the defining feature of cancer, that is uncontrolled cell division. So how is cell division controlled in the first place? There are certain checkpoints and landmarks that happen in the cell that allow it to enter the next phase of cell division. If these goals are not met, then the cells can not procede to divide. One of these checkpoints is on the size of the cell. Growing cells divide once with each doubling of mass and size. So a cell must reach a certain mass and size before it is allowed to divide, this checkpoint is located between G2 and M (Mitosis) phase. Cells maintain the same average size over many generations. What happens if the cell does not meet the size standards? Either it is allowed to grow more or it undergoes programmed cell death (apoptosis). The two regulatory molecules are cyclin and CDK, the chemical interactions mostly phosphorylation between these allow entry into the next phase. Tumor suppressor genes interact with these molecules to inhibit cell division if the cellular DNA is damaged in anyway. More info of the general mechanism can be found at Picture citation - 10

11 DNA can only replicate once with each cell divison.
A cell with to much DNA material does not behave correctly so DNA must only replicate once with each cycle and each daughter cell must have the correct amount of genetic material. Purpose of this slide- This slide is supposed to show an example of a cell regulation in the cell cycle. One of the checkpoints in the cell cycle is to make sure that DNA is only replicated once with each cell division. This is to ensure that each cell contains the right amount of genetic material. Once DNA replication has started, it must be completed. So in terms of the cell cycle, once a cell has entered S phase it must complete the cell cycle or undergo programmed cell death (apoptosis). Chromosome separation in mitosis must not begin until all the chromosomes are attached to microtubules and properly aligned. This is to ensure that each daughter cell receives the right amount of genetic information. Defects in any of these proteins that control the checkpoints could cause the cell to transform in a cell with uncontrolled cell division which a key feature of cancer. The cell must not divide before DNA replication is complete. This is another checkpoint that allows a smooth transition between S phase and G2 phase. 11

12 DNA Damage must be repaired before replication.
To prevent a cell from having the ability to become cancerous, damage must be repaired. Purpose of this slide- The purpose of this slide is to explain why it is so important to repair DNA damage. Tumor suppressor proteins halt the cell cycle for the damage to be repaired or for the cell to undergo programmed cell death. Damage to genes that encode cell cycle regulators or tumor suppressor genes will lead to cancer so the damage must be stopped from being passed on. If DNA is damaged it must be repaired before replication. Another key cell cycle regulator is the p53 protein, a tumor suppressor absent in many cancers. If there is DNA damage, p53 prevents entry into S phase until the DNA is repaired. If the damage is excessive, p53 will trigger apoptosis (programmed cell death). In many tumors the p53 gene becomes mutated, the protein is inactive or not expressed, and so it no longer prevents progression through the cell cycle after DNA damage. If damaged DNA is replicated, tumors accumulate more mutated DNA, and the cancer becomes more aggressive. Most cancer treatments (radiation, chemotherapy) work by damaging DNA and stimulating apoptosis. If p53 is absent, however, then the tumor cells are often unresponsive to such treatments. In general, tumors with mutated p53 have a bad prognosis. 12

13 If a cell fails to pass a checkpoint…
Purpose of this slide: The purpose of this slide is obviously to be a little humorous, but also to introduce an important concept which is programmed cell death. Programmed cell death is a defensive mechanism that the body has to kill cells infected with a virus and also badly damaged cells. Picture citation- If a cell fails to pass a checkpoint… It will undergo programmed cell death, also known as apoptosis. This prevents damaged cells from dividing and leading to cancerous cells. 13

14 Class Demo Purpose of this slide- This class demo is intended to give the students a conceptual understanding of cancer. Depending on how many iterations you let it go, you are going to need a few volunteers. Have 1 cell (student) “divide” (get another student volunteer) and perform a task such as use a spoon to spoon beans into a cup. Once the task is done, the student “dies” (sits back down) Allow this to go on for a few cycles. Next, to represent uncontrolled cell division, do not allow the students to use their hands, but instead their mouth to spoon beans (expect some spills). And instead of “dying” have that student come back and “divide”. This will show how quickly numbers can add up and also shows an interesting characteristic of cancerous cells which is that they are in a sense immortal. Most normal cells have a certain number of cell divisions they go through before they die, cancer cells seem to have an unlimited amount. 14

15 What are some causes of cancer?
Goal: Have the students list out what they think are possible causes of cancer. Then hit enter on slide to show the causes listed and explained later in this powerpoint. The images are used to give a visual idea of the different possible causes. Expected responses: smoking, sun, family Sun: rest of images from clipart environment (ex: sun), chemicals, infection, genes, toxins etc.

16 Cancer has multiple causes
-mutated tumor suppressor genes -mutated cell cycle regulators -mutated repair proteins -mutated receptor signaling constant division, etc. Purpose of this slide- The student should know that its best to think of cancer as not just one disease, but many different diseases with similar underlying causes because there are so many things that could have caused the cell to divide out of control. 16

17 How can one’s environment affect their chances of getting cancer
How can one’s environment affect their chances of getting cancer? Example: UVA and UVB light exposure By damaging the skin’s cellular DNA, excessive UV radiation produces genetic mutations that can lead to skin cancer. Goal: To show how UV light from the sun can cause skin cancer Images: Chose a cartoon to represent sunbathing so less sexual, used image of light rays going through skin to show how it affects it Details: By damaging the skin’s cellular DNA, excessive UV radiation produces genetic mutations that can lead to skin cancer. Both the U.S. Department of Health and Human Services and the World Health Organization have identified UV as a proven human carcinogen. UVA is the dominant tanning ray, and we now know that tanning, whether outdoors or in a salon, causes cumulative damage over time. A tan results from injury to the skin’s DNA; the skin darkens in an imperfect attempt to prevent further DNA damage. These imperfections, or mutations, can lead to skin cancer. Tanning booths primarily emit UVA. The high-pressure sunlamps used in tanning salons emit doses of UVA as much as 12 times that of the sun. Not surprisingly, people who use tanning salons are 2.5 times more likely to develop squamous cell carcinoma, and 1.5 times more likely to develop basal cell carcinoma. According to recent research, first exposure to tanning beds in youth increases melanoma risk by 75 percent.

18 How Can Chemicals Cause Cancer?
Purpose of this slide- To get students to think about all the bad stuff in a cigarette and also all the chemicals that cause cancer.

19 By causing DNA Damage Chemicals can cause mutations in DNA such as missense and nonsense. They can cause the bases to stick together in a process called dimerization. Various chemical modifications. Cancer causing chemicals are known as carcinogens. Purpose of this slide- To remind the students about mutations. More info can be found at-

20 How can viruses cause cancer?
Purpose of this slide: To inform students on how viruses can cause cancer and also to think critically about what a virus does. It has been known since 1911 that some animal tumors can be transmitted by what is now known to be a tumor virus. The ability to induce tumors in animals is useful for finding drugs to treat cancer. Moreover, a virus contains just a few genes (1:1,000,000 th the size of humans), providing an early clue that one or a few defective genes could trigger cancer growth. These cancer-causing genes are called oncogenes. In tumor viruses they must act in a dominant manner. Although tumor viruses rarely cause cancer in humans, tumor virus genes that affect growth are often related to human genes that become activated or over-expressed in human cancers. The picture can be found at- More info can be found at- 20

21 Think about it! Viruses insert their own DNA into our cells so our cells will make more viruses. The viral genes that cause cancer activate or over express similar human genes that cause the cells to exhibit uncontrolled cell divison. Purpose of this slide: To get students to actually think about what a virus does. You can even tie this in to the car factory analogy. Image location- 21

22 Cell communication gone awry
One way viruses have been found to cause cancer is through mutated receptors on the cell surface. What might the receptor be for? Purpose of this slide- To get the students thinking of how an outside force like a virus can cause cancer. The receptor is for the signal that tells a cell to divide. The reason I chose this picture is because it is a good diagram of how cells communicate with each other. Image Location- Background info- Oncogenes promote cell growth through a variety of ways. Many can produce hormones, a "chemical messenger" between cells which encourage mitosis, the effect of which depends on the signal transduction of the receiving tissue or cells. In other words, when a hormone receptor on a recipient cell is stimulated, the signal is conducted from the surface of the cell to the cell nucleus to effect some change in gene transcription regulation at the nuclear level. Some oncogenes are part of the signal transduction system itself, or the signal receptors in cells and tissues themselves, thus controlling the sensitivity to such hormones. Oncogenes often produce mitogens, or are involved in transcription of DNA in protein synthesis, which creates the proteins and enzymes responsible for producing the products and biochemicals cells use and interact with. Info can be found at- 22

23 Why does one family have a history of cancer?
A family can have a history of cancer due to their germ cells having damage in a cell cycle regulating gene or gene that triggers apoptosis once enough damage has accumulated. Hereditary cancer is a cancer that has developed as a result of a gene mutation passed down from a parent to a child. Inheriting a gene mutation does not necessarily mean that person will develop cancer, but increases their risk factor. Research and studies have found that certain gene mutations increase the chances of a person to develop certain kinds of cancers, depending on family history. Remember, cancer is not inherited, only the gene that increases the risk factor of developing it. Cancer More info- Heredity-This is the process by which an offspring cell or organism acquires or becomes predisposed to the characteristics of its parent cell or organism. 23

24 Xeroderma pigmentosum
Autosomal recessive disorder caused by mutations in genes that code for DNA repair proteins Goal: To explain how important the DNA repair genes are. Bio 202 notes: Autosomal recessive, defect in a nucleotide excision repair (NER) gene, NER is an extensively studied process which consists of the removal and the replacement of damaged DNA with new DNA. symptons: sensitivity to sunlight, skin cancer; homozygous recessive for mutations in 1 of 7 genes encoding enzymes that normally function in NER. People with this mutation cannot efficiently remove the thymine dimers caused by UV light exposure which causes base substitution mutations. As the person comes in contact with the sun , these mutations accumulate and eventually lead to skin cancer. Patients younger than 20 years have a 1000-fold increase in the incidence of nonmelanoma skin cancer and melanoma. The mean patient age of skin cancer is 8 years in patients with xeroderma pigmentosum, compared with 60 years in the healthy population. Actinic damage occurs between ages 1 and 2 years. Background info: Image:

25 Retinoblastoma and RB1 Purpose of this slide: This gives students a real world example and they can also tie in what they have previously learned. They know that we have two copies of a gene so if one copy is mutated, then the other one must have been mutated somehow. More info- Retinoblastoma is a form of cancer that young children usually get because of one mutated copy of a protein called RB1. What must happen for retinoblastoma to occur? 25

26 Remember we have two copies of a gene.

27 With only one good copy of the gene, all it takes is one hit on that gene for the stage to be set for retinoblastoma to occur. Purpose of this slide- To inform students that just becaus 27

28 Game Time! Game Purpose of this slide- This slide contains a link to a very informative game about cell cycle, damage, and general information about cancer. It’s a great way to end a lesson and cement what all the students know. 28

29 What can you and your body do to help prevent getting cancer?
Have students list ways to help prevent getting cancer Predicted responses: don’t smoke, wear sunscreen, eat healthy, exercise

30 Don’t Smoke! Tobacco smoke contains over 4,000 chemical compounds, many of which have been shown to be cancer-causing, or carcinogenic. The two primary carcinogens in tobacco smoke are chemicals known as nitrosamines and polycyclic aromatic hydrocarbons. The risk of developing lung cancer decreases each year following smoking cessation as normal cells grow and replace damaged cells in the lung. In former smokers, the risk of developing lung cancer begins to approach that of a nonsmoker about 15 years after cessation of smoking. Cigarette smoke contains about 4,000 chemical agents, including over 60 carcinogens (8). In addition, many of these substances, such as carbon monoxide, tar, arsenic, and lead, are poisonous and toxic to the human body. Nicotine is a drug that is naturally present in the tobacco plant and is primarily responsible for a person’s addiction to tobacco products, including cigarettes. During smoking, nicotine is absorbed quickly into the bloodstream and travels to the brain in a matter of seconds. Nicotine causes addiction to cigarettes and other tobacco products that is similar to the addiction produced by using heroin and cocaine (9). Researchers discovered that the production of a protein called FANCD2 is slowed when lung cells are exposed to cigarette smoke. Low levels of FANCD2 leads to DNA damage, triggering cancer. Cigarette smoke curbs the production of 'caretaker' proteins, like FANCD2, which normally prevent cancer by fixing damages in DNA and causing faulty cells to commit suicide. The researchers studied how DNA methylation contributes to lung cancer development in former smokers. Methylation is an important event regulating gene expression during normal development. As we age and in cancer, proper patterns of DNA methylation become deregulated throwing off the tight control of gene activity that normally exists. "Alteration to DNA methylation might potentially explain why some former smokers sustain additional genetic damage resulting in lung cancer," Vucic said. "As methylation is a reversible DNA modification, this knowledge could prompt the development and application of chemopreventive agents and unique therapeutic strategies that target DNA methylation in these patients. "Exposure to cigarette smoke is a major culprit in disease development. "In addition to DNA sequence mutations, cigarette smoke also causes widespread errors in DNA marks, such as DNA methylation, used to regulate gene function and genome stability," Vucic said. Cigarette smoke exposure has been shown to activate genes that promote cancer and deactivate genes that stop tumor growth, she said. Image:

31 What can I eat to help prevent me from getting cancer?
Goal: Show students foods that can help them not to get cancer. Background: Broccoli, Brussels sprouts, Cabbage, Cauliflower, Carrots, Red peppers, Tomato, Sweet potato, Collard greens, Green Tea, Kale, Spinach, Apricot, Cantaloupe, Grapefruit, Orange, Papaya, Peach, Plum, Watermelon Images:

32 Why do these foods help prevent cancer?
Goal: Explain the science behind why these foods are so good for you! Background: Antioxidants neutralize free radicals as the natural by-product of normal cell processes. Free radicals are molecules with incomplete electron shells which make them more chemically reactive than those with complete electron shells. Exposure to various environmental factors, including tobacco smoke and radiation, can also lead to free radical formation. In humans, the most common form of free radicals is oxygen. When an oxygen molecule (O2) becomes electrically charged or "radicalized" it tries to steal electrons from other molecules, causing damage to the DNA and other molecules. Over time, such damage may become irreversible and lead to disease including cancer. Antioxidants are often described as "mopping up" free radicals, meaning they neutralize the electrical charge and prevent the free radical from taking electrons from other molecules. Antioxidants are abundant in fruits and vegetables, as well as in other foods including nuts, grains and some meats, poultry and fish. The website below also provides a list that describes food sources of common antioxidants. Antioxidants are substances that may protect your cells against the effects of free radicals. Free radicals are molecules produced when your body breaks down food, or by environmental exposures like tobacco smoke and radiation. Free radicals can damage cells, and may play a role in heart disease, cancer and other diseases. More Info: Cancers Linked to Diet Several types of cancer are directly linked to diet, according to research. In the typical American's diet, about 40% of calories come from fat. "Some evidence indicates that diets high in fat might increase the risk of cancers of the colon, breast, prostate, and the lining of the uterus (the endometrium). Diets low in fat may reduce these risks while they help to control weight and also reduce risk of heart attack and stroke," McDowell said. Obesity is also a risk factor for kidney, pancreatic, and oral/esophageal cancers. "To reduce the fat in your diet, choose more low-fat or fat-free dairy, legumes, lean meats, poultry or fish. Skip rich sauces that are made with butter, cream or mayonnaise, and limit fried foods," McDowell said. Diets rich in foods containing vitamin A, vitamin C, and beta carotene may also reduce the risk of certain cancers, such as bladder, breast, colorectal, and stomach cancer. Many vegetables and fruits contain vitamins A and C and beta carotene, such as dark green leafy vegetables, red, yellow and orange vegetables and fruits and citrus fruits and juices. The website below also lists several foods and what the foods contain that help in the fight against cancer. ANTIOXIDANTS Antioxidants are substances that may protect your cells against the effects of free radicals. Free radicals can damage cells, and may play a role in heart disease, cancer and other diseases.

33 How can my body fight cancer?
The Immune System Goal: For students to briefly understand how the immune system works like an army in our body to ward off foreign material such as cancer. The immune system is a complex network of specialized cells and organs that has evolved to defend the body against attacks by "foreign" invaders. When functioning properly it fights off infections by agents such as bacteria, viruses, fungi, and parasites. When it malfunctions, however, it can unleash a torrent of diseases, from allergy to arthritis to cancer to AIDS. The immune system, which equals in complexity the intricacies of the brain and nervous system, displays several remarkable characteristics. It can distinguish between "self" and "nonself." It is able to remember previous experiences and react accordingly; thus, once you have had chicken pox, your immune system will prevent you from getting it again. The immune system displays both enormous diversity and extraordinary specificity; not only is it able to recognize many millions of distinctive nonself molecules, it can produce molecules and cells to match up with and counteract each one of them. And it has at its command a sophisticated array of weapons. The immune system provides one of the body's main defenses against cancer. When normal cells turn into cancer cells, some of the antigens on their surface change. These new or altered antigens flag immune defenders, including cytotoxic T cells, natural killer cells, and macrophages. According to one theory, patrolling cells of the immune system provide continuing bodywide surveillance, spying out and eliminating cells that undergo malignant transformation. Tumors develop when the surveillance system breaks down or is overwhelmed. Some tumors may elude the immune defenses by hiding or disguising their tumor antigens. Alternatively, tumors may survive by encouraging the production of suppressor T cells; these T cells act as the tumor's allies, blocking cytotoxic T cells that would normally attack it. Image and also good info:

34 The Immune System Goal: Briefly explain immune system
Helper T cells are the major driving force and the main regulators of the immune defense. Their primary task is to activate B cells and killer T cells. However, the helper T cells themselves must be activated. This happens when a macrophage or dendritic cell, which has eaten an invader, travels to the nearest lymph node to present information about the captured pathogen. The phagocyte displays an antigen fragment from the invader on its own surface, a process called antigen presentation. When the receptor of a helper T cell recognizes the antigen, the T cell is activated. Once activated, helper T cells start to divide and to produce proteins that activate B and T cells as well as other immune cells.

35 The Immune System The killer T cell is specialized in attacking cells of the body infected by viruses and sometimes also by bacteria. It can also attack cancer cells. The killer T cell has receptors that are used to search each cell that it meets. If a cell is infected, it is swiftly killed. Infected cells are recognized because tiny traces of the intruder, antigen, can be found on their surface.

36 The Immune System B Cells
   The B lymphocyte cell searches for antigen matching its receptors. If it finds such antigen it connects to it, and inside the B cell a triggering signal is set off. The B cell now needs proteins produced by helper T cells to become fully activated. When this happens, the B cell starts to divide to produce clones of itself. During this process, two new cell types are created, plasma cells and B memory cells.The plasma cell is specialized in producing a specific protein, called an antibody, that will respond to the same antigen that matched the B cell receptor. Antibodies are released from the plasma cell so that they can seek out intruders and help destroy them. Plasma cells produce antibodies at an amazing rate and can release tens of thousands of antibodies per second. The Memory Cells are the second cell type produced by the division of B cells. These cells have a prolonged life span and can thereby "remember" specific intruders.

37 Statistics How common is cancer?
Approximately 6 of 10 people in will have children 2,3,5,6 stand Approximately 3 in 10 of the people in the room will be involved in an alcohol-related automobile accident sometime in their lifetimes. 3 and 6 stand Approximately 1 in 3 (or in this case, 2 in 6) of the people in the room will develop cancer sometime during their lifetimes. 1 and 4 stand Approximately 25 % of the U.S. population who will die of cancer. ¼ of people standing should sit Goal: For students to visually see how many people may get cancer based on the present statistics and for students to understand why they should be interested in learning about cancer because of the affect it may have on them later on in their life. This leads into how to treat people with cancer since so many folks have it. Have students number themselves 1-6. Then get the appropriate number of students to stand for each statistic. The number of the students numbered off is given as a bullet point under each statistic given. One uses other common statistics to show the prevalence of the possibility of getting cancer. Ask students if they were surprised by these statistics. Background Each of us has a chance of developing cancer sometime in our life. On average, in the United States, men have a 1 in 2 lifetime risk of developing cancer and women, a 1 in 3 risk. Many Americans, however, have a higher-than-average chance of developing particular forms of cancer. For example, smokers have a 10-fold higher risk of developing lung cancer compared with nonsmokers. Likewise, women who have a mother, sister, or daughter who has had breast cancer have about a 2-fold higher chance of developing breast cancer compared with women who do not have such a family history. The National Cancer Institute estimates that approximately 8 million Americans alive today have a history of cancer. In 1998, more than 1 million new cases were diagnosed. In fact, cancer is the second leading cause of death in the United States, exceeded only by heart disease.

38 What are some of the common treatments for cancer?
Ask students if they know anyone that has had cancer treatments before and ask what treatments they received. Expected responses: chemotherapy, surgery, radiation Biological therapy image: Surgery Image: Radiation image: Chemotherapy image:

39 How does biological therapy work?
It uses the body's immune system, either directly or indirectly, to fight cancer or to lessen the side effects that may be caused by some cancer treatments. Biological therapy (sometimes called immunotherapy, biotherapy, or biological response modifier therapy) is a relatively new addition to the family of cancer treatments. Biological therapies use the body's immune system, either directly or indirectly, to fight cancer or to lessen the side effects that may be caused by some cancer treatments. Biological response modifiers (BRMs) occur naturally in the body and can be produced in the laboratory. BRMs alter the interaction between the body's immune defenses and cancer cells to boost, direct, or restore the body's ability to fight the disease. Biological therapies include interferons, interleukins, colony-stimulating factors, monoclonal antibodies, vaccines, gene therapy, and nonspecific immunomodulating agents. Image: This drug (Erbitux) is an example. It blocks the growth receptors on cancer cells.

40 How does surgery help? Surgery may be used for cancer prevention to remove tissue before cancer develops, diagnosis to determine if tumor is cancerous or not, staging to see how advanced the cancer is, and primary treatment to remove cancerous tumors. Cancer surgery — an operation to repair or remove part of your body to diagnose or treat cancer — remains the foundation of cancer treatment. Your doctor may use cancer surgery to achieve any number of goals, from diagnosing your cancer to treating it to relieving the symptoms it causes. Cancer surgery may be your only treatment, or it may be supplemented with other treatments, such as radiation, chemotherapy, hormone therapy and biological therapy. How is cancer surgery used in treatment? Cancer surgery may be used to achieve one or more goals. Common reasons you might undergo cancer surgery include: Cancer prevention. If there’s reason to believe that you'll develop cancer in certain tissues or organs, your doctor may recommend removing those tissues or organs before cancer develops. For example, if you have a genetic condition called familial polyposis, your doctor may use cancer surgery to remove your colon and rectum because you have a high risk of developing colon cancer. Diagnosis. Your doctor may use a form of cancer surgery to remove (biopsy) all or part of a tumor — allowing the tumor to be studied under a microscope — to determine whether the growth is cancerous (malignant) or noncancerous (benign). Staging. Cancer surgery helps your doctor define how advanced your cancer is, called its stage. Surgery allows your doctor to evaluate the size of your tumor and determine whether it's traveled to your lymph nodes. Additional tests might be necessary to gauge your cancer's stage. Primary treatment. For many tumors, cancer surgery is the best chance for a cure, especially if the cancer is localized and hasn't spread. If there’s evidence that your cancer hasn't spread, your doctor may recommend surgery to remove the cancerous tumor as your primary treatment. Debulking. When it's not possible to remove all of a cancerous tumor — for example, because doing so may severely harm an organ — your doctor may remove as much as possible (debulking) in order to make chemotherapy or radiation more effective. Relieving symptoms or side effects. Sometimes surgery is used to improve your quality of life rather than to treat the cancer itself — for example, to relieve pain caused by a tumor that's pressing on a nerve or bone or to remove a tumor that's obstructing your intestine. Image:

41 How does chemotherapy work?
It uses drugs to destroy cancer cells, stop cancer cells from spreading, and slow the growth of cancer cells. It can be given through an IV, a shot into part of the body, a pill or liquid to swallow, or a cream to rub on skin. Chemotherapy is a cancer treatment that uses drugs to destroy cancer cells. It is also called "chemo." Today, there are many different kinds of chemotherapy. So the way you feel during treatment may be very different from someone else. Chemotherapy can be used to: Destroy cancer cells Stop cancer cells from spreading Slow the growth of cancer cells Chemotherapy can be given alone or with other treatments. It can help other treatments work better. For example, you may get chemotherapy before or after surgery or radiation therapy. Or you may get chemotherapy before a peripheral blood stem cell transplant. Chemotherapy can be given in these forms: An IV (intravenously) A shot (injection) into a muscle or other part of your body A pill or a liquid that you swallow A cream that is rubbed on your skin Images:

42 How does radiation work?
It uses high powered x-rays or radioactive seeds to damage the DNA and kill cancer cells. Other rapidly growing cells may also be damaged in the process. Definition Radiation therapy uses high powered x-rays or radioactive seeds to kill cancer cells. Alternative Names Therapy - radiation; Radiotherapy Information Cancer cells usually multiply faster than other cells in the body. Because radiation is most harmful to rapidly growing cells, radiation therapy damages cancer cells more than normal cells. Specifically, radiation therapy damages the DNA of cancer cells. Doing so prevents the cancer cells from growing and dividing. Unfortunately, certain healthy cells can also be killed by this process. The death of healthy cells can lead to side effects. Radiation therapy is used to fight many types of cancer. It is often used to shrink a tumor as much as possible before surgery. Radiation can also be given after surgery to prevent the cancer from coming back. For certain types of cancer, radiation is the only treatment needed. Radiation treatment may also be used to provide temporary relief of symptoms, or to treat malignancies (cancers) that cannot be removed with surgery. There are two forms of radiation therapy: External beam radiation is the most common form. This method carefully aims high powered x-rays directly at the tumor from outside of the body. Internal beam radiation uses radioactive seeds that are placed directly into or near the tumor. Internal beam radiation is also called interstitial radiation or brachytherapy. The following are some commonly used radioactive substances: Cesium (137Cs) Cobalt (60Co) Iodine (131I) Phosphorus (32P) Gold (198Au) Iridium (192Ir) Yttrium (90Y) Palladium (103) Radiation therapy can have many side effects. These side effects depend on the part of the body receiving radiation, the dose of radiation, and how often you have the therapy. Hair loss Skin pain Red, burning skin Shedding of the outer layer of skin (desquamation) Increased skin coloring (hyperpigmentation) Death of skin tissue (atrophy) Itching Fatigue and malaise Low blood counts Difficulty or pain swallowing Erythema Edema Changes in taste Anorexia Nausea Vomiting Increased susceptibility to infection Fetal damage (in a pregnant woman)

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