Health
CLEARLAKE, Calif. – Tuesday, April 3, marked the first campaign cabinet meeting of the St. Helena Hospital Clear Lake Development Office.
Gathered at the hospital campus, the cabinet met to discuss strategies for the “Building for the Future” campaign under way to raise the final $1.8 million to complete the new emergency department, expected to be finished mid-2013.
“Our Emergency Department is the front door to our hospital, the place where our patients get their first and most lasting impression of the quality of our hospital,” said David Santos, vice president of Operations. “The community support of this critical project demonstrates its commitment to making St. Helena Hospital Clear Lake a place for our patients to experience the highest level of care.”
Adventist Health, St. Helena Hospital’s parent organization, provided the first $9 million for the $12.1 million project, and challenged the hospital to fund the remainder from within the community.
Redbud Health Care District pledged $1 million in 2010. In January 2012, the Rotary Club of Clearlake pledged $25,000.
Since the beginning, the Building for the Future campaign has raised an additional $1,236,510 from community donors, including hospital employees and volunteers.
Local businesses and organizations such as Lake Pharmacy, Wells Fargo, Bikram Yoga Lake County and Coastal Mountain Electric also have been supporters.
The hospital’s emergency department – one of the smallest yet busiest in the state – currently handles about 16,000 visits per year.
With the projected increase in the county population in the future, this number may rise to as many as 35,000 visits per year.
The renovations include expanding and upgrading the original cramped 1960s-era emergency room to provide faster precision care for patients, better access, and an increase in patient care staff.
With just one year to complete the funding, the cabinet faces this tight timeline with enthusiasm for being involved in this new phase of the hospital’s future.
Leaders were identified based on individual abilities and traits such as integrity, respect among peers, the willingness to connect others, a feeling of social responsibility, and managed time to spend on a worthy cause.
“Our cabinet members will take the lead in representing the Development Office and the hospital in the Building for the Future Campaign,” said Development Officer Melissa Kinsel. “All our members bring extraordinary personal gifts and heart to this effort. I am so encouraged by their involvement.”
“I see the emergency department from the bedside and I know the incredible transformation that will occur because of the cabinet’s fundraising efforts,” said Dr. Rockwell, medical director of the Emergency Department. “We will be transformed from a small, outdated Emergency Department to an Emergency Center of excellence.”
Two key positions have been filled by well-known Lake County community members: Celia Hoberg, a longtime resident and West America Bank representative, has accepted the position of campaign cabinet chair and Rick Hamilton, owner of RAHamilton Co., and resident of Hidden Valley Lake, has agreed to be co-chair.
“As a patient I felt as though my health was the most important to everyone who was involved,” said Hoberg. “This hospital is here for the whole Lake County Community. I am proud and honored to be involved with the task of helping raise the additional funds needed to complete the remodel. A very worthy cause indeed.”
For more information or if you would like to donate please visit us at www.newERforyou.com/donate .
- Details
- Written by: Editor
Scientists at the BC Cancer Agency and University of British Columbia have identified new breast cancer genes that could change the way the disease is diagnosed and form the basis of next-generation treatments.
Researchers have reclassified the disease into 10 completely new categories based on the genetic fingerprint of a tumor. Many of these genes could offer much-needed insight into breast cancer biology, allowing doctors to predict whether a tumor will respond to a particular treatment. Whether the tumor is likely to spread to other parts of the body or if it is likely to return following treatment.
"Breast cancer is a global problem and it's exciting to see a new framework for the understanding of breast cancer emerge from our partnership with colleagues in the UK.
"This is a major step forward in building the genetic encyclopedia of breast cancer and in the process we've learned there are many more subtypes of breast cancer than we imagined,” said Dr. Sam Aparicio, study co-lead author and professor in the Department of Pathology and Laboratory Medicine UBC; BC Cancer Agency Chair of Breast Cancer Research.
“The new molecular map of breast cancer points us to new drug targets for treating breast cancer and also defines the groups of patients who would benefit most,” Aparicio added.
The study, published online in the international journal Nature, is the largest global study of breast cancer tissue ever performed and the culmination of decades of research into the disease.
In the future, this information could be used by doctors to better tailor treatment to the individual patient.
"Our results will pave the way for doctors in the future to diagnose the type of breast cancer a woman has, the types of drugs that will work, and those that won't, in a much more precise way than is currently possible,” said Professor Carlos Caldas, study co-lead author and senior group leader at Cancer Research UK's Cambridge Research Institute and the Department of Oncology. "This means that women who are diagnosed and treated fairly uniformly today will in the future receive treatment targeted to the genetic fingerprint of their tumor.”
Caldas added, “We've drilled down into the fundamental detail of the biological causes of breast cancer in a comprehensive genetic study. Our results have reclassified breast cancer into 10 types – making breast cancer an umbrella term for an even greater number of diseases.”
He said the next stage is to find how tumors classified under each sub group behave. “And we need to carry out more research in the laboratory and in patients to confirm the most effective treatment plan for each of the 10 types of breast cancer.”
The team at the BC Cancer Agency, in collaboration with Cancer Research UK's Cambridge Research Institute and Manitoba Institute of Cell Biology at University of Manitoba, analyzed the DNA and RNA of 2,000 tumor samples taken from women diagnosed with breast cancer between five and 10 years ago.
The sheer number of tumors mapped allowed researchers to spot new patterns in the data.
Study milestones include:
- Classified breast cancer into 10 subtypes grouped by common genetic features, which correlate with survival. This new classification could change the way drugs are tailored to treat women with breast cancer.
- Discovered several completely new genes that had never before been linked to breast cancer. These genes that drive the disease are all targets for new drugs that may be developed. This information will be available to scientists worldwide to boost drug discovery and development.
- Revealed the relationship between these genes and known cell signaling pathways – networks that control cell growth and division. This could pinpoint how these gene faults cause cancer, by disrupting important cell processes.
This is the second major breakthrough announced by BC Cancer Agency scientists in as many weeks.
On April 4, a team led by Dr. Sam Aparicio celebrated the decoding of the genetic makeup of the most-deadly of breast cancers, triple-negative breast cancer, which until then was defined by what it was missing, not what it was.
Similar to that announcement, the new discovery identifies genes that were previously unknown to be linked to breast cancer and makes it clear that breast cancer is an umbrella term for what really is a number of unique diseases.
While the research is unlikely to benefit women who currently have breast cancer, it substantially advances how scientists approach further research and clinical trials by providing them with a springboard to develop new treatment options and drugs targeted to specific genes.
The research was carried out in collaboration with the following institutes:
- British Columbia Cancer Agency, Vancouver
- University of British Columbia, Vancouver
- Department of Oncology, University of Cambridge
- Department of Applied Mathematics and Theoretical Physics, University of Cambridge
- Department of Genetics, The Institute for Cancer Research
- Oslo University Hospital
- Department of Histopathology, University of Nottingham
- Cambridge Breast Unit, Addenbrooke's Hospital, Cambridge University Hospital NHS Foundation Trust and NIHR Cambridge Biomedical Research Centre
- King's College London, Breakthrough Breast Cancer Research Unit
- Manitoba Institute of Cell Biology, University of Manitoba
- NIHR Comprehensive Biomedical Research Centre at Guy's and St Thomas' NHS Foundation Trust and King's College London
- Institute for Clinical Medicine, Faculty of Medicine, University of Oslo
- Cambridge Experimental Cancer Medicine Centre.
- Details
- Written by: Editor
One in eight women will be diagnosed with breast cancer during her lifetime. The earlier cancer is detected, the better the chance of successful treatment and long-term survival.
However, early cancer diagnosis is still challenging as testing by mammography remains cumbersome, costly, and in many cases, cancer can only be detected at an advanced stage.
A team based in the Department of Biomedical Engineering at McGill University's Faculty of Medicine has developed a new microfluidics-based microarray that could one day radically change how and when cancer is diagnosed.
Their findings are published in the April issue of the journal Molecular & Cellular Proteomics.
For years, scientists have worked to develop blood tests for cancer based on the presence of the Carcinoembryonic Antigen (CEA), a protein biomarker for cancer identified over 40 years ago by McGill's Dr. Phil Gold.
This biomarker, however, is also found in healthy people and its concentration varies from person to person depending on genetic background and lifestyle. As such, it has not been possible to establish a precise cut-off between healthy individuals and those with cancer.
"Attempts have been made to overcome this problem of person-to-person variability by seeking to establish a molecular 'portrait' of a person by measuring both the concentration of multiple proteins in the blood and identifying the signature molecules that, taken together, constitute a characteristic 'fingerprint' of cancer," explained Dr. David Juncker, the team's principal investigator. "However, no reliable set of biomarkers has been found, and no such test is available today. Our goal is to find a way around this."
Dr. Mateu Pla-Roca, the study's first author, along with members of Juncker's team, began by analyzing the most commonly used existing technologies that measure multiple proteins in the blood and developing a model describing their vulnerabilities and limitations.
Specifically, they discovered why the number of protein targets that can be measured simultaneously has been limited and why the accuracy and reproducibility of these tests have been so challenging to improve.
Armed with a better understanding of these limitations, the team then developed a novel microfluidics-based microarray technology that circumvents these restrictions.
Using this new approach, it then became possible to measure as many protein biomarkers as desired while minimizing the possibility of obtaining false results.
Juncker's biomedical engineering group, together with oncology and bioinformatics teams from McGill's Goodman Cancer Research Centre, then measured the profile of 32 proteins in the blood of 11 healthy controls and 17 individuals who had a particular subtype of breast cancer (estrogen receptor-positive).
The researchers found that a subset of six of these 32 proteins could be used to establish a fingerprint for this cancer and classify each of the patients and healthy controls as having or not having breast cancer.
"While this study needs to be repeated with additional markers and a greater diversity of patients and cancer subsets before such a test can be applied to clinical diagnosis, these results nonetheless underscore the exciting potential of this new technology," said Juncker.
Looking ahead, Juncker and his collaborators have set as their goal the development of a simple test that can be carried out in a physician's office using a droplet of blood, thereby reducing dependence on mammography and minimizing attendant exposure to X-rays, discomfort and cost.
His lab is currently developing a hand-held version of the test and is working on improving its sensitivity so as to be able to accurately detect breast cancer and ultimately, many other diseases, at the earliest possible stage.
- Details
- Written by: Editor
A team of researchers at Case Western Reserve University School of Medicine have identified a new mechanism by which colon cancer develops.
By focusing on segments of DNA located between genes, or so-called "junk DNA," the team has discovered a set of master switches, i.e., gene enhancer elements, that turn "on and off" key genes whose altered expression is defining for colon cancers.
They have coined the term Variant Enhancer Loci or "VELs," to describe these master switches.
Importantly, VELs are not mutations in the actual DNA sequence, but rather are changes in proteins that bind to DNA, a type of alteration known as "epigenetic" or "epimutations." This is a critical finding because such epimutations are potentially reversible.
Over the course of three years, the team mapped the locations of hundreds of thousands of gene enhancer elements in DNA from normal and cancerous colon tissues, pinpointing key target VELs that differed between the two types.
"What is particularly interesting is that VELs define a 'molecular signature' of colon cancer. Meaning, they are consistently found across multiple independent colon tumor samples, despite the fact that the tumors arose in different individuals and are at different stages of the disease," said Peter Scacheri, PhD, senior author of the study and assistant professor, Genetics and Genome Sciences, School of Medicine, and member, Case Comprehensive Cancer Center at Case Western Reserve University. "The set of common VELs govern a distinct set of genes that go awry in colon cancer."
"The VELs signature is notable because it cuts through the complexity of the many genes that are changed in colon cancer, to identify genes that are direct targets of alterations on chromosomes,” said Sanford Markowitz, MD, PhD, Ingalls Professor of Cancer Genetics in the Division of Hematology-Oncology at the School of Medicine, member, Case Comprehensive Cancer Center, and oncologist at University Hospitals Seidman Cancer Center, whose team collaborated on the study. "The key next step will be to determine whether we can use VELs for 'personalized medicine,' to molecularly define distinct groups of colon cancers that differ in their clinical behavior, and to enable selection of specific drugs that will best treat a given colon tumor."
In addition to finding that VELs are a "signature" of colon cancer, the team showed that genetic variants which predispose individuals to colon cancer are located within VELs. This suggests that individual differences within VELs may play significant roles in determining different individuals' susceptibility to colon cancer.
"Epigenetics has transformed the way we think about genomes. The genetic code isn't just a series of As, Ts, Gs, and Cs strung together. Epigenetic 'marks' on DNA tell genes when, where, and how much to turn on or off to keep cells healthy," said Batool Akhtar-Zaidi, PhD candidate in Dr. Scacheri's lab and lead author of the study. "When this epigenetic machinery is disrupted, as we see with VEL events, this can tip the balance to cancer."
Co-authors on the study, "Epigenomic enhancer profiling defines a signature of colon cancer" published advanced online in Science Express, include Olivia Corradin, Alina Saiakhova, Cynthia F. Bartels, Dheepa Balasubramanian, Lois Myeroff, James Lutterbaugh, Paul J. Tesar, Thomas Laframboise, Joseph Willis at Case Western Reserve School of Medicine; Awad Jarrar, Matthew F. Kalady at Cleveland Clinic; and Richard Cowper-Sal lari, Jason H. Moore, Mathieu Lupien at Dartmouth Medical School.
This research was supported by the National Cancer Institute, as well as the Case Comprehensive Cancer Center.
- Details
- Written by: Editor