You have probably already heard about the advantages of eating soy beans and their association with the lower risk of developing certain types of cancer.  This theory stemmed in the 1930s from the fact that females of Asian decent have lower chances of developing breast cancer. During the National Cancer Institute’s environmental and lifestyle experiments on animals & humans, their scientists theorized that diets higher in soy, and similar foods containing isoflavones can lead to lower chances of developing specific types of cancer.

Isoflavones

Isoflavones mimic the effect of estrogen that is produced in humans and animals and this effect is what helps avoid the cells from turning cancerous.  The antioxidant properties help fight against free radicals, which can cause damage to cells through oxidation. The specific isoflavones (phytoestrogens) that contribute to this “cancer-preventing” effect are genistein, daidzein, and glycitein. This is not a point-blank theory - it revolves around the age that isoflavones are consumed and results have only been identified for certain types of cancer.

Cancers

The biggest reason that it’s been especially challenging to discover a cure for cancer is that all cancers are different - they all develop, grow, advance, and attack neighboring cells differently. This is also why the “Soy Theory” does not pertain to all types of cancer. Laboratory studies have found the most substantial evidence pertaining to isoflavones aiding in the prevention of the development of breast and prostate cancers, however this is still just a theory and not enough evidence has been found to make this a fact. Colon and endometrial cancer research are also underway, but have less evidence pertaining to their prevention.

The bottom line is that this research is still underway and the theories are strongly supported - but if anything soy is still high in protein and helps lower blood pressure and cholesterol. Stick to consuming these healthy items and living a healthy lifestyle to help reduce your risk of developing cancer.

Learn more from The American Cancer Society, About Breast Cancer, and Cornell University.

HALO received national attention The Doctors TV show with a segment on HALO. “One Life to Live” soap star Crystal Hunt (“Stacy”) was shown having the HALO procedure and was presented her results in front of the live audience. Show host Dr. Lisa Masterson gives an enthusiastic overview of what HALO is all about.

Tamoxifen is a widely-used breast cancer drug which 500,000 women in the United States are taking to prevent their estrogen-dependent breast cancer from recurring. The FDA plans to warn doctors about a recent breakthrough in which evidence has been gathered about the interaction between tamoxifen and antidepressants. Certain anti-depressants, when taken with tamoxifen can actually increase a women’s risk of breast cancer recurrence by two-fold.

The study used to discover these findings involved 1300 women over a one year period of time. All the women were monitored, their breast cancer recurrence rates were compared in different groups of women taking no antidepressants, Zoloft, Paxil, and Prozac all along with tamoxifen. The results yielded a 7.5% recurrence rate for women not taking antidepressants and a recurrence rate of 16% for women taking any of the 3 mentioned types of antidepressants. Other antidepressants studied that did not significantly affect breast cancer recurrence rate were Luvox, Celexa, and Lexapro.

Now that the FDA has proof through clinical outcomes that this drug interaction can actually increase a women’s risk of recurring cancer, the FDA is opting to add information to tamoxifen’s label.  Although placing information on FDA-approved labels is a start to informing health care providers and patients about this drug interaction, further vehicles will be needed to educate the breast cancer survivor community on this issue.

Medco’s cheif medical officer, Robert Epstein, explained that over 500,000 U.S. women are taking tamoxifen, of which 30% are simultaniously perscribed antidepressants.  This indicates that many health care providers are not aware of this dangerous interaction, so patient awareness is key, especially for patients treated by multiple doctors.

This article was written by Amy Shah, however facts were obtained from an article by Jennifer Corbett Dooren.

Natural Genetics just published the discovery of a mutation responsible for the progression of cancer.  This finding has the potential to help treat against numerous types of cancers since the mutation can be linked to various types of malignancies, rather than just in one type of cancer like many previous discoveries.

This mutation was discovered through the study of MicroRNAs (miRNAs).  Normally, the data stored in DNA is translated into RNA and the RNA is then translated into proteins, which then regulates gene expression.  In this study, the small pieces of RNA, miRNAs, were found to be blocking their translation into corresponding proteins.  Some of the miRNAs are hypothesized to suppress tumor formation and it was found that unusual levels of these molecules were present in all cancers studied.  This implies that this type of mutation could be responsible for cancer growth and progression in all types of cancers.  Following this hypothesis, continued research could possibly lead to a therapy that could reverse abnormal miRNA levels to treat multiple types of cancer.  The scientists working on this project believe that they could lead to an incredible discovery in cancer treatment.

Moving forward with the research, Sonia Melo is planning to analyze 12 different types of cancer in search of mutations in the pathway of miRNA formation.  In preliminary studies, she and her team found a protein called TARP2 that caused mutations in the pathway of miRNA formation, leading to low amounts of miRNA.  Upon the discovery of this protein and its pathway, the team later found that when functional TARBP2 was introduced to those cancerous cells, the miRNA returned to its normal levels.  In turn, those normal levels of miRNA that were reintroduced into the cancerous cells suggested to initiate tumor suppression functions.  This was found by comparing the levels of several known oncoproteins that promote tumorous functions when activated.

In vivo studies were performed by Melo and her team to verify their findings in SCID mice.  The team injected SCID some mice with new TARBP2 cells and other SCID mice with old TARBP2 from mutated cancer cells and compared the two groups.  The first group of mice with new TARBP2 cells either didn’t form tumors or formed a negligible amount of cancerous cells, while the second group of mice with old TARBP2 cells formed tumors relatively quickly.  This result confirmed the group’s theory that aberrant TARBP2 promotes tumor growth by reducing the amount of miRNA in cells.

A TARBP2 mutation in human cancer impairs microRNA processing and DICER1 function

Chemotherapy is any treatment that utilizes the use of chemicals to stop cancer cells from continuing to flourish.  This type of treatment is used on 50% of all people diagnosed with cancer.  It can eliminate cancer cells that have been metastasized as well. Chemotherapy has saved millions of peoples lives, but it doesn’t save every cancer patient.

Chemotherapy works wonders for some people and not at all for others.  The cause of this was not known until recently when the Center for Environmental Health Sciences (CEHS) and Departments of Biological Engineering and Biology from MIT discovered a group of 48 genes.  Several of these 48 genes have been linked to cancer, but what they all have in common is that they can all show how susceptible a patient is to MNNG, which is a DNA-damaging agent present in chemotherapeutic agents.

MNNG induces unstoppable DNA damage by creating lesions in the DNA, thereby killing the cells.  Everyone’s DNA reacts to MNNG by attempting to repair itself, however some people’s DNA reacts more strongly while others’ reaction can be more passive.  Everyone’s DNA is so different that two seemingly equally healthy individuals were tested by MIT researchers and it was found that they could have completely different responses to the same chemotherapy treatment.

The MIT team continued with this research by measuring the expression of each of the 48 genes in every cell line.  They measured the sensitivity of each gene to MNNG several times and found they were 94% accutrate in their results.  They followed by measuring responses to other common chemotherapeutic toxic agents that are typically used to treat cancer patients.  They have discovered how and why different patients react differently to the same chemotherapy treatments.  This means that chemotherapy may not be the right cancer treatment for every patient, it depends on their genetic reactions to MNNG and other toxic agents.

Glioblastoma, with an average survival rate of only five years, is the most common and aggressive type of brain tumor. It affects over 50% of all brain tumor victims and is infamous for being highly resistant to traditional cancer therapies, such as radiotherapy, chemotherapy, and surgery. Dr. Gordon Gribble of Dartmouth College has lead a team of researchers to discovering a high performance compound that can kill 50% of glioblastoma cells at its lowest dosages. In experiments run so far, this recently patented drug can out-perform current anti-brain cancer drugs on the market such as Procarbazine, Nitrosourea, and Carmustine. This new drug has a cytotoxic effect on cancerous cells by binding tightly to their DNA and poisoning the cell through a process called bis-intercalation, in which the DNA is double-binded and the cell cannot replicate because its DNA fails to unravel (due to the double binding of the two strands of DNA).

The figure above shows a green molecule bis-intercalated to DNA.  This demonstrates how the nucleotides can adjust their bonding in reaction to a chemical reagent.

The researchers are continuing to perform in vitro studies on this anti-brain cancer drug with a partnership through PhytoMedical Technologies, Inc. (located in Princeton, NJ).

For more detailed information, please see PhytoMedical’s press release.

-Amy Shah

John Hopkins University is the top biomedical engineering university in the entire nation. Their Urology Robotics lab has successfully built a robot out of plastic, ceramics, and rubber that is powered by light and air; therefore it can function during an MRI (magnetic resonance image) scan without disrupting the reading or breaking down. This robot can precisely remove an organ biopsy while the patient is in the MRI machine. This is important because it can improve the treatment of prostate cancer since prostate cancerous cells are extremely difficult to see outside of the MRI scan. This means that surgeons won’t have to perform a blind cut surgery on the patient.

WOW! No metal. No electronics.

-Amy Shah

Campath is a breakthrough drug used to help patients with chronic lymphocytic leukemia (CLL). CLL is cancer of white blood cells which leads to weakening of the immune system. It affects over 12,000 people a year in the United States alone and there is no largely successful therapy for it. The most common drug used in chemotherapy for CLL patients is chlorambucil, which only about 55% of all patients respond to. However, William Wierda, assistant professor of medicine at the University of Texas, encourages usage of Campath for chemotherapy on CLL patients. Although Wierda’s patients have been responsive, many people are spectacle of this drug because it’s usually involved in excess infectious. At the 48th American Society of Hematology meeting that took place from December 9th to 12th, proof was presented that 83% of test subjects responded to Campath. An amazing 24% of patients responded completely to Campath, which is an explosion compared to the mere 2% of patients that respond completely to chlorambucil. “We can’t really say we can cure this disease,” Wierda said, “but we can change it into something that is truly chronic such as diabetes.”

More Information On Campath

-Amy Shah

A Device for Ankle Physical Therapy for a Child with Leukemia

In 2005, about 1,790 U.S. residents were diagnosed with Acute Lymphoblastic Leukemia (ALL) (American Cancer Society, Inc. 2006). One third of every cancer case in children is diagnosed to be ALL. It is the most common disorder diagnosed in children, with peak ages between 2 and 5 years old (Satake 2006). ALL is a cancer of lymphoid white blood cells, the cells responsible for fighting infection in the body. Cancerous lymphoid cells cannot perform their usual function, so children with ALL get sick extremely easily because their bodies are not equipped to fight infections (National Cancer Institute 2002). The acute part of this disease indicates rapid growth of immature blood cells which occupy so much space that bone marrow is not able to produce new, healthy blood cells. If immediate treatment is not sought for ALL in children, the result is more than often death in a few months or even weeks (National Cancer Institute 2002).

Factors that May Cause Reduced Ankle Dorsiflexion in Childhood Leukemia

It has been proven that survivors of childhood ALL have reduced ankle movements when compared to healthy children. Reduced ankle dorsiflexion is a prevalent problem in childhood leukemia in which dorsiflexion (upward movement of the ankle) is damaged and has a limited range of motion. These victims can only move their ankles less than five degrees up and down. A person with healthy ankles should be able to move their ankles at least twenty degrees up and thirty-five degrees down to be able to perform all daily activities (Wright et al. 1999).

Chemotherapy, the most common treatment for childhood leukemia, is the introduction of cytotoxic (anti-cancer) drugs into the body to attack cancer cells. These drugs are generally delivered via the bloodstream so that they can reach cancer cells in any part of the body. The drugs will attack cancer cells by inhibiting their growth cycle or keeping them from dividing. Although this is a widely used treatment for ALL, and many other types of cancer, it does have many side effects that can lead to reduced ankle dorsiflexion (Cancerbackup 2006).

One of the most common side effects of chemotherapy in ALL patients is thrombocytopenia (decreased platelet count). Platelets are present in the blood to help clot blood when someone gets a wound, a decrease in the amount of platelets results in increased bleeding and bruising. When this happens in children, their parents are often hesitant to let their children play sports or even go to the park. When the child stays in bed or is sitting at home, their dorsiflexor and plantar flexor motions (downward motion of the ankle) are not being utilized (Anon 2006).

Another common side effect of chemotherapy is fatigue. This fatigue can be caused by anemia (reduction of red blood cells, which is another side effect of chemotherapy) or chemotherapy itself. Regardless, fatigue in children isn’t healthy because this tiredness is another factor that causes them to stay in bed or in a constant sitting position (Anon 2006).

Cardiotoxicity is also a side effect of chemotherapy. This occurs when the heart muscle is damaged and doesn’t pump enough blood throughout the body. Blood especially has trouble reaching the extremities and can make it difficult for a child to have enough energy to want to exercise that part of the body (Cancerbackup 2006).

When lack of physical activity occurs by decreased platelet count, fatigue, cardiotoxicity or for any other reason, it is a problem. Leaving the muscles in one position for too long can cause muscle atrophy. Atrophy is the loss of muscles tissue due to lack of use. When someone is not regularly physically active, their muscles literally shorten to an appropriate length for everyday use. This is what causes reduced ankle dorsiflexion. The muscles’ shortening restricts dorsiflexor and plantar flexor ankle movements and therefore causes reduced ankle dorsiflexion (Medline Plus 2005).

Common Physical Activities that may be Affected by Reduced Ankle Dorsiflexion

Since reduced ankle dorsiflexion can damage your ankle movement to only five degrees up and five degrees down, many daily physical activities are affected. Reduced ankle dorsiflexion also affects the calf muscles, which are responsible for jumping and sit and reach flexibility. Children with reduced ankle dorsiflexion will not be able to play volleyball. This has been proven through a study of patellar tendon health, which is affected by damaged dorsiflexion motion (Mallarias et al. 2006). This will also affect playing basketball, tennis, soccer, and many other sports that require a great amount of physical strain. Almost all activities will be limited by reduced ankle dorsiflexion because walking and stair-climbing are severely altered due to limitations on ankle movement (Wright et al. 1999).

Device to Practice Ankle Exercises to Prevent Reduced Ankle Dorsiflexion

To prevent reduced ankle dorsiflexion, appropriate exercise must take place everyday. The idea of a bouncing ramp has been proposed for a four year old victim to exercise on while she brushes her teeth. There is a current design out on the market called Prostretch, but this doesn’t have enough resistance to help increase ankle range of motion. This ramp is invalid due to the fact that it doesn’t exercise the full range of ankle motion. Although this ramp has a good active component when the patient bounces forward, the passive component of the ramp isn’t sufficient to exercise her because she is simply leaning back on her heals rather than plantar flexing (Kuzma 2005).

To create a device that sufficiently exercises the appropriate muscles, both active and passive components of muscles need to be considered (Herzog 2003). Dorsiflexion and plantar flexion need to be stretched to their full capacity with the appropriate resistance to this motion as well. To effectively do this, a special bicycle-like device has been proposed. This device will have pedals that are attached to gears that rotate with an adjustable resistance. This device does not have any wheels, however it must have a seat and handle bars.

Pedals: This device’s pedals are specially designed so that the patient cannot rotate them in a full circle unless she is pedaling at the proper angle. When she pedals down, the pedals will have resistance until she angles her ankle downwards exactly twenty degrees to practice plantar flexion. When she pedals back up, the pedals will have resistance until her ankle pushes upwards exactly thirty-five degrees to practice dorsiflexion. The patient’s feet will be strapped onto the pedals to ensure proper movement along with the pedal angles.

Resistance: The resistance of these gears can be adjusted by the patient’s parents according to her weight and strength. Resistance adjusts simply just like the hand gears on a bicycle.

Seat: The seat will be raised higher than a normal bicycle so that the patient can keep her legs almost straight. This is because on a normal bicycle, one exercises their thigh muscles, but by increasing the height of the seat, the patient will be forced to pedal with her ankle motion rather than her full leg motion.

Balance: The handle bars are for balance because this device is meant for young children. This device can be mounted into the ground to provide further stability. This is so that the patient will not fall off of the device if she fools around.

Entertainment: Due to the balance of the device, the patient can watch television while exercising. There will also be a display screen in the middle of the handle bars with the alphabet running across it. This screen will also indicate the number of calories burned and how long the patient has been exercising for.

This device will sufficiently exercise the passive and active components of dorsiflexion and plantar flexion.

To measure the whether or not the amount of exercise is successful on dorsiflexion and plantar flexion, a device called chatillon dynamometer is available. This device can be used anywhere at anytime. The patient’s foot must simply be placed flat on the ground. Someone then needs to hold the device directly below her toe line and instruct her to raise her foot with her heal remaining on the ground. The chatillon dynamometer then measures the resistance of the foot to the machine and calculates the force exerted by the foot. This machine can also measure plantar flexion motion (Anon 2005).

Even if the patient uses this device everyday, there are also other factors that need to be considered to keep her healthy. She needs to keep a well-balanced diet because children on chemotherapy often have fluctuating weight and poor nutrition. This is because chemotherapy alters the metabolism of nutrients so that fats, carbohydrates, and proteins are metabolized too quickly (Picton 1998). To avoid depression, children are encouraged to play outside and visit friends daily. Chemotherapeutic drugs often cause depression and physical activities raise the levels of serotonin in the body to keep people happy and healthy (Anon 2006). The most important thing that a patient can do to avoid reduced ankle dorsiflexion is to stretch and jog. Studies have shown that less than fifteen minutes of stretching a day can increase dorsiflexion range of motion (Radford 2006). Overall, this young patient can live a normal life with the proper combination of chemotherapy, exercise, diet and emotional support.

-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