Category: Recent News
In This Issue:
- Message from the President: Dr Kenneth E. Thummel
- EB2016 Meeting Highlights
- Feature Article: Sleepy Sickness, Oliver Sacks, and the Early Days of L-Dopa
- Science Policy News
- Education News
- Journal News
- Membership News
- Members in the News
- Division News
- Chapter News
- Meetings and Congresses
Joon Ying Boon and Megan Varnum Participate in the 25th Annual BUMC Art Days and GMS Student Art Exhibit
Joon Ying Boon and Megan Varnum, Program in Biomolecular Pharmacology Ph.D. graduate students, contributed to the success of 25th Annual BUMC Art Days, March 30-31, 2015. BUMC students, faculty and staff were invited to contribute paintings, photos, poetry, sculpture, needlework, etc. for the event. This year’s keyword was INTERSECT and a special display section was set aside in Hiebert Lounge devoted to works focused on “Intersect.” On Tuesday, April 14, 2015, Joon’s and Megan’s art works were also displayed at a special exhibit sponsored by the Division of Graduate Medical Sciences featuring paintings and photographs by DGMS graduate students.
Joon Ying Boon has entitled her piece, “Grandfather Trees.” She explains that “somewhere in the overcrowded, busy and skyscrapers-filled urban Hong Kong, there is an old park with old trees where one can find peace and serenity.”
Joon is also a senior Ph.D. student pursing her dissertation research on the identification of proteins that bind to and regulate LRRK2 in the Laboratory of Neurodegeneration, under the mentorship of Principal Investigator and Professor of Pharmacology and Neurology, Benjamin Wolozin, M.D., Ph.D.
The banner painting above was done by Megan Varnum’s and is entitled, “A Mexican Hillside”. Megan elaborated on that, “Mexicans incorporate vibrant color into nearly every aspect of their culture, and I wanted to reflect that in this painting. Although I cannot personally take credit for taking the photo from which this was painted, it reminds me of the times my family would go to Mexico and how inspired I would be by all the colors.”
Megan is a senior Ph.D. student doing her dissertation research on traumatic brain injury (TBI) in the Laboratory of Molecular NeuroTherapeutics under the direction of mentor, Principal Investigator, and Professor of Pharmacology and Neurology, Tsuneya Ikezu, M.D., Ph.D.
These two aspiring young scientists inspire us with their creativity. Beautiful work, Joon and Megan!
Dr. Carol Walsh Presents BUSDM Dental Pharmacology Integrated Problem Session to ADEA Annual Meeting
Carol Walsh, Ph.D., Pharmacology Vice Chair for Education, presented a description of the innovative Integrated Problem Sessions of the BUSDM Dental Pharmacology course at a symposium held March 9 at the American Dental Education Association (ADEA) annual meeting in Boston. The symposium, organized by Aldo Leone, D.M.D.,Associate Dean for Academic Affairs at BUSDM, was entitled “Igniting Minds through Student Self-directed Group Learning: Integrated Problem Sessions” and included presentations by Dr. Leone, Drs. Whitney and Pessina from the Anatomy and Neurobiology Department, and Dr. Sarita-Reyes from the Pathology Department. The presenters were honored by special recognition of the symposium by the Chair of the ADEA Board of Directors.
University-wide Graduate Program for Neuroscience Receives BU Provost’s CEIT Interdisciplinary Course Development Grant
Congratulations go to Shelley J. Russek, Ph.D., Professor Pharmacology & Experimental Therapeutics and Biology, and the University-wide Graduate Program for Neuroscience (GPN) on being awarded the Boston University Provost’s Center for Excellence and Innovation in Teaching (CEIT) Interdisciplinary Course Development Grant. As GPN Director, Shelley spearheads a university-wide team of outstanding faculty who do an exceptional job in preparing graduate students for careers in neuroscience.
GPN is a University-wide Ph.D. degree granting program uniting the graduate training faculty of the BU Charles River Campus and the BU Medical Campus to serve as the nexus point for all neuroscience training missions at Boston University.
Neil J. Ganem, Ph.D., Assistant Professor of Pharmacology & Experimental Therapeutics and Medicine at the Boston University School of Medicine, has received a 2014 Smith Family Foundation Award for Excellence in Biomedical Research.
This prestigious, highly competitive three-year award of $300,000 is intended to help launch the careers of newly independent biomedical researchers. Since 1992, the program has funded 130 investigators for a total investment of $23 million. Applications focus on all fields of basic biomedical science as well as research in physics, chemistry and engineering. Applicants, who are nominated by their institutions, must be full-time faculty at nonprofit academic, medical, or research institutions.
Dr. Ganem received his Ph.D. from the Geisel School of Medicine at Dartmouth and was a postdoctoral fellow at the Dana-Farber Cancer Institute/Harvard Medical School. His research focuses on the causes and consequences of chromosomal instability, broadly defined as the persistent acquisition of both numerical and structural chromosomal aberrations. Chromosomal instability is a hallmark of solid cancers and is known to facilitate tumor initiation, progression, and relapse. The Smith Family Foundation Award will support Dr. Ganem’s research to examine how cancer cells adapt to abnormal chromosomal content.
Boston University Medical Campus is located in the historic South End of the capital city of Massachusetts. Well-known for the high quality of teaching, research, and community service, the school provides an exceptional learning environment for its students in the heart of the city.
Article originally posted on BestMedicalDegrees.com.
The Laboratory of Cancer Cell Biology has identified the tumor suppressor mechanism that prevents the oncogenic growth of cells harboring an abnormal number of chromosomes. The study, published in the journal Cell, was led by Neil J. Ganem, PhD.
Tetraploid cells, which are a common byproduct of cell division failure, are genomically unstable and have the capacity to facilitate tumorigenesis. Recent estimates suggest that ~40% of all solid tumors have undergone a transient tetraploid intermediate at some point during their evolution, suggesting that tetraploidy plays significant roles in both the development and/or progression of human malignancies. Given the potentially oncogenic consequences of tetraploidy, it is not surprising that tumor suppression mechanisms have evolved that prevent the proliferation of these cells. However, unlike other common cellular insults that trigger cell cycle arrest, such as DNA damage, the mechanisms governing cell cycle arrest in response to tetraploidy have been poorly defined.
To understand the mechanism of growth arrest in tetraploid cells, Dr. Ganem and colleagues combined genome-wide RNAi screening and in vitro evolution approaches to comprehensively identify all of the genes required to stall the growth of tetraploid cells. Collectively, these data revealed that the Hippo tumor suppressor pathway is specifically activated in tetraploid cells, both in vitro and in vivo, and that this is the pathway that prevents tetraploid proliferation. The authors pinpointed that defects in the cytoskeleton of tetraploid cells represented the initial trigger for Hippo pathway activation. Notably, analysis of a broad spectrum of human cancers revealed that near-tetraploid tumors frequently adapt to overcome Hippo signaling, suggesting that inactivation or bypass of this pathway may be a prerequisite for the development of high-ploidy tumors. “This work may help guide the development of new therapies that specifically target tumor cells with abnormal numbers of chromosomes, while sparing the normal healthy cells from which they originated,” explained corresponding author Dr. Ganem, PhD, Assistant Professor of Pharmacology & Experimental Therapeutics and Medicine in the Shamim and Ashraf Dahod Breast Cancer Research Laboratories at BUSM.
The study was highlighted with a preview article in Cell and by the journals Science Signaling, Cancer Discovery, and Nature Reviews Cancer. The article can be read online at: http://www.cell.com/cell/abstract/S0092-8674(14)00820-4.
Researchers at Boston University School of Medicine (BUSM) have uncovered important clues about a biochemical pathway in the brain that may one day expand treatment options for cognitive deficits seen in schizophrenia. The study, published online in the journal Molecular Pharmacology, was led by faculty members David H. Farb, PhD, Terrell T. Gibbs, PhD, and Shelley J. Russek, PhD in thedepartment of pharmacology & experimental therapeutics at BUSM.
Patients with schizophrenia suffer from a life-long condition that can produce cognitive deficits, delusions, disordered thinking, and breaks with reality. A number of treatments are available for the treatment of schizophrenia, but many patients do not respond to these therapies or experience side effects that limit their use. There is no current treatment for the cognitive deficits experienced in schizophrenia.
The healthy brain is made up of billions of cells including the primary signaling cells called neurons, that are responsible for managing everything the body does: including movement, eating behavior, and memory formation. These neurons acts like a miniature computer and are controlled by substances called neurotransmitters that, like bits in a computer chip, may be “turned on” or “turned off” depending on the specific signals being integrated. Neurotransmitters latch onto a cell via a specific receptor, like a key fits into a lock.
In schizophrenia, it is thought that certain neurons don’t “turn on” as well when exposed to a certain neurotransmitter, the amino acid glutamate, may not be sensed by one of its key receptors (the NMDA receptor) whose diminished function may be the possible culprit for these sluggish cells. It is thought that this deficit can at least partially be responsible for symptoms seen in schizophrenics.
Currently the therapeutic means for making these cells more “sensitive” to glutamate can be toxic to the brain.
In this study, researchers discovered that another, naturally occurring steroid within the brain, known as PregS, may be able to bypass this toxic effect, and “turn on” neuron communication safely through a novel mechanism. The implication is that a deficit in the amount of this novel steroid may underlie deficits in signaling and that stimulation using therapeutics that elevate its levels in the brain may decrease or eradicate some of the debilitating symptoms seen in schizophrenia.
Although still in the early stages, further research in this area may be instrumental in the identification and development of treatments not only for schizophrenia, but also for other neurological conditions, such as age-related decreases in memory and learning ability.
Earl Gillespie, Ph.D., a Postdoctoral Researcher at Boston University School of Medicine and an alumni of the Biomolecular Pharmacology Program, will join Avalere Health in Washington, DC as an FDA Policy Fellow this summer.
According to the Avalere Health website, the highly selective FDA Policy Fellowship Program allows participants to, “spend 6 months immersed in health and life science regulatory policy and strategy issues to help support the efforts of Avalere clients that include some aspect of FDA related issues. Fellows will collaborate within [the] existing FDA team to increase Avalere’s presence and visibility as experts and thought leaders in the FDA space.”
Dr. Earl Gillespie completed his dissertation work under the mentorship of Dr. Susan E. Leeman, Professor of Pharmacology, and Dr. Arthur F. Stucchi, Research Associate Professor of Surgery, and graduated in January 2013. The title of his dissertation was “Colonic Epithelial Genes in the Transition From Chronic Inflammation to Carcinoma in Colitis-Associated Cancer: Focus on the Truncated Neurokinin-1 Receptor.”
We are so very proud of Earl and wish him the best in this new phase of his career!
Researchers in the Laboratory of Addictive Disorders have discovered that impulsivity is a risk factor for food addiction . Results of the study, published online in Neuropsychopharmacology , suggest that impulsivity promotes pathological overeating.