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AH-Lewis Ch 16
Cancer
Question | Answer |
---|---|
What is cancer? | uncontrolled and unregulated growth of cells |
What type of cancer is growing faster than any other type in the US? | Melanoma |
Melanoma is a combined result of? | genetic predisposition and sun exposure |
Cancer incidence is higher in? | men |
What is a second most common cause of death? | cancer |
Cancer incidence is higher in what ethniticity? | African American |
Survival from cancer are attributed primarily to a combination of what factors? | poverty, difficult access to and poor quality of health care, comorbid condition, and difference in tumor biology |
Who is in the strategic position to lead efforts at changing attitudes and behaviors about cancer? | Nurses |
What are two major dysfunctions present in the process of cancer? | cellular proliferation and defective cellular differentiation |
Cancer can arise from any cell of the body capable of? | evading reulatory controls over proliferation and differenctiation |
Most tissues of the human adult contain a population of predetermined, undifferentiated cells known as? | stem cells |
What does predetermined cell mean? | the stem cells will differentiate and become mature, functioning cells of that tissue and only that tissue |
Cells proliferation originates in the? | stem cells |
What does cell proliferation begin? | when stem cells inters the cell cycle |
What is the generation time of the cell? | the time from when a cell enters the cell cycle to when the cell divides into two identical cells |
All cells of the body are controlled by? | intracellular mechanism that determines when cellular proliferation is necessary |
Normally cellular proliferation and division is activated only in the presence of? | cellular degeneration or death |
What will occur if the body has physiologic needs for more cells? | cellular proliferation |
What is contact inhibition? | where the cells respect the boundries of the cells around them |
The rate of normal cellular proliferation differs in? | each body tissue |
Where is cellular proliferation rapid? | bone marrow, hair follicles, apithelial lining |
Where is cellular proliferation slow? | myocardium and cartilage |
Cancer cells respond differently than normal cells to the? | intracellular signals that regulate the state of dynamic equilibrium |
The stem cell theory proposes that the loss of? | intracellular control of proliferation results from a mutation of the stem cells |
What is viewed as the target or orgin of cancer development? | stem cells |
What happens to DNA in stem cells when there is cancer? | the DNS is substituted or permanently rearranged |
Once a stem cell has mutated what can occur? | Cell can die, the cell can recognize the damage and repair itself, or the mutated cell can survive and pass along the damage to other cells |
What is apoptosis? | cellular suicide |
The rate of _______ is more rapid in cancer cells than normal cells? | proliferation |
The proliferation of cancer cells is? | indiscriminate and continuous |
What is the time required for tumor mass to double in size? | doubling time |
What is the pyramid effect? | 1-2-4-8-16 |
What is cellular differentiation? | orderly process that progresses from a state of immaturity to maturity |
All cells have the potential to perform all? | body functions |
What is dedifferentiate of a cell? | revert to a previous undifferentiated state |
What are 2 types of normal genes that can be affected by muturation? | protooncogenes and tumor suppressor genes |
What are normal cellular genes that are important regulators of normal cellular processes? | protoonocogenes |
Protoonocogenes do what? | promote growth |
Tumor suppressor genes do what? | suppress growth |
Mutations that alter the expression of protooncogenes can activate them to function as? | oncogenes |
What has been described as the genetic lock that keeps the cell in its mature functioning state? | protoonocogene |
What are agents that cause cancer? | carcinogens |
Oncogenes interfere with? | normal cell expression under some conditions, causing the cell to become malignant |
Cancer cells produce that protiens? | Cacionoembryonic antigen and A-fetoprotien (in the cell membrane) |
Tumor suppressor genes function to? | regulate cell growth |
What are types of tumor suppressor genes? | BRCA 1, BRCA 2 |
Alteration in tumor suppressor genes increase? | a person's risk for breast and ovarian cancer |
Alterations in what gene increase a person's risk for familial adenomatous polyposis, colorectal cancer? | APC |
What p53 suppressor gene has been seen with wat cancers? | bladder, breast, colorectal, esophageal and lung |
Benign neoplasms are? | well differentiated |
Malignant neoplasms are? | well differentiated to undifferentiated |
What are the three stages of the development of cancer? | initiation, promotion, and progression |
What is the first stage of cancer development? | initiation |
What is initiation? | mutation in the cell's genetic structure resulting from an ingerited mutation, or following exposure to a chemical, radiation or viral agent |
What is a clone? | group of identical cells |
Initiation is? | IRREVERSABLE |
Not all altered cells go on the establish a tumor because many undergo? | apoptosis |
Why is a initiation cell not yet a tumor cell? | because it does not have the ability to self replicate and grow |
Many cancinogens are detoxified by? | protective enzymes and are harmlessly excreted |
Carcinogens may be? | chemical, radiation, or viral in nature |
UV radiation secondary to sunlight exposure is linked to the development of? | melanoma |
What is oncogenic? | DNA and RNA viruses |
DNA and RNA viruses can? | transform the cells they infect and induce malignant transformation |
Only 10% of cancers have a strong? | genetic link |
What is the second stage of the development of cancer? | promotion |
What is promotion in the development of cancer? | the reversible proliferation of the altered cells |
promotion is? | REVERSABLE |
What are promoting factos of cancer development? | fat, smoke, and drinking |
What are complete carconogens capable of? | initiating and promoting the development of cancer |
What is the latent period? | a period of time that elapses between the initial genetic alteration and the actual clinical evidence of cancer |
What is the final stage of cancer development? | progression |
What happens in the progression stage of cancer development? | increased growth of the tumor, increased invasiveness, and spread of cancer to a distant site |
What are the most frequent sites of metastasis? | lungs, brain, bone, liver, and adrenal glands |
How does metastasis begin? | with the rapid growth of the primary tumor |
What is tumor angiogenesis? | formation of blood vessels within the tumor itself |
What are metalloproteinase enzymes? | a family of enzymes that are capable of destroying the basement membrane |
What routes to cancers metastisize? | lymph and hematogenous |
HOw does hematogenous metastasis begin? | penetration of blood vessels by promary tumor cells via the release of metalloproteinase enzymes |
Most tumor cells do not survive what? | metastisize through blood because of immune system and mechanical mechanism |
What protects some tumor cells from destruction in blood vessels? | tumor cells, platelets, and fibrin deposits |
What is skip metastasis? | where tumor cells bypass first lymph nodes and travel to more distant nodes |
Vascularization is critical to the supply of nutrient to the? | metastatic tumor and to the removeal of waste products |
The immune system may not be able to? | identify cancer cells because they are from normal cells |
What are tumor associated antigens? | cancer cells that display altered cell surface antigens as a result of malignant transformation |
What is immunologic surveillance? | response of the immune system to antigens of the malignant cells |
Immune responses involve? | cytotoxix T cells, natural killer cells, macrophages, and B lymphcytes |
What plays the dominant role in resisting tumor growth? | Cytotoxic T cells |
What do cytokines do? | stimulate T cells, natural killer cells, B cells, and macrophages |
What are able to directly lyse tumor cells? | natural killer cells |
What do B lymphocytes do? | produce specific antibodies that bind to tumor cells and can kill these cells by complement fixation and lysis |
Where are B lymphocytes detected? | serum and saliva |
What is immunologic escape? | where cancer cells evade the immune system |
What are oncofetal antigens? | type of tumor antigen |
Where are oncofetal antigens found? | surfaces and inside of cancer cells |
What are onocofetal antigens a sign of? | the shift of cancerous cells to a more immature metabolic pathway |
What are examples of onocofetal antigens? | carcinoembryonic antigen and A-fetoprotein |
Where is carcinoembryonic antigen found? | surfaces of cancer cells derived from the GI tract and from normal cells from the fetal gut, liver, and pancreas |
A-fetoprotein is produced by? | malignant liver cells |
Tumors can be classified according to? | anatomic site, histology, and extent of disease |
What is the anatomic classification of tumors? | where the tumor is identified by the tissue of origin, the anatomic site and the behavior of the tumor |
Carcinomas originate from? | skin and glands and mucous membranes |
Sarcomas originate from? | connective tissue, muscle, bone and fat |
Lymphomas and leukemias originate from? | the hematopoeitic system |