On Stage for the Opening Ceremonies of the 2011 Event:
Aaron Goldman, PhD
Post Doctoral Research Fellow, Harvard Medical School
Division of Biomedical Engineering, Brigham and Women's Hospital
65 Landsdowne St. Cambridge, MA 02139
|Breast cancer recurrence is often accompanied by the acquisition of
chemotherapy-resistance. We now know that within breast cancer, some cells are sensitive to chemotherapy while others resist treatment and regrow more aggressively than before. My research elucidates novel cellular processes which allow certain populations of breast cancer cells to tolerate the effects of chemotherapy. Using this knowledge, we engineer nano-scale therapeutics to specifically target chemotherapy tolerant breast cancer cells, prevent relapse and reduce the side-effects associated with treatment.
All the best, Aaron
University of Alabama at Birmingham for his four year research titled:
Former U.S. President George H.W. Bush • former First Lady Barbara Bush • Lance Armstrong •
The late Honorable Edward M. Kennedy, Senator from Massachusett • George N. Papanicolau, M.D., inventor of the Pap test • Robert C. Gallo, M.D., recognized for his achievements in pioneering the field of human retrovirology • Judah Folkman, M.D., a leading researcher in the field of antiangiogenesis • C. Everett Koop, M.D., former U.S. Surgeon General • Advice Authors Ann Landers and Abigail Van Buren • Benno Schmidt Sr., former chairman of the board of Memorial Sloan-Kettering Cancer Center
Dennis Slamon, M.D., director of the Revlon/ UCLA Women’s Cancer Research Program at UCLA’s Jonsson Cancer Center, who contributed to the development of the drug Herceptin® (trastuzumab), a therapy that treats an aggressive form of breast cancer
by targeting the HER2 protein
And recipient of SPINODYSSEY funding within our first 3 years!
Words cannot begin to express my gratitude toward SPINODYSSEY 2011, and ACS for
funding my project. The pressure is now on us to produce meaningful results!
|Metastasis is the major reason for morbidity and mortality of breast cancer patients. Every sequential step in the process of metastasis requires specific sets of genes to be turned on or off. These gene sets are regulated in part through large protein complexes that re-organize the structure of DNA and how it is interacting with associated proteins (chromatin). The current focus of our lab is to characterize the composition and enzyme activity of these chromatin modifying complexes that regulate the process of breast cancer metastasis. These studies will provide the necessary groundwork for the identification of novel targets to enable treatment of metastatic breast cancer.
Gayle Alswanger of ACS • Pameeka Smith-Pearson, PH.D. (Fully Funded 2010)
Jenifer Prosperi, Ph.D. (Fully Funded 2010) • Brian Lehmann (Fully Funded 2010)
Marc Menillo (Fully Funded 2009) • Ronit Elk with ACS
p53 Signaling Axis and Triple Negative Breast Cancer
(Vanderbilt University Medical Center 7/1/10-6/30/2013) $150,000
My research is focused on identifying novel therapeutic targets for triple negative breast cancer (TNBC). We have recently demonstrated that TNBC is a heterogeneous disease composed of at least six distinct subtypes that display unique gene expression and display differential sensitivity to targetedtherapy. Currently we are conducting a large screen to identify new drug targets. This work hassignificant potential for biomarker selection, drug discovery, and clinical trial design that will enable alignment of TNBC patients to appropriate targeted therapies.
Impact of APC loss in mouse models of human breast cancer
(University of Chicago 7/1/10 – 6/30/2012) $102,000
Cancer is often driven by the loss of a class of genes that normally control cell growth and death called tumor suppressors. My project is aimed at understanding the role that the adenomatous polyposis coli (APC) tumor suppressor plays in the development of breast cancer. By using tumor models that closely mimic human disease, the long-term goal of my work is to develop novel approaches for therapeutic intervention in breast cancers in which APC is lost.
The role of Abl kinases in cancer and metastasis
(Duke University Medical Center 7/1/10 – 6/30/2012) $102,000
My name is Pameeka Smith-Pearson and I am a postdoctoral fellow at Duke University in the Department of Pharmacology and Cancer Biology. I am performing research in the laboratory of Dr. Ann Marie Pendergast. The primary interest of our laboratory is delineating the role of Abl kinases in cancer as well as normal cellular function. Abl kinase activity is elevated in a number of metastatic cancers and these kinases are activated downstream of several oncogenic signaling pathways. My project investigates the role of Abl kinases in cancer, invasion, and metastasis.
Featured from Left to Right:
Committee Members: Barry Ficken, Sharon Simon, Shelley Goldman (in back),
Cathy Beckman, Dr. Stevens (with ACS), Marc Menillo (2009 Researcher), Herb Wexler (in back - SO),
Don Stillman (SO), Amelie Babkie (SO Co-Founder, Creative Director, Web Site Designer),
John Dugdale (SO), Jenna Brien (SO). Down in Front: Ginny O'Neil (SO), Judy Samuels (SO),
Emm Koteka-Wiki (ZumbaOdyssey), Patty Kondub (SO Co Chair).
Member, Whitehead Institute
Professor of Biology, MIT
Investigator of the Howard Hughes Medical Institute
CAMBRIDGE, Mass. (October 15, 2010) – President Obama
today named Whitehead Member Susan Lindquist, a recipient of the
National Medal of Science, the nation’s highest scientific honor.
2009 SPINODYSSEY Researcher Marc Mendillo is doing his research at Whitehead Institute at MIT.
Boris Wilson (fully funded) -
The Swi/Snf Tumor Suppressor in Stem Cell Self -
renewal and Pluriptency (Dana Farber 7/1/07-6/30/2010)
Here's the article (translation of the Cell articlefrom DFCI's intranet page:
October 18, 2010
Study examines role of 'antagonist' proteins in cancer
In many cancer cells, the chromosomes look like a truck stop after a tornado – a havoc of broken and mangled pieces. In a few forms of cancer, including some highly aggressive types, however, the cells' genetic material is quite stable, suggesting that something else is spurring the cells' unbridled growth.
That "something," in many cases, may be epigenetic alterations, changes in the cell's machinery for switching genes on and off. While epigenetics has received increasing attention in recent years, scientists still know little about the role of individual enzymes in operating this machinery. In a study in the October issue of Cancer Cell, Dana-Farber investigators show how an imbalance of two such enzymes can spur tumor formation, and that shutting one of them down can make tumor growth stop.
The work is particularly intriguing because, unlike gene mutations, epigenetic changes are potentially reversible, suggesting that therapies directed against epigenetic enzymes could be effective in treating cancer, the study's authors write.
The study involved two proteins, known as SNF5 and EZH2, that control genes' activity. The authors demonstrated that the duo have a see-saw, or 'antagonistic' relationship with each other: when one is in decline, the other is on the rise. When SNF5 is lost, as it is in some lethal pediatric solid tumors, the sudden upsurge in EZH2 produces epigenetic changes associated with certain cancers. When they deactivated EZH2 in mouse models, the formation of tumors driven by SNF5 loss was blocked.
"Epigenetic alterations may well contribute to the formation of most, if not all cancers," says the study's senior author, Charles Roberts, MD, PhD, of Pediatric Oncology. "In cancers with a great deal of chromosomal instability, however, it's been difficult to determine which epigenetic alterations are actually contributing to tumor formation and which are more in the nature of collateral damage.
"Given the genomic stability in the cancers we're studying, our experimental models offer a powerful system for defining the role of epigenetic alterations driving cancer formation," Roberts continues. "Our study shows that a balance between these two epigenetic regulators serves to prevent tumor formation – and that correcting an imbalance may hold hope for future cancer therapies."
Contributing to the study were lead authors, , and Xi Wang, PhD, and co-authors Xiaohua Shen, PhD, Elizabeth McKenna, Madeleine Lemieux, PhD, Ted Koellhoffer, and Stuart Orkin, MD, of Dana-Farber.
Read more from the original article:
Members of SPINODYSSEY presented a check for $12,000 to
Norwalk Hospital's Whittingham Cancer Center earlier this year.
From left: Mary Heery, APRN, AOCNS and Breast Health Specialist; SPINODYSSEY Wine Tasting Committee Volunteer
Michele Lamothe; Breast Cancer Researcher Dr. Richard Zelkowitz;
SPINODYSSEY Co-Chairwoman Patty Kondub; Jennifer Long, APRN; and Rita Ort, RN.
(some fully funded, others partially)
- Leon Murphy - Fos Phosphorylation and Cellular Transformation
- David Wah - Analysis of the Molecular Determinants in Proten Degradation
- John Wysolmerski - Role of PTHrP in Breast Cancer Metastases to Bone
- Michael DiGiovanna - Targeting HER2 and Estrogen Receptor in Breast Cancer
- Graham Colditz - Breast Cancer Epidemiology and Prevention
(Brigham and Women's Hospital 7/1/03-6/30/08)
- Dennis Slamon - Her-2 Alteration in Human Breast Cancer: Delineation of Downstram Molecular Events & Identification of Additional Potential Therapeutic Targets
(Univ. California Los Angeles 7/1/04-6/30/09)
- Kevin Janes (fully funded) - Cell Specification During Mammary Acinar Morphogenesis in Vitro (Harvard 7/1/05-6/30/08)
- Ryan Jensen - Delineating the Role of BRCA2 in Regulating Rad51 Mediated Recombination
(Univ. California Davis 7/1/05-6/30/08)
- Victor Grann (fully funded) - Decision Analysis of Population Screening for BRCA1/2 Mutations (Columbia Univ. 1/1/06-12/31/09)
- Meredith Crosby (fully funded) - Hypoxia-Induced DNA Repair Pathway Regulation
- Eric Smith (fully funded)-Causes and Consequences of Adaptive Evolution in Dosage Compensation (Fred Hutchinson Cancer Research Center 7/1/07-6/30-2010)
- David DeNardo (fully funded) - Role of Adaptive Immunity in Breast Cancer Progression (Univ. California San Francisco 7/1/07-6/30/2010)
- Boris Wilson (fully funded) - The Swi/Snf Tumor Suppressor in Stem Cell Self - renewal and Pluripotency (Dana Farber 7/1/07-6/30/2010)
- Josh Anderson (fully funded) - Saspase 2 Mediated Apoptosis
(Duke University 7/1/08-6/30/2011)
- Rachel Dusek (fully funded) - The Role of Perp in Mammary Gland Morphogenesis and Cancer (Stanford University 1/1/08-12/31/2010)
- Christopher Veldkamp (fully funded) - Novel Inhibition of Cancer Cell Metastasis with an Engineered Chemokine (Medical College of Wisconsin 7/1/08-6/30/2011)
- Traci Lyons (fully funded) - Mammary Gland Imicroenvironment in Breast Cancer Metastasis after Pregnancy (University of Colorado 7/1/08-6/30/2011)
- Marc Mendillo (fully funded) - The Role of HSF1 in Tumorigenesis
(Whitehead Institute at MIT 7/1/09-6/30-2012)
- Daniel Nomura (fully funded) - Annotating Metabolic Pathways that Support Cancer Pathogenicity (The Scripps Research Institute 7/1/09-6/30/2012)