4. (3pts) In class we discussed the multihit hypothesis in detail. a. Define the multihit hypothesis as it relates to
Posted: Thu Jun 30, 2022 6:37 pm
4. (3pts) In class we discussedthe multihit hypothesis in detail.
a. Define the multihit hypothesis as it relates tocancer. This definition has expanded since the first week ofclass! We now know specific functions of genes that increasecancer risk. A 20 point question on your final will ask youto tell a story about how a cell in your body became cancer usingmutations in genes that encode for proteins you learned in Unit 1,2, 3, 4, and 5! Let's practice here.
Illustrate your definition using the gene that is associatedwith your own cancer that I assigned to you in cancer journal#1. Do some quick research and see if the gene is aproto-oncogene or a tumor suppressor.
So the gene above will be 1-2 hits depending on what youfind. To get to the number of hits associated with cancerlook back at genes/proteins we have already learned about in thiscourse.
Now, use the gene I gave you and some of the genes you havealready learned about to illustrate the number of hits that wouldhave made one cell in your body a cancer cell. First, definethe multi-hit hypothesis adding examples of genes that are "hits".Second, Tell a story about one cell in your body becoming cancerthat illustrates your definition. Rubric(3): Complete definition-updated with what we know now! (1) with example (2)
Gene: MDM2
Example Story
· I was born with every cell of mybody having a mutation in the Chk2 gene......one hit.
· One adult stem cell in my pancreaswas exposed to a carcinogen while I was being breast fed by my Mom.This carcinogen caused a LOF mutation to occur in one copy of theBRCA1 gene of that cell. (one hit).
· While a teenager, I was exposed toradiation which caused a GOF mutation in CDC20 (one hit) whichcould lead to early onset of anaphase. But likely the othercheckpoints in the cell cycle of this cell are still ok.
· Sadly, I started smoking when Iwas 20 (stress relief) and another LOF mutation occurred in CHK2 ofthe adult stem cell I have been reporting on. This means that thisCHK2 protein no longer acts as a checkpoint to inhibitcdc25...meaning that CDK-Cyclin will not pause if there is DNAdamage from G1àS or G2àM. This adult stem cell is starting todivide more than its neighbors (total of 4hits).
· I continued to smoke and since mycells are less likely to pause to fix the DNA of this adult stemcell it received another LOF mutation, but this time in the BRCA1gene. Now my cells will be less able to pause in the cell cycle andinitiate DNA repair. 5 hits total.
· This pancreatic adult stem cell isdividing out of control and likely mutating morefrequently.....cancer.
a. Define the multihit hypothesis as it relates tocancer. This definition has expanded since the first week ofclass! We now know specific functions of genes that increasecancer risk. A 20 point question on your final will ask youto tell a story about how a cell in your body became cancer usingmutations in genes that encode for proteins you learned in Unit 1,2, 3, 4, and 5! Let's practice here.
Illustrate your definition using the gene that is associatedwith your own cancer that I assigned to you in cancer journal#1. Do some quick research and see if the gene is aproto-oncogene or a tumor suppressor.
So the gene above will be 1-2 hits depending on what youfind. To get to the number of hits associated with cancerlook back at genes/proteins we have already learned about in thiscourse.
Now, use the gene I gave you and some of the genes you havealready learned about to illustrate the number of hits that wouldhave made one cell in your body a cancer cell. First, definethe multi-hit hypothesis adding examples of genes that are "hits".Second, Tell a story about one cell in your body becoming cancerthat illustrates your definition. Rubric(3): Complete definition-updated with what we know now! (1) with example (2)
Gene: MDM2
Example Story
· I was born with every cell of mybody having a mutation in the Chk2 gene......one hit.
· One adult stem cell in my pancreaswas exposed to a carcinogen while I was being breast fed by my Mom.This carcinogen caused a LOF mutation to occur in one copy of theBRCA1 gene of that cell. (one hit).
· While a teenager, I was exposed toradiation which caused a GOF mutation in CDC20 (one hit) whichcould lead to early onset of anaphase. But likely the othercheckpoints in the cell cycle of this cell are still ok.
· Sadly, I started smoking when Iwas 20 (stress relief) and another LOF mutation occurred in CHK2 ofthe adult stem cell I have been reporting on. This means that thisCHK2 protein no longer acts as a checkpoint to inhibitcdc25...meaning that CDK-Cyclin will not pause if there is DNAdamage from G1àS or G2àM. This adult stem cell is starting todivide more than its neighbors (total of 4hits).
· I continued to smoke and since mycells are less likely to pause to fix the DNA of this adult stemcell it received another LOF mutation, but this time in the BRCA1gene. Now my cells will be less able to pause in the cell cycle andinitiate DNA repair. 5 hits total.
· This pancreatic adult stem cell isdividing out of control and likely mutating morefrequently.....cancer.