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51 Cards in this Set

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What are the 8 characteristics of a cancer cell?
a. Disregard internal signals anti-growth…
b. avoid apoptosis…
c. avoid senescence and differentiation…
d. genetically unstable…
e. escape home tissue (invasive)…
f. Metastasis (survive and proliferate in foreing tissue.)…
g. sustained angiogenesis…
h. limitless replicative potential.
How many mutations does an pro-oncogene need to become an oncogene?
One allele (thus, it's a dominant effect)
What type of gene (onco or TS) is NMyc?
What type of mutation is seen in NMYC?
Amplification, which leads to increased DNA, which leads to increased mRNA and increased protein
What sort of tumor does NMYC cause?
With respect to cancer, what type of gene (TS or oncogene) would you worry about it being mutated to cause it to be constitutively active?
What type of mutation is M4eo an example of?
Oncogene: chromosome inversion of Flt3 (receptor tyrosine kinase) causing to be constitutively active [can also be caused by a point mutation]
What clinical relevance is the chromosomal inversion of M4eo?
WBC do not differentiate, which leads to Acute myologenous leukemia type 4 (with eosinophils)
What are two possible outcomes of translocations? And why?
overexpressed (due to new promoter) and missexpressed (novel protein)
Give 2 general outcomes of Translocation (Hint: what happens in a translocation)
fusion of proteins and switch to different promoter
What type of translocation do these examples demonstrate? PML/RAR and Burkitt's Lymphoma.
Fusion of 2 proteins-PMLRAR and Swith to different promoter- Burkitt's Lymphoma
1. What pathogen is Burkitt's caused by? 2. What causes large B-cell lymphoma?
1. Burkitt's is caused by the translocation a immunoglobin promoter of a being moved to a Myc gene.

2 Diffuse large B-Cell lymphoma is also caused by transocation of a promoter (TTF, PIM1, IgH) to the Bcl6 gene
What type of mutation WBCs to get stuck in the promyolocytic stage, causing promyelocytic leukemia?
fusion of proteins (RAR with PML)
What does RAR stand for?
Retinoic acid receptor
Would the transcriptions of an mRNA transporter be considered an oncogene or a TS?
oncogene: Overexpression
What type of mutation is E14E? What type of tumor is this related to?
abberant transport of mRNA out of the nucleus --> overexpression --> Solid tumor
Match the following characteristic with either TS or oncogene: loss of function, misexpressed, only one mutated copy is needed, inherited, loss of apoptosis pathway, genomic instability, acts in dominant fashion, usually involved in growth, release cells from growth control, usually loss of both wild type genes
TS: Loss of function, loss of both alleles, loss of apoptosis pathway, genomic instability, release cells from growth contorl… ONCOGENE: misexpressed, acts in dominant fashion, usually involved in growth, only one mutated allele is needed
How do you inactivate a TS?
mutations and hypermethylation
What is associated with "loss of heterozygosity", TS or oncogene?
TS now only one gene and that gene is mutated Loss of function
With respect to tumor suppressor genes, what is dominant negative?
when the product of one allele affects the normal function of the product of the other allele.
Given a loss of one wild type allele at birth, name 5 ways a tumor suppressor gene can be inactivated.
1) dominant negative, 2) Dominant active, 3) imprinted, 4) LOH, 5) mutation
What are 6 ways to have a LOH?
a) nondisjunction (chromosome loss)… b) nondisjunction and duplication… c) mitotic recombination… d) gene conversion… e) deletion… f) point mutation
In tumor suppressor genes, what is the most common way for a person to lose the normal allele?
What type of gene TS or oncogene would methylation have an increased cancer risk?
TS, since methylation silences a gene
What are 2 causes of increased methylation of Tumor suppressor genes?
a) aging and 2) chronic ulcerative collitis
what are Rb, p16, p15, p14, p73, caspase-8, DAP kinase, E-cadherin, APC, Arf, and BRCA1 and 2?
tumor suppressors
Do tumor suppressors have to lose both alleles to be inactivated?
What is APC mutation associated with?
FAP (APC is a tumor suppressor that gets truncated in FAP.. CRC)
Which is related to inheritance, TS or oncogenes?
what decade would you expect to find sporadic cancer and inherited cancer?
Sporadic after 5th decade, and inherited 2nd and 3rd decade.
Which chromosome is BRCA1 and BRCA2 found on ?
BRCA1=chr 17… BRCA2=chr 13
Which chromosome would you find APC gene on?
What chomosome would you find mismatch repair mutation (HNPCC)?
Match the gene with the CRC: FAP and HNPCC
FAP: APC truncation… HNPCC: MSH2 and MLH1
Which protein and cancer is the Wnt pathway impliated?
APC truncation --> FAP
What is the RET gene implicated in?
Oncogene inheritance, which usually presents late in life with neoplasm of the endocrine system… seen also in sporadic
1) What contribution do SNPs and haplotype blocks have in familial risk to cancer? 2) Which has a higher incidence in a population, high penetrance alleles like BRCA1 or SNP (haplotype blocks)?
low (as compared to alleles like BRCA), 2) SNPs and haplotype blocks
What significance do SNPs and haplotype block for patient care in the future?
microarray predictors for cancer
1) Match the following with either TS or oncogene… 2) which are transcription factors and which are signal transduction mediators?: Flt3, p53, Rb, AKT, RAS, Myc
Transcription Factors: p52 (TS), Rb (TS), Myc (oncogene)… Signal transduction: Flt3 (TKR… oncogene), RAS (oncogene), AKT (oncogene)
1) Put these in order to show which suppresses which… 2) state which are TS and which are oncogenes: Cyclin-D, Rb protein, p16
p16 (TS) supresses cyclin D (oncogene), cyclin D suppresses Rb (TS)
1) Put these in order to show which suppresses which… 2) state which are TS and which are oncogenes: ARF(p19), MDM2 and p53
ARF-p19 (TS) suppresses MDM2 (oncogene), Mdm2 suppresses p53 (TS)
What is the healthy response (non cancer) to an oncogene mutation?
up regulation of one of the TS, like p53 or Rb… which leads to apoptosis or senescence
What is the progression to cancer? What can cause these progressions?
1) Normal –(1) --> Hyperproliferative –(2)--> early adenoma --> late adenoma --> carcinoma --> metastasis… 2) loss of TS or activation of an oncogene
In terms of cancer, what effect does HPV have? (Hint: E7 and E6)
HPV --> E7 --> suppresses Rb which will then allow expression of E2F1 (cell cycle promoting)… 2) HPv --> E6 --> suppresses p53, which will indirectly inhibit p21 and bax (TS)
What histologic presentation does Promyelocytic leukemia have?
blast promyelocytes with rods --> lead to bleeding by using up coagulation factors
What does the fusion of the PML/RAR protein cause physiologically? What disease does this protein fusion cause? How is it treated?
1) the retinoic acid receptor causes the the retinoic acid receptor to become less sensitive. 2) Acute promyelocytic leukemia… 3) retinoic acid (vit-A which drives the cells to neutrophils) and block the Flt3
Besides the PML/RAR protein fusion, what 2nd hit is seen in mice with APL (acute promyelocytic leukemia)?
Flt3 (tyrosine kinase receptor) mutation
What does a flt3 mutation give a cell?
survival advantage
Which type of gene mutation (TS or oncogene) is likely to end in genetic instability?
What is a good explanation for tumor resistance?
tumors are heterogenic
What are 4 methods for observing gene function in cells?
cell lines with gain of function (oncogene)… cell lines with loss of function (TS)… RNAi (knock-down of gene expression)… Viral vectors (to transport a transcript for gain of function)