In a new cancer treatment, a cold virus is genetically...

In a new cancer treatment, a cold virus is genetically modified so that it binds to, enters, and is replicated in cells, causing them to burst. The modified cold virus cannot replicate when wildtype p53 protein is present in the cell. How does this treatment treat cancer without harming healthy cells? a. The modified virus only infects and enters cancer cells. b. The modified virus replicates in normal and cancer cells. c. The modified virus only infects and enters normal cells. d. The modified virus replicates only in cancer cells.

In a new cancer treatment, a cold virus is genetically modified so that it binds to, enters, and is replicated in cells, causing them to burst. The modified cold virus cannot replicate when wildtype p53 protein is present in the cell. How does this treatment treat cancer without harming healthy cells?
a. The modified virus only infects and enters cancer cells.
b. The modified virus replicates in normal and cancer cells.
c. The modified virus only infects and enters normal cells.
d. The modified virus replicates only in cancer cells.

Key Concepts

Oncolytic Virotherapy

Oncolytic virotherapy utilizes viruses that selectively infect and destroy cancer cells, leveraging their ability to replicate within and lyse tumor cells while sparing normal healthy cells. This approach takes advantage of vulnerabilities in cancer cells that can be exploited by engineered viruses, making it a promising method for targeted cancer treatment.

p53 Tumor Suppressor Protein

The p53 protein is a crucial tumor suppressor that plays a significant role in regulating the cell cycle and initiating apoptosis in response to DNA damage. In many cancers, p53 is mutated or inactivated, which allows cancer cells to escape normal growth controls. Understanding the role of p53 is fundamental in therapies that differentiate between normal and cancer cells.

Genetic Modification for Selectivity

Genetic modification in the context of oncolytic viruses involves altering the viral genome so that replication and cytotoxicity occur preferentially in cancer cells. This modification often includes mechanisms that restrict the virus's ability to replicate in normal cells where tumor suppressors like p53 are active, thereby ensuring that healthy cells remain unharmed.

Selective Replication in Cancer Cells

Selective replication refers to the engineered ability of the virus to replicate only in cancer cells that lack normal tumor suppressor functions, such as an intact p53 pathway. By designing viruses that are unable to thrive in normal cells, this approach minimizes collateral damage and improves the safety profile of the oncolytic virus therapy.

Transcript

00:02 We are being asked about a scenario in which you come up with an effective treatment by getting a virus to interact with the p53 gene.

00:16 So before we look at our scenario, real quickly, let's look at what the p53 does.

00:22 The p53 gene is a tumor suppressor.

00:26 And like all genes, the p53 gene encode.

00:32 Which is up here in codes for some sort of protein so that protein undergoes transcription and that gene undergoes transcription and translation in order to produce the p53 protein the p53 protein is itself a transcription factor and it is a transcription factor for the p 21 gene i know it's a lot of acronyms but just follow along okay so p53 is a transcription factor for the p21 gene.

01:05 So it promotes the transcription of p21.

01:09 And that results in the production of p21, the protein p21.

01:15 P21 stops the activity of cdks, which are cycling -dependent kinases.

01:22 And cycling -dependent kinases promote division.

01:27 Okay so let's now kind of write it in shorthand okay me i needed a different color pan p53 promotes production of p21 which stops cdks from acting that should be a d which promote division okay so if you have more if you have more if if you increase p53, let me draw a better arrow there.

02:14 Should be an up arrow.

02:16 Okay, if you increase p53, you increase p21, which means that you lower the activity of cdks and you prevent cell division.

02:30 So that's how p53 is a tumor suppressor gene.

02:35 Because if it can detect their something severely wrong with a cell its production is increased and its production results in increased production of p21 increased production of p21 blocks the activity of cdks let me not make that a plus sign just meant to connect these two lines so p21 blocks the activity of cdks and by blocking the activity of cdks you ultimately block division so if you're creating a virus that is interoperating with p53, the virus needs to be inside the cell because all of this is happening inside the cell.

03:16 And that's a key thing to remember when we're answering this question.

03:22 Actually, there are two things we need to remember here.

03:25 One is that the virus is interacting with the p53, right? because we are told in the question that this virus is active, only when p53 is mutated.

03:44 If p53 is wall type, the virus will not replicate...

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