BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: cancerous cells

Preserve Biodiversity & Save Lives

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On October 20, 2019

In Student Post

How elephants are crucial to cancer research

Over the course of the past few years intensive research has been done on elephants specifically on studying their cells. Elephant’s cells can play an extensive role in advancing cancer research for humans. You may be wondering why is this? How is an elephant’s cell so unique? Well elephants rarely get cancer. This may seem impossible since they weigh tons which means their cells are significantly bigger than a human sized cell, and they should be more prone to getting cancer. In addition, elephants have “hundreds of times the number of cells — and have similarly long natural lifespans — but their cells mutate, become cancerous, and kill them less frequently”. This peculiar trait is being studied by the ACE team, they have given it the name ‘Peto’s Paradox’ named for Richard Peto, a British epidemiologist.” Elephants make multiple copies of their genes, so if a mutation does occur in an elephant’s cell thus becoming cancerous “..instead of reproducing, just kill themselves.”

African bush elephants (Loxodonta africana) female with six-week-old baby.jpg

African bush elephants (Loxodonta africana) female with six-week-old baby

Researchers now are trying to work with human cells and see if this “cancer-fighting technique” used by elephants could lead to new medical treatments. Peto’s Paradox seems to work on every type of cancer that it was tried on. Which would really cut down on the time and money needed to study every form/type of cancer. If  Peto’s Paradox were to work on human cells on a bigger scale than just the “petri dish” used in this study more time could be devoted to just perfecting this technique in human cells and would for the first time ever be a revolutionary cure for every cancer known to man.  

Protecting Elephants

Gabon Rainforest

According to research African forest elephants help fight against climate change. There is a direct correlation between African forest elephant eating patterns and a reduction in carbon emissions released in their ecosystem. “African forest elephants need to eat 5-10 percent of their body weight (about 200-600 pounds) every day. They mostly feed on trees with lower wood density — leaving more room in the forest for the growth of high-wood-density trees that more efficiently absorb carbon in the environment, reported Ahimsa Campos-Arceiz from University of Nottingham.” Sadly, this species faces constant threats from poachers and the ever rising issue of deforestation. It’s essential to protect elephants and their habitats so they don’t go extinct. “[I]f African forest elephants go extinct, above-ground biomass — the organic materials such as trees that live above soil, essential to storing carbon — would decrease by 7 percent in Central Africa’s rainforests. Tropical forests can provide at least 30 percent of the mitigation needed to limit global warming, making their protection vital not only for the elephants’ diets and habitats, but for the planet.”

As mentioned earlier elephants rarely get cancer so if their species die off, so would the key to finding a cure for cancer in humans as many leading scientists believe. Elephants are virtually on the edge of extinction, their disappearance could have far-reaching effects for both public health and cancer research. As a result, scientists are trying to quickly gather as much data as they can while elephants are still here. However not all hope is lost. Conservation International is working hard to protect species such as elephants, the habitat they live in, and to help stabilize climates all around the world.

The Oxygen Sensing Discovery: A Huge Impact on Cancer Research

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On October 19, 2019

In Student Post

On October 7, 2019, three scientists- William G. Kaelin, Gregg L. Semenza, and Peter J. Ratcliffe- won the 2019 Nobel Peace Prize in Physiology or Medicine for their groundbreaking discovery in the 1990’s of how cells detect and respond to the presence of oxygen. That may not seem very significant-even Ratcliffe’s colleague’s dimissed his facination with how organs respond to oxygen availability-but the applications are profound. In fact, the Nobel prize was not awarded until recently for this very reason: to evaluate the “when the full impact of the discovery has become evident” (Ralf Pettersson, a former Nobel Selection comittee chairman). Well, their research has provided an possible explaination for the rapid metastasis for which cancer cells are notorious.

An image released by the National Cancer Institute, part of the National Institute of Health, that depicts malignant breast cancer cells (brown stained) metastasizing within the liver.

According to Ratcliffe’s research, cells produce a complex of proteins called the hypoxia-inducible factor, HIF, that help increase the level of oxygen when cells are oxygen deficient. The HIF turns on genes necessary for the production of the hormone erythropoietin, EPO. In turn, the EPO protein hormone signals for red blood cells to be produced in the bone marrow. Through oxygen-carrying hemoglobin, the red blood cells carry more oxygen to tissues and cells. For example, when the body undergoes hypoxia in response to lack of oxygen, like when people occupy high altitudes, HIF turns on production of EPO.

However, when the oxygen levels are sufficient in the cell, proteins called ubiquitin will bind to the HIF and induce it’s destruction. In this way, cells sense when oxygen levels are low or high and can respond accordingly by regulating the presence of HIF.

That’s pretty cool right? It gets better.

Through the individual work of Semenza and Kaelin, cancer cells were discovered to sense oxygen levels by manipulating VHL. While conducting their separate research, both Semenza and Kaelin hypothesized that cancer cells were searching for oxygen when they spread. Kaelin, as a cancer biologist, took specific interest in von Hippel-Lindau disease, a rare hereditary disease in which either malign or benign tumors form in mostly in the nervous system, pancreas, adrenal glands, and kidneys. The VHL protein, which the VHL gene codes for, in humans helps prevents tumor formation by recognition of the indicator hydroxyl groups placed on HIF by enzymes when the oxygen level are normal. In this case, VHL knows to destroy HIF. On the other hand, if the oxygen levels are low, the HIF lack the hydroxyl groups and are ignored by VHL. During research, he discovered that in these type of cancers, the VHL genes are mutated so that VHL becomes inactive. As a result, it can no longer regulate the quantity of HIF proteins thus, the HIF level increases. Increased HIF levels mean more oxygen for cancer cell, which multiply rapidly because of their now readily available supply of oxygen. This knowledge is vital since Harvard cell biologist Andrew Murray say that “tumors can grow to only about 1 millimeter across without making new blood vessels, because oxygen can diffuse only about half a millimeter away from a capillary before cells consume it”.

The trio’s research is fascinating to me, because this knowledge could be revolutionary in preventing the development and spread of cancer cells. What other biological issue do you think that the discovery of oxygen sensing could solve?

 

 

How Mesh in a Cell Can Cause Cancer

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On October 12, 2016

In Student Post

Warwick Press Release In July 2015 researchers at the University of Warwick discovered, accidentally, how the structure of a cell can cause cancer development.  The mesh that holds microtubules together also assists the mitotic spindles (made of microtubules) in cell division.  To learn more about cell division click here.  Mitotic spindles are responsible for making sure new cells have a complete genome: the correct number of chromosomes.  To learn more about spindle structures click here.  It has been known that a cell with too many or too little chromosomes, called aneuploidy, can cause diseases, including cancer.  Mesh gives structural support to mitotic spindles.  Too little or too much support from the mesh causes mitotic spindles to be too weak or too strong (cannot correct mistakes).  The discovery of the mesh occurred when Warwick researchers looked at microtubule structures in a 3D shape and saw that the bridges that hold microtubules together were not “single struts,” but “web-like structures.”  The next step in this research is to determine if it is possible to prevent mesh from giving not the right amount of support.  Could medicine ensure that the mesh supports the mitotic spindles just enough so that a  shared number of chromosomes is guaranteed during cell division?

Kinetochores on chromosomes attach to spindle fiber during cell division

Kinetochores on chromosomes attach to spindle fiber during cell division

To Know or Not to Know: Cancer Risk Gene Testing

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On September 25, 2014

In Student Post

Breast Cancer Cells

Genetic mutation testing has been a hotly debated and controversial topic since its initial prevalence in 1990.  Originally genetic testing was used to test females who have cancer in their family history for the BRCA 1 and 2 gene mutations.  Early detection of these mutations allowed for precautionary measure sure to be exercised prior to cancer even being diagnosed. The hereditary breast cancer risk testing was done mainly by Myraid Genetics but just last year the Supreme Court invalidated Myraid’s patents on the testing of the BRCA genes.  This ruling opened up many windows for the competition of Myraid in the field of genetic testing.  Many other companies and Myraid itself began not only offering BRCA testing but also more elaborate multi gene testing for the same price (apron $4000) as it would have been to test just the two BRCA genes.  This “bargain” influenced many patients to have more genes (up to 25) tested for mutations despite the fact that they may not have a family history to tendency towards certain cancers.  This multiplex testing has raised many eyebrows in the medical field because patients and doctors are getting information that sometimes they are unsure as to what they should do.  Doctor Kenneth Offit of Memorial Sloan Kettering Cancer Center stated when referring to multiple gene mutation testing, “because they could be tested,not necessarily because they should be…individuals are getting results we’re not fully educated to council them on. ” However Memorial Sloan Kettering Cancer Center is working on setting up a database for more knowledge on genetic testing.  This online forum, the Prospective Registry of Multiplex Testing (PROMPT) will allow for more research to be done and for patients to learn more.   Often genetic mutations are found and doctors are unsure how to react to the information due to lack of knowledge in that specific field of mutation leading to a specific type of cancer with out any family history.   Professor Mary-Claire King of the University of Washington voiced her opinion that, “We need to report back only what is devastating and clearly devastating.”  Meaning she felt that patients and physicians should only receive specific information as opposed to a full list of all the genetic mutations that tested position or inconclusive.  When do we know when to much information become frivolous? When it come to human health, the more we know the better the outcomes.  How will doctors be able to sift through extraneous data to find what truly are indications for higher risk of cancer?  Is this “extra” testing and information skewing the data and prognosis of many patients?

 

Main Article Used:

http://www.nytimes.com/2014/09/23/health/finding-risks-not-answers-in-gene-tests.html?ref=health&_r=0

 

Getting closer to a cure for cancer!

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On January 11, 2012

In Student Post

Many cancer cells can be detected because the sugars on their surface proteins undergo specific changes from regular cells. The tumors produce a lot of the protein known as MUC1. Our immune systems have trouble recognizing the difference between these cancerous cells and the healthy cells because they both develop within the body.

Researchers have been testing a new vaccine on mice with cancers similar to the ones that develop on human cell. Luckily, the mice have been showing promising results and responding well to the vaccine! “This is the first time that a vaccine has been developed that trains the immune system to distinguish and kill cancer cells based on their different sugar structures on proteins such as MUC1,” Dr. Gendler says.  The MUC1 can be detected on 70% of all cancer cells. Can this really be the answer?!

It’s suppose to help with breast, pancreatic,  ovarian and multiple myeloma cancer. The vaccine will help the immune system recognize the MUC1 as a harmful foreigner. The vaccine has 3 parts. As we learned recently in our AP Biology class, the immune system attacks foreign cells with antibodies. Therefore the vaccine first has the immune system recognize the cells with MUC1 has harmful bacteria and then the immune system can send out the antibodies to fight off the cancer. Lastly, the  vaccine stimulates a response from a lymphocyte.

This vaccine should be ready by 2013 to improve cancer treatment! The vaccine would be life changing for many patients out there that experience triple – negative deadly cancers. I am looking forward to hearing more about this research and hearing the wonders its will do!

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