cancer cells – BioQuakes

Tag: cancer cells

There are more than 500 different types of human cancers. Wouldn’t it be wonderful if scientists could develop cures for all of them? Scientists believe that CRISPR gene-editing can be used to cure some cancers. CRISPR (an acronym for clustered regularly interspaced short palindromic repeats) is a way of targeting a specific bit of DNA inside a cell which can then be gene-edited to change such bit of DNA. CRISPR has also been used for other purposes, such as turning genes on or off without changing their DNA sequence.

Recent research has found a link between CRISPR gene-editing and mutated cancer cells. Scientists believe that a further understanding of this link can identify a group of genes which should be monitored for mutations when cells are subjected to the CRISPR gene-editing method. Although CRISPR gene-editing holds promise for cell repair, the application of CRISPR gene-editing, which is meant to identify and correct damage in cells, can also cause damage to cells in a controlled manner. Such damage activates a protein, p53 (“also known as the guardian of the genome”), which helps repair damaged DNA.

P53 is a transcription factor, which is a protein that regulates the rate at which DNA is transcribed into RNA. These transcription factors bind to regulatory sequences in proteins, thus changing the shape of DNA, ultimately making them the most vital form of gene regulation. Transcription factors include many proteins but exclude RNA polymerase, which pries two strands of DNA apart and joins two strands of DNA together (Campbell, 280). P53 works by sliding along the damaged DNA, seeking a critical site to which it attaches and then sends a message to halt cell division until the DNA is repaired. In other words, p53 acts as a checkpoint in the cell cycle, preventing cell from proceeding though the G1 and G2 phases of the cell division cycle. In mice, the same exact transcription factor exists; those that lacked the Trp53 gene developed tumors at a far faster rate than those with the functioning gene.

By using CRISPR technology to damage DNA at the same cite at which DNA damage occurs, scientists are able to identify the protein responsible for cellular proliferation. If damage to the cell is too severe then p53 triggers apoptosis (the death of cells which occurs as a normal and controlled part of an organism’s growth or development) so that the damaged cell is destroyed. However, sometimes p53 is itself damaged which prevents such protein from binding to the damaged DNA in order to repair it or otherwise signaling destruction of the cell. When this occurs, the damaged cells multiply and grow, resulting in tumors. Scientists have found alterations in p53 in more than half of all cancers and thus, consider p53 the most common event in developing cancer.

New studies show that p53 inhibition can make CRISPR more effective thus, counteracting “enrichment” (the process of purifying cells for downstream applications such as qRT-PCR, cell polarizations ex vivo, or to enrich cells for use in a flow cytometry experiment) of cells with p53 mutations which has been observed to occur in cell cultures when such cells have been subjected to CRISPR. In other words, there is in vitro evidence that CRISPR technology causes harmful p53 mutations to be more prevalent in the population that has been subjected to the CRISPR technique. These findings suggest that there is a group of genes that should be monitored for mutations when the CRISPR gene-editing method is applied to cells.

Cancer is a devastating disease that has taken the lives of many people. Members of my family have suffered and lost their battle to cancer (most recently my dear aunt this past weekend). CRISPR presents the possibility of finding cures to cancer which are specifically designed to target the particular genetic mutations that are unique to each individual. Perhaps, the cure to cancer will be achieved sooner than we realize, although clearly not soon enough.

Works Cited:

Reece, Jane B, and Neil A. Campbell. Campbell Biology. Boston: Benjamin Cummings / Pearson, 2011. Print.

How Does Activation of p53 Effect the Use of CRISPR?

By sydeousmembrane

On March 16, 2022

In Student Post

In a study conducted at Karolinska Institutet in Sweden, researchers looked into CRISPR gene editing and how that can play a critical role in mutated cancer cells as well as the medical field. CRISPR is “programmed to target specific stretches of genetic coding and to edit DNA at the precise location;” specifically, the CRISPR system binds to the DNA and cuts it, therefore, shutting the targeted gene off. Researchers can also permanently alter genes in living cells and organisms, and in the future, using this method they may even be used to treat genetic causes of diseases. Although CRISPR sounds amazing, will it really be as great as it seems?

CRISPR

There are a few obstacles that need to be overcome before CRISPR can even become regularly administered in hospitals. The first is to understand how cells will behave once they are subjected to DNA damage which is caused by CRISPR in a controlled manner. When cells are damaged they activate a protein called p53 which has negative and positive effects on the procedure. The technique is less effective when p53 is activated, however, when p53 is not activated cells can grow uncontrollably and become cancerous. Cells, where p53 is not activated, have a higher survival rate when subjected to CRISPR and because of this can accumulate in mixed cell populations. Researchers have also found a network of linked genes that have a similar effect to p53 mutations, so inhibiting p53 also prevents these cells from mutating.

Long Jiang, a doctoral student at the Department of Medicine at Karolinska Institutet, says that “it can be contrary to inhibit p53 in a CRISPR context. However, some literature supports the idea that p53 inhibition can make CRISPR more effective.” By doing this it can also counteract the replication of cells with mutations in p53 as well as genes that are associated with the mutations. This research established a network of possible genes that should be carefully controlled for mutations during CRISPR. This will hopefully allow for mutations to be regulated and contained more efficiently.

DNA, or deoxyribonucleic acid, is a long molecule that contains a genetic code; “like a recipe book it holds all the instructions for making the proteins in our bodies.” Most DNA is found in the nucleus of the cell, but a small amount can also be found in the mitochondria. DNA is a key part of reproduction because genetic heredity comes from the passing down of DNA from parents to offspring. Altering this DNA can have an impact on a number of someone’s physical characteristics. CRISPR does just that. It can be used to edit genes by finding a specific piece of DNA inside a cell and then modifying it. Since CRISPR is so new, it has its positives and negatives, but overall it is a groundbreaking discovery.

DNA

In conclusion, even though cells seem to gain p53 mutations from CRISPR, it has been discovered that most of the cell mutations were there from the start. Even though this is still an issue, we don’t know to what extent it can cause greater harm, so it will be exciting to see the new discoveries in the future!

New research further advances the understanding of DNA repair

By chrisynthesis

On March 16, 2022

In Student Post

In a study recently published in Nature Cell Biology, there’s been a discovery that alters our understanding of how the body’s DNA repair process works and may lead to new chemotherapy treatments for cancer and other disorders. Because DNA is the repository of genetic information in each living cell, its integrity and stability are essential to life. DNA, however, is not inert. Rather, it is a chemical entity subject to abuse from the environment and any resulting damage, if not repaired, will lead to mutation and possibly disease.

DNA Polymerase

The fact that DNA can be repaired after it has been damaged is one of the great mysteries of medical science, but pathways involved in the repair process vary during different stages of the cell life cycle. In one of the repair pathways known as base excision repair (BER), the damaged material is removed, and a combination of proteins and enzymes work together to create DNA to fill in and then seal the gaps. In addition to genetic insults caused by the environment, the very process of DNA replication during cell division is prone to error. The rate at which DNA polymerase adds incorrect nucleotides during DNA replication is a major factor in determining the spontaneous mutation rate in an organism.

Researchers discovered that BER has a built-in mechanism to increase its effectiveness, it just needs to be captured at a very precise point in the cell life cycle. In BER, an enzyme called polymerase beta (PolyB) fulfills two functions: It creates DNA, and it initiates a reaction to clean up the leftover chemical waste. Through five years of study, scientists learned that by capturing PolyB when it is naturally cross-linked with DNA, the enzyme will create new genetic material at a speed 17 times faster than when the two are not cross-linked. This suggests that the two functions of PolyB are interlocked, not independent, during BER.

Cancer cells replicate at high speed, and their DNA endures a lot of damage. When a doctor uses certain drugs to attack cancer cells’ DNA, the cancer cells must cope with additional DNA damage. If the cancer cells cannot rapidly fix DNA damage, they will die. Otherwise, the cancer cells survive, and drug resistance appears. This research examined naturally cross-linked PolyB and DNA, unlike previous research that mimicked the process. Prior to this study, researchers had identified the enzymes involved in BER but didn’t fully understand how they work together. This research improves the understanding of cellular genomic stability, drug efficacy, and resistance associated with chemotherapy, which, as previously stated, can lead to new chemotherapy treatments for cancer and other disorders.

For Cancer Cells, it’s Halloween All Year Long– New Research Finds That They Masquerade as Normal Cells by Covering Themselves in “Sugary Costumes”

By rileybosome

On October 27, 2021

In Student Post

Dr. Rachel Willand-Charnley and her team of biochemist researchers at South Dakota State Univerity have achieved a “sweet victory” in cancer research. Their recent findings determine how cancer cells utilize sugar to deceive our immune systems. Their research suggests that cancerous cells mimic normal cells’ glycans due to genetic mutations, and because of this similarity, the immune system then confuses the cancer cell for a normal, healthy cell. This is because glycans on cell membranes of the cell are inspected by T-cells belonging to the immune system.

This is revolutionary to understanding the behavior and function of cancer cells which could help create more effective cancer treatments. Potential new treatment methods include stripping or altering the sugary layer of the cancer cell, allowing the immune system to recognize it as a threat and take care of it itself.

Milestones in cancer research are significant because as of right now, there is no cure for it. As we have learned in AP Biology, normal cells comply with signals that direct themselves into apoptosis, or programmed cell death. This process involves the expulsion of lysosomal enzymes into the cytosol which kills off the cell. This occurs when the cell is deemed inefficient or unable to function. If cancerous cells are detected by the immune system, those cells could avoid destruction by evading apoptosis signals and continue to progress within the human body which often leads to death.

How could a cancer cell bypass something like this? Well, it seems that their newly adapted sugary coating could play a role in avoiding those signals. This is because T-cells from the immune system inspect glycans in the extracellular matrix for deviations. When deviations are present, an immune response is triggered, which could also trigger apoptosis of the deviated cell. So, the modified glycans on the cancer cell’s extracellular matrix help cancer evade a process like apoptosis.

Isn’t it astonishing that a single genetic modification could actually make cancers resistant to immunotherapy and chemotherapeutics? What do you think about this discovery?

How Cancer Cells Spread Using Nerve-Cell tricks

By droeschdna

On October 15, 2020

In Student Post

In this article, Cancer cells use nerve-cell tricks to spread from one organ to the next, it explores how cancer cells are able to reproduce and spread into the bloodstream and other organs as well. Specifically in Breast and Lung Cancer, the cells are able to create signaling pathways that neurons use, in order to metastasis, or reproduce. I am really interested in going into the medical field so I decided to choose an article that relates to current research. Cancer research relates back to the basics of cells, which is such a crucial foundation to learning biology. I found it interesting how this article spoke about cell reproduction and organic compounds as well. It is neat to learn about current research after learning the fundamentals of biology throughout this unit.

Sohail Tavazoie, a scientist, found that cells located in the inner blood vessels can tell the cancer cells to metastasize in the tumor. Tumors are able to attach to the body’s nutrient supply and oxygen. I wanted to find out a little bit more about metastasis so I read an article to learn more about it and better my understanding of the process. Metastasis is when cancer spreads to another part of the body from where it started originally. Metastases, the plural of metastasis form when some of the cancer breaks off from the cell and enters the bloodstream. These metastases carry fluid and can form tumors in other locations in the body. Bernardo Tavora, who is a research associate, used a modified version of TRAP, which was developed in Nathaniel Heinz’s lab. This helps to pinpoint subtle differences between cells that are similar and have produced similar proteins. To further develop my knowledge and research of TRAP, I read this article. In this article I learned that TRAP stands for Translating Ribosome Affinity Purification. TRAP has been used to study the aging of neurons to further research diseases such as Huntington’s Disease. In order to use this technique, scientists needed to understand translation. When DNA turns into mRNA in the nucleus it is transported to the cytoplasm or the ER. This is then recognized by ribosomes and then the ribosomes turn the mRNA into proteins.

Cancer cells replicating

Tavora and his colleagues discovered that the signal is Slit2, which is a protein that is made by neurons. Slit2 helps to guide nerve-cell extensions when they go through different parts of the brain. Researchers found that cancer cells use a process to make blood-vessel cells make and release Slit2. This dose helps the cancer cells to start spreading throughout the body, making the cancer worse. The cells activate DNA so that it makes RNA, and then it acts like a signal, which triggers them to move into the bloodstream and other organs. This protein along with other molecules could help with diagnostics. Doctors could identify cancers that have left the primary tumor before it is too late. This could also help develop drugs to stop metastasis in cancer cells.

This topic raketes a lot to what we have learned in biology so far this year. Cancer is made up of cells which can multiply and spread to other parts of the body through reproduction, or metastasis in this case. We learned about Slit2 which is the protein made by neurons, and helps to guide nerve-cell extensions. The cancer cells can use this protein to “trick” and then spread throughout the body by acting like a signal. We also learned that proteins are transported from cell to cell by being released from the plasma membrane. Proteins are crucial for many functions in the body such as speeding up chemical reactions, responding to stimuli, etx.

This article helped me to understand how biology works in research and how the fundamentals are so pertinent to understanding complex research.

BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: cancer cells

Cell Cycle Regulation in Revolutionary Gene Editing Technique (a.k.a. CRISPR)

How Does Activation of p53 Effect the Use of CRISPR?

New research further advances the understanding of DNA repair

For Cancer Cells, it’s Halloween All Year Long– New Research Finds That They Masquerade as Normal Cells by Covering Themselves in “Sugary Costumes”

How Cancer Cells Spread Using Nerve-Cell tricks

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