메뉴로 건너 뛰기 내용으로 건너 뛰기
COMMUNITY
Title [Roy Lee] AP Bio - 4.7 질문
4.7 Regulation of Cell Cycle 24
Author ych*** Date Posted 2023-07-24 오전 6:18:54

안녕하세요 선생님, 


문제풀이에서 q10) part c(FRQ)에 잘 이해가 안되는 부분이 있는데요.. 


By preventing the ligand (EGF) from binding onto the active site of EGFR, the signaling cascade is not initiated so the cell cycle is discontinued, but wouldn't this stop the production of the skin cell that EGFR is in rather than the production of EGFR itself? Then how would this be a reason for the therapy being effective for treating cancer since the question states that an increase in the production of EGFR is associated with skin cancer?


Also, does the antibody therapy have to prevent EGF from binding onto EGFR through competitive inhibition or would it be okay to state that the therapy could also operate through noncompetitive inhibition? 


(영어로 쓰는게 더 편해서 영어로 질문 보내드려요... 죄송합니다..!)

2023-07-25 오후 6:29:52

안녕하세요!

 

Feel free to ask questions in English! It's easier for both of us :D

 

The reason for your question is based on understanding the mechanism behind targeted antibody therapies,

which isn't technically part of the AP Bio curriculum,

but is still something you can deduce based on what you have learned so far.

 

First off, some basic information about antibodies.

Antibodies are proteins created by the immune cells in the human body.

They are weapons used by our immune system to destroy foreign substances that can cause disease.

 

Antibody proteins work by binding to and completely surrounding exposed parts of a virus or a bacteria,

preventing them from attaching to or invading into human cells.

 

Imagine antibody proteins forming a layer of protective coating around a bacteria

that essentially quarantines the bacteria from the environment,

neutralizing it and preventing it from spreading.

 

In order for this strategy to work, these antibodies have to be very selective in terms of what they bind to.

They can't bind to any normal human cell because that will cause disease;

they have to be designed to bind only to specific bacteria or viruses which you want to destroy.

You don't have to know the details here, 

but just know, there are processes in the human body that can selectively create antibodies that only bind to specific things, 

such as a bacterial plasma membrane, or a viral DNA fragment.

 

Now, in the modern day, human beings have studied these antibodies and found 

that there are ways we can manipulate the antibody genes itself,

allowing us to create antibody proteins that only bind to things we want them to bind to, not just bacteria or viruses.

 

One example would be EGF-receptors found in the neck or head region.

 

We have been able to create antibodies that can bind to normal EGFR in a human being.

The amazing part is antibodies binding to the receptors are NOT the same as activating these receptors.

Again, antibodies simply bind and create a protective coat that surrounds the ligand-binding site, 

preventing actual signals from interacting with receptors and activating the signal cascade.

 

Now, going back to the question,

we are asked about anti-cancer treatments, 

specifically "antibodies against the extracellular portion of EGFR".

We have established that the cause of cancer is due to mutations that lead to overproduction of EGFR,

where a small amount of EGF signal is picked up by way too many EGFRs, causing too large of a response of cell division.

 

The initial EGF signal came from somewhere (it doesn't really matter where, because that's not the point)

carried by blood or lymph into a region of the neck or head, 

where there is a group of cells with overproduction of EGFR.

 

Here, our antibody treatment injects the body with proteins that can specifically bind to EGFRs and surround them,

preventing these receptors from being activated.

 

 

In terms of the second part of your question,

it wouldn't be entirely accurate to describe this process as either competitive or noncompetitive inhibition.

 

We are talking about the extracellular portion of the receptor,

which becomes flooded with and surrounded by antibody proteins,

that prevents the meeting of the actual ligand to the ligand-binding site.

 

The antibodies are not acting as molecules that just take up space in the ligand-binding site.

They are more like a heavy blanket thrown over the entire receptor, 

so it wouldn't be accurate to describe them as "out-competing EGF"

Similarly, the antibodies are not necessarily changing the structure of the ligand-binding site (just surrounding the outside)

therefore, it would be incorrect to describe this process as "noncompetitive inhibition" either.

 

 

Targeted antibody therapies are a hot topic in medicine right now,

specifically because of the reasons I have mentioned above.

Any treatment that requires very precise targeting and turning off a specific signals can be achieved

which is why it may potentially be a very effective treatment for cancer.

 

 

Again, your question is not based on misunderstanding,

but the confusion regarding what antibodies are and how they work,

which I repeat, isn't techically part of the AP Bio cirriculum anymore.

Nonetheless, hope this helps and let me know if you have additional questions! :D

 

 

 

 

 

 

 

 

Top