AAMC Scored B/B Questions

[kryptonxenon]

1) Based on the data presented in the passage, which statement best describes the HSP110ΔE9 allele?
I understand the cancer-suppressing part, but don't understand how to figure out that HSP110ΔE9 is dominant to HSP110WT.

3) A man with a CRC mutation that results in the synthesis of HSP110ΔE9 and a woman that does not carry this mutation in any of her tissues have a child. What is the percent chance that the child will inherit the CRC mutation?
I don't understand the explanation AAMC gives about why the gene is somatic and not germ line dependent.

5) The information in the passage best supports the conclusion that Intron 8 of HSP110most likely contains which of the following?
I completely do not understand how to approach this question.

24) Which mechanism best describes how P-gp facilitates drug resistance?
Please let me know if this is how the question should be approached: The passage says P-gp exhibits ATPase activity. This rules out D. Since P-gp is a transporter this rules out A and C. Thus, the answer is B.

26) What is the most likely location of P-gp within the plasma membrane?
Since P-gp (P-glycoprotein) has glycosylated chains I figured that it wouldn't be associated with the lipid bilayer. So I chose C. What about my reasoning is incorrect?

38) The lung cells of heavy smokers would be expected to have greatly increased concentrations of cP-450 and:
I ruled out A because every cell would have DNA sequences that code for cP-450. Ruled out B because mRNA is transient and is degraded easily so you can't have increased concentrations of it. Ruled out C because didn't think rRNA would be specific to each protein that's made. Cys residues were mentioned in the passage so I went with D.

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[theonlytycrane]

1) Based on the data presented in the passage, which statement best describes the HSP110ΔE9 allele?
I understand the cancer-suppressing part, but don't understand how to figure out that HSP110ΔE9 is dominant to HSP110WT.

The only thing to base this off is Table 2 in comparing the WT, deltaE9, and WT + deltaE9 rows. When combined, the induced protein aggregation and cellular localization of HSP110 looks similar to deltaE9. The apoptotic cells column is off though so I'm not sure what to make of that.

Did the deltaE9 mutation make sense to you? It says the mutant protein is found in cancer tissue, but then Figure 1 shows it suppressing the tumor growth?

3) A man with a CRC mutation that results in the synthesis of HSP110ΔE9 and a woman that does not carry this mutation in any of her tissues have a child. What is the percent chance that the child will inherit the CRC mutation?
I don't understand the explanation AAMC gives about why the gene is somatic and not germ line dependent.

The last sentence of paragraph 2 says that the mutation is in the cancerous tissue only, and the cancer is in the colon. This means that the germline cells are still okay and unaffected by the mutation. I wasted a few minutes searching the passage to tell me something about the mutation type for this one.

5) The information in the passage best supports the conclusion that Intron 8 of HSP110most likely contains which of the following?
I completely do not understand how to approach this question.

Seeing "intron" immediately rules out choice A (stop codon) because this would be on an exon and choice D (partial coding sequence) because introns are spliced out and don't code for proteins. Nothing is really mentioned about choice C (the promotor), but in paragraph 2 it says that deletions of 3-8 base pairs in intron 8 then cause exon 9 (adjacent to intron 8) to be omitted from the final sequence. We know introns get spliced out so choice B (splice acceptor site) is a reasonable choice.

24) Which mechanism best describes how P-gp facilitates drug resistance?
Please let me know if this is how the question should be approached: The passage says P-gp exhibits ATPase activity. This rules out D. Since P-gp is a transporter this rules out A and C. Thus, the answer is B.

P-gp is a transporter and uses ATP. The first paragraph says that it helps the tumor cells from building up drug levels in the cytoplasm. To me, it sounds like it's pumping the drugs out. Choice (A) would be something more like a protease. Choice (C) is wrong because the transporter isn't blocking entry of the drugs, it's just getting the drugs out of the cell. Choice (D) isn't really supported since nothing is mentioned about increased membrane permeability. This would also be pretty detrimental for the cell in general if stuff was able to just flow out.

26) What is the most likely location of P-gp within the plasma membrane?
Since P-gp (P-glycoprotein) has glycosylated chains I figured that it wouldn't be associated with the lipid bilayer. So I chose C. What about my reasoning is incorrect?

Choices A-C describe locations that are only on one side of the membrane but this thing has to pump out drugs so it needs to span the full membrane. Being on a lipid raft doesn't necessarily imply this, but the other choices describe the protein being located only on one side.

38) The lung cells of heavy smokers would be expected to have greatly increased concentrations of cP-450 and:
I ruled out A because every cell would have DNA sequences that code for cP-450. Ruled out B because mRNA is transient and is degraded easily so you can't have increased concentrations of it. Ruled out C because didn't think rRNA would be specific to each protein that's made. Cys residues were mentioned in the passage so I went with D.

cP-450 breaks down the toxins and the smokers need all of those carcinogens broken down. cP-450 is the protein and the q-stem says that the protein levels are increased. mRNA levels would also be increased to code for more of these proteins. I think that tRNA and rRNA upregulation just for a specific protein to be upregulated is less clear. mRNA gets translated and degraded quickly, but I think the answer is implying that mRNA concentrations increase more than normal to upregulate cP-450 concentration.

 

[kitkat13]

Can anyone explain #1 to me? In terms of why it is cancer suppressing? Why would a Cancer suppressing mutation be found in cancerous tissue?

 

[aldol16]

Can anyone explain #1 to me? In terms of why it is cancer suppressing? Why would a Cancer suppressing mutation be found in cancerous tissue?

Normally, cells have genes that function to kill off cells that are dividing too rapidly/proliferating. These genes have "cancer-suppressing" activities and thus are called "cancer-suppressing genes." In order for a cancer cell to divide rapidly, it must shut off these genes, thereby releasing the molecular brakes on its own rapid division. Put another way, imagine these genes as cages that keep rapidly-dividing cells contained. If a cell wants to divide rapidly, i.e. become a cancer cell, then it must break out of this cage - that's what a mutation to a cancer-suppressing gene does.

 

[DSM_302.0]

What is a lipid raft?! I assumed it was something floating in the cytoplasm or in the extracellular fluid.

 

[bonedoc82]

Congrats to everyone and good luck to others! 4th year Orthopedic surgery resident here! Contact here or PM with questions!

Dr. Webb

 

[garbageman]

P-gp is a transporter and uses ATP. The first paragraph says that it helps the tumor cells from building up drug levels in the cytoplasm. To me, it sounds like it's pumping the drugs out. Choice (A) would be something more like a protease. Choice (C) is wrong because the transporter isn't blocking entry of the drugs, it's just getting the drugs out of the cell. Choice (D) isn't really supported since nothing is mentioned about increased membrane permeability. This would also be pretty detrimental for the cell in general if stuff was able to just flow out.

Also, to make this type of question go by extremely fast, know that the whole point of an MDR (which says that it is in the passage) is to pump drugs that can harm it out of the cell, which is why cancer cells are extremely hard to treat b/c they have multiple MDR-ABC transporters