Question 1: Discuss the practical implications that genetics research is playing in our lives today. Discuss where is might lead us in the next 10 years.

First Place

Kristin Young (11)
Athol High School

As I spin around in my computer chair, I see many different things. I see a picture of my friends, one of whom has watched her mother battle breast cancer over the last few years. Through the doorway I spot my parents making salad out of, what I feel safe assuming are, genetically modified vegetables. Then I pass by the television, knowing that, were I to turn it on, I could probably catch a news story about one of the many continually emerging biological controversies of today. The one thing that all of these thoughts have in common is the same thing that every living being has in common: genetics. Everything from a weed to an elephant has DNA, and advancements in the field of genetics are helping us to understand and, in more recent years, manipulate these complex macromolecules that determine who and what we are.

Work on genetics began in the middle of the 19th century with experiments such as Gregor Mendel’s careful statistical analysis of pea plant traits over generations of hybridization (Spangenburg). Through the 20th century, more information about genes came to light as technology advanced and scientists such as William Bateson and Thomas Hunt Morgan continued to experiment and analyze in the same way Mendel had (Spangenburg). Today, some of the breakthroughs of these early geneticists are common concepts for any biology class, but modern genetics developments are influencing many aspects of our lives.

Many foods in our grocery stores are in some way genetically modified. Plants can be altered genetically to be more nutritious, cheaper to produce, and resistant to many forces that can lower crop yield (Morris). Questions have been raised as to how safe and how ethical this ability to tamper with products of nature is, but, for the time being, many unsuspecting Americans are less concerned about their consumption of these subjects of strong debate and more worried about the more obviously consequential role genetics research plays in our lives.

Medical advances are almost definitely the most important way in which genetics research is affecting our lives today. With the aid of advanced technology, scientists are able to pinpoint specific genes that cause thousands of diseases. For example, we know that there are genes on chromosomes 1, 14, 19, and 21 that can all contribute to Alzheimer’s disease (Wynbrandt). This knowledge allows for early diagnosis, but, unfortunately, that only lets us start treatments that will make the disease more bearable. It allows for earlier use of drugs known as cholinesterase inhibitors, which help slow “the breakdown of acetylcholine, a neurotransmitter that occurs in abnormally low levels in patients with Alzheimer's” (Turkington). These drugs can help to slow the development of early stages of Alzheimer’s by keeping the levels of acetylcholine up, allowing the brain to transmit normally for longer, but they’re no cure (Turkington). Similar situations exist for large numbers of other disorders, and though there is no current cure for Alzheimer’s and these many other genetically linked diseases, the future of genetics is very bright, and we are learning more every day.

I firmly believe that the one thing genetics research requires most for more significant advances is time. It doesn’t seem as if we don’t know things because we don’t have the proper tools or knowledge to figure them out. I think that they just haven’t been discovered yet. It takes time to notice patterns and draw proper conclusions, which is exactly what scientific discovery is all about. It may take decades for scientists to figure out whether or not GM foods and certain genetic treatments are safe because they must observe whether or not people who have eaten the foods or received the treatments are negatively affected. And if these things do appear to be safe, I think, more than anything else, it will take time to convince the general population that these innovations are not physically dangerous, and it will take even longer for people to decide (if they ever do) that these advances are ethical. Over another ten years of time, I believe that, once they have been proven safe, gene-therapy will be a common treatment and possible cure for many diseases, and advances in epigenetics will provide a way to drastically improve the health of those with genetic diseases without actually changing their genes. It may mean more controversy over morals and more doubts about safety, but I believe that the pros of genetics discoveries will eventually outweigh the cons. All we need is time.


Morris, Jonathan. "Ethics and Politics of Genetically Modified (GM) Foods." The Ethics of Biotechnology: Biotechnology in the 21st Century. New York: Chelsea House Publishing, 2005. Science Online. Facts On File, Inc. 14 March 2008. 

Spangenburg, Ray and Diane Kit Moser. "Discovery of Heredity and Genetics." Modern Science: History of Science. New York: Facts On File, Inc., 2004. Science Online. Facts On File, Inc. 13 March 2008. 

Turkington, Carol. "Drug Treatments For Alzheimer's Disease." The Encyclopedia of Alzheimer's Disease. New York: Facts On File, Inc., 2003. Health Reference Center. Facts On File, Inc. 14 March 2008. 

Wynbrandt, James and Mark D. Ludman. "Alzheimer's Disease and Genetics." The Encyclopedia of Genetic Disorders and Birth Defects, Second Edition. New York: Facts On File, Inc., 2000. Health Reference Center. Facts On File, Inc. 13 March 2008. 

Second Place

Elaine Chung (11)
Montgomery Blair High School

Using Genetics to Find the Right "Fit"

What do running shoes and prescription drugs have in common? Running shoes are clearly not one-size-fits-all, but depending on the shape of your feet and how they hit the ground, you will need a different shoe, specialized to fit you. Have flat feet? You might want a pair of motion control shoes. High arches? A neutral cushioned shoe may help. Wide feet? You might want to avoid brands whose shoes tend to be more narrow, or opt for a wider version of a shoe. Even among these categories of shoes, not every shoe will be a perfect fit. A shoe may need to be more flexible or more cushioned depending on the runner.

Similarly, different drugs and dosages are needed for patients depending on many factors, especially their genes. Last May, after receiving warfarin to treat a blood clot in her lungs, Karen Schmale had to return to the hospital to treat excess bleeding caused by the drug (Mathews). Although the gender, age, and weight of a patient can influence the optimum dosage of warfarin, the expression of two genes, CYP2C9 and VKORC1, determines “about 40 percent of a person's response to the drug” (Brown). The two genes control the speed at which the drug is “burned off” and affect how sensitive the patient is to the drug. Schmale’s reaction to warfarin was a result of a variation in these genes. Because of patients like Schmale, the U.S. Food and Drug Administration (FDA) updated the label for warfarin this August, warning that “people with variations of the genes CYP2C9 and VKORC1 may respond differently to the drug.” A month later, the FDA approved a genetic lab test that identifies variations in the two genes. With the results of this test, physicians can prescribe patients a specific dosage to strike a balance between blood clots as a result of too little warfarin, and excess bleeding as a result of too much. Combined with a regular prothrombin time test to check how the blood is clotting, the risk of excess bleeding due to warfarin will be much lower in the future.

Since a third of the two million warfarin-receiving Americans react differently to the drug than expected (FDA), personalizing the drug dosage is a necessary step in reducing its risks. In the coming years, more studies can be conducted on the genetic similarities between patients with adverse reactions to other common drugs. These comparisons may point out genes that play a role in determining the drug’s effectiveness and reactions in the body. If these studies can find genes that affect the sensitivity of a patient to a particular drug, then physicians will be able to give patients a personalized dose, or even recommend the patient a different drug altogether.

Genetic testing is a necessity in personalizing medications. In the future, with more genes being identified that affect a patient’s reaction to a drug, people will no longer have to take a genetic test for each drug. Instead a more efficient approach would be to simply map the patient’s genome. This advancement can lead to a positive feedback cycle; with more patients getting their genomes mapped, scientists will be able to identify genes that determine how patients react to medications, thus giving people more of an incentive to get their genomes mapped.

An ill-fitting running shoe can lead to injury. Likewise, a drug whose dosage is not “fitted” according to a patient’s genes can be dangerous as well. As scientists continue to research genes and their effect on how patients react to medications, identifying the right drug for a patient may become as easy as finding the right shoe. Medications tailored to your specific needs are not far in the future.


Brown, David. “For the First Time, FDA Recommends Gene Testing.” Washington Post. 17 Aug. 2007.

“FDA Clears Genetic Lab Test for Warfarin Sensitivity.” U.S. Food and Drug Administration. 17 Sep. 2007. 1 Jan. 2008 .

Mathews, Anna Wilde. “In Milestone, FDA Pushes Genetic Tests Tied to Drug.” Wall Street Journal.

Third Place

Christian Fagel (12)
Archmere Academy

Health care in the US is founded primarily upon the relatively inefficient method of reacting to symptoms as patients encounter them. From brain tumors to heart disease, various illnesses are rarely detected until patients become physically aware of the symptoms and see their physicians for diagnosis. This problem of delayed discovery and intervention often results in less effective treatment as the small window of opportunity during which the disease could be most easily stopped had most likely passed. Furthermore, our current methods of treatment and administration of drugs are rather indiscriminate. About 100,000 cases per year results in adverse reactions due to usage of mass-produced, “one-size-fits-all” drugs (Philipkoski).

The condition of our health care system will change dramatically over the coming years as genetic and genomic research continues to advance. The Human Genome Project, an effort to identify all the genes in human DNA and determine its sequence of 3 billion chemical base pairs, was completed on April 14, 2003 (Human Genome Project). This full set of genes does not provide sufficient information to begin treatment planning; however, it affords a foundation from which to continue analysis. This continued examination is in the study of single nucleotide polymorphisms, or SNPs. These variations in the genetic code occur only at certain places, in certain individuals (Genovations). Many SNPs have no effect on our health, but some can predispose us to disease or influence our response to a food or drug. About 1.8 million SNPs have been identified so far (Human Genome Project). Continued study of the human genome will help us understand the genes’ expressions and resulting functions subsequently allowing us to apply genomic information to the diagnosis and treatment of diseases (Genomic Health). Additionally, our study of the human genome will confer us the ability to define disorders by their genetic basis, rather than by their symptoms alone.

The knowledge obtained through genomic research will undoubtedly change the face of health care significantly. DNA tests in the future can provide physicians with critical information to better prevent or treat disease. Examination of each individual’s genetic makeup for problem-causing SNPs in conjunction with careful analysis of their current medical records, family history, and lifestyle will provide a more accurate portrayal of the patient’s predisposition to disease. Armed with this invaluable intelligence, doctors can more effectively promote the health of their patients in the long term through diet management, lifestyle alteration, and drug administration. The phrase “preventative medicine” will take on a new, revolutionary meaning as physicians tailor their patients’ treatment plans to combat their specific health risks before disease even develops. For instance, presymptomatic medical therapies such as antihypertensive agents can be dispensed before hypertension arises or regiments of diet and exercise can be assigned to diabetes prone patients thus stalling or even completely preventing the onset of the disease. In addition, access to patients’ genetic variations will allow doctors the capability to determine whether a patient will have an adverse reaction to a certain treatment. Also, this genetic information will allow doctors to give personalized medication capable of treating chronic conditions that were previously unresponsive to conventional treatment (Genovations). This method of targeted gene treatment coupled with the preventative benefits that genomic health care provides, will indoubitably increase the quality of life and prolong its duration.

On a nationwide scale, the switch to genomic health care will mean alterations in personnel training. In order to make sense of genetic tests and devise an appropriate treatment strategy, physicians will need to take into account the patient’s environmental influences and behavioral tendencies such as bed rest or use of oral contraceptives. Regulated training on genetic test interpretation will be necessary in order for genomic healthcare to become implemented nationwide (Brower). Despite the negative repercussions that genomic healthcare may bring to the United States, they are greatly outweighed by the potential benefits of improved life and disease prevention.


"About the Human Genome Project." Human Genome Project. 7 Dec. 2005. U.S. Department of Energy Office of Science. 27 Jan. 2008.

Brower, Vicki. "Genomics and Health Care." EMBO Reports. 2004. The European Molecular Biology Organization. 26 Jan. 2008.

"Patients Guide to Genomics." Genovations. 2002. Great Smokies Diagnostic Laboratory. 27 Jan. 2008.

Philipkoski, Kristen. "Health Care: Genomics' Final Act." Wired. 28 June 2000. 27 Jan. 2008.

"SNP Fact Sheet." Human Genome Project. 9 July 2007. 27 Jan. 2008.

"Understanding Genomics." Genomic Health. 2008. 26 Jan. 2008.

Question 2: If you were a genetics researcher, what would you like to study and why?

First Place

Laura Irei (11)
Aracdia High School

Alzheimer’s is a disease that afflicts about four million Americans, including my two surviving grandparents. Over the past five years I have watched first one and then the other struggle with the forgetfulness, withdrawal, and loss of independence that manifest themselves in Alzheimer’s disease. They have difficulty recognizing me and remembering conversations we have only moments before. Simple, everyday tasks have become laborious chores that others must help them execute. Alzheimer’s is the most common disease to affect the adult brain and takes its toll on families across the globe. Research is being done to accumulate knowledge of the disease and explore possible methods for preventing or alleviating its symptoms. If I were a human genetics researcher, I would find it thrilling to be a part of the encouraging headway being made in the research of Alzheimer’s disease.

Alzheimer’s disease is one type of a class of disorders clinically known as “dementias”. It is a progressive disease affecting the brain and eventually resulting in death, usually seven to ten years after diagnosis. Nerve cells in the brain die as a result of certain pathological events, especially plaques and tangles. Plaques consist of a protein called beta amyloid, of which high amounts build up in the brain and clump together. Tangles consist of a protein called tau, which becomes chemically altered and accumulates tangles that prevent it from functioning in the nerve cells. Dr. Alois Alzheimer observed these aberrations of the brain when examining brain tissue from a post mortem patient who suffered from dementia. Some people may have a genetic predisposition to develop Alzheimer’s disease. “Familial” Alzheimer’s disease is the result of mutated genes, and causes the early onset of the disease. Another genetic risk factor besides mutation is the inheritance of the ApoE4 gene, a variant of the apoE gene. If a person inherits one ApoE4 gene from one parent, they have three times the risk of suffering from Alzheimer’s disease. If they inherit an ApoE4 gene from both parents, their risk increases to ten times. When the patient crosses a certain age threshold, it triggers the genes to become activated and the disease to develop. However, not everyone with this gene develops Alzheimer’s disease, and scientists are searching for even more definitive genetic answers as well as treatment possibilities.

Stem cell research is occurring for Alzheimer’s disease. Stem cells are stimulated to become nerve cells by growth factors, and then implanted into the brain to replace damaged nerve cells. It is also theorized that resident stem cells can become nerve cells spontaneously and assist areas of the brain where there has been cell loss. This may become an area of long-term research for Alzheimer’s disease. Other research is being conducted with Nerve Growth Factor, a substance that is involved in keeping nerve cells healthy. Scientists are implanting genetically engineered cells that produce Nerve Growth Factor into the brains of animals, and results are positive. This exciting research is still occurring, and hopefully new breakthroughs will be achieved in the future.

If I were a human genetics researcher, I would search for genetic risk factors for Alzheimer’s disease. I would select a large test group of people suffering from Alzheimer’s disease and sequence their DNA. I would then compare their DNA and locate areas that they have in common. I would also sequence the DNA of people not suffering from Alzheimer’s disease as control group. In this way, more genes could be discovered that contribute to the development of Alzheimer’s disease. Treatment could be tailored to fit patients’ specific genetic makeup and people could be more accurately tested for their genetic predisposition to developing the disease.

I believe that the research occurring for Alzheimer’s disease is incredibly important. As the baby boomers age, the number of people with the disease will increase. The cost of the disease, both financially and socially, will be overwhelming. The more effective treatments developed, the better. Screening processes will also improve, enabling doctors to make accurate diagnoses in the earlier stages of the disease. I think that more will be learned on the inheritance of Alzheimer’s disease through genes. This will mean that people might be tested for certain genes and told their likelihood of developing the disease. They could then be given preventative treatment and have a treatment plan tailored to fit their needs. Alzheimer’s is a devastating disease affecting millions of people, and research on this topic is crucial.


Antuono, Piero. “Current Research on Alzheimer’s, Memory Loss, and Aging.” (Online) Available, March 3, 2008.

Diamond, Jack. “A Report on Alzheimer’s Disease and Current Research.” (Online) Available, March 3, 2008. 

Second Place

Briana Skalski (12)
Archmere Academy

An Alternative to Alzheimer’s

The human nervous system is the epicenter of everything that is human, while the brain is the powerhouse, the control room. When this control system goes awry due to genetic abnormalities, fascinating, yet deadly changes may occur. Scientists recognize that thousands of diseases and conditions are the result of this genetic misinformation. The prevention and cure for these diseases may come with an understanding of how these genes function. My grandfather passed away recently due to this disease, thus my father is concerned with the recognized hereditary implications. If I were a genetics researcher, I would study the genetics of Alzheimer’s disease.

My Dad has a right to be concerned, as do I, because “people with at least one first-degree relative (parent or sibling) with Alzheimer’s disease are 3.5 times as likely to develop the disease” (Adams). At least 25% of all Alzheimer’s disease patients have a familial form of the disease, while other instances are considered random forms. The disease is characterized by memory loss, speech difficulties, behavioral changes, confusion, restlessness, and complications with daily activity. Mutations in several genes results in this often hereditary disease. Although scientists do not know the genes responsible for late onset of Alzheimer’s, they do know the gene mutations that trigger early onset of the disease. All the early onset gene mutations are inherited in “a dominant fashion” (Adams). They include presenilin 1 (PS1), presenilin 2 (PS2), and APP. The APP gene is responsible for making amyloid precursor protein; however, the six mutations of this gene will create beta amyloid protein, a segment of the amyloid precursor protein and also a component of the amyloid plaque that builds up in the brain of an Alzheimer’s sufferer. Scientists are uncertain of the role of the gene PS1 in our bodies; however, they have recognized at least 40 mutations of this gene that cause about 50% of early onset Alzheimer’s. As expected, PS2 gene and PS1 gene have similar genetic sequences; in turn, scientists are unsure of PS2’s role in the body. Differentially, mutations in the PS2 gene are very rare and at times the mutations do not cause Alzheimer’s disease; thus, researchers suggest that mutations of this gene cause a weak form of the disease.

Researchers today have found that genetic therapy can affect the progression of Alzheimer’s. Scientists have successfully injected patients with skin cells genetically altered to rejuvenate neurons. As a genetics researcher, I would like to pursue further research on gene therapy. My experiments would focus on the human APP gene, the gene responsible for the build up of amyloid plaque. The mutated gene damages neurons by producing a mutated amyloid precursor protein which blocks protein transports in the mitochondrial membrane of neuron cells. The blockage makes it impossible for mitochondria to import proteins and produce metabolic energy, causing the neuron to die and plaque to build from beta amyloid protein. Scientists are unsure what characteristics of the protein create blockage within mitochondria of neurons; however, they are led to believe the blockage results from its partial negative charge or large size as a result of improper protein folding. Interestingly, one of the six APP gene mutations does not create a blocking amyloid precursor protein. In my experiment, I would like to analyze six groups of mice, each with one of the six APP gene mutations. First, I will work with the mice with the mutated APP gene that does not block mitochondrial pathways. With information on the genetic sequence, I will compare it to the other five sequences and decipher the reason for the blockage, whether it is the negative charge or incorrect folding of the amyloid precursor protein. After successfully isolating the part of the sequence causing the harmful blockage, I will use RNA interference (RNAi) to silence the gene. Silencing the gene will make it unproductive in nervous tissue, yet productive and harmless in other tissues. If successful, this experiment will partially solve one of Alzheimer’s related gene mutations.

Alzheimer’s affects more than 5 million Americans alone, and by 2050 this number is expected “to more than triple” (U.S. Medicine). With knowledge of the symptoms and causes of this disease, some patients may be able to avoid the earlier stages of Alzheimer’s through genetic therapy or by actively using their minds working through crossword puzzles etc. Although my suggested experiment potentially corrects only one aspect of the disease, it could hopefully preserve someone’s memory and improve their quality of life for many more years.


Adams, Amy. Alzheimer’s Disease: Genes Can Cause Alzheimer’s Disease. 3 Sept 2000. Genetic Health 2000-2001. 3 Jan. 2008. 

Bradt, Steve. Alzheimer’s protein jams mitochondria of affected cells; resulting ‘energy crisis’ kills neurons. 14 Apr 2003. University of Pennsylvania. 18 Jan 2008. 

Hitti, Miranda. Alzheimer’s Gene Therapy Slows Mental Decline. 25 Apr 2005. WebMD Medical News: Alzheimer’s Disease Health Center. 18 Jan 2008. 

Panno, Joseph. Gene Therapy: Treating Diseases by Repairing Genes. New York: Facts On File, 2005.

Russell, Doug. Preventing & Treating Alzheimer's: Prevention, Treatment & Slowing Down the Progress. 18 Dec 2007. 18 Jan 2008. 

U.S. National Library of Medicine. Alzheimer’s Disease. Oct 2006. Genetics Home Reference: Genetic Conditions. 3 Jan 2008. 

Third Place

Razan Dababo (10)
Mercy High School

About a century and a half ago, in an abbey garden, a monk named Gregor Mendel commenced a breeding experiment that shed light on the “heritable factors” that are passed from parents to offspring. According to the Mendelian model of inheritance, discrete factors, known today as genes, account for traits present in offspring. However, it is evident today that genes and the sequence of bases found in DNA are not the sole determinants of traits. Epigenetics, an emerging science, confirms that a variety of factors, including chemicals, influence gene expression, and thus, phenotype and predisposition to disease. A clear understanding of and extensive experimentation on these external factors and how they affect gene expression holds great therapeutic and scientific potential, and as a genetics researcher, this would be a field I would definitely investigate.

A myriad of epigenetic interactions have been identified by researchers, including histone acetylation. Chromatin is composed of tightly packed nucleosomes. Each nucleosome consists of DNA wrapped around histones (proteins), which have protruding tails. The tight binding of nucleosomes to one another prevents transcription agents from interacting with the gene. During acetylation, acetyl groups are joined to histone tails, and this process loosens the tight coiling of nucleosomes in chromatin, thus allowing transcription agents to access the gene. This phenomenon poses two crucial questions: (1) Can one apply enzyme inhibition to prevent acetylation of certain genes that cause disease? And (2) Can one deacetylate disease-causing genes so that they are no longer transcribed? As a researcher, I would focus on answering these questions through experiments on mammalian cell cultures genetically predisposed to disease.

Another interesting epigenetic process is DNA methylation. This process involves the attaching of methyl groups to specific places in DNA, such as CpG sites (sections of DNA in which a cytosine nucleotide is followed by a guanine nucleotide). Methylating CpG sites present within promoters of genes (regions of DNA that signal where to launch transcription) can silence the genes. For instance, when researchers analyzed identical genes of different tissues, they noticed that the greatly methylated genes were usually not expressed. Furthermore, researchers have observed that some proteins that attach to methylated DNA sites also recruit enzymes that deacetylate histones. Hence, researchers have arrived at a dual theory, in which DNA methylation and histone deacetylation function together to repress transcription, and thus gene expression. Using DNA methylation and deacetylation to treat cancer is an intriguing idea which I deem holds great potential. As a researcher, I would attempt to methylate and deacetylate oncogenes of cancerous mammalian cultures while removing methyl groups from tumor-suppressor genes. Such an experiment is bound to yield results for cancer treatment.

Gene expression could be inhibited by yet another process—RNA interference. The RNA interference pathway was first discovered by biologists who observed that when double-stranded RNA molecules were injected into a cell, genes with complementary bases to those RNA molecules were silenced. This silencing occurs in a multi-step process. First, double stranded RNA is injected into a cell, where it is immediately cut by an enzyme into short interfering RNAs (siRNAs). These siRNAs join a silencing complex known as RNA-induced silencing complex (RISC). RISC then finds and destroys complementary messenger RNAs. Destroying messenger RNA is in effect silencing the gene from which the messenger RNA was transcribed; if there is no messenger RNA, there is no protein. If RNAi could be used for mammalian therapeutic purposes, it would revolutionize the way we look at medicine. It may pose expense issues, but its potential benefits outweigh all disadvantages. Its sequence-specific nature might allow researchers to inhibit precisely the unwanted expression of certain genes, such as oncogenes. This would yield major breakthroughs for treatments of fatal and debilitating diseases such as cancer.

Apparently, mapping the human genome was definitely not the concluding step in understanding human genetics. Genes are far from being unchanging, mechanical units; in fact, they are very interactive. Their interactions with each other and their surrounding environment affect their expression. Chemical modifications are capable of interfering with protein synthesis, either by turning genes off directly or rendering chromatin difficult to loosen. Chemical interactions such as these comprise epigenetics. Understanding epigenetic processes is crucial for unlocking hidden therapies. It holds enormous potential, both scientific and therapeutic. Understanding the role of RNA in inhibiting gene expression is equally important. RNA interference offers an effective and specific way to destroy a gene’s message. Indeed, the Human Genome Project was just the first step in unlocking the mystery of genetics.


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