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Pathology 3-2
Duke PA pathology
| Question | Answer |
|---|---|
| What some examples of pre-neoplastic disorders? | cirrhosis, HPV, UC |
| What are some factors that affect cancer risk? | tobacco smoke, asbestos, radiation exposure, alcohol abuse |
| How do genetics affect cancer risk? | cancer results from non-lethal genetic damage |
| Genetic hypothesis of cancer | tumor arises from clonal expansion of the damaged cell |
| More on genetic hypothesis of cancer | prediction that tumors have a monoclonal origin has been confirmed experimentally |
| carcinogenesis - molecular basis of cancer | a multistep process at both phenotypic and genetic levels |
| tumor progression | progressive acquisition of mutations leading to malignancy or metastasis |
| initiators | stimulate mutation |
| promoters | stimulate cell division |
| Damage to growth-promoting proto-oncogenes can result in what? | cancer |
| Damage to growth-inhibiting tumor suppressor genes can cause what? | cancer |
| Damage to genes that regulate cell death can cause what? | cancer |
| Damage to genes that affect DNA repair can cause what? | cancer |
| What is needed for cancer to allow unlimited cell division? | activation of telomerase |
| oncogenes | cancer-causing genes, drived from proto-oncogenes |
| Proto-oncogenes | cellular genes that control normal growth and differentiation |
| insertional metagenesis | retroviral promoter insertion near gene dysregulates its expression |
| What can activates oncogenes? | insertional mutagenesis, point mutation, amplification, chromosomal translocation |
| mutation of ras oncogene | mutant ras is always on |
| Where is ras anchored? | cytoplasmic domain of growth factor receptors via a lipid group |
| What prevent addition of the lipid group, preventing ras localization? | inhibitors of farnesyl transferase |
| What does translocation do to proto-oncogenes? | places expression of protooncogenes under control of highly active promoters |
| What is the result of translocation? | formation of hybrid genes that encode growth-promoting chimeric proteins |
| What gene does translocation occur in with Burkitt's lymphoma? | c-myc |
| Are coding regions changed in Burkitt's lymphoma? | they are unchanged |
| Over-expression due to translocation in mantle cell lymphoma | cyclin D1 gene placed adjacent to IgH locus |
| Over-expression due to translocation in follicular lymphoma | bcl-2 gene placed adjacent to IgH locus |
| Tumor suppressor genes | products of these genes regulate cell growth (usually negatively) |
| What has to happen to tumor suppressor genes for cancer to take over? | both copies of the gene have to inactivated - "recessive" cancer gene |
| What are the functions of tumor suppressor gene products? | regulate the cell cycle, regulate nuclear transcription, cell surface receptors |
| What is the purpose of cell surface receptors? | growth inhibition, adhesion |
| What does tumor growth depend on? | balance between cell growth and cell death |
| What does dysregulation of apoptosis allow? | accumulation of mutations that would otherwise by lethal |
| What is an example of dysregulation of apoptosis? | bcl-2 overexpression in lymphoma |
| genes that regulate DNA repair | mismatch repair genes |
| Are mutations in DNA repair genes oncogenic in and of themselves? | no |
| What do mutations in DNA repair genes allow? | allow mutations to occur in other genes during normal cell division |
| Can mutation of one gene transform cells? | no - every human cancer has multiple genetic alterations including oncogenes and tumor suppressor genes |
| What does the rate of tumor growth depend on? | growth fraction and the rate of cell loss |
| What does the growth fraction of tumors have an effect on? | has a profound effect on susceptibility to chemotherapy |
| Crude indication of growth rate? | frequency of mitoses |
| What is the first step for metastasis? | loosening of intercellular junctions |
| In metastasis, what happens after loosening of intercellular junctions? | attachment |
| In metastasis, what happens after attachment? | degradation |
| In metastsis, what happens after degradation? | migration |
| "soil and seed" theory | different organs provide growth conditions optimized for certain cancers |
| Homing theory | different organs have special abilities to attract cancer cells |
| Cartilage and skeletal muscle are rarely targets of metastasis, helping prove what theory? | soil and seed |
| What are three ways tumors cause disease? | tissue destruction, organ compression, obstruction |
| What are three more ways tumors cause disease? | infection, anemia, soluble products |
Created by:
ges13
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