Carcinogenesis – Flashcards
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Cause of carciogenesis
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Abnormal cell growth and development caused by mutation to DNA
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Genes typically involved in carcinogenesis
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Proto-oncogenes Tumor suppressor genes
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Most widely adapted theory of carinogenesis
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Initiation-Promotion-Progression model
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Initiation
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First phase of carcinogenesis in which the initial mutation occurs
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Characterization of the initiation phase of carinogenesis
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Exposure to factors causing irreversible DNA damage (ie, muation) on one cell
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Factor that begins the process of normal cell transformation to a cancer cell
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Mutation
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Mutation
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Spontaneous and/or induced genetic changes
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Proto-oncogenes
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Genes that normally direct controlled mitosis and differentiation
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Oncogenes
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Tumor promoters
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Factor that drives mutation to oncogenes
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Genetic changes
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Way oncogenes induce hyperactive cell growth
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By stimulating protein synthesis
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Growth factors
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Chemicals (usually proteins) that stimulate cell reproduction
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Function of growth factor receptors
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Form chemical bonds with growth factors
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Cytoplasmic signal transducers
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Chemicals that work directly inside the cell's cytoplasm to begin the process that will lead to uncontrolled cell reproduction
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Proteins synthesized in greater quantity than normal during mutation transformation
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Growth factors Growth factor receptors Cytoplasmic signal transducers
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Process that elevated levels of growth factors trigger
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Cell growth
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Promotion
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Second phase of oncogenesis in which the mutated cells are stimulated to divide
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Way elevated levels of growth factors trigger cell growth
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By binding to an increasing number of growth factor receptors
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Function of the cytoplasmic signal transducers
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Amplify the signals sent from the growth factors binding to the receptors
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Function of transcription factors
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Initiate transcription of RNA
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First step to making any protein
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Transcription of RNA
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Purpose of transcription factors
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Enables genes to produce larger numbers of messenger RNA for increased protein synthesis
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Function of the tumor suppressor gene
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Supresses runaway cell reproduction
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Metaphor for proto-oncogenes
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Green light
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Metaphore for tumor suppressor genes
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Red light
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Examples of tumor suppression genes
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Rb P53
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Impact mutation initiation has on the tumor suppressor gene
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Causes it to lose its suppressor ability
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Result of the tumor suppressor gene losing its ability to suppress runaway cell production
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Uncontrolled cell reproduction
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General impact mutation initiation has on proto-oncogenes and tumor suppressor genes
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Cause them to become defective
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Normal function of Rb and P53 genes
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Trigger apoptosis
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Result of Rb and P53 genes becoming defective
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Fail to trigger apoptosis
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Anaplasia
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Loss of differentiation
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Cause of anaplasia
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Accelerated cell reproduction and mitotic rate
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Structural result of anaplasia
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Lose their adult form and more closely resemble some form of undifferentiated precursor cell (ie, embroyonic stem cell or cell formed later in development)
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Functional result of anaplasia
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Loss of normal function
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Reproductive result of anaplasia
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Lose ability to divide into adult cells. More undifferentiated cells are produced that never develop into functional adult cells
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Lifespan of mutated cells
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None. Immortal
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Mechanism in which mutated cells become immortal
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Mutated cells produce a telomerase enzyme to repair the telomeres after each subdivision, so they don't shorten and never become too short to reproduce
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System responsible to destroy mutated cells
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Immune
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Second phase of carcinogenesis
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Promotion
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Phase of carcinogenesis that is necessary in the progression of a single mutated cell to become an entire population
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Promotion
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Process that characterizes promotion
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Proliferation of many cancer cells from one population of transformed cells
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Monoclonal origin
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Descendants from one cell
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Phenomena that can promote a group of mutated cells
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Nutrition Immunosuppression Hormones
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Effect on promotion if a promoter is removed
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It will stop
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Role of nutrition in cancer promotion
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Nutrition must be sufficient to support growth and since
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Reason why cancer cells have a high demand for nutrient energy
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They grow very rapidly
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Role of immunosuppression in cancer proliferation
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Allows cancer growth to go undetected by the immune system
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Role of hormones in cancer growth
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They promote cancer cell promotion
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Cause of tumor development
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Increased mitotic rate of a small group of transformed cells
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Density-dependent inhibition of growth
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Normal cells will not divide if they are close to other cells
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Reason tumor cells continue to grow, even when in contact with other cells
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Increased amounts of growth factor Decreased adhesiveness Lack of cell-cell communication
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Requirement that stimulates normal cells to divide mitotically
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High concentration of growth factor proteins
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Autocrine growth factors
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Growth factor produced by tumor cells
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Growth factor requirements of tumor cells
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Very little and produce their own
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Anchorage dependence of normal cells
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Firmly connected by tight junctions, desomosomes, gap junctions, etc.
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Anchorage dependence of tumor cells
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None. The display degeneration of cell-cell attachments
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Impact of tumor cells not being securely attached to their surroundings
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Greater liklihood of detaching from their original development site and spreading throughout the body
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Morphology of tumor cells
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Variable in size and shape May contain large abnormal nuclei Bear little resemblance to normal adult cells
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Reason for tumor cell morphology
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Increased mitotic rate Abnormal chromosome structure Loss of normal cellular arrangement
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FMP
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Fibronectin membrane glycoprotein
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Fibronectin membrane glycoprotein
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Intercellular "glue"
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Impact of cells not anchored to their neighbors
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Far more likely to metastasize
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Relative amount of FMP in tumor cells
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Decreased
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Plasminogen
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Plasma protein that slowly digests a blood clot
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Plasminogen activator
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Enzyme that converts plasminogen (inactive) to plasmin (active)
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Impact of plasminogen secreted by tumor cells
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Loss of adhesion Decreased FMP Decreased anchorage dependence
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Role of plasminogen in tumor cells
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Tumor cells secrete their own plasminogen activator that converts plasminogen to plasmin
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Tumor cell action on actin filaments
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Degeneration
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Impact of tumor cell degeneration on actin filaments
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Reduces adhesion to neighboring cells Ultimately loss of density-dependent inhibition of growth
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Tumor cell markers
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Hormones Enzymes Antigens Antibodies
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Types of markers secreted by tumor cells
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Those normally secreted by substances and those just secreted by cancer cells
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Markers secreted in thyroid cancer
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Calcitonin
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Markers secreted in prostate cancer
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Prostate-specific antigen (PSA)
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Markers secreted in liver, ovaria, and testicular cancers
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Alpha-fetoprotein
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Oncogenesis
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Carcinogenesis
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Stages of oncogenesis
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Initiation Promotion Progression
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Progression
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Third phase of oncogenesis in which the tumor cells compete with one another and develop more mutations which make them more aggressive
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Cancer control genes
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Proto-oncogenes Tumor-suppressor genes Apoptotic genes
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Function of proto-oncogenes
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Promote normal growth with direct controlled mitosis and differentiation
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Function of tumor-suppressor genes
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Prevent the growth of mutated cells
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Function of apoptiotic genes
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Promote programmed cell death
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Result of mutated proto-oncogenes
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Become oncogenes. Tumor promoters
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Protein synthesis stimulated by proto-oncogenes
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Growth factors Growth factor receptors Cytoplasmic signal transducers Transcription factors
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Malfunctions caused by a mutated proto-oncogene
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Production of too much or an abnormal protein Protein that turns on by itself Protein made when not needed Protein that cannot turn cell division off Protein that should be made by a different cell
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Result of mutated tumor suppressor genes
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Promotes growth
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Method by which tumor suppressor genes prevent runaway cell division
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Counteracts oncogenes and makes proteins for checkpoints that usually stop the division of mutated cells
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Role of microRNA
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Pairs to specific sequence on mRNA Blocks protein translation
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Ways that epigenetics can influence cancer manifestations
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Silence genes without changing DNA Hypermethylation of promotor region Environmental influences
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Epigenetics
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Mechanisms that involve changes in the patterns of gene expression without a change in the DNA
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Way promotion works in cancer progression
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Single, mutated cell proliferates into an entire poplulation of transformed cells
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Aneuploidy
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Abnormal number of chromosomes
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Types of cells that display aneuploidy
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Malignant
