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29 Cards in this Set
- Front
- Back
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What cancer type do fibroids fall under?
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Leiomyoma
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What is tumor heterogeneity?
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Refers to tumor undergoing additional mutations with each doubling and the subsequent gain of add'l abilities
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Role of telomerase in cancer cells.
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Limitless replication potential
Telomerase activation voids telomere time clock |
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Under what conditions are angiogenic factors produced? Ex. of angiogenic factor?
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Hypoxia; VEGF
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How do proteases from tumor/stroma mediate anti-angiogenic effects?
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Cleavage of plasminogen to angioSTATIN (anything -statin means STOPPING)
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Role of HIF-1alpha
Mechanism? |
Angiogenic switch:
HIF-1alpha binds VHL in presence of O2, and gets degraded In absence of O2, binds nuc and upregs VEGF |
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How do cells loosen from each other during cancer invasion? How do they enter the ECM?
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Downregulation of cadherins (intercell jn)
First have to adhere to ECM via expression of LAMININ receptors, then degrade matrix via Type IV COLLAGENASE and PLASMINOGEN ACTIVATORS |
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How does spread of carcinomas differ from spread of sarcomas?
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Carcinomas likely to spread to sentinel LN
Sarcomas likely to spread to blood flow |
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Two examples of growth stimulatory factors.
One example of growth inhibitory factor. One example of cell adhesion molecule. What do they have in common? |
PDGF, FGF: Growth stimulatory
TGF-beta: Growth inhibitory factor Cell adhesion: Cadherins---Catenins All result in intracellular PW with RAS (G-prot; and tyrosine kinase) |
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Effect of stimulatory factors on CDK?
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GF's upregulate CDK's
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Role of BCL-2
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Apoptotic INHIBITOR
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Effect of inhibitory factors on Rb
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IF's activate Rb (and CDK-I's)
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How do CDK's and CDK-I's interact with Rb?
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CDK Pi's Rb, releases EGF, allows progression into S phase
CDK-I's de-pi (?) |
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2 examples of CDK-I's. Role?
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p21 (produced by p53) - inhibits progression to G1, G2
p16 - inhibits progression to G1 |
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When is RAS activated? What happens it it's mutated at site of GTP hydrolysis?
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RAS activated by binding of GF to GF-r
If mutated at site of GTP hydrolysis, won't shut itself off and continuously drives cell proliferation |
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What would a blood smear show in chronic myelogenous leukemia? Hallmark?
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would demonstrate leukocytosis: mature neutrophils/immature myelocytes (young granulocyte)
Hallmark: balanced chrom translocn between 9 and 22 |
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What is the effect of a balanced chromosomal translocation in CML?
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Get a hybrid gene that acts as a non-localized tyrosine kinase; it's in cytoplasm and cells no longer require GF's
Unaffected by inhibitory factors, evade apoptosis |
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Genetic mechanism behind neuroblastoma.
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Amplification of N-myc gene (cell cycle stimulatory gene)
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Why is HER2/NEU an oncogene?
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It's a growth factor receptor; it's over-expression leads to cancer
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What is the Kanutzen hypothesis re: retinoblastoma?
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Rb can be hereditary (inherit first hit, develop 2nd hit) or sporadic (develop both hits via mutations in retinoblasts)
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Example of AD cancer syndrome. Associated symptom?
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Retinoblastoms is AD
AD Cancer syndromes often involve multiple (benign) cancers at many sites |
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Role of Rb?
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Impt in G1 checkpoint; normally bound to E2F, when CDK Pi's, E2F released and binds transcription factor, allowing progression to S phase
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What is p16? AKA?
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CDK-I
p16 = INK4a |
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What is epigenetic silencing and how does it occur?
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Silencing of a gene via methylation at promoter region, prevents transcription factor binding
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Via what agent does p53 mediate cell cycle arrest? Apoptosis?
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p21
Mediates apoptosis via increase in BAX |
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What disease are APC mutations associated with?
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Colon cancer; APC acts as tumor suppressor
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What is hereditary adenomatous polyposis syndrome? Cause?
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1000's of polyps developed at young age due to mutation of APC
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Mechanism of APC.
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APC binds beta-catenin in cytoplasm
when WNT binds extracell WNT-R, beta-catenin released and acts as transcription factor (increases proliferation) |
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Effect of knocking out APC.
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beta-catenin unbound and upregulated proliferation
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