Term
|
Definition
gain DNa
lose DNA
change in nucleotide
epigenetic effect |
|
|
Term
most tumors initally devlop as?
what happens over time? |
|
Definition
monoclonal
get more aberattions->heterogentity/polyclonal |
|
|
Term
non lethal genetic damage to _ initaties cancer?
what are these-4 |
|
Definition
cell regulation genes
DNA repair,
cell cycle,
cell signnaling/growth
apoptosis |
|
|
Term
| what are the protooncogenes-2 |
|
Definition
|
|
Term
| what are tumor suppression genes-2 |
|
Definition
|
|
Term
| what are the genes that regulate cell cycle |
|
Definition
|
|
Term
| what are the cell signal trnasduciton geneses |
|
Definition
|
|
Term
| what % of cancers are inherited? |
|
Definition
|
|
Term
| look at lside 5 for the heridiatry cancers |
|
Definition
|
|
Term
| to inherit breat cancer, a daughter gets a mutaiton in what gene? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| when a daughter gets the rbeast cancer mutation, its only 1 mutated and 1 normal alle. what happens over adolsesnce? |
|
Definition
| the other allele undergoes mutaiton to pave way for cancer in hormone tissues at early age |
|
|
Term
|
Definition
| # of copies of chromosomes |
|
|
Term
|
Definition
| 2 copies (1 chrom from dad and mom) |
|
|
Term
|
Definition
| mutlitple pairs of the chrom. beyond diploid set |
|
|
Term
|
Definition
| cell has abnormal non-integer ploidy |
|
|
Term
Def:
loss of heterozygoistiy |
|
Definition
| one chrom has normal allele and the toher has a mutant |
|
|
Term
| normally protoconocgenes do? |
|
Definition
| cell growth and proliferation |
|
|
Term
| in cancer cells what 2 gene splay majro role |
|
Definition
protooncogene-> oncogene (++ growth_
tumor supression gene (is inhibited) |
|
|
Term
this gene is the gas pedeal for cell proliferation
mutations cause- |
|
Definition
proto-oncogene
break pedeal to stick- too much prolif (-> onco-genes) |
|
|
Term
_ are the brakes for cell proliferation
mutation? |
|
Definition
tumor supressor genes (negatively regulate)
brake failure- too muhc prolif |
|
|
Term
|
Definition
| cancer causing dervied from proto-oncogene |
|
|
Term
|
Definition
| normal genes that promote cell prolfieration |
|
|
Term
|
Definition
| proteins of oncogenes that resemble protooncogenes, but DONT need growth facotrs for production in transfromed cells |
|
|
Term
|
Definition
| tell cells to grow/divide, but ONLY in response to signals (dont't listen to these signals when mutated) |
|
|
Term
| protooncogenes-> oncogenes results-4 |
|
Definition
overproduction growth factors
too many replication signals
uncontrolled stimulated in intermediary pathways
cell growth wiht increased trascription factors |
|
|
Term
| 3 specific ways proto-oncogenes become oncogenes |
|
Definition
deletion/point mutaitons
gene amplification
chromosome rearragnement |
|
|
Term
| cell protoncogenes can be mutated, captured by retrovirus, or have virus genes that mutate to oncogenes |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
what is the chrom trnaslocaiton in Burkitt lymphoma?
result? |
|
Definition
c-myc -> adjacnt IgG promoter
increased myc production |
|
|
Term
what is the chromosome trnaslocaiton for leukemia
result? |
|
Definition
Abl-> BCR locus (philedelphia chromosome)*
more potent tyrosine kinase activity |
|
|
Term
| slide 17 has the gene amplificaitons and the cancers caused |
|
Definition
|
|
Term
| example of molecular target therapy- |
|
Definition
|
|
Term
| what is the MOA of gleevac/imatinib |
|
Definition
| molecule inhibts Bcr-Abl tyrosine kinase overexpressed |
|
|
Term
| what cancer does gleevac target |
|
Definition
| chronic myloid leukemia (refractory) |
|
|
Term
what is the Ras inactive form?
active?
which is the mutation form always in? |
|
Definition
GDP bound
GTP bound
GTP bound/active |
|
|
Term
| what is the function of ras? |
|
Definition
| transduces signals to stimulate proliferation |
|
|
Term
| *in tumor cells there is abornmal amt of EGFR (epidermal growth factor recpotrs)that signal cell proliferation |
|
Definition
|
|
Term
| EGFR does signal transductin thru what? |
|
Definition
|
|
Term
| when do EGFR and other like it not need ligand stimulation? |
|
Definition
|
|
Term
| what molecules cna inhibit EGFR?-2 |
|
Definition
monclonal abs
small molecles |
|
|
Term
| what is the resting state in cell cycle? |
|
Definition
|
|
Term
| what is hte DNA synthesis pjase of cell cycle? |
|
Definition
|
|
Term
| what is the sequcne for cell cycle? |
|
Definition
|
|
Term
| cyclin dependent kinases drive ht cell cycle, are the kinases active on their own? |
|
Definition
|
|
Term
| what are the CDK inhibitors that bind and inhibit the regulation of the cell cycle progresision?-2 |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| what CDK makes G1 go to S? |
|
Definition
|
|
Term
| what CDK makes it go from S to G2? |
|
Definition
|
|
Term
| what CDK makes it go from G2 to M? |
|
Definition
|
|
Term
| what cell cycle check causes stop in S phase |
|
Definition
|
|
Term
| what causes a cell cycle stop in the G2 phase |
|
Definition
|
|
Term
| what if after G2 the cell has high MPF? |
|
Definition
|
|
Term
| what is the cell cycle check point that stops in M phase |
|
Definition
| improper spindle formation |
|
|
Term
| what if after M phase the cell has low anaphase inhibitor? |
|
Definition
|
|
Term
| what is the chekc point in G1 phase? |
|
Definition
|
|
Term
| deregulation of what is a hallmark of canceR? |
|
Definition
|
|
Term
| gene amplification of _ causes the cel cycle to progress faster? |
|
Definition
| CDKs (positve regulators) |
|
|
Term
| gene coding deletes/inhibits _ which causes cell cycle to go faster |
|
Definition
|
|
Term
| the _ protiens are mutated in cancer so more dysregulation |
|
Definition
|
|
Term
| both or only one gene copy of a tumor supressor gene has to be defective to cause cancer |
|
Definition
|
|
Term
what are the tumor suppressor genes?-3
what cancer do each cause? |
|
Definition
BRCA, P53, TGF-B
BRCA1=female, BRAC2= male and female breast
P53=most cancers
TGf-B: colon |
|
|
Term
what is the gaurdian of the genome?
when is it activated? |
|
Definition
|
|
Term
|
Definition
| stops cell cycle if damage for repairs. if too excessive->cell death |
|
|
Term
_ % of cancer have P53 mutaiton
if this mutation occurs ealy what happens? |
|
Definition
50
more likely aggressive malginnancy |
|
|
Term
| what tumor supporessor protein control moving past G1 checkpoint to S? |
|
Definition
|
|
Term
what is the MOA of Rb?
what happens when Rb is bound to it? |
|
Definition
phosphylation in G1->rlease E2F transscirption facotrs. G2-> dephosy and binds E2f= stops DNa synth
-no trnascirption/replicaiton |
|
|
Term
| Rb is inactive when its phosphyrlated/dephosphyrlated? what cycline does this? |
|
Definition
|
|
Term
| what is the consequcne of an inactive Rb |
|
Definition
| cells all go to S phase-> uncontrolled proliferaiotn-> cancer |
|
|
Term
what is the rpocess of cell death that causes bursting into other areas and inflammatory?
what is the one where it just shrinks and disentrgrates inside the one membrane |
|
Definition
|
|
Term
| chemo and radtion kill tumor cells how? |
|
Definition
| activaitng the orderly apoptotic pathways |
|
|
Term
| what is the anti-apoptotic/ prosurvivial gene? |
|
Definition
|
|
Term
| what is hte proapoptotic gene |
|
Definition
|
|
Term
| Bax nad Bcl2 are dimerizing proteins with _ domains |
|
Definition
|
|
Term
| pro and anti apoptotic genes are _ responsive |
|
Definition
|
|
Term
| _ modificaitons determine if apoptosis is active/inactive |
|
Definition
|
|
Term
| activaiton of pre-apoptotic members may inovle? |
|
Definition
|
|
Term
| balance btwn what 2 things determiens apooptosis or not? |
|
Definition
|
|
Term
BCL 2 control the permability of-
these 2 protiens cause perambility to it thru channels or PTPs to allow apoptsis molecules |
|
Definition
OMM (mitochondrial membrane)
Bax and Bak |
|
|
Term
| whcih pathway invovles stimulation of death receptors for apoptotiss |
|
Definition
|
|
Term
| whihc pathway for apoptosis incoled disruption of the mitochondiral permeaility releasing cytochrome C into cytoplasm |
|
Definition
|
|
Term
| in both pathways for apoptosis, _ are activaed and cell regulatory proetins are cleaved (by DNAase) |
|
Definition
| caspases (death proteases) |
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|
