BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: Tumors

One Giant Leap for Dead Cells

The fight against cancer may seem like a one-sided battle, though current findings bring us one step closer to victory. A recently published study found that dead cell injections directed mice’s immune systems to combat tumors.

Researchers placed an enzyme called (RIPK3) that induces necroptosis, meaning the cell self-destructs by filling itself with holes, in the rodent. When the gene calling for necroptosis was placed in a virus that infects tumor cells, the immune system’s response was to kill the virus and in turn, the tumor cell. 

Apoptosis vs. Necroptosis vs. Survival by Bram

This reaction is a great sign. Though the tumors in rats do not exactly mimic the cancers and tumors in human beings, they support the idea that the immune system responds to certain stimuli, among them necroptosis. 

As of now, the main treatments for those affected by cancer or tumors are chemotherapy and radiation therapy. The issue with these methods is that both cancerous and healthy cells die; there is no way to target just the harmful cells. The study involving necroptosis is a huge step forward as it provides a possible method to destroy only those cells which negatively affect the patient.

Whether or not the programmed death solution can apply to humans is still unknown. The rat experiment is among the first of its kind, and it may be too soon to say whether this is truly a viable option. Additionally, the tumor types in rats are quite different from cancers fostered human beings. 

Nevertheless, I think this experiment is hopeful as it has paved the way for so many other experiments to test; there is so much left to explore. This may be the beginning of something extraordinary. What do you think? Is this experiment promising or not? Let me know in the comments below. 

Your favorite muscular tube,

Jessophagus

How DNA damaged from radiation causes cancer

In a recent study, professors from the Wellcome Trust Sanger Institute sought to see the similarity between spontaneous cancerous tumors and cancer caused by ionized radiation. By looking at the molecular fingerprint of different types of cancers, they were able to differentiate between cancers that formed by radiation and cancers that were not formed by radiation.

In the study, they studied the mutational signatures of the DNA. Mutational signatures are just ways in which the DNA is affected by cancerous mutations. They studied the DNA mutational signatures from DNA exposed to radiation, but not necessarily cancerous, and the mutational signatures of the DNA of cancerous cells of which some were caused by radiation exposure and some were not. Both included the same signatures.

The two mutational signatures that were observed were deletion of segments of DNA bases and balanced inversion, where the DNA is cut in two places, the middle piece flips around, and the pieces are joined back in the opposite orientation from before the flip. High energy radiation is the cause for balanced inversion, since it does not happen naturally in the body. After the mutation, the DNA cannot repair itself.

This gives us a better understanding of cancer and how ionized radiation affects DNA and produces these mutational signatures. Knowing this information, this helps us recognize which tumors are caused by radiation. Once we have a better understanding of this, it will prove important for determining how each cancer should be treated. But for now, this is a strong step forward in the battle against cancer and every step of the way is crucial if we are to be victorious.

 

How A Chemical From the Cypress Tree Could Advance Epigenetics Against Cancer

by Czechmate on Wikimedia Commons

Found in the essential oil extracted from the bark of a cypress tree, a chemical named hinokitiol shows potential to impact epigenetic tags on DNA and stop the activity of genes that assist the growth of tumors.

In order to develop an of understanding cancer, researches have had to comprehend the DNA methylation, an epigenetic function which controls gene expression. In regular DNA methylation, genes that work to fight against tumors are turned on, reducing the risk of cancer. However, if DNA methylation is negatively altered, then those cancer-fighting genes will be silenced, helping to progress cancer development. Scientists have tried to combat irregular DNA methylation and over-silencing of genes by creating epigenetic anti-cancer medications that reverse non-beneficial methylation effects. Like in most cases of medication usage, the users face unappealing side effects. Hinokitiol is attractive to scientists because it is a natural compound with many health benefits and way less side effects than modified drugs that can possibly cause mutagenesis and cytotoxicity.

 

Researchers from the Korea University College of Medicine tested the productivity of the hinokitiol chemical in a study by giving doses of it to colon cancer cells. It was found that this chemical helped to inhibit the colon cancer cells efficiency without affecting the colon cells without cancer. The scientists also found through careful inspection that the presence of hinokitiol decreases the expression of proteins DNMT1 and UHRF1; both of which are proteins that encourage carcinogenesis. In summary, the doses of hinokitiol appear to have allowed normal cells to remain healthy, while reducing the ability for the colon cancer cells to thrive and ceasing the production of proteins that promote cancer maturation.

Researchers are continuing their search for natural compounds, as opposed to artificial medications, that can prevent the flourishing of cancer in our bodies through playing a positive role in gene expression and DNA methylation.

http://www.whatisepigenetics.com/cypress-trees-epigenetically-protect-cancer/

 

 

https://commons.wikimedia.org/wiki/File:Raindrops_on_leyland_cypress.jpg

The mutation and spread of Cancer caused by changes in Epigenetics

Epigenetics could be the key to understanding how cancer originates, when it mutates, and how it spreads. Researchers at the Boston University School of Medicine (BUSM) believe that different types of cancer are caused by an “on and off” switch in the epigenome. While many scientists believe  that many cancers originate in cells called progenitor cells, they cannot concoct a model that explains  how cancer spreads from the progenitor cell and mutates into many forms as it continues to grow in a person’s body.

One of the lead researchers, Sibaji Sarkar, posited “there should be a general mechanism that initiates cancer progression from predisposed progenitor cells, which likely involves epigenetic changes.” The researchers believe that the theory of an epigenetic switch is supported by the growth of tumors, which go through many different stages. The team believes that if cells can be altered to become cancerous and remain stuck in their stage of growth while they replicate out of control, then there must also be an off switch to this uncontrolled replication. They also suspect that epigenetic changes can determine the rapidity of growth and the mutability of the characteristics of the cancer and tumors.

Although Sarkar’s team has not yet found specific epigenetic code that causes these mutations and growth, he believes that their hypothesis will cause other scientists to focus their attention on the epigenome and find ways to prevent progenitor cells from spreading and mutating into malignant tumors.

This epigenetic research relates to our study of the relationship between the epigenome and cancer. Specifically the absence of an active p53 protein would prevent a certain part of the DNA from being  read and the cell would therefore lack a protein that inhibits the cell cycle. This would cause uninhibited cell division and the spread of cancer.

 

Methylation of DNA

640px-DNA_methylation

Text Away!!

Credit: samantha celera Flickr

Most of us worry, or at least acknowledge, that our beloved cell-phones may contribute to the forming of tumors. Fortunately, a recent study on the link between cell phone use and tumors found that there was actually no link!

The previous studies on cell-phones and tumors had been inconclusive and were prone to error. This new study, with probably some faults of its own, says that cell-phones do not contribute to the forming of tumors in the body. Danish scientists compared the cancer risk for all of the Danish cell-phone users, all 420,095 of them, from 1982 to 1995 and then compared it to the risk from 1996 to 2002, when more people had cell-phones. The study showed that there was not a link between cell-phones and tumors. They then extended the study to include cell-phone users from 2002 to 2007 with still not definitive link.

The researchers found that 10,729 people had tumors between 1990 and 2007. Using this number, they funneled it to just people who had been using cell-phones for more than 13 years. The rate of people with tumors was unrelated to whether or not they had a cell phone.

Unfortunately, the study did not focus on each person’s particular usage of their cell-phone or on people who have had cell-phones for more than 15 years. So, it’s probably best not to always be glued to the phone, but hey, one more text can’t hurt!

Powered by WordPress & Theme by Anders Norén

Skip to toolbar