Academy Scientific JUNE 2011
NAKED MOLE RATS
MEMORY OF BCA TEACHER
MICROBIOLOGY: GERM THEORY CONNECTIONS TO MEDICINE
CANCER STEM CELLS
NEW KIDS ON THE BLOCK
FOUNDING OF THE ACADEMY SCIENTIFIC
HISTORY IN THE MAKING
Academy Scientific Editor-in-Chief and Founder Aishwarya Raja Publisher and Layout Editor Emily Tu Managing Editor Tom Silver Publisher Emily Tu Co-Features Editors Jenny Yoon, Ryan Lee, and Michelle Rudshteyn Co-World News Editors Elizabeth Dente and Janet Park Co-School News Editors Jenny Chen and Maria Ilina Co-Photography Editor Simran Arjani and Anna Geduldig Webmaster: Jenny Chen
BERGEN COUNTY ACADEMIES 200 HACKENSACK AVE. HACKENSACK, NJ 201-343-6000 WWW.BERGEN.ORG 2 | ACADEMY SCIENTIFIC VOL 1.1
On the front cover: A cytotoxic lymphocyte (yellow) besides a large tumor cell. On the back cover: An image from BCAâ€™s SEM of BDCM (leukemia) cells.
contents Founding of the Academy Scientific
The Editor-in-Chief reflects on BCA’s new scientific journal.
Dr. Ostfeld Ryan Lee A BCA student reflects on the loss of Dr. David Ostfeld, a BCA chemistry teacher and the Dean of Admissions.
Jisoo Kim, Aishwarya Raja, Greg Loshkajian, Ana Song, Michelle Rudshteyn, and Elizabeth Dente
The recent scientific and technological advances, ranging from Provenge to global warming, are creating a buzz in the media.
11 Defining Cancer Jenny Yoon
This feature explores the meaning of cancer and discusses the more commonly seen types. FEATURE
13 Cancer Stem Cells Emily Tu
The dangers of cancer stem cells, their origins, and future applications interest researchers everywhere.
20 Why Anti-Cancer Drugs Are Flawed Andrew Cho
16 Customizing Blood Cells Jenny Yoon
Breakthroughs in leukemia treatment will improve the lives of millions of patients. FEATURE
18 The Incredible Mr. Naked Mole Rat
This feature discusses the downsides of current cancer treatment, and potentially devastating effects of anticancer drugs. FEATURE
22 Photos from BCA’S SEM
These photographs were taken with BCA’s scanning electron microscope, ranging from astrocytes, starshaped brain cells, to BDCM cells, cytotoxic lymphocytes.
David Heller and Stephanie Jeong
A cancer superhero sparks new research into the disease.
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23 Redefining Microbiology Michelle Rudshteyn Researchers are discovering bacteria in the most unlikely of places, leading to new breakthroughs in medicine.
26 Academy Abstracts
Thomas SIlver, Aishwarya Raja, Elizabeth Dente, and Michelle Rudshteyn
Featuring student research conducted at BCA, Academy Abstracts features project abstracts written by students.
28 Student Interview Interview conducted by Ariana Aimani
Bhasha Mukhopadhay talks about her senior internship.
30 Dr. Pergolizzi
Interview conducted by Aishwarya Raja Dr. Pergolizzi talks about his career, education, and humorous life experiences.
32 School News Teresa Fan and Jenny Chen
Recent news of BCAâ€™s math team and their successes.
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founding of the academy scientific In November of 2010, I approached Dr. Pergolizzi with a seemingly obvious question. If our school focuses so profoundly on the sciences, then why do we not have our own science journal? With rival schools like Thomas Jefferson already publishing their own scientific journals and winning numerous awards, it only seemed judicious that our school make a mark on the scientific world with a journal of our own. As I collaborated with Dr. Pergolizzi, my idea took off and I knew I was really onto something great. After eating a couple pieces of congratulatory Halloween candy from Dr. Pergolizziâ€™s desk, I began working with Tom Silver and the Research Club to officially establish the Academy Scientific. As Managing Editor, Tom helped me recruit a team of willing and ebullient students who were more than ready to take on a leadership role in the journal. One recruitment meeting later, we had a staff of 14 members who were extremely excited to found the very first scientific journal at BCA. We held weekly staff meetings and discussed the responsibilities of each position on the staff. The work was divided up and deadlines were established. Before we knew it, December break was fast approaching and time was running out. To meet the deadlines, we were forced to work quickly and efficiently, two adverbs that we, BCA students, were very familiar with. As it turned out, the process of publishing this first issue was definitely not as easy as I thought. Unwanted factors like time crunches, lack of sleep, and confusion struck the staff, and I often felt overwhelmed by how much work we still had left to complete. From finding content to laying out the issue on InDesign, the tasks were endless but time was not.
Brown/Photo Researchers, Inc.; Omikron/Photo Researchers, Inc
This photograph taken in 1953 shows Watson (left) and Crick (right) posing with one of their original models of DNA.
Now, as I look back on the last three months, I cannot help but feel overwhelmingly satisfied at how much we actually achieved. Just as Watson and Crick built the first DNA model, the Academy Scientific staff built the schoolâ€™s first comprehensive and visually appealing scientific journal, an accomplishment that will live on as our legacies.
I cannot thank the staff, the contributing writers, and Dr. Pergolizzi enough for their efforts. Because of them, this remarkable first issue was published and hopefully many more just like it will be published in years to come. By Aishwarya Raja, a junior in AMST and the Editor-in-Chief
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dr. ostfeld (1942 - 2010): a personal reflection To me, Monday was more of a shock than a tragedy, more so than any other event that happened over the course of my four years at BCA. Yesterday passed by in a daze; I was only coherent enough to send an e-mail to the Chemistry Team in memory and gratitude of someone who I still couldn’t believe I would never see again. Only today, twenty-four hours after the fact, has the real sadness set in - and I’m sure even that will pale in comparison once I return to school and realize as I pass Dr. Ostfeld’s office that he won’t be sitting there any longer. Why such surprise? Well, for one thing, Dr. Ostfeld was more of a father figure and mentor to me than anyone else I’ve ever met. With my father living and working in South Korea since I was in fifth grade, I was and am so grateful to find someone with whom I shared so many interests. They extended far beyond simply chemistry: in the months preceding the National Chemistry Olympiad Study Camp last year, I would regularly stop by and sit in his office to chat about everything from a recent article we had read Dr. Ostfeld (L) with Dr. Mayers (R). in The Atlantic to Sibelius’ Violin Concerto. We would
both stop and ponder the cosmos as we discussed recent developments in physics, debate the merits of the new iPad, or marvel at some breathtaking orchestration of the “Rite of Spring”. And as I listened to him talk, I never failed to regain a sense of composure and mirth, no matter what the situation. A long story short, it was to Dr. Ostfeld I looked for advice on everything from chemistry to personal matters. And as Dr. DeWitt (L) with Dr. Ostfeld (R). all children secretly and fervently believe, such paternal figures will always be there to watch over us - right? As seemingly embarrassing as it may sound, Dr. Ostfeld was that Marvel superhero to me that could never be vanquished; whatever trials arose, he would always bounce back the next day with a renewed vigor and an amused smile on his face. Yet the fact is, even our childhood heroes must age, and we are certainly not incarnations of Superman. And one day, I, too, will accept Dr. Ostfeld’s passing and be even more grateful for the time that I did get to know him. Perhaps this reflection was one step towards that final equanimity or perhaps not. But if it achieves one thing, I hope that it is to let the remembrance of Dr. Ostfeld live on in our memories - a remembrance not simply of an AP Chemistry teacher or admissions dean, but of a mentor whose intellect and personality soared the cosmos and sailed down to reflect all his well-earned counsel for the benefit of his students. Dr. Ostfeld, rest in peace.
By Ryan Lee, a senior in AAST and the Features Editor
Dr. Ostfeld with Dr.Grieco in front of the Hackensack River.
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Photos courtesy of Dr. Don DeWitt
UPDATES REGARDING THE SCIENCE, TECHNOLOGY, AND MATH NEWS AROUND THE WORLD
Ancient African Lizard: Ancestor of the Komodo Dragon? According to researchers at the University of Alberta, an ancient lizard in Africa and today’s widely known Komodo dragon in Indonesia may actually be long-lost relatives. Although the ancient lizard fossil is estimated to be about 33 million years old and its cousin, the Komodo dragon, has only been around for 700,000 years, the distinct connection between the two lies in the similar and unique shapes of their vertebrae. The old fossil believed to be of the lizard genus Varanus Brown/Photo Researchers, Inc.; Omikron/Photo Researchers, Inc was found in a desert This is a komodo dragon from the Thoiry Zoo in France. in Africa, land that had once been the bottom of a lake. According
to the fossil’s discoverer, biologist Rob Holmes, “Whether the animals lived in the water or surrounding land, we don’t know, but we do know that some modern day species of Varanus are comfortable swimming in fresh water.” Holmes’ claims that the African vertebrae fossils belonged to a lizard that had the ability to swim. This just might answer the question of why the two creatures could possibly be linked together. Even biologist Alison Murray claims, “From about 100 million years ago until 12 million years ago, Africa was completely isolated, surrounded by ocean, but somehow they got out of Africa during that period.” Her views on ancient world geography may explain why the animals, which were worlds away from each other at different points in history, share such a special connection. However, time will only tell if a conclusive result can be determined from this extraordinary find. Until then, these long-lost relatives might as well get to know each other.
By Jisoo Kim, an junior in AVPA
Season of Birth Linked to Dramatic Differences in Personality According to a recent study published in Nature Neuroscience on December 5, the season in which babies are born may have a long-term effect on how their biological clocks run. Douglas McMahon, Professor of Biological Sciences at Vanderbilt University, as well as other students at the university, suspect their experiment to provide one of the first pieces of evidence of seasonal imprinting on mammalian biological clocks. The study was conducted on a special strain of baby mice that produces a fluorescent green protein which glows when the biological clock neurons are active. It may provide an answer for why babies born in the winter have a higher risk of certain neurological disorders such as seasonal affective disorder Public Domain (winter depression) and schizoThe internal biological clock monitors time and brings about changes that phrenia than those born in the influence the body. spring.
The strain of mice were subject to different artificial seasonal light cycles for three weeks until they were weaned; the cycles mimicked the various seasons including summer, winter, and equinox. After the mice were weaned, researchers switched the environment the mice were in for another 28 days as they matured, and then placed the mice in an environment of continuous darkness. The scientists then monitored the activity of the mammals’ master biological clocks, which are situated in the middle of their brains in the suprachiasmatic nucleus (SCN). It was at this stage in the experiment that researchers discovered a groundbreaking difference between summerborn and winter-born mice. They learned that the variations in the activity of the mice in the different cycles were produced by changes in the activity patterns of the individual neurons. McMahon concluded that the biological clock was indeed affected by the amount of light received by the mice at the time of birth.
By Aishwarya Raja, a junior in AMST and the Editor-in-Chief
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The Deeper Layers of Global Warming It seems that the greenhouse effect – the increase of carbon in the atmosphere that prevents heat from leaving the earth - has a much more complex effect on the Earth’s temperature than previously known. Studies published in November from NASA’s Jet Propulsion Laboratory show that the world’s largest lakes are in fact warming, but at significantly different rates.
The studies, led by Dr. Simon J. Hook and Philipp Schneider, utilized temperature data taken from 1987 to 2009 of 104 lakes in various locations around the world. Results indicate that the warming trend was most intense in northeastern Europe, where the temperature increase reached a high of 1.72oF. However, there were anomalies in various regions. For example, the warming trend for lakes in the Southern Hemisphere, as well as for those in the tropics, was much less significant. Even stranger, lakes in the same region had significant variations in their warming trends. For instance, data of lakes along an arc from the Great Lakes to Canada’s Lake Athabasca showed an appreciable difference in the warming rates. Of these inconsistencies, Hook said: “You will get some lakes that, for reasons we really don’t know, will not be showing as much warming as other lakes, even in the same region.” This research could reap many benefits for climate scientists. According to Hook, since this research provides independent data sets which run parallel to the measurements of air temperatures, it provides yet another piece of evidence for global warming. Groups concerned about the fate of lakes would also benefit from this research, since warming water quickens the growth of deadly algae blooms.
The Caspian Sea in 2010 is one of the few lakes saved from global warming.
Future research aims to compare these results with the predictions that climate models provide for various regions. Such data would allow scientists to test the accuracy of the models that are currently being used to predict the future of global warming.
By Gregory Loshkajian, a junior in AAST
Provenge®: The First FDA-Approved Cancer Vaccine The use of cancer vaccines to treat diseases has always been a controversial issue. Because of their high cost and general ineffectiveness, critics have been reluctant to apply them to clinical settings. Regardless, in the last couple of years, there have been rumors about the development of more reliable cancer vaccines that will help the immune system fight tumors. This report was largely unsubstantiated, until now. A biotechnology company called Dendreon recently developed a cancer vaccine called Provenge® that the Federal Drug Administration (FDA) approved on April 29, 2010. Provenge® will have its own place in scientific history as the first cancer vaccine to be approved by the FDA. Soon to be released in the United States, Provenge® is a cancer treatment that aims to cure advanced prostate cancer. Its general mechanism is relatively simple; immune system cells will be taken 8 | ACADEMY SCIENTIFIC VOL 1.1
from a patient’s blood and exposed to a protein called prostatic acid phosphatase in the lab. After exposure, the cells will be directed back into the patient’s body. As a result, the patient’s own T-cells will be now programmed to attack his or her tumors.
Ledford, Heidi. “Controversial Vaccine Fights Prostate Cancer: Nature News.” Nature Publishing Group: Science Journals, Jobs, and Information. 29 Apr. 2009.
Although the FDA has approved this vaccine, nobody is calling it a cure. Patients who received this treatment have only lived approximately 4 months longer than those who did not. The company claims that Provenge® is far more effective than other cancer drugs because those treatments only extend a patient’s life by a few weeks or months. Also, Provenge® requires three injections, costing $31,000 each, but many patients are willing to pay the price because of the drug’s promising results. Although more research must be done to develop a more effective drug, Provenge® has laid the foundation for the future of cancer vaccinations.
This is the vaccine Provenge, which is administered intravenously.
By Ana Song, a freshman in AMST
Inheriting Negative Interactions: Yellow-Bellied Marmots
Hulse, Ben. Yellow-bellied Marmots. ScienceNews. 29 Nov. 2010.
Yellow-bellied marmots show that victimization could be genetic.
A yelllow-bellied Marmot lying on a rock.
In marmot social networks, victimization may be heritable. As humans, we make complicated networks of social interactions and feelings that define how we feel about our friends, relatives, and classmates. Every disagreement, grouchy interaction, or warm hug is an individual decision characteristic of who we are as complex human beings- right?
overlooked aspect of a valuable social and evolutionary trait. Being able to survive in a group may involve dealing with conflict. Organisms that are faced with more negative interaction have to be better prepared to tolerate and deal with negative relations, rather than shying away from the conflict.
It may seem difficult to believe, but a new set of studies published in the Proceedings of the National Academy of Sciences found in a population of animals closely related to squirrels that genetics plays a role in social interactions. The results suggest that negative interactions could be inheritable.
Previous studies have focused on genetic explanations for ...the marmots who rebeneficial relationships, but ceived negative interactions this recent report has shown were more often genetically that we may need to reevalusimilar, suggesting that being ate our perception of which the victim in a social interac- traits are socially bad. The tion could be hereditable. authors of the paper hope to study the social interactions of humans next, in order to see if victimization is truly linked to genetics.
The studies were conducted on yellow-bellied marmots, which are ground squirrels native to the western United States. Studying their social interactions and genetic material gave researchers from the University of California in Los Angeles a better understanding of the genetic components of social relationships. The animals are an effective model population because they live in colonies of ten to twenty, which provide scientists with an opportunity to observe all their social interactions. The researchers identified positive interactions, which included grooming a neighbor, and negative interactions, which included biting. Regardless of the nature of the interactions, there was no evidence of heritability in the initiation of the interactions. However, according to coauthor Daniel Blumstein, “It’s receiving incoming social attention, particularly in grouchy interactions, that showed a small but intriguing genetic influence”. The researchers found that the marmots who received social interactions were linked genetically; the marmots who received negative interactions were more often genetically similar, suggesting that being the victim in a social interaction could not be inherited.
Similar studies in human populations have thus far been relatively limited, because it is more difficult to maintain a controlled human population. Also, humans have many more complex behaviors, which are not always as obvious as biting or pushing. If these researchers’ findings end up applying to humans, we may have to accept that who we are, and how we are treated in society, is not so much an individual choice. We will also have to acknowledge that a species of marmots may actually have taught us something crucial about genetics and the way our societies function.
By Michelle Rudshteyn, a junior in AMST and the Features Editor
Blumstein also reported that finding a genetic influence on the animals that endured the negative interactions may reflect an ACADEMY SCIENTIFIC VOL 1.1 | 9
Ancient Astronomer’s Hollywood-Worthy Murder What do you get when you combine a well-known Danish astronomer, his mentally unstable German assistant, a Swedish hit man, and a jealous Danish king? The sudden and mysterious death of a Danish astronomer. Half a century later, this real-life mystery has been given blockbuster potential. Professor Jens Vellev, a Danish archaeologist, and his team of scientists were given permission this past month to exhume the remains of Tycho Brahe, a 16th century Danish astronomer. To their surprise, they might have dug up a five-hundred-yearold murder plot that seems to have been taken straight from a movie script. But how did the young Danish astronomer wind up dead in the first place? In the late 16th century, Tycho Brahe became famous in the science community for identifying new stars, and even a supernova under the patronage of the king of Denmark. But once his royal patron died, Tycho found that the new Danish king, Christian IV, despised him. Therefore, Tycho traveled to Prague and found a new patron: Rudolf II, the Holy Roman Emperor.
Tycho ill. The second time when Tycho was exposed to a high dose of mercury was on the final day of his life, suggesting that this second mercury exposure was the cause of death. Many scholars point to Kepler as the prime suspect. Kepler described himself as having an “uncontrollable spirit” as well as an “eagerness for trickery”. Kepler was also eager to prove his own model Public Domain The astronomer Tycho Brahe of the universe, and resented Tycho for was famous in the scientific not allowing him access to essential community, until his untimely death. data. Kepler desperately desired access to Tycho’s data in order to prove his own theories. However, this could only happen if Tycho were out of the picture. Another suspected individual is Eric Brahe, a Swedish relative of Tycho who was staying at his home during that time. In his diary, Eric wrote numerous incriminating entries that are extremely suspicious.
At this point, the astronomer was preparing to publish his many celestial observations but quickly found that he But in the 1990s, hair could not accomplish this samples from Tycho were on his own. He then enlisted analyzed and were shown the help of Johannes Kepler, to have been exposed to a 28-year-old astronomer elevated levels of mercury at with his own strong opintwo separate times. ions about the model of the universe. But less than a year later, Tycho suddenly became ill and died within 11 days.
Adding another layer of intrigue to the story, Peter Andersen, a literature professor at the University of Strasbourg in France, argues that Eric Brahe was actually hired to carry out the murder by King Christian IV of Denmark. But why did Christian IV want to kill Tycho? Rumor has it that Tycho had an affair with Queen Sophie, who was Christian’s mother.
Until the late 20th century, the death of Tycho Brahe was believed to be the result of kidney problems. But in the 1990s, hair samples from Tycho were analyzed and were shown to have been exposed to elevated levels of mercury at two separate times. The first dose was believed to be what initially made
Fortunately, a lack of data has never stood in the way of Hollywood masterminds.
Amidst all the speculation, lead investigator Professor Vellev has chosen to focus instead on CT scanning, DNA testing, and PIXE analysis of these samples. These tests are meant to uncover information relating to the scientist’s health as well as the cause of his death. Professor Vellev insists that even if the tests proved that Tycho was poisoned with mercury, this would not necessarily identify the killer.
By Elizabeth Dente, a junior in AMST and the World News Editor
References Ancient African Lizard: Ancestor of the Komodo Dragon? “Link between Ancient Lizard Fossil in Africa and Today’s Komodo Dragon in Indonesia.” Science Daily: News & Articles in Science, Health, Environment & Technology. 30 Dec. 2010. Seasons of Birth Linked to Dramatic Differences in Personality Christopher M Ciarleglio, John C Axley, Benjamin R Strauss, Karen L Gamble, Douglas G McMahon. “Perinatal photoperiod imprints the circadian clock,” Nature Neuroscience 14, 25-27. The Deeper Layers of Global Warming Barringer, Felicity. “Lakes Around the World Are Warming - NYTimes.com.” Energy and Environment - Green Blog - NYTimes.com. 1 Dec. 2010.
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Provenge: The First FDA-Approved Cancer Vaccine Couzin-Frankel, J. First U.S. ‘Cancer Vaccine’ Approved. Science Magazine. 29 Apr. 2010. Smith, R. P. Cancer Vaccines: Between the Idea and the Reality. OncoLink. 24 Jul. 2004. Inheriting Negative Interactions: Yellow-Bellied Marmots Hulse, Ben. Yellow-bellied Marmots. ScienceNews. 29 Nov. 2010. Ancient Astronomer’s Hollywood-Worthy Murderer Tierney, John. “Murder! Intrigue! Astronomers?” The New York Times. 29 November 2010.
Cancer is a disease in which abnormal cells divide uncontrollably and invade tissues and organs. There are many different cancer types, but they can be grouped into broad categories. Carcinomas are cancers that begin in the skin or tissue of internal organs. Sarcomas are cancers that begin in connective or supportive tissue while leukemia is a cancer that starts in blood-forming tissues such as bone marrow. Lymphoma and myeloma are cancers that start in the immune system cells, and central nervous system cancers begin in the brain and spinal cord tissues. Not all tumors are cancerous; harmless tumors are called benign tumors while cancerous tumors are labeled as malignant tumors. The latter type of tumor is able to spread throughout the body and cause further damage. This process is known as metastasis.
Wellcome Image Awards A tubular adenoma is a benign epithelial tumor in which the cells form recognizable glandular structures.
Breast cancer, a malignant tumor that starts from breast cells, is one of the most widespread diseases for women. About 12 percent of women in the United States will develop invasive breast cancer sometime in her life.
foreign substances. Through the lymph nodes, the cancerous cells are free to travel throughout the body. Breast cancer is always caused by a genetic abnormality, and about 90 percent of breast cancer cases are results of genetic abnormalities that come with age and time.
Usually, the cancer begins either in the cells of the lobules, milk-producing glands, or the ducts, the passages that drain milk from the lobules to the nipple. The cancer cells eventually invade healthy breast tissue and advance into the underarm lymph nodes, small organs that filter ACADEMY SCIENTIFIC VOL 1.1 | 11
Smoking & Cancer
linked with an increased risk in lung cancer; smoking being responsible for 9 out of 10 lung cancer cases.
In the United States, smoking is the major single cause of cancer mortality. The CDC reported that 20.6 percent of all US adults were smokers in 2009, but the number is gradually decreasing. Cigarette smoking is not only hazardous for the general health, but it is also the cause for at least 30 percent of all cancer deaths. It is most frequently
Lung cancer is the leading cause of cancer deaths in the United States for both men and women, and it is the most preventable form of cancer death in our society because smoking and tobacco use is an acquired behavior that people choose to do.
Healthy lung tissue, showing the hollow cavities where gas exchange occurs with the blood known as alveioli.
An image of lung cancer cells, starkly contrasting the healthy lung tissue seen in the previous image.
Prostate Cancer The prostate gland, which is only found in men, contains cells that make some of the semen that protects and nourishes sperm. There are various cell types in the prostate gland, but the gland cells are prone to develop into a serious cancer, called adenocarcinoma. Most prostate cancers grow slowly, and studies show that 7 to 9 males out of 10 had prostate cancer by age 80. The causes of prostate cancer are uncertain, but researchers believe that it begins with minimum changes in the size and shape of the prostateâ€™s gland cells. Age and family history are strong factors that can determine oneâ€™s chances of acquiring prostate cancer. The four standard treatments for prostate cancer are monitoring the patientâ€™s condition, surgery, radiation therapy, and hormonal therapy.
Robyn Schlicher, Robert Apkarian, and Mark Baran
A transmission electron microscope image of a prostate cancer cell.
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By Jenny Yoon, a junior in AMST and the Features Editor
Cancer Stem Cells
e have all heard the words “cancer” and “stem cell,” but have you ever heard these words put together? Research has now discovered a new disease-causing agent: cancer stem cells.
Cancer stem cells are a subset of cancer cells that have the potential, like stem cells, to self-renew. Self-renewal is the process in which a cell gives rise to more cells through differentiation. Usually the self-renewal of stem cells is a process that is regulated, but in the case of cancer stem cells, the opposite is true. Cancer stem cells with this ability to self-renew help transfer disease or form tumors after transplantation. These cells give rise to phenotypically diverse cancer cells and cancer stem cells and cancer cells that are formed from these stem cells have a greater ability to form tumors than do tumor cells or non-tumorigenic cancer cells. As a result, cancers cells that were originally non-tumorigenic may form tumors. Overall, these cells promote metastasis and relapse in multiple cancer patients.
The reasons that cancer stem cells exist is a consequence of the similar signaling pathways and mechanisms that regulate Cancer stem cells self-renewal in both stem cells and cancer have already been found cells. The Wnt, Shh, and Notch pathways are all found in the signaling pathways of in human acute myeloid leukemia, breast cancer, and stem cells and cancer cells. Mutations in glioblastomas. these pathways may give rise to tumors, most notably colon carcinoma and epidermal tumors through the Wnt pathway, medulloblastoma and basal cell carcinoma through the Shh, and T-cell leukemia through the Notch. Currently, the origins of cancer stem cells are unknown. In some cases, cancer stem cells have been shown to arise from mutational transformation of normal stem cells. In other cases, cancer stem cells have been shown to arise from mutations that cause a restricted progenitor or mature cell, giving these cells the ability to self-renew. This theory draws parallels to normal somatic cells, which arise from embryonic precursors.
On The Flip Side… Teratomas are stem cells formed from the three embryonic germ layers (endoderm, mesoderm, and ectoderm). As a result, teratomas which range from benign lesions to malignant tumors contain derivatives of all three germ layers. While cancer stem cells are cancer cells with stem cell characteristics, teratomas are stem cells that may develop to be cancerous. The word teratoma itself comes from the Greek word teras meaning monster. The name is a suitable one, as teratomas contain many different tissue types including hair, bone, teeth, and sometimes even complex organs such as eyes, hands, or feet. Teratomas have been known to exist throughout history, and early beliefs blamed ingestion of teeth and hair, curses from witches, and adultery with the devil. However, the common belief held nowadays is that teratomas arise from germ cells. The most common occurrence of teratomas is in infants, but they may also appear later in life. Treatment is usually surgery; however, teratomas with malignant transformation will contain elements of malignant tumors such as leukemia, carcinoma, or sarcoma, and chemotherapy is needed to treat these tumors. Although horrifying, teratomas are relatively rare – about 10,000 cases are diagnosed worldwide each year.
These embryonic precursors are able to give rise to normal fetal stem cells that are then able to self-renew. Thus, mutations in this process allow normal stem cells to become malignant cancer stem cells. Cancer stem cells have already been found in human acute myeloid leukemia, breast cancer, and glioblastoma. Researchers have successfully determined surface markers to discern cancer stem cells from cancer cells. Treatments are currently being researched to inhibit the differentiation of cancer stem cells and consequently stop the rise of cancer cells. Scientists are also determining approaches to convert malignant cancers into benign tumors. As a consequence, this targeted treatment of cancer stem cells will undoubtedly improve the quality of cancer treatment in the future.
By Emily Tu, a junior in AMST, the Publisher and Layout Editor
References T. Reya, S. J. Morrison, M. F. Clarke, and I. L. Weissman. Stem cells, cancer, and cancer stem cells. Nature 414 (2001): 105-111. R. Pardal, M. F. Clarke, and S. J. Morrison. Applying the principles of stem-cell biology to cancer. Nature Reviews Cancer 3 (2003): 895-902.
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Teratomas may contain hair, bone, and teeth.
Reya, T., Morrison, S.J., Clarke. M.F., and Weissman, I.L, “Stem cells, cancer, and cancer stem cells.” Nature 414: 105-111 (2001).
Mutations in the Wnt, Shh, and Notch pathways may give rise to tumors.
Pardal, R., Clarke, M.F., and Morrison, S.J. “Applying the Principles of Stem-Cell Biology to Cancer.” Nature Reviews Cancer 3, 895-902 (2003).
In a., normal somatic stem cells arise from embryonic precursors during fetal development. These fetal stem cells selfrenew and become normal adult stem cells. The adult stem cells are able to undergo differentiation and become adult tissues. In b., cancer stem cells arise from the acquisition of self-renewal potential in restricted progenitor cells, or from mutations in normal stem cells. Thus, benign cancer cells are formed.
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Customizing Blood Cells for
Leukemia Treatment Clinical Center Communications
eukemia is a disease caused by the overproduction of white blood cells, which fight invading organisms such as bacteria and viruses. When these white blood cells are overproduced, they do not have the ability to mature properly, and therefore are ineffective in fighting off foreign bodies. They also begin to crowd the space in the bone marrow, which inhibits the growth of red blood cells that carry oxygen from the lungs to the rest of the body. As a result, the body grows weak from the lack of oxygen and defenseless from the weakening immune system. Treatment plans for leukemia are often personalized depending on the progress of the disease and the patient’s individual health. There are five general treatments for leukemia. Chemotherapy involves strong anti-tumor drugs that usually bring both mild and severe side effects. Interferon therapy tries to slow the reproduction of leukemic cells, while radiation therapy attempts to kill cancer cells by fatally modifying their DNA using high-energy radiation exposure. Additionally, 16 | ACADEMY SCIENTIFIC VOL 1.1
stem cell transplantation exists, which involves the use of both radiation therapy and chemotherapy. Lastly, surgery can be used to remove tumors or withdraw blood and tissue samples. Recently, scientists have been playing around with a unique method of replacing faulty blood cells with healthy cells as a treatment for leukemia. The technique could create and swap blood cells to help the body efficiently fight foreign bodies and have a constant supply of healthy cells. These blood cells would be created from adult skin cells that scientists altered and “reprogrammed.” A team of scientists from McMaster University in Hamilton, Canada created new red blood cells by inserting a gene OCT4, which reprograms adult cells, into human fibroblasts, or skin cells. As a result of this gene insertion, fibroblasts became more specialized and organize themselves into blood-forming cells much like the ones found inside the human bone marrow. These reprogrammed cells efficiently produce a normal amount of hemoglobin, which is the body’s oxygen-carrying protein, and transport oxygen throughout the body.
By way of this treatment, blood cells could constantly be replaced, and the patient be kept healthy. Digital Image
These re-created blood cells proved to be both suc- References Treatment - Leukemia - Oncology Channel.” Cancer, Tumors, Patient Ed, cessful and efficient for treating leukemia. Although “Leukemia Physician-Developed - Your Oncology Community - Oncology Channel. scientists feared that these cells would become Conversion of Human Fibroblasts to Multilineage Blood Progenitors : Nature : Nacancerous over time, when grown in a culture dish, “Direct ture Publishing Group.” Nature Publishing Group: Science Journals, Jobs, and Information. the cells only divided a finite number of times. Additionally, in a mice model, the cells did not overgrow abnormally into structures called teratomas. By observing the mice models, scientists discovered that the recreated blood cells adjusted to the organisms’ bodies well. The mice did not reject the cells and after eight weeks of cell growth, 20 percent of the new cells had grown into completely human cells within the mice’s bone marrow. Although more research must be conducted as to whether or not cells created from specific adult skin cells, will exist normally and efficiently after a long period of time, this technique looks promising as a treatment option for leukemia and other bloodrelated disorders. By Jenny Yoon, a junior in AMST and the Features Editor
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The Incredible Mr. Naked Mole-Rat W
hen one pictures an organism that is both resilient and strong, one will most likely picture a creature that is twenty feet tall and weighs thirty tons. However, the naked mole-rat, a tiny, 35-gram rodent living in Africa, is considered to be one of the most resilient creatures to walk the Earth. Earning its name because of its remarkable hairless coat, the naked mole-rat has become a commonly-used animal in scientific experiments. Why is it used so frequently when there are many other animals that are easier to obtain? The truth is that it is remarkably resistant to senescence. Senescence, or biological aging, is a process all species have been known to undergo. Humans, which are a reactive oxygen species (requiring oxygen-rich ions to repair cells), have been known to age due to oxidative stress. This means that the body can no longer detoxify the reactant used to repair cells. As a result, the oxidative stress that builds up can lead to a host of conditions and diseases. Researchers have conducted studies on the naked mole-rat to see if the same 18 | ACADEMY SCIENTIFIC VOL 1.1
aging processes take place inside them. When compared to other species of mice, results showed that these rats contained very high concentrations of oxygen-rich molecules after a period of two years. As a result, it was hypothesized that the naked mole-rat has the ability to essentially stop the biological aging process by producing large amounts of molecules that are responsible for counteracting senescence without succumbing to oxidative stress. Another reason that naked mole-rats have recently been in the spotlight is their remarkable ability to resist forming cancerous tumors. Cancer is a disease that affects almost all living organisms and kills an average of 7.6 million humans every year. The disease commonly begins when cancer cells start to divide uncontrollably as a result of mutations in the proto-oncogenes, which normally regulate apoptosis, or cell death, and tumor-suppressing genes, which stop mutated cells from dividing. These mutated cells contain no signals telling them when to stop, so they continue to produce more and more mutant copies of themselves. These copies build up in the body and eventually form a tumor. Naked mole-rat cells, however, exhibit a behavior called
contact inhibition. This means that once their cells reach a certain density, they stop growing to avoid overcrowding. Researchers at the University of Rochester recently discovered the reason for this strange phenomenon: the mole-rats’ unique tumor suppressor pathways. The p27 gene is responsible for suppressing cancer in human and mouse cells; if this gene becomes mutated in a person, that person is very likely to develop cancer. Naked mole-rat cells, for some reason, use the p16 gene as well as p27 to control contact inhibition. Scientists observed that one stage of contact inhibition is controlled by p16, while the other stage is controlled by p27, thus giving the naked mole-rat its remarkable resistance to cancer. If the p16 gene does not do an adequate job in preventing early contact inhibition, p27 steps in later on to Even when injected make sure that the cells are with chemicals that turned not overcrowded. In other mouse fibroblasts into words, the p16 gene gives cancer cells, the naked the naked mole-rat an extra mole-rat cells resisted converting into cancerous layer of protection. Even when injected with chemicells. cals that turned mouse
A photo of a naked mole rat, the size of a person’s hand.
fibroblasts into cancer cells, such as Ras and SV40 LT, the naked mole-rat cells resisted converting into cancerous cells. While other rodents have a higher probability of succumbing to cancer, the naked mole-rat has nothing to fear. Therefore, the naked mole-rat is the longest living rodent, with a maximum lifespan exceeding 28 years. Students at Bergen County Academies such as Jennifer Chan, a sophomore in AMST, have also realized the tremendous potential of working with naked-mole rat cells. Chan’s research project titled “Naked Mole-Rats: Digging for the Underground Secret to Cancer Resistance” focuses on the distinct properties of naked mole-rat cells to resist cancer. It is not difficult to guess why she chose this distinctive rodent to focus on. It is incredible that such a seemingly insignificant organism that is as long as a human hand has evolved to become one of the most intriguing creatures in the world. With its abilities to counteract cancer and slow down the biological aging process, the naked mole-rat is one of the most studied species on Earth. Scientists are in awe at the potential of these tiny yet resilient rats that may one day save millions of lives.
By David Heller, a freshman in AMST and Stephanie Jeong, a sophomore in AAST
Sluanov, Andrei et. al. “Hypersensitivity to contact inhibition provides a clue to cancer resistance of naked mole-rat.” PNAS. 26, Oct. 2009.
A model comparing contact inhibition in naked mole-rat to mouse and human. Naked molerat cells have two tiers of contact inhibition: early contact inhibition mediated by p16 and regular contact inhibition mediated by p27. In contrast, human and mouse only have regular contact inhibition. The presence of two-tiered contact inhibition may provide naked mole-rats and increased protection against tumor development.
Perez, Viviana et. al. “Protein Stability and Resistance to Oxidative Stress Are Determinants of Longevity in the Longest-living Rodent, the Naked Mole-rat.” PNAS 106 (2009). Print.
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why anti-cancer drugs are
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n the past several decades, the development of anticancer drugs, commonly referred to as chemotherapy, has prolonged the lives or even cured thousands of cancer patients. Unfortunately, not every patient that takes anti-cancer drugs is cured or treated; far more often than should be the case, the anti-cancer drugs fail to work. To understand why chemotherapy is not effective all the time, one must first understand how they are supposed to work in the ideal scenario: their mechanisms of action. Available anti-cancer drugs vary widely in their mechanisms, which makes their effects dependent on the types of cells they are used to treat. Of these methods, though, the most commonly used anti-cancer drugs seek to accomplish one or more of three seminal goals, which all decrease the growth rate of the cancer cells: to damage the DNA of cancer cells, to inhibit the replication of cancer cells by stopping the synthesis of new DNA strands, and to stop the process of mitosis, or the splitting of one cancer cell into two new cancer cells. As there are over 100 types of cancers and few biochemical differences between cancerous cells and normal cells, many anti-cancer drugs are limited in their effectiveness. This is partly because they are as equally toxic to normal rapidly growing cells as they are to cancer cells. A particular example of casualties is the cells in the bone marrow, which are necessary for human survival. The cancer that is being treated may also develop resistance to the drugs, so chemotherapy usually consists of several different drugs Public Domain such as capecitabine, Capecitabine (Xeloda®) inhibits DNA synthesis. which inhibits DNA synthesis, and docetaxel, which interferes with cell division in breast cancer cells. For example, for cancers, such as ovarian cancer, which remain an ongoing challenge because of the appearance of resistant forms of the tumor that the specific chemotherapy cocktail fails to suppress, combination therapies using drugs with different mechanisms of action offer a means of overcoming the drug resistance and treating the cancer.
...the most commonly used anti-cancer drugs seek to accomplish one or more of three seminal goals, which all decrease the growth rate of the cancer cells: to damage the DNA of cancer cells, to inhibit the replication of cancer cells by stopping the synthesis of new DNA strands, and to stop the process of mitosis, or the splitting of one cancer cell into two new cancer cells. Yet another way that the anti-cancer drugs can fail is by causing a second cancer in the patient after the chemotherapy treatment. The use of alkylating agents, which insert foreign molecules into the DNA of dividing cancer cells to stop their dividing, has been linked to the development of second cancers in patients. The foreign molecules present an additional disadvantage in that they kill healthy cells by disrupting their normal functions and preventing their proliferation. The death of the cells leads to toxic side-effects such as nausea, vomiting, hair loss, anemia, infection, and blood clotting problems. Also, the alkylating agents sometimes produce mutations in cells similar to those produced by radiation, which can also lead to a second cancer, necessitating another round of anti-cancer drugs and resulting in a never-ending cycle of recurrence and therapy. Strides have been made by medical researchers to overcome the failures of current anti-cancer drugs. There are many promising anti-cancer drugs that are currently in development or in clinical trials, such as cyclopamine, which uses a novel mechanism of action to shut down critical cell-signaling pathways in gliobastomas, an aggressive brain cancer, to stop tumor growth. We can only hope that advances in these new anti-cancer drugs will improve the process of chemotherapy and increase the chance of survival against cancer.
By Andrew Cho, a freshman in AAST References Tucker, Margaret A. “Anticancer Drugs.” National Cancer Institute. Web. Yunos, Nurhanan M. et al., “Studies on Combinations of Platinum with Paclitaxel and Colchicine in Ovarian Cancer Cell Lines — Anticancer Research,” Anticancer Research 30, 4025-4037 (2010). Johns Hopkins Medical Institutions. “Experimental Anti-cancer Drug Kills Brain Tumor Stem Cells.” ScienceDaily 31 August 2007.“Capecitabine (Xeloda®) and Docetaxel (Taxotere®) Chemotherapy - Cancer Information - Macmillan Cancer Support.” Macmillan Cancer Support, 1 Dec. 2009.
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TAKEN WITH BCA’S SCANNING ELECTRON MICROSCOPE
BDCM M5a myeloid leukemia cells
BDCM M5a myeloid leukemia clumps
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t first glance, Dr. Jillian Banfield and Dr. Michael Morowitz could not be more different. Dr. Banfield works in some of the most treacherous settings on Earth. In September, she studied the dark, hot, sulphurous grottos of Richmond Mine inside Iron Mountain, California, where the most acidic water in the world can be found. Last year, she worked underneath a former nuclear-processing site in Colorado digging beneath years’ worth of uranium, arsenic, molybdenum, and other radioactive metals. Dr. Morowitz is a neonatal surgeon studying necrotizing enterocolitis (NEC), a potentially fatal disease in the intestines of premature babies. However, a recent collaboration between these two scientists has led to new discoveries in microbiology, a field that studies microbes including bacteria, archaea, viruses, and fungi. In the extreme environments where Dr. Banfield performs research, she studies how the bacteria that inhabit those areas have adapted to survive. Now, these scientists, along with Dr. David Relman of Stanford University, are applying Banfield’s techniques to human beings by sequencing and analyzing microbial genes in close detail, to determine which strains of microbes correlate to NEC and other intestinal diseases. Affecting 7% of severely premature infants, NEC is often not diagnosed until the late stages of development. If treatment is not begun in time, surgeons must remove part, if not all, of the intestine, a procedure which is often fatal for infants. Medical researchers have been searching for the cause of this disease for decades, but the only discovery that has been made is that more than one microbe is involved. In a Nature News article, Morowitz reported, “I had a suspicion that we weren’t going to find a [pathogenic] smoking gun, so I was looking around for different ways to study the problem.” He understands that new, more effective methods of data organization and analysis will be crucial. “I became interested in people who were looking at entire communities of organisms,” he said. This collaboration comes at a crucial time for microbiology research. Human microbiologists have already succeeded in building up a large genetic catalogue of different microbes that live in humans, but also have realized the complexity of microbiology in humans. There are hundreds of interrelated 24 | ACADEMY SCIENTIFIC VOL 1.1
microbial overflow From the moment an infant slips out of his or her mother’s vaginal cavity, he or she encounters a flood
of microbes, whether it is in the intestines, eyes, skin, or lungs. The germ theory of disease, discovered by Robert Koch in the nineteenth century, has fueled research into these diverse human microbes that surround us from the day we were born. However, clinical microbiologists who were studying foreign pathogens such as Salmonella and Ebolavirus in the twentieth century were dismissing those agents found in the human body as inconsequential to health. At the same time, microbial ecologists were following an entirely different course of action. They realized that the approach that the clinical microbiologists were pursuing was inaccurate because of factors such as “the great plate count anomaly”, a discrepancy that resulted in fewer cell counts of an original sample after plating. Because of these flaws, clinical microbiologists were actually losing a great chunk of microbial samples after plating. Through genetic surveys such as the sequencing of the 16S ribosomal RNA gene, these microbial ecologists advanced the germ theory tremendously by allowing for a more in-depth pursuit of the genetic makeup of all samples. In 1999, however, the merge was finally made when David Relman of Stanford University performed a 16S survey on a sample of human teeth plaque before and after plating and discovered that after plating, much of the diverse samples were lost. After another decade of research, scientists were able to successfully evaluate the diverse nature of the microbiota in nature. They are discovering that these organisms display a wide array of functions that prove useful to humans on a daily basis. From synthesizing proteins to providing immune function, they are essential to human well-being and survival. According to Jeff Gordon, a gut microbiologist at Washington University, “The microbiota are bringing a series of utensils to the dining-room table that the human host doesn’t have.” He even goes on to say that humans and microbes have coevolved to become a “superorganism” and that a human is indeed 99% microbial. Other research including that at the US National Institutes of Health in Bethesda, Maryland, which launched the Human Microbiome Project (HMP) in 2007, is also exploring this pivotal connection between humans and microbes. Through the analysis of millions of genetic samples of microbes from all parts of the worlds, NIH researchers such as Lita Proctor hopes to explore “something that’s a hundred times bigger [than the human genome] that we don’t have a handle on, that’s intimately tied to our own health and vitality.”
By Aishwarya Raja, a junior in AMST and the Editor-in-Chief
and different species of bacteria living in each human Reference being, that have little to do with the humans them- Buchen, Lizzie. “Microbiology: The new germ theory.” Nature 468 (2010): 492-495. Print. selves, which makes it more difficult to know which bacteria are beneficial and which cause diseases. The challenge is now to effectively organize the collected data in order to make significant conclusions. By Michelle Rudshteyn, a junior in AMST and the Features Editor
clinical applications Banfield, after discovering the sample from the Richmond Mine, immediately began her genetic analysis to determine the metabolic functions and structures of these hardy microbes. She had a looming task in front of her though: to pinpoint the specific species and strains of microbes from clumps of fragmented DNA samples. Instead of using techniques such as 16S surveys, which cannot reveal subtle genetic differences between closely related strains, Banfield and her team decided to take these clumps and construct them into full fledged genomes. Afterwards, they performed fine-grain analyses and inspected by-hand the parts of the genome where specific strands did not line up.
“He just called me out of the blue one day,” Banfield recalls, and spoke to her about NEC. “He was really concerned about this terrible disease. I was sort of taken by how passionate he was, and hoped I’d be able to do something that might be useful,” Banfield said. As it turned out, the population of microbes in the guts of infants with NEC was very similar to that of microbes in the Richmond mines because only a dozen or so species of microbes exist. Therefore, these infants proved to be the best experimental models for Banfield’s technique. Currently, this trio is taking samples from healthy babies, sequencing the microbial populations, and trying to determine a strain of bacteria that is correlated with NEC development. By Aishwarya Raja, a junior in AMST and the Editor-in-Chief
Through this, they were able to differentiate different strains of the dominant species of the microbe more accurately. The genes were also an indicator of the biogeochemical processes these microbes were performing. Relman, however, wanted to expand Banfield’s research on this small community of microbes in a mine where the dominant population accounts for 40% of the population, to the diverse groups of microbes in the human gut where the dominant population is only about 4% of the total. “It was reasonably straightforward to see that this kind of approach would really be important,” he notes. Morowitz, also recognizing the importance of Banfield’s technique, decided to call her up.
Buchen, Lizzie. “Microbiology: The new germ theory.” Nature 468 (2010): 492-495. Print.
A researcher collects samples of the pink biofilm floating atop hot, green, acidic pools in the Richmond Mine at Iron Mountain, California.
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THE FOLLOWING ABSTRACTS SHO SEVERAL BERGEN ACADEMIES RESEARC
A Genetic Approach to Alzheimer’s Disease: Is a Longevity Gene the Answer? Alzheimer’s disease (AD), a neurodegenerative disorder characterized by an accumulation of amyloid beta protein (Aβ) and tau protein in the brain, contributes to neuronal dysfunction. The role of the human sirtuin 1 gene (SIRT1), a survival gene that protects cells from stress, in the accumulation of Aβ and tau proteins in the SH-SY5Y neuroblastoma cell line will be investigated through this experiment. Herein, SIRT1, which is overexpressed in the SH-SY5Y cell line, will be silenced with SIRT1 shRNA. SIRT1, Aβ, and tau ELISA assays from Invitrogen will be used to quantify protein levels before and after the application of shRNA. The effect of SIRT1 inhibition on the protein levels of cell division protein kinase 5 (CDK5) and glycogen synthase kinase 3 beta (GSK3B), two genes associated with the tau pathway in Alzheimer’s disease, will also be quantified with respective ELISA assays. Cell apoptosis levels will be measured before and after the treatments as well as the levels of reactive oxygen species (ROS) via a fluorescence technique. As a result of this experimentation, a direct relationship between SIRT1 and Aβ and tau accumulation in neuroblastoma cells will be observed: as SIRT1 gene expression decreases, Aβ and tau protein production will increase. Comparatively, levels of apoptosis and ROS will be significantly higher in the treated SH-SY5Y cells than in the control because of the accumulation of Aβ and tau proteins in the former. Lastly, CDK5 and GSK3B genes will be more expressed in the treated SH-SY5Y cells because of the accumulation of characteristic Alzheimer’s proteins in the cells. Overall, these results are indicative of a regulatory role of SIRT1 on the production of Aβ and tau proteins as well as on other genes on the tau pathway; therefore, SIRT1 activation is a viable strategy to combat AD and perhaps other neurodegenerative diseases.
Author: Aishwarya Raja AMST 2012
Aishwarya participates in choir and is the Junior Editor in Chief of the Academy Chronicle. She enjoys reading and writing in her spare time. Castle and Pretty Little Liars are her favorite telelvision shows.
Altering Lentiviral Tropism by Pseudotyping with Specific Receptor-Mediated Proteins One major obstacle in gene therapy has always been the lack of vector specificity. The scientific community has no effective method of transporting genes to specific cells if a naturally occurring virus or other vector does not already exist. This experiment outlines a method of directing viruses to cell lineages of choice, via a modification of the process known as “pseudotyping”, which is the modification of proteins on the surface of enveloped viruses: viruses are pseudotyped with proteins that specifically attach to naturally unique receptors on the cell lines that are to be infected. To prove the viability of pseudotyping, lentiviral particles expressing the green fluorescent protein (GFP) were pseudotyped with Vesicular Stomatitis Virus Protein G (VSV-G) and introduced to a gastric adenocarcinoma cell line (AGS) in vitro. After 24 hours, flow cytometry revealed that 48% of the AGS cells had been infected, in comparison to nonpseudotyped viruses, which only infected 10% of cells. To demonstrate the effectiveness of the specific receptor-mediated protein pseudotyping concept, this experiment utilized pseudotyped lentiviruses with gastric inhibitory polypeptide (GIP), a protein which attaches to GIP receptor (GIPR). GIPR is a receptor which is unique to pancreatic beta cells, and thus these viruses will specifically target pancreatic beta cells. This method can be applied in order to deliver genes to any cell line that has a unique protein receptor.
Author: Thomas Silver AMST 2012
Tom enjoys playing lacrosse and piano in his free time. He is President of HOSA and President of the Junior Class Council. His guilty pleasures are watching White Collar and Glee.
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OW A GLIMPSE OF WHAT PROJECTS CH STUDENTS ARE COMPLETING AT BCA
Benzoin’s anti-aging properties: A new frontier for skin care Benzoin, first synthesized in 1832 by Justus von Liebig and Friedrich Woehler, is an organic compound. Benzoin is synthesized from benzaldehyde, which is the primary component of bitter almond oil. Bitter almond oil has been claimed mostly by folklore to have beneficial effects on the skin such as anti-itching, anti-inflammatory, antioxidant, and antiseptic. Bitter almond oil has even been claimed to prevent evil spirits. However, the ability of Benzoin to have anti-aging properties on the skin has not been scientifically proven. Certain enzymes, in particular, the matrix metalloproteinase (MMP) family are involved in the breakdown of the extracellular matrix (ECM), which gives skin tissue its firmness and elasticity. MMP-9 was specifically chosen in this experiment because it is mostly responsible for the degradation of skin’s elasticity and firmness. When the activity of MMP-9 is inhibited, the skin can maintain a healthier, youthful structure. It was hypothesized that if the concentration of Benzoin was introduced and increased in the skin cells human keratinocytes (HaCaT cells) and dermal fibroblasts, the levels of MMP-9 in these cells would decrease in a dose-dependent manner. A spectrophotometer was used to assay the levels of MMP-9 in the cells. Statistically significant assay results showed that the amount of MMP-9 in the cells decreased as the concentration of Benzoin increased (p<0.05). Viability results show that concentrations less than .01 μL Benzoin were nontoxic, with the aforementioned concentration being toxic to 40.5% of the cells. These results clearly state that Benzoin possesses the ability to decrease the levels of MMP-9 in HaCaTs and dermal fibroblasts. In the future, Benzoin, synthesized from benzaldehyde, deserves further recognition for its anti-aging effects on the skin as a result of its ability to downregulate MMP-9 in human keratinocytes.
Author: Elizabeth Dente AMST 2012
In addition to research, Elizabeth is also a violinist. She performs with her school orchestra and a string quartet that she formed with her friends. She is a youth leader in her church youth group and is currently planning a trip for the youth at her church to go to World Youth Day in Madrid, Spain. Her greatest passion being medicine, she hopes to work hard and someday become a doctor.
Gene Silencing of DARPP-32 in the Dopamine Pathway using Nanorod-mediated RNAi Nicotine addiction is a global health issue and is one of the leading preventable causes of death around the world. This experiment uses a newly discovered method of gold nanorod-mediated delivery of RNAi against the DARPP-32 gene. DARPP-32 regulates the dopaminergic signaling pathway in the brain, which is activated during addiction. Suppression of this gene was shown to lead to significant behavioral inhibition of the addiction process. Gold nanorods were electrostatically bound with RNAi, and these complexes were delivered into dopaminergic neuronal cells. The embryonal carcinoma cell line, P19, was differentiated into neuronal cells using retinoic acid. Dark field microscopy and gel electrophoresis were used to evidence the improved uptake of the nanorod/RNAi complexes in the cells, as compared to free RNAi. An immunofluorescence assay was used to show the direct impact of silencing the DARPP-32 gene on the dopamine pathway by using specific antibodies to fluorescently label the protein DARPP-32. Neuronal cells with inhibited levels of DARPP-32 can be exposed to the dopamine stimulator nicotine and have a reduced response, indicating the potential application of gold nanorod/ RNAi complexes to addiction therapy. These complexes appear to be an effective method of facilitating the delivery of RNAi to specific, targeted cellular sites.
Author: Michelle Rudshteyn AMST 2012 Besides research, Michelle enjoys swimming and ballroom dancing. She likes to read and write, and dreams of writing a bestselling novel. Her perfect day would involve reading a good book at the beach, discovering a new, life-saving medicine, and winning a Nobel Prize in Medicine.
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a student interview
INTERVIEW WITH BHASHA MUKHOPADHYAY AMST ‘11 What is your internship? As an intern of Dr. Tengson at St. Joseph’s Children’s Hospital (which is a part of St. Joseph’s Regional Medical Center in Paterson, NJ), we shadow the attending physician on their rounds and meetings, attend lectures, see patients and their conditions up close, and learn about many new conditions, as well as have fun! What is your day like?
Our day is flexible, but we set up a 8 AM to 3 PM day. We start by checking in with Sister Mary Rose, and then we move on to the Pediatric floor and attend Morning Report with the medical students and residents, where the attending physicians and everyone else discuss special and interesting patient cases. From there, we go with the medical students and residents to do rounds (check up on all the patients on the floor), and as we go around to the patients (more long-term patients who need to stay overnight), we learn about their conditions and the attending physician gets an update on each patient’s condition. After rounds, we talk to Dr. Tengson, who usually serves as a school doctor early in the morning, about the cases that we saw. We also do rounds with Dr. Tengson for a different set of patients. Does your mentor give you external assignments to do? Dr. Tengson assigns us homework based on the patients we see. For example, if we see a patient who has a certain condition, he will assign one of us to write a one-page paper on that condition and add a little write-up of the patient. Through this assignment, we learn about a lot of conditions, as well as technical terms used in the medical profession. We discuss our homework assignment from the week before each
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Wednesday after rounds with Dr. Tengson. Then, if there is a lecture that we are interested in, we go to the one-hour lecture at 12 PM. We then go to lunch with the medical students, and stop by the library to find some sources for our homework assignment at the medical library for the staff, since they have access to some sources not available to us otherwise. After lunch, we join Dr. Tengson in the St. Joseph’s outpatient clinic, where we see short-term patients who make emergency appointments to see him. We stay with him as he goes into the exam rooms and sees the patients, and unless the patient has any problem with us being there, we also go in with him to observe how he interacts with the patients. Based on the patients’ conditions, he takes us to his office and asks us to find the causes, diagnoses, exams, and treatments for that particular condition and then give him a “work-up,” meaning what we saw and what we would do with a patient in that situation. Since Dr. Tengson wants to have the “full experience,” meaning not only see what doctors do, but he wants us to also see what medical students and residents go through academically, physically, as well as socially, and to see if we want to go through all of this in the future. Had you always wanted an internship like this? If so, what was it that made you always want this? Yes, I always wanted an internship like this! What I was wanted in my internship was to have a mentor who was open to teaching us as much as he can, while giving us valuable hands-on experience. What I got is so much more - my mentor treats us like residents, so we get not only amazing learning experiences and patient interactions, but also he teaches us the social aspects to be a doctor, like how to communicate with patients and lots of patient signs to look out for. Also, since we are in Paterson, we see lots of interesting cases from patients over-exaggerating their symptoms to get out of school to cases of gang violence. He also introduces us to the medical students and residents, so we also get a lot of valuable advice from them. There is so much to my internship that I cannot even explain it all! There is so much to it that I didn’t expect to experience,
but Dr. Tengson makes sure we can do as much as possible in our short time with him. What did you consider when looking for an internship? I honestly just wanted to have a good time while learning a lot and seeing interesting cases. I wanted to be at a renowned hospital’s pediatric department, or at a pediatric clinic that never had a dull moment. I got both and so much more!
What is your favorite part of your internship? Why? My favorite part is the rounds. During rounds, we go around to each patient’s room and first stand outside, discussing the patient’s case and overnight changes with the attending physician. Then, we (attending physician, residents, medical students, and us) go to the patient and see how they are doing and answer any of their questions. If the doctor thinks that there is something to hear or see with this patient, the doctor will show us, as well as answer any questions we may have. In order to make sure we understand exactly what is going on with the patient, the doctor also gives us a background. Whether we know the condition already or not, it is comforting to know that nothing we ask will be naive or laughed at. We are really taken seriously and everyone makes sure that they can give us the full internship experience!
offered to us, we can certainly ask to see if it’s possible for us to sit in. For instance, one day Dr. Tengson had told us that he would be one hour late to the hospital, so we asked our secondary mentor, Sister Mary Rose (the internship and mentoring coordinator) if we could go to another pediatric specialty. She took us to Labor and Delivery, where we had the opportunity to see a C-section! What I really value about this internship that I hope anyone who wants to go into the field experiences is that I get to have not only the medical lessons and I not only see the medical aspects of this internship, but I am also taught about the other qualities that medical professionals need, like the ways of communication and interaction that they need to have, and also the social aspects. If there is a party going on, we are invited - this way we see the lives of residents and medical students. Dr. Tengson wants to make sure that we are positive that we want to go down this road we have chosen for ourselves. Based on your internship, would you still want to pursue this as a career? Definitely! I went in wanting to be a pediatrician, and I now have more of an urge to become one! Now that I have gotten the know-how with residents, I want to go straight into residency and save the time! Well, even though that isn’t possible, now there is no gray area. I definitely want to go down this road and I know I’ll have fun during this journey!
Do you work with a team of people at your internship? The amount of people we work with depends on the type of job we are doing. Rounds are a group job - we go around with the doctor and usually three medical students, and sometimes one or two residents. However, when we are in the outpatient clinic, it is usually Dr. Tengson and just us (there are two of us interning with Dr. Tengson). When we attend the Morning Report at 9 AM, it is usually a meeting with two or three doctors, a few residents, and a few medical students, as well as the two of us. Would you recommend your internship to anyone else? I would DEFINITELY recommend this internship! I have such an amazing time and get to have so many cool experiences. I also have freedom, so the hours are flexible, and we have the right to be vocal, so if we don’t want to do something we can tell our mentor, or if we do want to have an experience that has not yet been
St. Joseph’s Regional Medical Center in Paterson, NJ
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a teacher interview
INTERVIEW WITH DR. ROBERT PERGOLIZZI
What is your philosophy of education? Your education is the one thing no one can ever take from you. They can take your arm, or your freedom, but not your education. If you do it properly, it should almost kill you. In what ways have your college experiences prepared you for a career? When I went to college, the Vietnam War was raging, students were protesting everywhere, and we all came to believe that you had to be bold and fearless about expressing your beliefs and feelings. You should never back down. I have never wavered from that approach to life, and I feel it has served me very well throughout my career. What jobs did you have before you were a teacher? My first job was soldering parts together for Bell Telephone, if I ignore the lemonade stand and paper route I had as a child. I had jobs working in a giant refrigerator at a dairy farm, as a sporting goods manager at a department store, and as a clerk in a bookstore. After college I got my first real â€œscienceâ€? job, working as a technician, first at a lab doing cancer research and then for the Pediatrics Department at North Shore Hospital on Long Island. Then I went to graduate school, got a few degrees, including a PhD in Biochemistry, and then did a post-doctoral fellowship in Human Genetics and Development. Then I joined a biotech company, when the field was just beginning, as the Director of Recombinant DNA Research. I left four years later to become the Director of Molecular Genetics and Gene Therapy at the North Shore-Long Island Jewish Health System, where I also became Associate Professor of Pathology at the Weill Cornell Medical College. I was then recruited to the Weill Cornell Department of Genetic Medicine as Associate Professor and Director of the National Gene Vector Lab. Finally, four years ago, I came to BCA. When did you first become interested in teaching? Last week. Just kidding. I have always been interested in teaching and I have always taught in some capacity, 30 | ACADEMY SCIENTIFIC VOL 1.1
but as a full time pursuit, teaching at BCA is my first experience. I am in love with the material I teach, and I need to have students who share my enthusiasm. Medical students are boring, hardened cases that only rarely stop to listen. They think they know everything they need to know. They do learn eventually, but it is often painful. We enjoyed knocking them off their pedestals. What are your greatest strengths as a teacher? I love what I teach, I have boundless energy and I believe that despite the things I have done and the places I have been, the most important job I have ever had was being a Dad. I feel a parental sense about every student I encounter, and it makes me do whatever it takes to help them. What is your biggest weakness as a teacher? I wish I knew more about everything. I wish I had more time to spend with each student. I wish I were younger. I suppose my biggest weakness is that I am a pussycat
or an easy A. Some students do take advantage of that, believe it or not. I should take toughness lessons from my wife. How do you determine or evaluate success? That is an excellent question. Do you mean my success or the success of my students? I do not think about my success. I live my life according to an ancient Chinese proverb: â€œLive every day as if it were your last, and one day you will be right!â€? We must evaluate the success of students, although I would prefer not to do that. I think tests are weak indicators of success in learning; they are imperfect instruments. Grades have become an evolutionary vestige, like the coccyx. They may have been important once, but now they are just one more thing to injure. What two or three accomplishments have given you the most satisfaction? Why? I took great satisfaction from a project I did at Cornell where we cured a genetic disease in an animal model. This was published in Nature Medicine, and is probably one of my favorite papers. This was done with a brilliant Japanese post-doc in my lab, Minoru Tahara, who died tragically a few years later. Nothing is ever an unqualified success. I developed a strategy to increase the amount of information a virus can carry, and a diagnostic test for the Fragile X syndrome; I am quite satisfied with those. I also feel a great sense of satisfaction stemming from the fact that I did not die from some of the stunts I pulled in college. Ask me again when you are older. As you might have guessed from one of my previous answers, I am enormously satisfied with my beautiful, talented children, one of whom will no doubt bite my head off for having said that.
it or not I loved English classes the best. I love the way different people express their feelings and experiences, and how different they often are from how I would have described them. It makes the world a bigger, deeper and more complex canvas. English classes also always had the best looking girls. What school subjects did you like the least? Why? For four years of high school I was forced to take various forms of mechanical drawing. I must have sharpened a billion pencils. I still have all my compasses, S-curves, stencils, and lousy grades that I got in those classes. That was in the sixties. Do you know what happened since then? COMPUTERS! You think anybody draws with a pencil anymore? I feel like I got bad grades for cave drawing. Beware easily replaced technologies; we puny carbon-based life forms are easily seduced by such things. What is one piece of advice you would give to BCA students? Say yes to everything. Figure out what you need to know later.
What would be most important to you in your job? The most important thing would be a sense that something I had done or taught played a part in the success of my students, especially if they did something magnificent such as curing a disease, feeding the hungry, that sort of thing. I would also love to stop filling out paper work. That would be great. After the first hundred grant applications, you tire of that sort of thing.
Weill Cornell Medical College
What school subjects did you like best? Why? Although I studied every science that I could, believe ACADEMY SCIENTIFIC VOL 1.1 | 31
UPDATES REGARDING THE SCIENCE AND MATH DEPARTMENTS AT BERGEN COUNTY ACADEMIES
8th Annual BCA Math Competition is Once Again a Success Each year, the Bergen County Academies Math Team and Math Booster Club hold a math competition for local middle school students in grades 4 through 8 known as the BCA Math Competition, or the BCAMC. This year’s event was held at BCA on October 17, 2010 and there were roughly 500 participants, mostly from Bergen County, although some came from as far away as Massachusetts. Sponsors of the event were Wolfram Research Inc., Art of Problem Solving, Key Curriculum Press, Texas Instruments, and Ralph and Kathryn Armenta, who generously provided the prizes. The prizes included engraved crystals, TI-Nspire calculators, trophies, origami activity books, and math posters. The competition, as always, was staffed and organized entirely by volunteers; BCA Math Team students, teachers, and parents planned the event, handled registration, and acted as proctors for the tests. This year, the student coordinators and competition editors of the event were BCA seniors Victoria Png and Michael Tan. Several seniors and juniors also acted as exam leaders and were responsible for leading the other volunteers. Many students from all grades, mostly members of the Math Team, wrote questions for the exams. The exam itself was an individual, grade-specific test, consisting of 50 numerical response questions. Students were given one hour and thirty minutes, and calculators were not allowed. The test was quite challenging, but there were many students that earned impressive scores. The scores were posted on a later date on the competition website, along with the original tests and their solution guides so that students could review their mistakes, or practice for next year’s exam. After BCA student proctors graded the tests, the event concluded with an awards ceremony, marking the end of yet another successful BCAMC, a product of combined efforts. According to Victoria Png, the volunteers “put a lot of time and effort into making this year’s math competition a successful event. We really could not have controlled all the participants [and their parents] as easily without their help. Everything went smoothly and I am happy that all the events ran on schedule.” For more information regarding the competition and for a list of the top ten scorers in each grade level, visit the BCAMC The committee members that made the event possible! website: http://sites.bergen.org/mathcompetition/index.asp
By Teresa Fan, a junior in AAST and volunteer at the 2010 BCAMC
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AAST Math Team Successful at the Princeton University Math Competition On the morning of the November 20th, 32 students from the AAST Math Team boarded the bus and headed for Princeton to compete in the Princeton University Math Competition (PUMaC). Before the competition started, each team handed in their completed Power Round, which was completed a week in advance. Austin Wang, a senior and one of the captains of the AAST Math Team said, “For the power round, members on all four teams gathered with their respective teammates at some point after school to work on the contest, which is commendable.” The real competition, which consisted of an Individual round and a Team round, then began. After the exam was over, the students took part in mini-events, such as a Math Bowl, Chess, and a Scavenger Hunt, while others met up with friends that attended Princeton. “The exam problems were pretty interesting and the activities after all of the exams were relaxing,” said Wang. After the exams were graded, the Awards Ceremony began. In Division A, Mu A, consisting of Michael Tan, Robert Lin, Alex Zhu, Licheng Rao, Michael Sun, Jongwhan Park, Alex Radek, and Andrew Cai, took third place overall and tied for 4th place in the Power round. Alex Zhu placed 1st with a perfect score on the Algebra exam and 4th on the Number Theory exam. Licheng Rao tied for 4th place on the Geometry exam. In Division B, Mu C, consisting of Mark Aksen, Isabel Juniewicz, Ben Lam, Daeyoung (David) Lee, I-Jui Lee, Sungjae Lee, James Mayers, and Victoria Png, tied for 6th place in the power round. David Lee and Eric Lee, both from Mu C, won 3rd and 7th place on the Algebra exam, respectively. Wang also added, “Considering that the AAST Math Team lost many of its best members with the graduating class last year, the fact that the top teams can perform the way they did is fantastic.” Overall, PUMaC was another success for the AAST Math Team.
By Jenny Chen, a junior in AMST on the AAST Math Team and the School News Editor
AAST Math Team Takes 3rd and 4th Place at Duke Math Meet On the morning of November 12th, 49 students from the AAST Math Team headed for Duke University to compete in the Duke Math Meet. After the ten hour bus ride, the team finally arrived in Durham, North Carolina. After a restful night, the competition began the next day, consisting of the Power Round, the Team Round, the Individual Round, and the Relay Round. The Power Round and Team Round came first, and after lunch, students moved to an auditorium for the Individual and Relay Rounds. The AAST Math Team put in much effort into practicing for the competition, and did well this year. AAST Mu A, consisting of Michael Tan, Robert Lin, Alex Zhu, Licheng (Chan) Rao, Michael Sun, and Jongwhan Park, won 3rd place. AAST Mu B, consisting of Andrew Cai, Alex Katz, David Lee, James Mayers, Justin Zhang, and Kelley Zhao, won 4th place. Alex Zhu and Robert Lin placed in the top 10 in the individual round. Austin Wang, a senior and one of the captains of the AAST Math Team commented, “I think Mu A did a great job preparing for the competition.” The Duke Math Meet was another victory for the AAST Math Team.
By Jenny Chen, a junior in AMST on the AAST Math Team and the School News Editor
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Bergen County Technical Schools â€œThe Bergen County Technical School District is an educational model that prepares students to live, work and lead in a global community.â€?
Bergen County Technical Schools Board of Education Lazaro Carvajal................................................................................................................................................................... President William Connelly........................................................................................................................................................Vice President Robert M. Gilmartin.............................................................................................................Executive County Superintendent Jason Kim...................................................................................................................................................................Board Member Thomas H. Richards................................................................................................................................................Board Member Central Office Administration Dr. Howard Lerner ................................................................................................................................................ Superintendent Andrea Sheridan.................................................................................................................................. Assistant Superintendent Richard Panicucci..................................................................... Assistant Superintendent for Curriculum and Instruction John Susino............................................................................................................... Business Administrator/Board Secretary Bergen County Executive Kathleen A. Donovan Board of Chosen Freeholders John Driscoll, Jr..................................................................................................................................................................Chairman Maura DeNicola................................................................................................................................................. Vice Chairwoman John D. Mitchell................................................................................................................................................Chair Pro Tempore John A. Felice ...................................................................................................................................................................Freeholder David L. Ganz ...................................................................................................................................................................Freeholder Robert G. Hermansen....................................................................................................................................................Freeholder Bernadette P. McPherson..............................................................................................................................................Freeholder BCA Campus Administration Russell Davis......................................................................................................................................................................... Principal Raymond Bath..................................................................................................................................................................Supervisor Dr. David Niedosik...........................................................................................................................................................Supervisor
This first issue is dedicated to Dr. David L. Ostfeld, 1942-2011, Academy Admissions Director since 1992. Designed & Printed by Students and Staff at BCA
Published on Aug 11, 2011
This is the first issue of the Academy Scientific, BCA's first premier scientific journal. Please feel free to leave any comments or suggest...