Patho Cancer Test – Flashcards
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Social Control genes
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-Genes that regulate cell birth and death
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Tumors (cancer)
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-Abnormal cells that fail to regulate cell proliferation, cell growth and cell division
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Genes implicated in cancer
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-Signal transduction -Cell cycle control -DNA repair -Cell growth -Differentiation -Transcriptional regulation -Apoptosis
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BRCA - 1 and 2
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-DNA repair
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Bcl-2
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-Apoptosis inhibitor
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ß- Catenin
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-Inhibits signal transduction
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CDK inhibitor
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-Cell cycle regulator
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Mutational Pathway to Uncontrolled Proliferation
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1. Stimulation - Hyperactivity gene altered 2. Inhibition - inhibition gene
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Oncogene
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-Over expression of growth regulating genes -Resulted in tumor formation
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Proto-oncogene
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-Normal hyperactivity gene, does not generate cancer
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Major properties of cancer
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1. Autonomy 2. Anaplasia
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Autonomy
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-Cancer cells are independent of normal cellular controls
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Anaplasia
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-Loss of differentiation -Lose ability to have a specialized function as in normal cell
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Neoplasms
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-Resemble undifferentiated cells -Pathway to differentiation is blocked -Cells locked in an undifferentiation and rapid proliferation stage
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Anaplastic
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-The further tumor cells are from normal cell structure and function the more undifferentiated they are
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Tumor grading
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-Estimates of differentiation -Estimates the tumors degree of malignancy
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Mechanisms in differentiation could lead to tumor growth
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1. More than 50% of daughter cells remain stem cells 2. Differentiation process becomes altered
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Immortialized cells
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-Cells will multiply indefinitely
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Growth inhibitory proteins that regulate senescence
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-Retinoblasoma -p53 gene
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Telomeres
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-Count number of replicative generations cells go through -After a specific number of cell divisions they induce senescence and crisis
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Telomere caps
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-At the end of a chromosomes -Shortens after each chromosome division -Induces senescence and crisis
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Telomerase gene
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-Gene codes for the telomerase enzyme that rebuilds the telomere -Allows tumor cells to divide endlessly
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Epithelial cells
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carcinomas
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Connective tissue
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sarcomas
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Lymphatic tissue
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lymphomas
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Nervous tissue
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gliomas
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Bone marrow
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Leukemias
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Carcinoma "in situ"
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-Preinvasive epithelial tumors of glandular or squamous cell origin -Tumor cells have not broken through basement membrane of the epithlial cells
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Characteristics of Cancer cells
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-Local increase in cell number -Loss of normal arrangement of cells -Variation in shape and size -Increase in nuclear density -Increase mitotic activity
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Tumor Cell Markers
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-Substances produced by cancer cells and found on tumor plasma membrane or in blood or urine
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Types of tumor cell markers
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-Hormones, enzymes, genes, antigens, antibodies
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HER-2/neu (c-erbB-2)
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-protein receptor found on breast tumor cells -Can be treated with special immunotherapy
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Steroid receptors (estrogen/progesterone)
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-Tumors with these receptors can be treated with anti-steroid therapy
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Carcinoembryonic antigen (CEA)
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-Some tumors (ovarian/breast) produce this antigen (in blood)
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Ectopic hormone production
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-Production of hormones by tumors of "nonendocrine origin"
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p53 gene
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-Tumor suppressor gene -Mutated in 50% of tumors -If mutated it will not block tumor formation
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Oncogenic Viruses
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-Viruses cause cancer transformed into normal animals -True pathogenic agent - cause specific type of cancer
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DNA viruses life cycle
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1. DNA virus penetrates the host 2. Inside the cell viral DNA enters the nucleus 3. Integrates into the host DNA 4. VIral DNA is transcribed - makes mRNA 5. Viral DNA is transcribed at two different times
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v- onc
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Virus possesses oncogenes
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c-onc
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-oncogenes in normal cells -Collectively termed proto-oncogenes -Likely to be important in normal cellular function
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Viral carcinogenesis theory
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-Oncogenic viral infection can lead to the transformation of normal cells to neoplastic cells
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Mechanisms of Viral Carcinogenesis
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1. Direct mechanism-"insertional mutagenesis 2. Indirect
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Carcinogenesis
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-process of tumor development -Evidence indicates multiple mechanisms
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Mechanisms of carcinogenesis
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1. Cell is unable to terminally differentiate 2. Unable to control growth 3. Increased ability to move to distant tissues 4. Invade and establish cells in these tissues
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Monoclonal Origin Theory
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-Cancer begins with a single abnormal cell
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Evidence that cancer is a stem cell disease
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1. Stem cells and cancer cells rapidly proliferate 2. Stems and cancer cells self-generate 3. Both cell types respond to radiation therapy in a similar manner 4. Terminal differentiation can be induced in both cells using differentiation factors
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4 types of human cancer that are hormone sensitive
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1. Breast cancer 2. Endometrium 3. Ovary 4. Prostate
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Estrogen replacement therapy (ERT=HRT=HT)
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-Treatment of perimenopausal symptoms -Osteoporosis
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Diethylstilbestrol (DES)
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-synthetic estrogen -Stimulates enhanced estrogen response - Linked to breast cancer
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Estrogen and cancer
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1. Estrogen stimulate breast cells to proliferate/grow 2. Estrogen metabolism results in production of free radical 3. Estrogen withdrawal stimulates apoptosis and decreased proliferation
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Prostate regulation- growth
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-DHT and other hormones -IGF-I (insulin like growth factor) -Estradiol (E2) -Progesterone levels
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Age Related Changes in Endocrine factors in Men
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1. Testosterone levels decline 2. Progesterone levels decline 3. Lower progesterone 4. Increases in 5 alpha reductase activity 5. Causes increased production of DHT 6. This stimulates prostate growth 7. Estrogen aslo increases
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Factors leading to prostate cancer
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-Androgens (and receptors) act as tumor promoters -Endogenous DNA toxicity due to estrogen metabolic free radicals and prostate free radicals -Initiates normal cell transformation to neoplastic cells
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General Mechanism- tumor progression
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1. Cell transformation-normal to neoplastic 2. Growth of transformed cells 3. Local invasion by transformed cells 4. Distant metastasis
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Local Invasion
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-Required for metastasis to occur -Cells break away and invade other tissues
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Cellular multiplication
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-invasion depends on cellular multiplication rate
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Mechanical Invasion
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-Mechanical pressure from tumor growth -Pressure disrupts circulation to local normal tissue -Enhances tumor spread
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Decreased Cell-cell adhesion
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-Tumor cells do not adhere to each other or normal cells -Thus cells more likely to spread or break off from the initial mass
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Fibronectin
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-Important in cell attachment -Cancer cells may produce abnormal this -Or cancer cells may breakdown this during growth
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Increased motility
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1. Tumor cells infiltrate adjacent tissues 2. Pass through the vascular walls - enter circulation 3. Cells leave the circulation and pass into the vascular walls of vessels
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Proteases
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inhibited by antiproteases present in normal cells
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Classes of Tumor proteases
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-Serine -Cysteine -Matrix metalloproteinases (MMPs)
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MMPs
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-Increased in epithelial cancers -Have a role in producing new blood vessels (angiogenesis)
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Urokinase type plasminogen activator (uPA)
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-Increased in tumor cells -This converts plasminogen (proenzyme) into protease plasmin (active) -Degrades extracellular matrix during tumor cell invasion
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Theory of Tumor Invasion
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1. Tumor cell attachment to the matrix 2. Degradation of the matrix 3. Locomotion into the matrix
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RNAi
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-Blocks cancer specific genes (eg. Protein degrading enzymes)
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siRNA
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-Type of double stranded RNA -Consists of sense and anti sense RNA
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Direct or continuous extensions-Metastasis
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-Cancer cells extending from the primary tumor without breaking away
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Potential regions of tumor spread
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-Tissue spaces -Lymph Vessels -Blood vessels -Body Cavities -Cerebral spinal spaces
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Metastasis by lymphatics
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1. Invasion of local tissue 2. Penetration in vessels or body cavity 3. Transport to a new secondary site 4. Cells stabilize and proliferate at the secondary site 5. Clumps of cells have a better chance of survival 6. Most common metastatic route is lymph 6
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Metastasis by blood stream
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1. Cell penetrate blood vessels 2. Within the blood stream tumor cells must -Survuve immune attack -Survive mechanical stress of blood flow -Attach and break through the vessel walls
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Angiogenesis
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-New blood vessels development
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Pro-angiogenic factors
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-Vascular Endothelial growth factor (VEGF) -Platelet-derived growth factor (PDGF) -Transforming growth factor (TGF) -Fibroblast growth factor (FGF)
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Inhibitors of angiogenesis
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-Platelet factor-4 -Angiostatin -Endostatin -Vasostatin
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Thrombospondin
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-Normal cells block angiogenesis using this
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Chemotherapy
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-Directed at destroying tumor cells -Small tumors are more sensitive to this
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Taxotere
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-Disrupts cellular microtubules -Microtubules are important in cell division -Rapidly dividing cells are sensitive to these agents
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Abraxane
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-Taxol analog bound to albumin -Water soluble does not not require chemicals to solubilize chemotherapy -"vechicles" to drive chemotherapy drugs into solution cause side effects -Avoid pre-medicating before giving drug
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Multidrug resistance protein (MDR)
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-Tumors expressing a cell membrane surface glycoprotein termed (P-170) -Protein functions as a transporter moving chemotherapy drugs out of the cell
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Radiation therapy
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-Rapidly dividing cells (cancer cells) are sensitive to ionizing radiation -Will die after appropriate exposure
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Advantages to immunotherapy
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-Generally reduced side effects -Specific for cancer cells -Normal cells are spared
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Immunomodulating Agents
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1. Adjuvant- inactivated bacteria or parts of bacterial cell wall 2. Stimulates the patients immune system 3. Adjuvant is injected into or near the tumor 4. Activates the immune system 5. Tumor mass is reduced 5
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Adjuvant
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Inactivated bacteria or parts of the bacterial cell wall
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alpha interferon
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-From activated leukocytes -Inhibits tumor growth -Activates NK cells -Increases cancer cell surface protein expression
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Effector Cells and Lymphokines
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1. Lymphokine activated killer cell therapy (LAK) 2. LAK cells cultured with interleukin-2 3. Inject these LAK cells and interleukin back into the patient 4. LAK cells attack tumor cells and interleukin activates other immune system cells interleukin activates other
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Monoclonal Antibodies
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-Highly specific antibodies -Used to detect tumor cell antigens -Conjugated to radioisotopes visualize tumor sites
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Herceptin
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-Monoclonal antibody against the HER2 receptor -Growth hormone receptor -Commonly used to treat some forms of breast cancer -Tumors the HER2 gene becomes amplified -Results in high amounts of mRNA for HER2 protein -Produces high amounts of the HER2 receptor
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Breast Cancer therapy regimen
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1. Adjuvant chemotherapy- 3 rounds 2. Surgery - remove tumor or lymph 3. Chemotherapy - single round 4. Radiation 4-6 weeks 5. Immunotherapy - 1 year
