Duke PA pathology
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| What some examples of pre-neoplastic disorders? | cirrhosis, HPV, UC
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| What are some factors that affect cancer risk? | tobacco smoke, asbestos, radiation exposure, alcohol abuse
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| How do genetics affect cancer risk? | cancer results from non-lethal genetic damage
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| Genetic hypothesis of cancer | tumor arises from clonal expansion of the damaged cell
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| More on genetic hypothesis of cancer | prediction that tumors have a monoclonal origin has been confirmed experimentally
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| carcinogenesis - molecular basis of cancer | a multistep process at both phenotypic and genetic levels
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| tumor progression | progressive acquisition of mutations leading to malignancy or metastasis
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| initiators | stimulate mutation
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| promoters | stimulate cell division
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| Damage to growth-promoting proto-oncogenes can result in what? | cancer
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| Damage to growth-inhibiting tumor suppressor genes can cause what? | cancer
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| Damage to genes that regulate cell death can cause what? | cancer
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| Damage to genes that affect DNA repair can cause what? | cancer
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| What is needed for cancer to allow unlimited cell division? | activation of telomerase
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| oncogenes | cancer-causing genes, drived from proto-oncogenes
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| Proto-oncogenes | cellular genes that control normal growth and differentiation
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| insertional metagenesis | retroviral promoter insertion near gene dysregulates its expression
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| What can activates oncogenes? | insertional mutagenesis, point mutation, amplification, chromosomal translocation
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| mutation of ras oncogene | mutant ras is always on
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| Where is ras anchored? | cytoplasmic domain of growth factor receptors via a lipid group
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| What prevent addition of the lipid group, preventing ras localization? | inhibitors of farnesyl transferase
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| What does translocation do to proto-oncogenes? | places expression of protooncogenes under control of highly active promoters
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| What is the result of translocation? | formation of hybrid genes that encode growth-promoting chimeric proteins
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| What gene does translocation occur in with Burkitt's lymphoma? | c-myc
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| Are coding regions changed in Burkitt's lymphoma? | they are unchanged
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| Over-expression due to translocation in mantle cell lymphoma | cyclin D1 gene placed adjacent to IgH locus
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| Over-expression due to translocation in follicular lymphoma | bcl-2 gene placed adjacent to IgH locus
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| Tumor suppressor genes | products of these genes regulate cell growth (usually negatively)
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| What has to happen to tumor suppressor genes for cancer to take over? | both copies of the gene have to inactivated - "recessive" cancer gene
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| What are the functions of tumor suppressor gene products? | regulate the cell cycle, regulate nuclear transcription, cell surface receptors
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| What is the purpose of cell surface receptors? | growth inhibition, adhesion
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| What does tumor growth depend on? | balance between cell growth and cell death
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| What does dysregulation of apoptosis allow? | accumulation of mutations that would otherwise by lethal
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| What is an example of dysregulation of apoptosis? | bcl-2 overexpression in lymphoma
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| genes that regulate DNA repair | mismatch repair genes
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| Are mutations in DNA repair genes oncogenic in and of themselves? | no
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| What do mutations in DNA repair genes allow? | allow mutations to occur in other genes during normal cell division
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| Can mutation of one gene transform cells? | no - every human cancer has multiple genetic alterations including oncogenes and tumor suppressor genes
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| What does the rate of tumor growth depend on? | growth fraction and the rate of cell loss
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| What does the growth fraction of tumors have an effect on? | has a profound effect on susceptibility to chemotherapy
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| Crude indication of growth rate? | frequency of mitoses
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| What is the first step for metastasis? | loosening of intercellular junctions
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| In metastasis, what happens after loosening of intercellular junctions? | attachment
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| In metastasis, what happens after attachment? | degradation
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| In metastsis, what happens after degradation? | migration
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| "soil and seed" theory | different organs provide growth conditions optimized for certain cancers
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| Homing theory | different organs have special abilities to attract cancer cells
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| Cartilage and skeletal muscle are rarely targets of metastasis, helping prove what theory? | soil and seed
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| What are three ways tumors cause disease? | tissue destruction, organ compression, obstruction
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| What are three more ways tumors cause disease? | infection, anemia, soluble products
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