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BIO170 - Obj 12
BIO170 - Obj 12 - Carcinogenesis
| Question | Answer |
|---|---|
| What is carcinogenesis? | abnormal cell growth & development caused by DNA damage leading to malfunction of 2 sets of control genes: proto-oncogenes and tumor suppressor genes |
| What is the cancer theory we are studying? | initiation - promotion - progression theory |
| What is initiation? | Phase 1 of the Initiation-Promotion-Progression Theory; a single exposure to factors causing irreversible DNA damage (mutation) of one cell -> transformation to a cancer cell |
| What are mutations? | spontaneous and/or induced genetic changes |
| What are 2 types of mutations that enable the transformation to a cancer cell? | mutations of proto-oncogenes to oncogenes (tumor promoters) and mutation of tumor suppressor genes |
| What is the function of proto-oncogenes? | proto-oncogenes normally direct controlled mitosis and cell differentiation |
| How do oncogenes promote tumors? | oncogenes induce hyperactive cell growth by stimulating protein synthesis; they initiate/promote tumor cell transformation |
| Describe the protein synthesis changes induced by oncogenes: | proteins are synthesized in greater quantity than normal during tumor cell transformation; these proteins include growth factors, growth factor receptors, cytoplasmic signal transducers (i.e. ras gene), transcription factors; tumors are autocrine cells |
| What is an autocrine cell? | autocrine cells produce substances needed for their own growth |
| What is the significance of the increase in growth factors and cytoplasmic signal transducers produced by the tumor cell? | growth factors: trigger cell growth by binding to an increasing # of growth factor receptors; cytoplasmic signal transducers: amplify the signals sent from the growth factors binding to the receptors |
| What is the significance of the increase in transcription factors produced by the tumor cell? | enable genes to produce more mRNA for increased protein synthesis |
| What is anaplasia? What causes it? | anaplasis is the loss of structural differentiation; it is caused by accelerated cell growth and mitotic rate |
| What do anaplastic cells look like? What ability do they lose? | transformed cells lose their adult morphology; they lose any ability to divide into adult cells and more closely resemble undifferentiated embryonic cells |
| What is the significance of the loss of morphology? | loss of morphology is associated with loss of function |
| What happens during mitosis of the anaplastic cell? | more undifferentiated cells are produced from mitosis which will never develop into functional adult cells |
| What is the function of the tumor suppressor gene? What happens as a result of the initiation phase? | it normally regulates controlled cellular growth; the initation phase causes the tumor suppressor gene to become defective, allowing them to become autonomous, lose senescence and become immortal |
| How do damaged tumor suppressor gene cells become autonomous? | by losing dependence from normal cellular controls |
| What are 3 genes involved in normal cellular control? What types of genes are these? | the bcl gene and the Rb and P53 genes; these genes are tumor suppressor genes |
| What is the function of the bcl gene? | it blocks growth; damage to this gene eliminates normal growth inhibition |
| What is the function of the Rb and P53 genes? What happens when these genes become defective? | the normal functiono of Rb and P53 genes is to trigger apoptosis - pre-programmed cell death in damaged cells; defective genes fail to trigger apoptosis of damaged cells, allowing them to lose senescence and become immortal |
| What is senescence? | aging |
| What are telomeres? What is their significance? | telomeres are segments at the ends of DNA which are terminators (terminal sequence); the telomeres shorten after each cell division; after a set number of mitotic divisions (perhaps 50-60), the cells have lost all their telomeres |
| What triggers apoptosis? | the loss of telomeres signal Rb or P53 genes to trigger apoptosis |
| How do transformed cells avoid apoptosis? What is the significance of this? | cells initiated to transform make a telomerase enzyme which repairs the telomeres after each cell division; since the telomeres never shorten, the cells are immortal |
| What are some known carcinogens? | radiation, chemicals, certain compounds, microorganisms, DNA & RNA type viruses, heliobacter pylori |
| Describe the carcinogenic effect of radiation: | UV light and X-rays cause skin cancer |
| What are some carcinogenic chemicals? | nickel, chromium, and cadmium metals; also, asbestos and arsenic |
| What are some the known carcinogenic compounds? What types of cancer do they produce? | benzene, tar, mineral oil, mustard gas, soot, vinyl chloride; many induce skin cancer on contact or lung cancer if inhaled |
| Describe the carcinogenic effect of microorganisms: | some microorganisms carry their own oncogenes similar to cellular proto-oncogenes |
| What are some DNA type viruses and the types of cancer they initiate? | HPV (human papilloma virus) causes genital warts and can initiate cervical cencer; Epstein-Barr virus initiates lymphoma; Hepatitis B & C can cause hepatic cancer |
| What are RNA type viruses? What is an example and what type of cancer does it cause? | RNA type viruses are retroviruses; an example is the human T-cell leukemia/lymphoma virus (HTLV) which causes T-cell lymphoma |
| What type of cancer is heliobacter pylori responsible for? | heliobacter pylori causes ulcers and possiblly leads to stomach cancer |
| How prevalent are inherited cancers? | inherited cancers are rare as it would indicate DNA damge to germ cells; DNA damage is more common to somatic cells than to germ cells |
| What is neurofibromatosis? | aka elephant man; this is an inherited cancer |
| What is promotion? | the 2nd phase of carcinogenesis; it is characterized by multiple exposures to factor(s) causing irreversible proliferation of many cancer cells from one transformed cell |
| What are the descendants of a single transformed cell called? | they are said to be of monoclonal origin |
| What are the 4 factors that allow for promotion? | genetic, nutrition, infection, and hormones |
| What is the genetic component of promotion? | oncogenes are turned on while tumor suppressor genes are turned off |
| What is the role of nutrition on promotion? | nutrition must be sufficient to support cancer cell growth |
| What is the role of infection on promotion? | immunosuppression allows cancer cell proliferation to go undetected by the immune system |
| What is the role of hormones on promotion? | estrogen promotes female reproductive cancer proliferation; testosterone promotes male reproductive cancer (i.e. prostate) proliferation |
| What is progression? | the 3rd stage of carcinogenesis |
| What stage is tumor development? What is is caused by? | progression; increased mitotic rate of a small group of transformed cells |
| What is a cancerous tumor? | an abnormal, undifferentiated mass of cells which ultimately exhibits malignant behavior |
| What is malignancy? | the spread (metastasis) of the tumor cells to distant sites |
| What are the characteristics of malignant tumors? (10) | density, growth factor requirements, anchorage dependence, proliferative life span, adhesiveness, morphology, fibronectins membrane glycoprotein, plasminogen activator, actin filaments. tumor cell markers |
| What is the significance of density regarding cancerous tumors? | tumor cells display continuous growth even when in contact with other cells (i.e. no contact inhibition) due to increased, growth factors, decreased adhesion (anchoring junctions) and cell-cell communication (gap junction) |
| What is the significance of growth factor requirements regarding cancer tumor cells? | tumor cells need little growth factor and produce their own (autocrine); tumor cells ignore growth inhibition factors (i.e. interferon, tumor necrosis factor) |
| What is the significance of anchorage dependence of cancer tumor cells? | tumor cells display degeneration of cell-cell attachments (i.e. anchoring junctions for structure and gap junctions for communication) leading to metastasis |
| What is the significance of a proliferative life span of cancer tumor cells? | tumor cells display accelerated mitotic rate, increase in chromosomal abnormalities, and incress in cell numbers; tumor cells become immortal |
| What is the significance of adhesiveness in tumor cells? | tumor cells are not connected to each other and have a greater chance of metastasis |
| What is the significance of morphology in tumor cells? | tumor cells are variable in size/shape, contain large abnormal nuclei, bear little resemblance to normal adult cells (undifferentiated); these changes are due to increased mitotic rate, abnormal chromosome structure, & loss of normal cellular arrangement |
| What is the significance of fibronectins membrane glycoprotein? | because tumor cells lose their normal adult shape and adhesion to neighboring cells leading to metastasis; fibronectins function as adhesive ligand-like molecules and therefore their number is reduced in tumors |
| What are tumor cell markers in tumors? | tumor cells secrete tumor cell markers, which are chemical substances, and include hormones, enzymes/isoenzymes, antigens, and antibodies |
| Are tumor markers chemicals that are only secreted by cancer cells? | sometimes tumor markers are substances secreted only by cancer cells (ex: PSA, alpha-fetoprotein); in other cases, tumor markers are elevated levels of normally secreted substance (ex: estrogen in reproductive cancers) |
| What is PSA and alpha-fetoprotein? | PSA is prostate specific antigen, a tumor marker, which is screted by prostate cancer cells; alpha-fetoprotein is a tumor marker secreted by liver, ovarian, and testicular cancer cells |
| What is plasminogen activator? | a protease secreted by tumor cells that converts plasminogen to plasmin; this protease degrades the extracellular matrix leading to loss of adhesion |
| What is the significance of actin filaments in tumor cells? | tumor cells display degeneration of actin filaments which reduces adhesion to neighboring cells and ultimately loss of density-depending inhibition of growth |
Created by:
debmurph
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