Category: Press Release
Press: October 16th 2014, written by Todd Feathers | Boston Globe
Five eminent Boston researchers will officially join forces Thursday to tackle one of the most perplexing questions about breast cancer: Why do so many people with no family history of the disease get it?
The researchers will examine whether common man-made chemicals are responsible for the disease, which increasingly strikes men and women.
In 2014, breast cancer will be the second-most-diagnosed form of cancer and the third- deadliest form of the disease, according to the National Cancer Institute. But unlike with some other cancers, the vast majority of breast cancer diagnoses — more than 90 percent — cannot be traced to a hereditary cause, the institute said.
“I think what we’re going to be doing is adding the weight of evidence that environmental chemicals contribute significantly to [breast] cancer, more than most people expect,” said David H. Sherr, of the Boston University School of Public Health. He is leading the team.
The research is backed by a three-year, $5 million grant from ART beCAUSE, a breast cancer foundation.
Ellie Anbinder, its cofounder, spearheaded the funding effort. She survived breast cancer but was left wondering why she developed it in the first place.
“The bottom line is that there is not a lot of coordinated research around the environment and breast cancer,” she said. “We felt that in order to have some kind of strong impact on the field of environmental causes of breast cancer we needed to put together a large project.”
Most cancer research is dedicated to developing drugs or cures, Sherr said. But the Boston consortium’s ultimate goal is finding a way to prevent the cancer from ever taking hold.
Sherr studies receptors in cells that detect chemicals in their vicinity. Fellow researchers Gail Sonenshein, of Tufts University School of Medicine, and Dr. David C. Seldin, of the Boston University School of Medicine, will examine signaling pathways that tell a cell when and how to change once it interacts with a chemical.
Charlotte Kuperwasser, also of Tufts, is a pioneer of the theory of cancer stem cells.
Rounding out the team is Stefano Monti, of BU, a computational biologist who uses algorithms to project how cells will react to certain chemicals.
Press release: September 4th 2014
SOUTH SAN FRANCISCO, Calif., Sept. 4, 2014 /PRNewswire/ — Veracyte, a molecular diagnostics company pioneering the field of molecular cytology, today announced an agreement to acquire Allegro Diagnostics Corp. based in Maynard, Mass., for $21.0 million, comprised of $7.8 million in cash and $13.2 million in Veracyte common stock. Allegro is a privately held company focused on developing genomic tests to improve the preoperative diagnosis of lung cancer.
Veracyte plans to commercially launch Allegro’s lead lung cancer test in the second half of 2015, with meaningful revenue expected in 2017.
Allegro’s lung cancer test is designed to help physicians determine which patients with lung nodules who have had a non-diagnostic bronchoscopy result are at low risk for cancer and can thus be safely monitored with CT scans rather than undergoing invasive procedures. The gene expression test uses Allegro’s proprietary “field of injury” genomic technology platform to circumvent the traditional challenge of obtaining accurate lung nodule samples for testing, without surgery or other invasive, risky and expensive procedures.
“With Allegro and its novel, clinically validated lung cancer test, we plan to accelerate our entry into the pulmonology market, enabling us to improve care for patients with lung nodules while creating long-term growth opportunities,” said Bonnie H. Anderson, Veracyte’s president and chief executive officer. “Allegro is a natural fit for us and we believe this move further establishes our leadership in molecular cytology, using genomics to resolve diagnostic ambiguity preoperatively and thus spare patients from unnecessary invasive procedures and reduce associated healthcare costs.”
Allegro’s technology detects molecular changes that occur throughout the respiratory airways in response to smoking – the cause of almost all lung cancers – and that are correlated with disease. These changes can be detected in a gene expression signature from cytologically normal airway cells and indicate the presence of malignancy or disease processes from distant sites in the lung. The lung cancer test is performed on cytology samples obtained through bronchoscopy, a minimally invasive procedure that enables a physician to access airways in the lung. The molecular classifier’s performance has been established in two prospective, multicenter clinical validation studies, involving 25 centers and nearly 1,000 patients.
“We are excited for our lead test to become available to patients, helping to reduce unnecessary diagnostic surgeries and other procedures among the hundreds of thousands of patients with lung nodules who undergo bronchoscopies each year in the U.S to rule out cancer,” said Michael D. Webb, president and chief executive officer of Allegro Diagnostics. “We believe Veracyte is uniquely poised to commercialize and gain reimbursement for our test, given the rapid success the company has achieved with its Afirma® solution in endocrinology.”
About Lung Cancer Diagnosis
Lung cancer is the leading cancer killer in the U.S., with an estimated 225,000 new cases diagnosed and approximately 160,000 deaths caused by the disease each year. Recent guidelines recommend annual CT screening for high-risk patients, with an estimated eight million Americans falling into this category based on smoking history and age. Among the approximately 250,000 bronchoscopies currently performed each year in the U.S. to evaluate lung nodules – a potential sign of cancer – up to 40 percent produce non-diagnostic results, based on pathology. Approximately half of these patients undergo surgery or other invasive procedures to obtain a diagnosis. Data show that approximately 40 percent of lung nodule patients who undergo surgery prove to have benign nodules. Thus, a better way to risk-stratify patients at high risk of lung cancer could help determine which patients can be safely followed with CT scans versus invasive procedures.
Veracyte is pioneering the field of molecular cytology, focusing on genomic solutions that resolve diagnostic ambiguity and enable physicians to make more informed treatment decisions at an early stage in patient care. By improving preoperative diagnostic accuracy, the company aims to help patients avoid unnecessary invasive procedures while reducing healthcare costs. Veracyte’s first commercial solution, the Afirma® Thyroid FNA Analysis, provides a comprehensive approach for assessing thyroid nodules, centered on the proprietary Gene Expression Classifier (GEC) to resolve ambiguity in diagnosis. Each year, of the more than 525,000 thyroid nodule FNAs performed in the U.S., approximately 115,000 patients undergo diagnostic thyroid surgery, with 70% to 80% of nodules proving benign and thus the surgery unnecessary. Veracyte commercially launched Afirma in January 2011. As of June 30, 2014, the company has received nearly 115,000 FNA samples for evaluation using Afirma and has performed over 20,000 GECs to resolve indeterminate cytopathology results. Backed by multiple, peer-reviewed, published studies and included in leading medical guidelines, Afirma is covered by Medicare and major commercial payers, which collectively represent more than 135 million covered lives. Afirma is marketed and sold through a global co-promotion agreement with Genzyme Corporation, a subsidiary of Sanofi. Veracyte intends to expand its molecular cytology franchise to other clinical areas and is in product development for its first product in pulmonology. For more information, please visit www.veracyte.com.
This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, including statements relating to the company’s belief that the acquisition of Allegro will accelerate Veracyte’s entry into the pulmonology market and allow it to improve patient care while creating long-term growth opportunities, the company’s plans to launch Allegro’s lung cancer test in the second half of 2015 and its beliefs regarding when it expects to derive meaningful revenue from the test, the company’s beliefs regarding the benefits of its tests and Allegro’s tests to physicians, patients and payers, and the company’s intent to expand its molecular cytology business into other clinical areas. Forward-looking statements involve risks and uncertainties, which could cause actual results to differ materially, and reported results should not be considered as an indication of future performance. These risks and uncertainties include, but are not limited to: our ability to close the acquisition; our limited operating history and history of losses; our ability to increase usage of and reimbursement for Afirma and any future products we may develop or sell, including the Allegro lung cancer test; our ability to continue our momentum and growth; our dependence on a few payers for a significant portion of our revenue; the complexity, time and expense associated with billing and collecting from payers for our test; laws and regulations applicable to our business, including potential regulation by the Food and Drug Administration or other regulatory bodies; our dependence on strategic relationships and our ability to successfully convert new accounts resulting from such relationships; our ability to develop and commercialize new products and the timing of commercialization, including our ability to successfully commercialize the Allegro lung cancer test; our ability to achieve sales penetration in complex commercial accounts; the occurrence and outcome of clinical studies; the timing and publication of study results; the applicability of clinical results to actual outcomes; our inclusion in clinical practice guidelines; the continued application of clinical guidelines to our products; our ability to compete; our ability to expand into international markets; our success integrating Allegro into our business; our ability to obtain capital when needed; and other risks set forth in the company’s filings with the Securities and Exchange Commission, including the risks set forth in the company’s Quarterly Report on Form 10-Q for the quarter ended June 30, 2014. These forward-looking statements speak only as of the date hereof and Veracyte specifically disclaims any obligation to update these forward-looking statements.
Veracyte, Afirma, the Veracyte logo, and the Afirma logo are trademarks of Veracyte, Inc. This press release also contains trademarks and trade names that are the property of their respective owners.
Burns McClellan, Inc.
Press Release from July 24th 2014
A new study has shown that it is possible to predict long-term cancer risk from a chemical exposure by measuring the short-term effects of that same exposure. The findings, which currently appear in the journal PLOS ONE, will make it possible to develop simpler and cheaper tests to screen chemicals for their potential cancer causing risk.
Despite an overall decrease in incidence of and mortality from cancer, about 40 percent of Americans will be diagnosed with the disease in their lifetime, and around 20 percent will die of it. Currently fewer than two percent of the chemicals on the market have been tested for their ability to induce cancer.
Using an experimental model, researchers from Boston University School of Medicine (BUSM), Boston University School of Public Health, the BU Bioinformatics Program and the National Toxicology Program at the National Institute of Environmental Health measured the effects on healthy tissue from few days of exposure to a given chemical and assessed the effects on the gene expression response in the liver. “By comparing the responses to known chemical carcinogens and non-carcinogens, we were able to extract a “signature” and an associated predictive model capable of discriminating with high accuracy between the two,” explained corresponding author Stefano Monti, PhD, associate professor of medicine at BUSM and a member of the BU Superfund Research Program. “Furthermore, by inspection of the coordinated set of genes driving the response to chemical exposure, we were able to zoom in to the potential mechanisms driving cancer induction,” he added.
According to the researchers there is growing recognition that the role played by environmental pollutants in human cancer is under-studied and that more formal approaches to the analysis of the biological consequences of prolonged exposure to pollutants are needed. “This work has confirmed that it is possible to predict the long-term cancer risk by measuring the short term effects,” said Monti. “As a result of our findings we expect that accurate and cost-effective screening for evaluating the carcinogenic potential of the more than the 80,000 chemicals currently in commercial use soon will be a reality.”
Publication: Daniel Gusenleitner, Scott S. Auerbach, Tisha Melia, Harold F. Gómez, David H. Sherr, Stefano Monti. Genomic Models of Short-Term Exposure Accurately Predict Long-Term Chemical Carcinogenicity and Identify Putative Mechanisms of Action. PLoS ONE, 2014; 9 (7): e102579 DOI:10.1371/journal.pone.0102579
Story Source: The above story is based on materials provided by Boston University Medical Center. Note: Materials may be edited for content and length.
Press Release: From October 28th 2013
Written by Jenny C Leary
Researchers at Boston University School of Medicine (BUSM) have discovered a molecule that could help lead to the non-invasive detection of lung cancer as well as its treatment. Using RNA sequencing, the team looked at airway epithelial cells and identified a regulatory molecule that was less abundant in people with lung cancer and inhibits lung cancer cell growth. The findings, which are published in the Proceedings of the National Academy of Sciences, suggest that this molecule may aid in diagnosing lung cancer in earlier stages and could potentially, when at healthy levels, aid in treating the disease.
According to the National Cancer Institute (NCI), lung cancer is the leading cause of cancer death among both men and women in the United States, and 90 percent of lung cancer deaths among men and approximately 80 percent of lung cancer deaths among women are due to smoking. The NCI also estimates that approximately 373,489 Americans are living with lung cancer and its treatment costs approximately $10.3 billion in the United States each year.
MicroRNA’s are a new class of molecules classified as important regulators of the activity of other genes. In this study, the research team used a next-generation RNA sequencing technology and identified that a microRNA named miR-4423 in epithelial airway cells plays a major role in how these cells develop. In epithelial cells from the airway of smokers with lung cancer, levels of miR-4423 were decreased.
“These results suggest measuring the levels of microRNAs like miR-4423 in cells that line the airway could aid in lung cancer detection through a relatively non-invasive procedure,” said Avrum Spira, MD, MSc, the Alexander Graham Bell professor of medicine and chief of the division of computational biomedicine at BUSM, one of the study’s senior authors.
Using experimental models in vitro and in vivo, the research team demonstrated that miR-4423 can both promote the development of the normal airway cells and suppress lung cancer cell growth. This suggests that miR-4423 plays a major regulatory role in cell fate decisions made by airway epithelial cells during maturation and low levels of miR-4423 contributes to lung cancer development. Interestingly, throughout the body, miR-4423 seems only to be present in high levels in the airway epithelium, suggesting this could be a very specific process occurring only in the lungs.
“Our findings open up the option to study whether returning the levels of miR-4423 to normal in the airway could help stop cancer growth and potentially be a way to treat lung cancer,” said Catalina Perdomo, PhD, a researcher in the division of computational biomedicine at BUSM who is the paper’s lead author.
“Interestingly, when we examined the genomes of other species for microRNAs that might function like miR-4423, we did not find anything in non-primates,” said Marc Lenburg, PhD, an associate professor in computational medicine and bioinformatics at BUSM who is one the study’s senior authors. “It makes us wonder what it is different about lung development in primates and excited that this could be a very specific process to target for lung cancer treatment.”
This study was funded in part by the National Institutes of Health’s National Cancer Institute Early Detection Research Network under grant award numbers R01 CA 124640 and U01 CA152751; the National Science Foundation Integrative Graduate Education and Research Traineeship under grant award number P50CA58184; and Merit Review grants 5I01BX000359 and R43HL088807-01.
Journal Reference: Perdomo C, Campbell J.D., Gerrein J, Tellez C, Garrison C.B., Walser T.C., Drizik E, Si H, Gower A.C., Vick J, Anderlind C, Jackson G.R., Mankus C, Schembri F, O’Hara C, Gomperts B.N., Dubinett S.M., Hayden P, Belinsky S.A., Lenburg M.E., Spira A (2013) MicroRNA 4423 is a primate-specific regulator of airway epithelial cell differentiation and lung carcinogenesis. Proc Natl Acad Sci USA, 10.1073/pnas.1220319110 PMID: 24158479
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Press Release : BU Today January 22 2013
Never Smoked. Lived Right. Died of Lung Cancer.
By Rich Barlow
Avrum Spira’s aunt died of lung cancer almost 20 years ago. She was a nonsmoking exercise buff in her 40s who hadn’t been exposed to any known toxins; she worked in a government office, not a coal mine. “One of the healthiest people you could imagine, did everything right,” says Spira (ENG’02), who at the time was an internal medicine resident at the University of Toronto.
The one thing she didn’t do right wasn’t her fault: she’d been born to a nonsmoking mother who had died from the same illness. “I’m absolutely convinced she had a genetic predisposition” to lung cancer, says Spira, a School of Medicine professor and chief of computational biomedicine. That conviction set him on a quest for the genetic key to a medical mystery: why some people who have never smoked fall victim to this scourge of cigarette users.
Lung cancer kills more Americans than any other cancer, and twice as many women die from it than from breast cancer, although the latter gets greater public attention, says Spira. In 2008, the last year for which data was available, more than 208,000 Americans were diagnosed with lung cancer and almost 158,600 died from it. Spira says between 10 and 15 percent of these annual victims are nonsmokers (the percentage has been edging up slowly in recent years) with no apparent exposure to other toxins—a crucial caveat. “How do you know someone has been or has not been exposed to something in the environment?” he asks. Some potential toxins, like radon, are invisible, he notes, “so people who we’re seeing now, with higher rates of nonsmoking lung cancer—is it because they were exposed to radon 20 years ago?”
It’s true that worldwide, the rise in the incidence of lung cancer—from the eighth leading cause of death in 1990 to fifth in 2010—is mostly a function, perversely, of good news: as living standards have improved in the developing world, more people survive into adulthood, meaning a decline in childhood deaths from malnutrition and infectious diseases. That has brought an accompanying uptick in the number of people dying from diseases mostly found in wealthier countries, among them cancer. Moreover, air pollution in industrializing countries has resulted in more lung cancer in nonsmokers there, Spira says.
But in the United States, he says, doctors believe there’s a similar spurt in lung cancers in nonsmokers who’ve had no apparent contact with other toxins. The most extensive studies, incorporating detailed questionnaires and visits to peoples’ homes to see their environment, show that “there hasn’t been a clear association among nonsmokers who are getting lung cancer with exposures to other things.”
An ongoing, as-yet-unpublished study by a team that includes Spira is looking at tumor tissue and adjacent, noncancerous tissue from the lungs of 32 subjects with lung cancer: 8 smokers, 11 former smokers, and 13 who never smoked and had no apparent exposure to other toxins. The researchers ran the samples through a gene sequencer at MED, which “can give us unprecedented insight into the genomic changes leading to lung cancer” in nonsmokers, says Rebecca Kusko (MED’14), a graduate student spearheading the study in Spira’s lab.
With the sequencer, “we study the normal cells from each person as a control,” says Spira, “and then what happens in their tumor right next door, and say, what’s changed?” Preliminary results suggest that in the smokers, “a huge number of cancer pathways are activated,” as genes controlling cell growth in the tumors turned on. But those pathways weren’t necessarily activated in the nonsmokers, who showed different gene changes between their healthy lung tissue and their tumorous tissue. The researchers’ hypothesis is that the nonsmokers had a genetic predisposition, a pathway, to cancer that was activated by something in their environment.
That trigger, Spira theorizes, may be a viral infection (cervical, liver, and head and neck cancers are all caused by viruses, he says). The researchers are now sequencing the tumor tissue of the nonsmokers to try and find any viral genes. “Even if there’s one viral gene per million human genes, we might pick it up, we believe,” he says. The work will take a year or two.
Potential therapies—which are many more years away, he warns—might include screening people with the genetic predisposition and then giving those with the predisposition regular lung scans to catch cancers early. Another possibility would be drugs that could turn off uncontrolled growth in cancerous cells. (Spira got attention in 2010 for research suggesting that the natural compound myo-inositolcould turn off incipient lung cancer in smokers.)
Those who walk Commonwealth Avenue and have to dodge fumes from smokers on break may wonder about secondhand smoke. Research is mixed, but Spira, who researches the amount of smoke necessary to change gene expression and possibly lead to lung cancer, believes that it takes a big dose—perhaps exposure over months or years.
Almost half a century after the surgeon general first warned of smoking’s dangers, Spira says that even Hollywood is catching on that not all cancer victims heedlessly bring the disease on themselves. In 2011, he was a presenter at the Prism Awards, given for accurate portrayals of illness in entertainment media. He handed an award to an actress whose character on the soap opera The Bold and the Beautifulhad lung cancer.
The character was a nonsmoker.
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