Small intestinal submucosa (SIS) is a biomaterial that can induce host tissue proliferation and regeneration when it is implanted at various tissue sites. This is made possible by SIS’s response to natural, site-specific stressors present in vivo. Upon implantation of the SIS biomaterial, it is quickly remodeled to mock the site-specific structure and function. SIS biomaterial has proven to be successful in rapid capillary ingrowth without any adverse immunologic reaction and is already available on the market. Through naturally occurring properties and proper biomaterial manufacturing, SIS biomaterial is able to successfully integrate itself into the existing tissue and become “self”. SIS biomaterial can be used in the treatment of serious joint, muscle, or tendon injuries and has been proven in vivo to integrate into the host tissue and degrade quickly.

SIS biomaterial is derived from the submucosal layer of the small intestine, typically from porcine. It is made up of mostly water, is translucent, resilient, and about 0.15 to 0.25 mm thick. Its aesthetics can be viewed in figure 1 or from this previous article on SIS, as can it be seen that the biomaterial possess the ability to be stretched. SIS is a cross-linked collagen-based extracellular matrix (ECM) that has very few connective tissue cells. Researchers believe that the properties of SIS have been proven to be ideal for multiple applications such as aid in soft tissue regeneration, treatment of dermal wounds, urinary bladder repair, hernia treatment and engineered tissue scaffolds (Brown-Etris 2002).

Figure 1

SIS biomaterial promotes the regeneration of host tissue via “smart remodeling”. This is a unique property of the biomaterial to be incorporated into new tissue in a short period of time where the biomaterial is almost indistinguishable from the natural tissue because SIS proliferates and regenerates the host tissue. Through various clinical trials, it has been shown that when a single layer of SIS biomaterial is implanted into a patient, multi-layered vessels have been formed in place of the biomaterial and the layers are thicker than the SIS layer! This means that the biomaterial implant supported the development of new arterial tissue in the intimal lining of endothelial cells with a supporting outer layer of smooth muscle tissue. SIS biomaterial has successfully been shown to mock the site-specific structure and function of the host tissue (Brown-Etris 2002, Ueno 2004).

Microscopic images of SIS biomaterial upon implantation into patient are shown in figure 2. The interface between the host tissue (left) and the biomaterial (right) seems sharp, but SIS is superior in biointegration. The cross-linked collagen fibers can be viewed in figure 2A where host cells begin to integrate into the SIS biomaterial scaffold (Brown-Etris 2002).

SIS also has the potential to induce rapid capillary ingrowth, which works with “smart remodeling” (figure 2B). Angiogenesis is a vital part of tissue implantation and the SIS biomaterial scaffold has proven successful in rapid cellular infiltration and angiogenesis in numerous clinical trials. In vascular implants, SIS biomaterial successfully promotes capillary ingrowth in just four days by migrating cells into the SIS ECM. This helps the tissue to fight bacterial infection. The quick and thorough distribution of capillaries throughout the tissue allows for rapid and resilient nutrient delivery and metabolic byproduct collection to and from the injury site. This leaves little time for the tissue to be deprived of nutrients, water, oxygen, and waste removal; which helps the tissue resist bacterial infection (Brown-Etris 2002).

Figure 2

A vital property of an acellular scaffold in an engineered tissue is that it should have the ability to degrade safely and quickly. SIS biomaterial has been proven to degrade quite rapidly. More than half of the biomaterial mass is lost one month after implantation. Tests were run and animal trials were preformed to show that after three months after implantation of the SIS biomaterial, it was completely resorbed into the host tissue. By this time, the SIS biomaterial implant area looks like figure 2C and is completely covered with a dense collagenous matrix that resembles the structure and function of the host tissue. Upon complete integration of SIS biomaterial into host tissue, the wound site appears as shown in figure 2D (Gilbert 2007).

Significance
There are over ten million cases of joint, muscle, and tendon injury in North America every year. When the injury results in a complete disunion of the tissue, it needs to be treated right away because the tissue doesn’t have the ability to heal this on its own. Treatment for complete disunion involves a surgeon invasively opening up the injury site, pulling together both ends of the broken tissue, and suturing them together. Tissue engineered constructs have been studied for this treatment and they strive to be integrated into the patient’s body between the two ends of the injured tissue. The biomaterial used for this treatment is required to functionally and histologically resemble the host tissue, actively fuse together the two ends of tissue, promote vascularization throughout the injury site, and illicit minimal immune response from the host. Small Intestinal Submucosa (SIS) is a naturally derived biomaterial that has been successfully tested in vivo for the treatment of this type of injury and can induce active regeneration of the tissue (Brown-Etris 2002, MacLoed 2004).

Background
SIS was accidentally discovered in 1987 at Purdue University when Dr. Stephen Badylak and his team were searching for a naturally derived vascular graft. Their goal was to discover a natural substitute to replace synthetic polymeric vascular grafts due to their 50% failure rate at five years in smaller blood vessels. Due to the small intestine’s tubular configuration, abundance in the body, and strength, the team searched to use small intestinal tissue as a vascular graft. Initially, every layer of the small intestine was used to conduct tests, however the enzymatic activity of this multi-layered material was too high. Therefore, researchers began pealing off various layers from the small intestine (see figure 1) and testing them individually. When the submucosal layer passed several clinical studies, it was named SIS, small intestinal submucosa, and utilized in further research (Badylak 2004).

Figure 1

When SIS treatments were proven successful in clinical trials on animals by Dr. Badylak and his team, they found that the extracellular matrix (ECM) was key in tissue healing. This lead the curious team into using SIS biomaterial for wound healing in patients. The team also discovered that this biomaterial could be converted into sheets, gels, powders, and/or multilaminates to be of use in numerous applications. A sample of the appearance of SIS sheet can be seen in figure 2. By 1994, Dr. Badylak and his team worked in conjunction with the Methodist Hospital in Indianapolis to receive four patents to use SIS biomaterial in humans. Human trials for numerous applications began in 1995. Not too long after, DePuy, Inc. aided the Badylak group in manufacturing SIS ligaments for human trails. Models like these SIS ligaments are now being used to treat joint, muscle, and tendon disunions (Badylak 2004). A start-up company called Cook Biotech, Inc. began near Purdue University to further research and commercial use of SIS biomaterial. The company is still rather successful and has many other products on the market now (www.cookbiotech.com).

Figure 2

Why SIS?
What sets SIS apart from other biomaterials is that it is completely naturally derived and it is capable of interacting with host cells to send and receive messages and signals of tissue growth and maintenance. SIS biomaterial provides a natural, cross-linked ECM with a three-dimensional structure that acts as a scaffold for host tissue remodeling (see figure 3). After SIS is implanted into the patient, tissues adjacent to it immediately begin to deliver cells and nutrients into its acellular construct. The cells rapidly invade the SIS material and capillary growth follows to allow nutrients to enter the SIS matrix. SIS is extremely strong at the time of implant and is gradually resorbed while the host tissue reinforces and remodels the damaged site with new cells. The integrity of the tissue is maintained and the new tissue quickly becomes completely “self” by integrating itself into the host tissue.

There are many applications for SIS, such as management of gastrochisis, coating stents, replacing dermal layers, repairing abdominal walls, and repairing bladder walls. SIS is used in tissue disunion to induce cell migration into the ECM, actively vascularize the ECM, and activate tissue regeneration into the ECM. This can successfully heal the injury or close the disunion in the tissue as the SIS biomaterial resorbs/degrades into the host tissue to become “self”. When disunion occurs in a tissue, it must be treated in order to restore functionality of the body part. The only way to do this is to “reattach” or regrow the two ends of tissue and immobilize the area to allow repair (Gilbert 2007). Tissue disunion is very painful and can cause great damage to a patient’s lifestyle, depending on where the injury occurs. Tendon disunion often occurs in the patellar area of a patient; without proper treatment, these patients would never be able to walk again (Kroeger 1999).

Disadvantages
Due to the fact that there is no “perfect” replacement material for natural body tissue, disadvantages of SIS biomaterial also need to be taken into consideration. Some of the disadvantages include the fact that although SIS biomaterial doesn’t demonstrate any adverse immunologic response in most trials, there is still possibility of rejection due to differences in individual immune systems. The “golden standard” will always be an autologous model, and SIS biomaterial is xenogeneic. Autologous samples are taken from another part of the patient’s body. These samples do not cause any averse immune response since they are from self. Xenogeneic is a tissue from a different species than the patient, as is SIS biomaterial. The complete degradation kinematics and communication between SIS and host tissue are not yet completely understood, therefore ongoing research is being conducted to fully understand the capacity of this multi-faceted biological system. Since SIS is a naturally derived material, batch-to-batch variations exist in every sample. When compared to synthetic biomaterials, natural materials are generally more difficult to process on a large scale. There is also no degradation control of SIS biomaterial, as may exist in certain synthetic materials. If a certain type of injury requires a slower degradation rate to heal, this is not adjustable when using SIS because the degradation rate is constant. Despite the shortcomings of SIS biomaterial, it is still an ideal choice for the treatment of many joint, muscle, and tendon injuries.

 -Amy Shah

Everyone knows that science has been booming at an insanely quick rate for the past decade. The world has erupted with stem cells, tissue engineering, cures for diabetes and Alzheimer’s Disease all in the past ten years! But what about the next ten years? MSNBC predicts that stem cells will be the norm, tissue engineering will be a replacement for most major surgeries with the remaining surgeries to be preformed by robots, and cures to widespread diseases will be perfected. If you’re not very fond of reading, watch this video The Year 2017 and get a glipse of what is to come (the video will play after a 30 second commercial).

Researchers from Queensland University of Technology learn out how bone cells work and figure out how they can heal them. Scientists are working on a device that will help heal bones in half the time. Being a person who breaks bones quite often (by quite often I mean once or twice a year) the minute I saw this I knew this could help change my life. Last Christmas I broke, fractured, dislocated, and had surgery on my wrist and it took about 8 months to fully recover from this unfortunate snowboard accident. If this device can cut the healing time in half then I can have more time to relax (break more bones). The next step for this bone healing theory is to test it. I will gladly volunteer myself for any test that Dr. Hannay (the person directly involved with this research) has to do.

“In the future we might be able to make a device utilizing these combined stimulants that could be attached to the body and help heal the bone.”
-Dr. Hannay

For more information check out QUT

-Sujan Patel

Just imagine not being able to feel any physical pain. The good part is, of course, that you can’t feel any pain. The bad part is that you can bleed to death and probably wouldn’t even think of going to a hospital.

Voltage-gated sodium channels are essential in pain perception. A gene called SCN9A is responsible for creating these channels so that when something painful strikes the skin, these voltage-gated sodium channels can open up and stimulate sensory neurons to send a pain signal to the brain.

No Pain!

A six-year-old Pakistani boy is a street performer who can stick knives in his body day in and day out and still be perfectly fine without fainting. He posses a rare genetic mutation that leaves gene SCN9A functionless, which in turn leaves him incapable of feeling any pain. He has no other defects or abnormalities; everything else in his body is perfectly fine. This turned on a light bulb in Dr. Geoffrey Woods’ head. He had been studying this SCN9A gene at the University of Cambridge for quite a while now and was linking this idea to the morphine receptor we possess in our bodies. The gears in Dr. Woods’ brain were grinding until he came up with a wonderful idea. Just as this SCN9A gene is blocked in the Pakistani street performer, he could temporarily block it in patients during surgery and other procedures. Dr. Woods studied this boy and six of his young relatives, who also had the mutation in their bodies. This would be better than using Morphine, which can cause addiction and drowsiness, or Celebrex, which can cause heart damage. Many researchers continue on this idea to try to find a healthy and effective way of temporarily blocking the SCN9A gene. This discovery will lead to a very helpful pain killer in medical settings in the recent future.

-Amy Shah

In 2005, approximately 200,000 people in the United States were diagnosed with breast cancer and 40,000 people died from breast cancer (American Cancer Society, Inc. 2006a); compared to the 14,000 people a year that die from HIV/AIDS (Central Intelligence Agency 2006), this is a prevalent problem. Breast cancer is the second most deadly type of cancer in the United States, exceeded only by lung cancer. More than 25% of all breast cancer incidents have an obstructed p53 protein (Itahana 1998). One could conclude that this protein is related to tumor growth, and researchers could use p53 to help fight against cancerous cells. This paper focuses mainly on how p53 and cancer are related; the potential of fighting breast cancer using p53; pros and cons to this p53 solution; and alternative solutions to this potential p53 solution.

The p53 Protein and Cancer

The obstruction of p53 in cells is the most common defect present in all types of cancers. Cells that lack even only a portion of this p53 protein are especially resistant to standard therapies that are used to help minimize the side effects of cancer (Center for Biotechnology Information 2005). Among the many proteins in a cell, p53 is statistically the most commonly mutated protein of all in any type of cancer (McGill 1999). The p53 protein was discovered in 1979 by Arnold Levine, David Lane, and Lloyd Old (Wikimedia Foundation, Inc. 2006b). It gained the reputation of being a protein produced by an oncogene, a gene that causes cancer, because it is overactive in cancer cells (Ko 1996). However, in 1989, Bert Vogelstein of John Hopkins School of Medicine (Wikimedia Foundation, Inc. 2006b) discovered that introduction of p53 into cells actually suppresses cellular growth (Ko 1996). Therefore, the reason that it is over-expressed in cancer cells is because it is trying to prevent cancer; it is a tumor suppressor protein. The function of a tumor suppressor protein is to kill cancerous cells, impede their cell cycle, or repair their mutation. Depending on how severe the mutation is, it may execute any or all of the previous cancer prevention methods (Gross 2006). Each cell contains two copies of p53, if only one copy is missing or obstructed, the cell will be especially vulnerable to becoming cancerous (Alberts et al. 2004).

DNA is essential in all cellular forms of life and controls the cell’s function, appearance, and biological development (Wikimedia Foundation, Inc. 2006b). When a cell replicates, it passes on identical copies of its DNA to new cells. A cell becomes cancerous when its DNA is mutated, which means it has been damaged or improperly replicated. If the DNA is mutated, all of the new cells’ DNA will be mutated as well and they will all be cancerous cells (Itahana 1998). While normal cells in the body will grow, divide, and then die; cancer cells do not die. Healthy cells realize the limitations of a physical body and will program themselves to die when there is not enough space for them or there are no more nutrients available in their area. Because cancer cells have a mutation that provides the cells with a selective growth advantage, they aggressively disregard all instructions to die (Itahana 1998). This selective growth advantage allows cancer cells to survive longer than normal cells because their programmed cell death is not active when p53 is obstructed. This causes the cells to divide uncontrollably and form a large group of cancer cells, called a tumor (American Cancer Society, Inc. 2006b). Cancer cells also have the ability to spread to other parts of the body where more resources are available, creating more tumors. When the tumor suppressor gene does not repair damaged DNA in cancer cells, the result could be long illness, death, or hereditary cancer (Wikimedia Foundation, Inc. 2006a).

All cells go through the cell cycle, which is their life cycle of growth, replication, division, and eventually death. The tumor suppressor protein, p53, plays a vital role in the cell cycle. After the cell’s growth phase, it has to pass a p53 checkpoint in order to proceed into the replication phase. At this checkpoint, p53 checks every single portion of the cell’s DNA for mutations. If small mutations are detected, p53 instructs the cell to repair the damage and then move on into the replication phase. If a large mutation is detected, p53 instructs to cell to die so that it cannot pass on this mutation (Anon 2006). When this checkpoint was discovered, p53 earned the title “the guardian of the genome” due to the fact that it protects the cell’s damaged DNA from replicating and being passed on to new cells (Anon 2001). If a questionable mutation is detected, p53 can slow down the cell cycle or stop it. Since p53 is obstructed in cancer cells, their cell cycle goes much faster due to absence of this checkpoint (Anon 2006).

Properly regulating p53 can keep cells healthy and prevent cancer (Wikimedia Foundation, Inc. 2006c). There is a delicate balance in p53 activity; unwarranted activation can be catastrophic to developing cells, but inactivity can lead to cancers. This tumor suppressor protein is regulated both negatively and positively. The stability of p53 is a complex process which involves many proteins and molecules that respond to overactive p53 in a negative feedback loop; this is when excess p53 activates certain proteins and molecules to reduce its affect. Positive feedback loops are activated by scarcity of p53 to increase its affect (Landes Bioscience 2005). In healthy cells, p53 is continually produced and degraded to maintain this balance; degradation plays a key role in overactive p53 (Lain 2003). These processes are sensitive to many forms of stress, such as, temperature, pH, and pressure. Homeostasis and the immune system help keep the body in a normal, healthy condition so that all of the processes can follow through smoothly.

Fighting Breast Cancer Using p53

Since p53 is obstructed in many cancer cases, restoring its innate tumor-suppressing mechanism will help fight against breast cancer. Since all healthy cells go through the p53 checkpoint during their development, inserting intact p53 into cancerous cells can activate this p53 checkpoint and cure cancer cells (Soussi 2006). Obstructed p53 proteins will not be a problem because new, healthy p53 can just be inserted into the cancer cells.

Although p53 is a powerful tumor suppressor protein, it does not work alone to fight cancer by simple insertion (Itahana 1998). Kinases and phosphorylating enzymes are proteins that “activate” or “energize” a molecule by adding a phosphate group to it from another high energy molecule (Ashcroft and Vousden 1999). Mdm2 is a protein that is stimulated by excess p53 and functions to minimize the amount of p53 in a cell. This is a key step in reducing overactive p53 in a healthy cell; however this is not a desirable effect in cancer cells (Gross 2006). Mdm2 binds to p53 and reduces its ability to activate gene expression and stop cell division, thereby interfering with p53’s control over DNA replication machinery. To restore p53’s function in cancer cells, kinases or phosphorylating enzymes need to be inserted into the cells to energize p53 and alter its structure. This allows p53 to carryout its function because Mdm2 cannot bind to p53’s new structure to deactivate it. By inserting kinases and phosphorylating enzymes into cancer cells, the p53 protein can activate the tumor suppressor gene to destroy cancer cells (Ashcroft and Vousden 1999).

Another tumor-suppressor protein, p14ARF, is known to be missing in about half of all breast cancer cases. However, missing p14ARF is not the sole component that can cause breast cancer in most cases. When p14ARF and p53 are both missing in a cell, a common result is cancer. This fact lead researchers to believe that p14ARF and p53 are somehow linked (Gjerset 2000). Additional research shows that p14ARF binds directly to Mdm2 on a different location than p53. Mdm2 can still interact with p53, but because p14ARF is also bound to Mdm2, it is deactivated. In this p14ARF-Mdm2-p53 protein complex, both Mdm2 and p53 are stabilized. This inhibits Mdm2’s activity and restores p53’s function. Therefore, the addition of p14ARF into breast cancer cells can lead to activation of p53 and stop cancer (Ashcroft and Vousden 1999).

Delivery of p53, kinases, phosphoylating enzymes, or p14ARF to cancerous cells can be a prevailing strategy in fighting breast cancer. However, these proteins cannot simply be injected into one’s blood stream or swallowed in a pill; they must be carefully inserted into the victim’s body and incorporated into their cells’ DNA. The proteins need to pass through the cell’s membrane, through the cell’s body, pass through the nuclear membrane, and be incorporated into the DNA. This can be done by gene therapy, which is when altered or foreign proteins are introduced into cells to fabricate a desired effect (Wikimedia Foundation, Inc. 2005). Experiments of introducing p53 into p53-deficient cells in a test tube have proven successful. The same experiments in rats depicted either the death of cancer cells or prevention of further division and survival of the rats. Although this has not been tested on humans yet, this hypothesis should still be taken into consideration (U.S. Department of Energy Office of Science, Human Genome Program 2005).

Injections of these proteins into a human body can be done through viral vector treatment. This procedure is a type of gene therapy that utilizes viruses to deliver genetic material into a cell, permanently changing that cell’s DNA. Since a virus infects its host by incorporating its DNA into the host’s DNA, scientists can modify viral DNA such that a desired protein is introduced to the host instead of a virus’s harmful effect. The specific virus used in this procedure is called a retrovirus. A retrovirus is a special type of viruses that can translate its own DNA into DNA that belongs in a living organism’s cell. The retrovirus’s ability to match these two different types of DNA together is what makes it so efficient in infecting its host cell (Wikimedia Foundation, Inc. 2006b). Viruses can therefore be used as a means of transportation to carry “good genes” into a cell. The virus functions to integrate a desired protein into the host’s DNA. As the cell replicates, the new cells created will also have the desired protein. Since the protein is now incorporated into the cells’ DNA, it can carryout its function (Gardlik et al 2005). If p53 is integrated into the DNA, it will follow through with its function and ignore the obstructed p53. If kinases or phosphorylating enzymes are integrated, they will alter p53’s structure to allow it to activate the tumor suppressor gene. If p14ARF is integrated, it will bind to Mdm2 to deactivate it and allow p53 to carryout its function. The p53 tumor suppressor protein is now ready to fight breast cancer.

p53 Solution - Pros

Fighting breast cancer using p53 is a very promising treatment for the future. This treatment uses p53, kinases, phosphorylating enzymes, or p14ARF, which are all proteins that exist naturally in the body. The concern of many people that choose not to use chemotherapy, the introduction of drugs into the victim’s bloodstream, is that unnatural chemicals are introduced to their bodies (MayoClinic 2006). Using gene therapy is another positive aspect of this p53 treatment. Gene therapy is a method that has already been proven successful in reducing tumor size and can differentiate cancer cells from healthy cells. This is why p53 treatment surpasses radiation therapy; X-rays focused on the victim’s tumor attack all cells, not only the tumor cells, and lead to unnecessary death of healthy cells. Using gene therapy spares the healthy cells and kills the cancerous cells (BBC News 2000). This solution is also ideal because it has been tested in great detail at the University of Pittsburgh Cancer Institute. The research at this lab has added normal p53 genes to groups of growing cancer cells in a petri dish and tumors in some animals. These cultures of growing cancer cells and tumors from test subjects prove that addition of the p53 gene to the groups of cancerous cells causes them to die (University of Pittsburg 1998).

p53 Solution - Cons

Although fighting breast cancer using p53 has much potential for the future, this treatment is limited by some constraints. First and foremost, this method is not in use yet. It needs to go through much more animal and human testing before it can be available on the market. Additionally, issues concerning the use of viruses as the choice of gene-carrier include weakening of the immune system and intoxication of DNA. If inserting a virus into one’s body weakens their immune system, there exist possibilities for sicknesses of other kinds to occur in the patient (U.S. Department of Energy Office of Science, Human Genome Program 2005). Scientists need to discover how much the immune system weakens, if this is a great amount, the treatment will not be worth the risk to the patient’s life. Given the nature of retroviruses, the inserted p53 gene is spontaneous and out of external control. The viral DNA may be integrated into many different parts of the host’s DNA and its effects may vary (U.S. Department of Energy Office of Science, Human Genome Program 2005). Since the p53 tumor suppressor protein is sensitive to many stresses, unwarranted activation may occur by external factors. This is bad because adding extra p53 to a cancer patient that has a low immune system, due to the virus used, can lead to over-active p53 because of the patient’s inability to maintain normal conditions in the body (Phillips 2006). Fighting breast cancer using p53 also has the common side effects of any other cancer treatment available today. Some of the most common side effects include bone marrow depletion, excessive bleeding, and hair loss (Phillips 2006). General constraints to this solution include the fact that every case of breast cancer is diverse and these differences need to be overcome in order to develop a universal treatment for breast cancer. Like all the different solutions available, this p53 solution has moral problems attached to it. Many researchers are arguing that the apoptotic death of cells isn’t necessary in fighting cancer. This type of cell death is immediate and programmed cell death that is induced by a protein, in this case the protein is p53. Radiobiologists have a particularly difficult problem with this type of cell death because slower, non-apoptotic death plays an important role in the cycle of a viable cell (McGill 1999). Finally, there is a major downfall in using p53 itself for any type of treatment. Although much more is known today about this tumor suppressor protein than was known in the 1970s, its function is still incompletely known. Researchers are working hard everyday to find out all they can about this powerful protein, but there are still limitations to what they can discover (McGill 1999).

Alternative Solutions

Since the p53 solution is not currently in use due to certain hurdles that science needs yet to cross, breast cancer patients still have options to alleviate their symptoms and prolong their life spans. Today, tumors can be alleviated with a combination of surgery, chemotherapy, hormone therapy and radiation therapy. Through surgery, the doctor will either remove the entire breast or just the affected part of the breast; this depends on how severe the tumor is. Chemotherapy relies on drugs that interfere with cell division to kill cells (Wikimedia Foundation, Inc. 2006a). Hormone therapy removes or inactivates hormones so that cells lack proper hormones to grow, however it only works in breast cancer cases that are caused by hormonal factors (National Cancer Institute 2005). Radiation therapy uses an X-ray beam to kill the cells in that target area. The X-ray damages the cell’s DNA to make it impossible for the cell to divide (Wikimedia Foundation, Inc. 2006a). Tumors are infatuated with certain proteins that are produced by oncogenes, but can be poisoned by tumor suppressor proteins. Essentially, the drug of choice would function to stop this infatuation or provide poison to the tumor cells. There are some drugs that exist today which follow this function, for example Gleevec and Herceptin (Brody 2003). However, due to the recurrence of cancer, these drugs aren’t sufficient. Even when surgery, chemotherapy, hormone therapy and radiation therapy are all combined to fight cancerous cells, tumors have a tendency to recur. The ideal counterattack against cancer is to suppress it before it begins because once cancer has begun to grow, the fight against it is an enormously rough battle.

-Amy Shah

 

Over 80,000 Americans have to deal with spinal cord injuries every year! Spinal cord injury is damage to one’s spinal column leading to loss of function and/or sensation to one or multiple body parts. Imagine the thousands of victims with spinal cord injury that have lost function of a body part, but not sensation. They are constantly in excruciating pain, yet can’t even move that body part. No one has been able to find a pain reliever for this…until now!

A drug called Pregabalin exists on the market, but is currently used as a pain reliever for diabetes. A research group in Australia discovered that Pregabalin can also be used to ease the pain for spinal cord injury victims. About 80% of their test group of patients with spinal cord injury confirmed a reduction of pain and anxiety over a 12 week test period. They also confirmed that Pregabalin improved their sleep and overall well-being. About 30% of the test group said that they has no pain or only mild pain!