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4. If the tumor cells were not _________, gene expression from both X chromosome

ID: 267972 • Letter: 4

Question

4. If the tumor cells were not _________, gene expression from both X chromosomes would be

expected in females, reflecting the random inactivation of one X chromosome in each cell lineage.

a. Telomerase     b. Senescence                   c.Clonal                                d.Gain-of-function

5. A large fraction of the acute leukemias involve

A) Chromosomal translocations B)Suppression of the origin recognition complex

C) Increased contact inhibition D)Epigenetic inheritance               E)All of the above

6. Cancers associated with defects in mismatch repair show

A) Epigenetic inheritance              B)X-linked inheritance                   C)Maternal inheritance

D) Dominant inheritance               E)Recessive inheritance

7. Uncovering of a recessive allele by various mechanisms is called

A) Senescence B)Loss of heterozygosity               C)Gain-of-function mutation       D)Processivity

8. Even in the absence of damage, normal cells cease to divide in culture after about 50 doublings ? a

process called cell _______, whereas cancer cells in culture divide indefinitely.

a. Telomerase    b. Senescence                                   c.Clonal                                d.Gain-of-function

9. The senescent behavior of normal cells is associated with

A) Activation of the maturation promoting factor B)Increase in mutation rate

C) Decrease in contact inhibition                               D)Loss of telomerase activity      

10. The senescent behavior of normal cells is associated with a loss of _________ activity.

a. Telomerase     b. Senescence                                   c.Clonal                                d.Gain-of-function

11. Tumor-supressor genes normally control

A) Sister chromatid separation   B)Cell proliferation or activation of apoptosis

C) DNA polymerase processivity   D)Telomerase activity E)Protein degradation

12. ____________ genes are genes that normally control cell proliferation or that activate the

apoptotic pathway, in which loss-of-function mutations contribute to cancer progression

a. Tumor-suppressor b.Apoptosis             c.Leukemias                       d.Processivity

13. The retinoblastoma protein controls

A) Activation of apoptosis               B)Expression of cyclin D               C)Contact inhibition       

D) Transition from G1 to S phase               E)A and C

14. Retinoblastoma is inherited in pedigrees as a

A) Simple Mendelian dominant B)Simple Mendelian recessive    C)polygenic trait D)X-linked

16. Loss of function of p53

A) Activates apoptosis                    B)Eliminates the DNA damage checkpoint C)Increases contact inhibition

D) Blocks activation of the anaphase promoting complex                E)Suppresses assembly of the spindle

17. Mdm2 protein binds to p53 transcription factor in order to:

A) Activate it                      B)Transport it from the cytoplasm to the nucleus               C)Acetylate it

D) Prevent it's phosphorylation E)Trigger a block in the separation of the sister chromatids

18. What is the expected result of p21 malfunction?

A) Activation of the apoptosis B)Polyploidization C)Centrosome duplication D)chromosome fragmentation

Explanation / Answer

4). b) Senescence

5) A) Chromosomal translocations

6) D) Dominant inheritance    

7) B)Loss of heterozygosity  

8) b. Senescence

9) D)Loss of telomerase activity   

10) a. Telomerase

11) B)Cell proliferation or activation of apoptosis

12) a. Tumor-suppressor

13) D) Transition from G1 to S phase   

14) A) Simple Mendelian dominant

16) B)Eliminates the DNA damage checkpoint

17) B)Transport it from the cytoplasm to the nucleus    

18) B)Polyploidization

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