Pathology 3-2 Word Scramble
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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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