 |
 |
to Douglas Hurst, Ph.D., University of Alabama at Birmingham for his four year research titled: |
||||
 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.
|
FULLY FUNDED 2010 RESEARCHERS
On Stage for the Opening Ceremonies of the 2011 Event:
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).
IMPORTANT RESEARCH INFORMATION!
 |
SUSAN LINDQUIST 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.
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, Boris Wilson, PhD, and Xi Wang, PhD, and co-authors Xiaohua Shen, PhD, Elizabeth McKenna, Madeleine Lemieux, PhD, Ted Koellhoffer, and Stuart Orkin, MD, of Dana-Farber. |
- WHITTINGHAM CANCER CENTER -
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)
|
|---|
| S |
|
|