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NURSING 3PA2 Final: Cancer Module Summary

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Kirsten Culver

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Cancer Module Summary CANCER AND CANCER TERMINOLOGY  Cancer – uncontrolled growth of abnormal cells in the body; other terms: malignant or malignancy  Malignant or cancerous cells – composed of less well-differentiated cells that have lost the ability to control both cell proliferation and differentiation into a mature cell  Oncology – study of tumors and their treatment including non-malignant or benign tumors INCIDENCE AND MORTALITY RATES  Risk of cancer increases with age – with a higher % of cancer cases occurring in those 70 or older.  More specifically, prostate cancer is the most common cancers among Canadian men and breast cancer is the most common cancer types among Canadian women in Canada.  In terms of estimated deaths, lung cancer is the leading cause of cancer death for both men and women, followed by colorectal cancer in men and breast cancer in women. CELL CYCLE AND CARCINOGENESIS CELL CYCLE  Cell cycle – sequence of events involved in replication and distribution of DNA to daughter cells in which a starting cell duplicates its contents and divides into two identical daughter cells  Five phases of the cell cycle  G zero, G1, S, G2, and M  Two major phases of cell cycle  synthesis or S phase (DNA is synthesized and chromosomes are replicated) and mitosis or M phase (cell divides and 2 daughter cells are formed).  The G phases are when the cell is metabolically active or growing enzymes or proteins in preparation for DNA synthesis or mitotic division.  After mitosis  daughter cells either go into a state of dormancy called the G zero phase (not actively proliferating) or the cell enters the G1 phase to begin the cell reproductive cycle again  Duration of the M, G2 and S phases is relatively constant, but G1 phase varies from hours to days. This determines the overall length of the cell cycle. Differentiation & Proliferation  Cells duplicate (and divide)  increase in number of cells  resulting daughter cells organize and become differentiated. Cell differentiation is where proliferating cells become specialized.  This is an orderly process, with increasing specialization occurring with each step.  3 main categories of cells produced through cell differentiation and proliferation  cells that never or rarely divide (ex. nerve cells), cells that continue to proliferate and then die, and stem cells which enter the cell cycle and produce progenitor cells when required.  Progenitor cells are early descendants of stem cells that can differentiate to form one or more kinds of cells but cannot divide and reproduce indefinitely (more limited in the kinds of cells it can become).  Stem cells can remain quiet until needed and then be called upon to produce daughter cells of the type required (it is a cell from which other types of cells develop). Checkpoints  Cancer cells are able to complete the cell cycle more quickly by decreasing the length of time spent in the G1 phase. They are also much less likely to enter or remain in the G zero phase of the cell cycle.  Several checkpoints in cell cycle  allow cycle to be stopped if previous events weren’t completed.  Example  G1-5 checkpoint monitors whether the DNA in the chromosomes is damaged by radiation or chemicals, and the G2 M checkpoint prevents entry into mitosis if DNA replication is not complete.  Transition from G2 to M is believed to be one of the most important checkpoints in the cell cycle. CARCINOGENESIS  Normal cells in the body follow an orderly path of growth, division, and death. A series of complex molecular processes are used to keep these cells growing in controlled and programmed fashion.  Carcinogenesis  process by which normal cells are transformed into cancer cells, caused by a mutation of the genetic material of normal cells (upsets normal balance between proliferation and cell death)  results in uncontrolled cell division and tumor development in the body.  Normal cells undergo a finite number of divisions before they stop completely, cancer cells have the capacity to undergo infinite number of cell divisions. Transformation  All cancer is genetic, in that it is triggered by altered genes. Genes that control the orderly replication of cells become damaged, allowing the cells to reproduce without restraint.  Cancer  disease in which a single normal body cell undergoes a genetic transformation into a cancer cell. This cell and its descendants produce the population of cells that we recognize as a tumor. Stages  Carcinogenesis  process in which normal cells become cancer cells. Three stages of this process: 1) initiation, 2) promotion, and 3) progression.  Initiation  exposure of cells to appropriate doses of carcinogenic agent (ex. chemicals, physical, or biological and produce irreversible changes) that makes them susceptible to malignant transformation.  Promotion  unregulated and accelerated growth of the mutated cells. Dysplasia – abnormality of cell development during the promotion stage, often indicative of an early neoplastic process.  Progression  process in which tumor cells acquire malignant changes and autonomous growth tendencies that promote invasiveness and metastatic capabilities.  Carcinoma in situ  transformation of a neoplastic lesion to one in which cells undergo no maturation so may be considered cancer like. Remains localized, hasn’t invaded past the basement membrane.  Invasive carcinoma is the final step in this sequence which is cancer that has invaded beyond the basement membrane and has the potential to metastasize or spread to other parts of the body. Gene and DNA Structure  Genes reside within chromosomes, the large DNA molecules, which are composed of two chemical strands twisted around each other to form a “double helix”.  Each strand is constructed from millions of chemical building blocks called “bases”.  DNA contains four different bases: adenine (A), thymine (T), cytosine (C), and guanine (G).  The sequential order of the bases in any given gene determines the message the gene contains. How does it occur?  In their normal forms, genes control the cell cycle, the sequence of events by which cells enlarge and divide. The cell division process is dependent on a tightly controlled sequence of events.  When this process does not occur properly, unregulated cell growth may be the end result.  Of the genes that exist, there is a small subset that seem to be particularly important in the initiation, promotion, and progression of all different kinds of cancer.  Two broad categories of genes that have been identified: proto-oncogene and tumor suppressor genes  Proto-oncogenes encourage cell division and tumor suppressor genes inhibit cell division. Together, they coordinate the regulated growth that normally ensures that each tissue/organ in the body maintain a size and structure that meet the body’s needs.  Mutated proto oncogenes become oncogenes, genes that stimulate excessive division. Mutations in tumor suppressor genes inactivate these genes, eliminating the critical inhibition of cell division that normally prevents excessive growth. Mutations in these two categories of genes account for much of the uncontrolled cell division that occurs in human cancers.  Oncogenes result from the activation or turning on of proto-oncogenes but tumor suppressor genes cause cancer when they are inactivated or turned off. Proto-Oncogenes and Oncogenes  Proto-oncogenes encourage normal cell division and when they become mutated, they are oncogenes.  Oncogenes can contribute to the development of cancer by instructing cells to make proteins or “go signals” that stimulate excessive cell growth and division. This causes a cell’s growth-signalling pathway to become hyperactive. This causes the cell to continually grow and divide.  Most cancer causing mutations involving oncogenes are acquired, not inherited. Tumor Suppressor Genes  Tumor suppressor genes  play a critical role in regulating when cells are allowed to divide and increase in number. When DNA damage is detected in a cell, some tumor suppressor genes can send “stop signals” to the cell to stop it from multiplying until the damage is repaired.  When they don’t function correctly, cells with DNA damage continue to divide and can accumulate further DNA damage that can lead to a cells to grow and divide in an uncontrolled fashion.  Individuals who inherit an increased risk of developing cancer often are born with one defective copy of a tumor suppressor gene. This will not cause cancer though because the other normal copy is still functional. But if the second copy undergoes mutation then the person may develop cancer. DNA Sequencing Gone Wrong  The DNA repair system also helps cells avoid runaway cell division by instructing a cell to repair damaged DNA. This system operates in every cell in the body, detecting and correcting errors in DNA.  Mutations in the DNA repair system can occur in several different ways.  Simplest type of mutation  a change in a single base along the base sequence of a particular gene  In other cases, one or more bases may be added or deleted. And sometimes, large segments of a DNA molecule are accidentally repeated, deleted, or moved.  Errors also occur during DNA replication. In most cases, such errors are rapidly corrected by the cell’s DNA repair system however, mutations in this DNA repair system can lead to a failure in repair, which in turn allows subsequent mutations to become a permanent feature in that cell and its descendants. Mismatch Repair  DNA polymerase copies both strands of the DNA – the top strand and the bottom strand.  Normally there is going to be an A opposite a T, and C opposite a G, but suppose it makes a mistake and copies a T where a C should be. That mistake is a potential mutation.  Fortunately cells have repair systems that can erase those mutations. These repair proteins recruit another enzyme called EXO1 – an exonuclease that chops off the mutant strand. This allows a DNA polymerase to come by and synthesize the correct strand, fixing up the DNA and making it normal. Apoptosis  This is another system that works in our body to balance the generation of new cells via cell division and the loss of cells through cell death. Old cells become damaged over time and are eliminated by a process termed programmed cell death or apoptosis.  Specific tumor suppressor genes can stimulate cells with damaged DNA to commit “cell suicide.”  In cells that have undergone DNA damage, the tumor suppressor p53 protein, initiates cells suicide, thereby preventing the genetically damaged cell from growing out of control. In a cell with a mutated p53 gene, cell suicide system is defective, and the damaged cell goes on in the cell cycle and divides. NK Cell & the Immune System  The immune system and natural killer cells is another back up system that affects the way cancer grows.  The immune system is the first and last defence against cancer. NK cells are a part of the immune system and are very important because they can target tumors and cancer cells and kill them.  A number of chemotherapeutic drugs need the immune system to be intact for the drugs to be effective.  Over 10,000 times each day our immune system destroys cells that could become cancerous. Metastasis  Tumor cells progress from a state of initiation to promotion to progression and finally metastasis.  The spread of cancer from its original location to other parts of the body is called metastasis. This is a critical event in cancer. Metastasis can occur in two ways.  Firstly, malignant cells can directly invade or extend into adjacent organs or sites. Secondly, individual cancer cells may move away from the primary tumor and enter the blood or lymph circulation.  Once tumor cells have successfully entered the blood and lymph circulation, they travel and get stuck in the capillary bed of a distant organ or site. They can continue to grow here until they burst.  The most common sites of cancer metastasis are the lungs, bones, and liver. ANGIOGENESIS  Angiogenesis is the process of forming new blood vessels which is needed for cancer metastasis. It begins when a tumor becomes large enough where it needs to increase the supply of nutrients and oxygen it receives.  Hypoxia triggers the tumor and its surrounding environment to release signals that result in the growth of blood vessels towards and into the tumor. These new vessels supply oxygen and nutrients that allow the tumor to continue growing. Normal Cell Angiogenesis  Angiogenesis occurs normally in the human body at specific times in development and growth.  For example, a developing child in a mother’s womb must create the vast network of arteries, veins, and capillaries that are found in the human body.  Also, angiogenesis is necessary for the repair or regeneration of tissue during wound healing. Tumor Cell Angiogenesis  Tumor angiogenesis is the proliferation of a network of blood vessels that penetrate into cancerous growths, supplying nutrients and oxygen and removing waste products. Tumor angiogenesis begins with cancerous tumor cells releasing molecules that send signals to surrounding normal host tissue.  This signalling activates certain genes in the host tissue that make proteins to encourage growth of new blood vessels. In a study, they found that without angiogenesis, tumor growth stopped. Angiogenesis Inhibitors  Researchers are now asking if inhibiting angiogenesis can slow down or prevent the growth and spread of cancer cells in humans. Angiogenesis inhibitors are currently being tested in cancer patients.  One class of angiogenesis inhibitors being tested in cancer patients are molecules that directly inhibit the growth of endothelial cells.  A second group of angiogenesis inhibitors being tested in human clinical trials are molecules that interfere with steps in the angiogenesis signalling cascade.  Avastin (a drug in this category) is the first to be FDA approved and has been proven to delay tumor growth and more important, to extend the lives of patients. BENIGN AND MALIGNANT TUMORS CHARACTERISTICS BENIGN TUMORS: CHARACTERISTICS  Benign tumors  composed of well-differentiated cells that resemble the cells of the tissues of origin, are characterized by a slow, progressive rate of growth that may come to a standstill or relapse.  Benign cells look like the tissues from which they arise. They grow by expansion and often remain localized to their site of origin, lacking the capacity to infiltrate, invade or metastasize to distant sites.  They develop a surrounding rim of compressed connective tissue called a fibrous capsule which is responsible for a sharp line of separation between the benign tumor and adjacent tissues known as encapsulated which is a factor that facilitates surgical removal.  Benign tumors are less of a threat than malignant tumors. They usually don’t cause death to tissues, blood vessels, or nerves unless they interfere with vital functions because of their location.  Benign tumors also can cause disturbances in the function of adjacent or distant structure by producing pressure on tissues, blood vessels, or nerves.  They can also cause alterations in body function by abnormally producing hormones.  Named by adding suffix “oma” to the tissue type from which the growth originated.  Papilomas  benign, microscopic or macroscopic finger-like projections that grow on any surface. MALIGNANT TUMORS: CHARACTERISTICS  Malignant neoplasms  less well differentiated tumors that have lost the ability to control both cell proliferation and differentiation into a mature cell.  Anaplasia  loss of cell differentiation in cancerous tissue  Poorly differentiated  poorly resembles the cell that it arose from. Undifferentiated  malignant cells are immature, embryonic in nature and no resemblance to the cell from which they arose.  Malignant cells grow rapidly and they grow in a disorganized and uncontrolled manner to invade surrounding tissues and blood vessels. They rob normal tissue of essential nutrients and they release enzymes, toxins and hormones called cytokines that destroy normal tissue.  They have cells that break loose and travel to distant sites to form metastases and inevitably cause suffering and death unless their growth can be controlled through treatment.  Named by adding suffix “carcinoma” or “sarcoma” to the tissue type from which the growth originated ETIOLOGY AND RISK FACTORS FOR CANCER ETIOLOGY  The etiology of cancer is multifactorial, with genetic, environmental, medical, and lifestyle factors interacting to produce a given malignancy.  One can look at this process of carcinogenesis as a cause of cancer – that is how cancer is caused by changes or mutations in a cell’s DNA or its genetic “blueprint”.  Heredity can pass on alterations in genes that make a person more susceptible to cancer.  Cancers come from random mutations that develop in body cells during one’s life, cancer is not considered an inherited illness.  Inheritance of certain kinds of genetic alterations can influence a person’s chances of developing cancer. All cancer is genetic (involving genes and DNA mutations) but small portion is inherited.  Sources of genetic information include DNA samples, and family history of disease. An accurate gene test can tell if a mutation is present, but that finding does not guarantee that disease will develop.  Inherited mutations can influence a person’s risk of developing many types of cancer.  Concluding that an individual is at increased risk of developing cancer may have important, potentially life-saving management implications and may lead to specific interventions aimed at reducing risk. RISK FACTORS Age  The chances of developing cancer increase as a person gets older because more time has been available for mutations to accumulate. Therefore, age is a risk factor for developing cancer.  Cancer screening  important as we age, involving checking for disease when there are no symptoms  Screening may find diseases at an early stage so there may be a better chance of curing the disease.  Canadian Cancer Society recommends that beginning at age 50, both men and women should be tested for polyps with sigmoidoscopy or colonoscopy every 5 years.  The Ontario Breast Screening Program recommends that women aged 50 to 74 years with an average risk for breast cancer receive a mammogram every two years, while women aged 30 to 69 years who are identified as being at high risk for breast cancer should be screened annually. Environment  Carcinogen (cancer causing agent)  mutations which trigger changes in a cells genes that may be caused by outside exposures. They are responsible for damaging DNA, promoting or aiding cancer.  Naturally occurring exposures (ex. radiation from sunlight) can cause cancer such as skin cancer.  Radiation exposure has been known to cause cancer. Exposure to certain chemicals such as benzene, asbestos and smoke are also carcinogenic.  Certain viruses that infect human cells can also cause cancer. For example, transmission of the human papillomavirus (HPV) during sexual relations can cause cervical cancer.  Even medical treatments such as chemotherapy, radiation and immune system suppressing drugs may make a person more susceptible to cancer. Lifestyle  Certain lifestyle risk factors that can be avoided increase the chance that a person will develop cancer.  People can help protect themselves by staying away from known risk factors whenever possible.  Having more than two alcoholic drinks each day for many years may increase the chance of developing cancers of the mouth, throat, esophagus, larynx, liver, and breast. For most of these cancers, the risk is higher for a drinker who uses tobacco which is one of the strongest cancer causing agents.  Obesity and physical inactivity may account for 25 to 30% of several major cancers.  People with a poor diet or whose diet is high in fat have an increased risk of cancer (ex. colon cancer).  The fluctuating levels of hormones in women such as during pregnancy, menstruation, etc. are linked to risks of hormone-related cancers, such as breast and uterine cancer.  Evidence from both animal and human studies suggests that chronic stress and sleep deprivation weakens a person’s immune system which in turn may affect the incidence of virus associated cancers. NOMENCLATURE FOR NEOPLASMS NOMENCLATURE: BENIGN TUMORS Epithelial (Gland) Tissue  Thyroid Adenoma  benign thyroid tumor, also known as a thyroid nodule. Patients may present with hyperthyroidism symptoms (excessive sweating, nervousness, agitation, rapid heart rate, weight loss, fatigue). Asymptomatic  warm or cold adenomas and symptomatic is referred to as hot adenomas.  Pituitary Adenomas  benign tumors arising from epithelial tissue in pituitary gland. They cause too much prolactin secretory which can trigger breast milk production in non-lactating females and males and amenorrhea (loss of menstrual periods) in females.  Fibroadenomas  composed of fibrous and glandular tissue in the breast. Biopsy may be done to rule out cancer. Fibroadenomas are easy to move with clearly defined edges.  Colon adenoma  benign growth on surface of the colon (called polyp). Develop when there are errors in the way cells grow and repair the lining of the colon. Some polyps have the potential to turn cancerous. Removing them early prevents colorectal cancer. Connective Tissue  Fibromas or skin tags  increase in frequency as we age, more common in obese people. Most skin tags are asymptomatic and benign. They can become irritated and inflamed. Recommended to remove skin tags only when they are irritated or source of discomfort. Removed by tying or cutting them after injecting a small amount of a local anaesthetic. They rarely become precancerous or cancerous.  Lipoma  benign tumor composed of connective adipose tissue. They are soft to touch, usually movable, and are generally painless. Many are small but can become bigger in size.  Osteoma  new piece of bone growing on another piece of bone, it is a benign tumor. Larger craniofacial osteomata may cause facial pain, headache, and infection due to obstructed nasofrontal ducts. Craniofacial osteoma presents itself through ocular signs and symptoms. Muscle Tissue  Leiomyoma  benign tissue of uterine muscle, commonly called uterine fibroids. They usually affect women over age 30. The cause is unknown but fibroid growth seems to depend on the hormone estrogen. Fibroid will continue to grow slowly as long as a woman with fibroids is menstruating. They can be very tiny but can also grow very large. Common symptoms include abdominal fullness, gas or constipation, bleeding between periods, increase in urinary frequency, heavy menstrual bleeding or menorrhagia, menstrual periods that may last longer than normal, pelvic cramping or pain with periods of sensation of fullness or pressure in the lower abdomen.  Rhabdomyoma  benign tumor of striated muscle. Commonly associated with the tongue and heart. Neural Tissue  Neuroma  benign tumor of nerve tissue, they can be applied to any swelling of a nerve.  Glioma  benign tumor that starts in the brain or spine, arises from glial cells, brain is common site.  Meningioma  benign tumor of the meninges. As they grow, they compress adjacent brain tissue. Symptoms are related to the compression of brain tissue. Most are considered non-malignant or low grade tumors. Some of these tumors can cause disability and may sometimes be life threatening. Endothelial Tissue  Hemangioma  benign tumor of the cells that line blood vessels, they are connected to the circulatory system and filled with blood. Sometimes they grow in internal organs such as the liver. They may present as a flat red or pink area. They are the most common childhood tumor, females are more likely to have them. Many are located in face and neck, and the liver is the next prevalent location.  Lymphangiomas  malformations of the lymphatic system (drains excess fluid from tissues). They can occur at any age and may involve any part of the body. They cannot become malignant. NOMENCLATURE: MALIGNANT TUMORS  These broad categories of tissue type help us to determine the types of cells affected. Epithelial Tissue  Epithelial tissue, as you recall, is basically skin tissue that covers and lines the body. 2 categories of epit
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