Tuesday, June 13, 2017
University of Rochester Medical Center researchers have discovered that loss of muscle stem cells is the main driving force behind muscle decline in old age in mice. Their finding challenges the current prevailing theory that age-related muscle decline is primarily caused by loss of motor neurons. Study authors hope to develop a drug or therapy that can slow muscle stem cell loss and muscle decline in the future.Read More: Stem Cells May Be the Key to Staying Strong in Old Age
Video of 3 Minute Thesis Event
Thursday, June 8, 2017
We have the video of the full event with all presentations fully captions and with the slides running in time with the videos.
3MT Presenters, Programs & Topics
Thesis presentations in order
- Stephanie Carpenter (Chemistry) - Solving the Mystery of Iron Chemistry
- Sarah Catheline (Pathways of Human Disease) - Inhibiting Inflammaging to Treat Osteoarthritis(OA)
- Scott Friedland (Genetics, Development & Stem Cells) - Pancreatic Cancer and the Tale of the Broken Librarian
- Claire McCarthy (Toxicology) - Investigating the Toxicological Effects of Dung Biomass Smoke Exposure
- Taylor Moon (Immunology, Microbiology and Virology) - The New Epidemic
- Thuy-Vy Nguyen (Social-Personality Psychology) - Solitude *Winner*
- Manisha Taya (Cellular & Molecular Pharmacology and Physiology) - Understanding Lymphangioleiomyomatosis (LAM): The “Other” Steroid-Dependent Cancer From Bed-Side to Bench and Back Again
- Janelle Veazey (Immunology, Microbiology and Virology) - Role of Protein Kinase D in Epithelial Cells During Respiratory Infection
Full 3MT 2017 Event Video (CC)
Monday, May 15, 2017
On May 11th, 2017, Scott Friedland took 2nd place in the Three Minute Thesis (3MT) competition with his talk entitled, “Pancreatic Cancer and the Tale of the Broken Librarian. 3MT, created at The University of Queensland in Australia, is an effort to bring awareness to research and scientific communication, in which competitors have 3 minutes to get across the thrust of their thesis to a general audience. Scott is an MD/PhD student currently working in the lab of Dr. Aram Hezel in the Genetics, Development, and Stem Cells program. His research focuses on defining the role of ARID1A and the SWI/SNF complex in pancreatic cancer and development.Read More: Scott Friedland takes 2nd place in the Three Minute Thesis (3MT) competition
29th Annual Genetics Day Symposium
Thursday, May 4, 2017
This year's Genetics Day provided another opportunity to celebrate the impact of Genetics on science and medicine. The program consisted of four short talks by U of R scientists, a poster session and the Keynote event, the Fred Sherman Lecture, delivered this year by Dr. David Sabatini from the Whitehead Institute for Biomedical Research at MIT. Dr. Sabatini talked about “Growth Regulation by the mTOR Pathway”.
This year’s Genetics Day Poster Session included posters from research laboratories across the University. Three graduate students and one post-doctoral associate were awarded poster prizes:
Andrew Allbee – Biteau Lab
dLMX1A is Required for Drosophila Ovary Stem Cell-Niche Unit Establishment
Amber Cutter – Hayes Lab
Molecular Characterization of Nucleosome Recognition by Linker Histone H1.0
Browyn Lucas – Maquat Lab
Evidence for Convergent Evolution of Sines for Staufen-Mediated Control of MRNA Decay
Janet Lighthouse – Small Lab
Expression Profiling Reveals the Cardioprototective Role of Metallothioneins in Exercise
Genetics Day has been a long-standing tradition at the University of Rochester and more recently includes the Fred Sherman lecture in memory of Fred Sherman a renowned biochemist and geneticist, who led international efforts to establish the yeast Saccharomyces cerevisiae as the premier genetic eukaryotic model system. The lecture is made possible by a generous fund endowed by Fred Sherman's wife, Elena Rustchenko-Bulgac, herself a research professor at the URMC.
GDSC Graduate Justin Komisarof successfully defends
Friday April 28
Tuesday, May 2, 2017
MD/PhD candidate Justin Komisarof presented his work on the hunt for a common cancer gene signature. Building on prior work by the Land and McMurray labs, Justin used bioinformatic approaches to search for the presence of a ‘cooperation response gene’ (CRG) cancer gene expression signature a broad panel of different tumors. Using microarray gene expression datasets from GEO in colon, pancreatic, prostate, and head and neck cancers, Justin found a core set of consistently disregulated CRGs. A more in-depth study of genotype-phenotype correlation in colon cancer samples revealed that this CRG dysregulation did not track with p53 or Ras mutations, suggesting that CRG dysregulation occurs in multiple human cancers, and that the CRG expression pattern is independent of mutational status and may emerges as a function of the malignant state. Justin also applied this CRG-based analysis to prostate cancer samples and identified a core set of CRGs that when combined with clinical staging predicts recurrent outcomes with greater than 80% accuracy – a highly significant improvement over current methods. Justin’s work provides an important step forward for both diagnostic and future therapeutic approaches.
A four gene signature predictive of recurrent prostate cancer.
Komisarof JMcCall M, Newman L, Bshara W, Mohler JL, Morrison C, Land H.
Oncotarget. 2017 Jan 10;8(2):3430-3440.
GDSC Students attend the March for Science
Tuesday, April 25, 2017
Students from the Genetics Program attended The Rochester March for Science on Saturday April 22
Fanju Meng (Biteau Lab), Sreejith (Biteau Lab), Emily Wexler (Portman Lab),
Sebastian Rojas Villa (Biteau Lab), Robert Hoff (Bohmann Lab), Andrew Allbee (Biteau Lab)
Michael John Beltejar awarded CTSI Pilot Trainee Grant
Thursday, April 13, 2017
Michael John Beltejar, a 4th year student in the Genetics, Development, and Stem Cells PhD program with a research focus in Genetic contributions to bone strength has been awarded CTSI Pilot Training Grant.
CTSI Pilot Trainee Grant RFA
A major priority for the CTSI is the active support of research collaborations via cross-disciplinary collaboration, and the support of research that addresses significant problems related to population health. Thus, applications directly addressing these areas are strongly encouraged. Trainee awards help awardees obtain the most prestigious fellowship possible following the project. The project should be part of a long-term plan to become an independent investigator. The award provides a maximum of $25,000 for a period of one year.
Osteoporosis remains a significant concern. By 2025, osteoporotic fractures are expected to increase to 3 million with an estimated cost of $25.3 billion. Morbidity and mortality increases following all major fractures in patients over 55 years of age. It is widely understood that compromised bone strength is the underlying pathophysiology of osteoporosis. Currently, bone mineral density (BMD), is the basis for diagnosis and the main target for osteoporosis therapy. BMD is an important clinical tool, but explains only 55 % of fractures, leaving the needs of 45% of patients unaddressed. Fundamentally, bone strength has two interconnected but distinct components: quantity and quality. While BMD reflects quantity, bone quality (BQ) reflects morphologic and compositional properties. However, developing therapies based on BQ is limited by two major gaps in knowledge: 1) Which genes regulate BQ and 2) Does estrogen deficiency modify the genetic regulation of BQ? Therefore, the objective of the work proposed is to construct a genetic network to identify candidate genes regulating bone composition(SA1) and determine if estrogen deficiency interacts with these genes(SA2).
The rationale for the proposed work is that bridging these gaps in knowledge is a crucial first step in the identification of novel therapeutics. The results produced from SA1 will inform ongoing research in the lab--in particular, a genome-wide association study identifying locations in the genome that are responsible for bone quality. Secondly, the results of SA2 have a strong potential to unlock research on multiple levels osteoporosis management. Identification of novel genes could be used as a new biomarker to identify at risk individuals earlier. Downstream activity of these genes could become additional metrics to monitor disease progression. Finally, these genes become putative targets for novel therapies. The research in this application is innovative because it is a significant departure which shifts focus from BMD to BQ as an equally important contributor of fracture resistance.