Boc 4 - Clapp

Front 1

peripheral blood smear showing immature myeloid cells (with bands) is suggestive of what condition?

Back 1

Chronic myeloid leukemia (CML)

Front 2

proto-oncogenes exist in normal cells and become an active oncogene by what mechanisms (3)

Back 2

point mutation, amplification of gene expression, translocation (of a promotor or of a gene fragment to form a chimeric protein)

Front 3

describe Ras gene activation in cancer

Back 3

Ras - normally quickly inactivated by the loss of GTP - becomes locked to GTP leading to continuous cell cycle progression

Front 4

what kind of mechanism leads to activation of Ras

Back 4

point mutation

Front 5

what mechanism is involved with the N-myc gene in causing neuroblastoma?

Back 5

gene amplification

Front 6

having >10 copies of N-Myc in neuroblastoma is correlated with what kind of outcome?

Back 6

poorer survival

Front 7

one of the fastest growing human cancers; a type of B cell lymphoma

Back 7

Burkitt Lymphoma

Front 8

genetic mechanism involved in causing Burkitt Lymphoma

Back 8

translocation of chromosomes 8 and 14 -- enhancer for IgH genes on chr 14 fuses with Myc gene on chr 8 leading to Myc enhancement

Front 9

What is the philadelphia chromosome and what condition is it involved in

Back 9

an unequal reciprocal translocation between chromosomes 9 and 22; causes CML

Front 10

what protein does the philadelphia chromosome encode

Back 10

BCR-ABL - a constituitively active tyrosine kinase that phosphorylates leading to cell growth

Front 11

How does Imantinib (Gleevec) work?

Back 11

it mimics ATP and binds to the ATP binding site on BCR-ABL; without bound ATP, BCR-ABL can't phosphorylate it's target

Front 12

what kind of experiment was used to determine whether the cancer "phenotype" was dominant or recessive? what was the outcome?

Back 12

cell fusion experiment; recessive (lead to discovery that there are normal mechanisms in the cell that prevent cancer)

Front 13

What is Knudson's "two-hit" hypothesis for the formation of retinoblastoma?

Back 13

a "hit" or mutation on both alleles is required to get tumor formation; in familial retinoblastoma, one hit is already inherited so it is easier to develop the other, somatic "hit"

Front 14

the two hit hypothesis applies to what types of genes

Back 14

tumor suppressor genes

Front 15

what is loss of heterozygosity?

Back 15

one allele is mutated (usually the germ line allele) and the second "hit" is a deletion, so the gene appears homozygous for the mutation

Front 16

The "molecular policeman" of the cell cycle that guards the G1/S phase transition is what?

Back 16

Rb

Front 17

explain the relationship of phosphorylation and Rb with progression of the cell cycle

Back 17

to suppress cell growth - Rb normally binds E2F to prevent progression into S phase

when phosphorylated by cyclin D or CDKs - Rb doesn't bind E2F and S phase is entered

Front 18

the most commonly mutated gene in cancer is _____.

Back 18

p53

Front 19

_________ controls the degradation of p53

Back 19

MDM2