News 15 mei 2009
Biological Timekeeper Studies
Reveal New Temperature Regulator and Track Clock Protein across a Day
Dartmouth Medical School geneticists have made new inroads into understanding the
regulatory circuitry of the biological clock that synchronizes the ebb and flow of daily
activities, according to two studies published May 15. Research on the relationship
between clocks and temperature, reported in Cell, offers insight into a longstanding
puzzle of temperature compensation: why the 24-hour circadian rhythm does not change with
temperature when metabolism is so affected. A related study, in Molecular Cell, tracks a
clock protein in action, mapping hundreds of highly choreographed modifications and
interactions to provide the first complete view of regulation across a day.
Chronic Infection Now Clearly Tied
to Immune-System Protein
he reason deadly infections like human immunodeficiency virus (HIV) and hepatitis C never
go away is because these viruses disarm the body's defense system. Researchers at the
University of Alabama at Birmingham (UAB) have discovered that a key immunity protein must
be present for this defense system to have a chance against chronic infection. Research up
to now has tried but failed to decipher the cross-talk between 'killer T-cells' and
'helper T-cells' in the fight against viruses. The new UAB study finds this cross-talk can
only happen in the presence of interleukin-21, a powerful immune system protein. If
interleukin-21 is missing for whatever reason, then the immune system's anti-viral efforts
fail, said Allan Zajac, Ph.D., an associate professor in UAB's Department of Microbiology
and lead author on the study.
A surprise 'spark' for
pre-cancerous colon polyps
Researchers at Huntsman Cancer Institute (HCI) at the University of Utah studied the
events leading to colon cancer and found that an unexpected protein serves as the
"spark" that triggers formation of colon polyps, the precursors to cancerous
tumors. "Our findings will certainly raise some eyebrows," says oncological
sciences graduate student Reid Phelps, first author of the study, which will be published
Friday, May 15 in the journal Cell. "We expect the conventional wisdom regarding
colon tumor development to be reconsidered, together with some resistance to our
alternative explanation." The study in zebrafish and human cells discovered that a
protein, known as C-terminal binding protein 1, or CTBP1, was the spark that initiated
colon polyp formation, not the protein beta-catenin, as previously thought. With this new
information, future treatments that prevent tumor progression can be developed. The
research centered on the mutation of a tumor-suppressor gene called APC – a mutation
previously found to be present in 85 percent of all colon cancers. Since then, research
labs around the world have developed theories about how the gene works in colon cancer
development. "Our work reveals new information about how the APC protein functions to
prevent colon tumor formation. This new information opens new possibilities treating and
preventing colon cancer. " says David Jones, Ph.D., a professor of oncological
sciences at the University of Utah and senior director of early translational research at
HCI. "We want to know what happens immediately following mutation of the APC gene
mutation as a way of understanding how we might intervene. If you're trying to match
therapies with a specific genetic mutation, it helps to understand the earliest steps in
tumor formation, as well as the downstream consequences." APC stands for adenomatous
polyposis coli. It is classified as a tumor suppressor gene. Before the new study,
scientists believed that following APC mutation, faulty cell communication caused by a
particular protein known as beta-catenin resulted in colon polyp formation. Colon polyp
formation precedes the development of colon cancer.
Ginger quells cancer patients'
nausea from chemotherapy
People with cancer can reduce post-chemotherapy nausea by 40 percent by using ginger
supplements, along with standard anti-vomiting drugs, before undergoing treatment,
according to scientists at the University of Rochester Medical Center. About 70 percent of
cancer patients who receive chemotherapy complain of nausea and vomiting. "There are
effective drugs to control vomiting, but the nausea is often worse because it
lingers," said lead author Julie L. Ryan, Ph.D., M.P.H., assistant professor of
Dermatology and Radiation Oncology at Rochester's James P. Wilmot Cancer Center. The
research will be presented at the American Society of Clinical Oncology meeting in the
Patient and Survivor Care Session on Saturday, May 30, in Orlando, Fla. "Nausea is a
major problem for people who undergo chemotherapy and it's been a challenge for scientists
and doctors to understand how to control it," said Ryan, a member of Rochester's
Community Clinical Oncology Program Research Base at the Wilmot Cancer Center. Her
research is the largest randomized study to demonstrate the effectiveness of ginger
supplements to ease the nausea. Previous small studies have been inconsistent and never
focused on taking the common spice before chemotherapy.
Early childhood health
interventions could save billions in health costs later in life
Promoting the health of young children, before five years of age, could save society up to
$65 billion in future health care costs, according to an examination of childhood health
conducted by researchers at the Johns Hopkins Bloomberg School of Public Health. The
results are published in the May 15, 2009, issue of Academic Pediatrics. "Our review
found convincing evidence that the four health problems we studied—early life tobacco
exposure, unintentional injury, obesity and mental health—constitute significant
burdens on the health of preschool-age children and are antecedents of health problems
across the life span," said Bernard Guyer, MD, lead author of the study and the
Zanvyl Kreiger Professor of Children's Health with the Bloomberg School's Department of
Population, Family and Reproductive Health. "These health problems affect
approximately one-third to one-half of children born in the U.S., and we estimated that
total lifetime societal cost could be about $50,000 per child—which translates to $65—100
billion for the entire birth cohort of children. The currently available research
justifies targeted investments in early childhood health promotion as a means to averting
future health costs and improving overall health during their life span." Researchers
conducted a systematic review of early childhood interventions using multiple health
databases: PubMEd, PsycINFO, National Health Service Economic Evaluation Database, the
National Bureau of Economic Research working paper database and EconLit. Guyer and his
colleagues examined the magnitude of the future effects of tobacco exposure, unintentional
injury, obesity and mental health. They looked at prevalence of these issues during the
target age period, their cost implications across the life span, the availability of
preventive interventions in this period of life and evidence indicating that prevention of
these problems early in life would pay off or save costs in the future. Researchers found
that the available evidence for the effectiveness of intervention in this age group was
strongest in the case of preventing tobacco exposure and controlling unintentional
injuries.
ISU study finds link between
individual stress and teens being overweight or obese
Stress may indeed be a direct contributor to childhood obesity. That's according to a new
Iowa State University study finding that increased levels of stress in adolescents are
associated with a greater likelihood of them being overweight or obese. The study of 1,011
adolescents (aged 10-15) and their mothers from low income families living in three cities
-- Boston, Chicago and San Antonio -- was posted on the Web site of the Journal of
Adolescent Health (http://www.jahonline.org/inpress), which will publish it in the August
issue. Forty-seven percent of the teens in the sample were overweight or obese, but that
percentage increased to 56.2 percent among those who were impacted by four or more
stressors. "We found that an adolescent or youth who's more stressed -- caused by
such things as having poor grades, mental health problems, more aggressive behavior, or
doing more drugs and alcohol -- is also more likely to be overweight or obese," said
lead author Brenda Lohman, an Iowa State assistant professor of human development and
family studies (HDFS).
Vitamin D insufficiency linked to
bacterial vaginosis in pregnant women
Bacterial vaginosis (BV) is the most common vaginal infection in US women of childbearing
age, and is common in pregnant women. BV occurs when the normal balance of bacteria in the
vagina is disrupted and replaced by an overgrowth of certain bacteria. Because having BV
puts a woman at increased risk for a variety of complications, such as preterm delivery,
there is great interest in understanding how it can be prevented. Vitamin D may play a
role in BV because it exerts influence over a number of aspects of the immune system. This
hypothesis is circumstantially supported by the fact that BV is far more common in black
than white women, and vitamin D status is substantially lower in black than white women.
This relation, however, has not been rigorously studied. To assess whether poor vitamin D
status may play a role in predisposing a woman to BV, Bodnar and coworkers at the
University of Pittsburgh and the Magee-Womens Research Institute studied 469 pregnant
women. The results of their investigation are published in the June 2009 issue of the
Journal of Nutrition. This prospective epidemiologic study investigated the relation
between vitamin D status and BV in 209 white and 260 black women at <16 wk of pregnancy
with singleton gestations. Blood samples were taken, and serum analyzed for
25-hydroxyvitamin D [25(OH)D], a marker of vitamin D status. 25(OH)D levels below 80
nmol/L are typically considered insufficient. Pelvic examinations were performed, and
Gram-stained vaginal smears were assessed to diagnose BV.
Cigarettes to the rescue?
veryone knows that smoking can kill you, but did you know that it may help with your
allergies? A new study shows that cigarette smoke can prevent allergies by decreasing the
reaction of immune cells to allergens. Smoking can cause lung cancer, pulmonary disease,
and can even affect how the body fights infections. Along with many harmful effects,
smoking cigarettes has a surprising benefit: cigarettes can protect smokers from certain
types of allergies. Now, a study recommended by Neil Thomson, a member of Faculty of 1000
Biology and leading expert in the field of respiratory medicine, demonstrates that
cigarette smoke decreases the allergic response by inhibiting the activity of mast cells,
the major players in the immune system's response to allergens. Researchers at Utrecht
University in the Netherlands found that treatment of mast cells with a cigarette
smoke-infused solution prevented the release of inflammation-inducing proteins in response
to allergens, without affecting other mast cell immune functions. The mast cells used in
the study were derived from mice, but it is likely that the same anti-allergy effect will
hold true in humans. While taking up smoking to cure allergies is unwise, Thomson
concludes that the findings presented in this study are "consistent with a dampening
of allergic responses in smokers."
Folic acid to prevent congenital
heart defects
The Canadian policy of fortifying grain products with folic acid has already proved to be
effective in preventing neural tube defects. The latest article published in the British
Medical Journal by a group of researchers from the McGill Adult Unit for Congenital Heart
Disease (MAUDE Unit), the Research Institute of the McGill University Health Centre (MUHC)
and McGill University, shows that folic acid also decreases the incidence of congenital
heart defects by more than 6%. According to Raluca Ionescu-Ittu, a PhD candidate on the
team, "this decrease is very significant and probably underestimated. During the
study period, there was an increase in other factors associated with a higher prevalence
of congenital heart defects, so without the fortification we would probably have seen an
increase in these defects." Since December 1998, all grain products sold in Canada
have been fortified with folic acid with 0.15 mg of folate per 100 g of flour. Thanks to
provincial databases, the researchers showed that the rate of congenital heart defects
between 1999 and 2005 was 1.47 per 1000 births compared to 1.64 per 1000 births between
1990 and 1999 for a decrease of 6.2% per year after 1999. Despite the success of this
initiative, prevention efforts are still necessary to encourage future mothers to take
folic acid supplements. "The level of fortification was established to avoid negative
side effects in the general population," explained Ms. Ionescu-Ittu. "However,
this level is not quite sufficient for women planning a pregnancy, who should start taking
folic acid supplements at least three months before becoming pregnant." Researchers
are constantly assessing the beneficial effects of folic acid on the various aspects of
embryonic and infant development. Natural sources of the vitamin, such as fruit or green
vegetables, might not provide sufficient doses for pregnant women. Most gynecologists
therefore recommend supplements in addition to a healthy diet rich in folic acid.
MDC researchers unravel key
mechanism in pathogenesis of osteoporosis
Osteoporosis, or bone loss, is a disease that is most common in the elderly population,
affecting women more often than men. Until now, it was not clear exactly how the disease
develops. Researchers of the Max Delbrück Center for Molecular Medicine (MDC)
Berlin-Buch, Germany, have now elucidated a molecular mechanism which regulates the
equilibrium between bone formation and bone resorption. Dr. Jeske J. Smink, Dr. Valérie
Bégay, and Professor Achim Leutz were able to show that two different forms of a gene
switch – a short isoform and a long isoform – determine this process. The MDC
researchers hope these findings will lead to new therapies for this bone disease. (EMBO
Journal)*. In osteoporosis, excessive bone resorption occurs. The bones lose their density
and are therefore prone to breakage. Even minor falls can lead to serious bone fractures.
The interplay between two cell types determines bone density: bone forming cells
(osteoblasts) and bone resorbing cells (osteoclasts). The equilibrium between these two
cell types is strictly regulated to prevent the formation of either too much or too little
bone.
Immunotherapy effective against
neuroblastoma in children
A phase III study has shown that adding an antibody-based therapy that harnesses the
body's immune system resulted in a 20 percent increase in the number of children living
disease-free for at least two years with neuroblastoma. Neuroblastoma, a hard-to-treat
cancer arising from nervous system cells, is responsible for 15 percent of cancer-related
deaths in children. The researchers reported their findings – the first to show that
immunotherapy could be effective against childhood cancer – online May 14, 2009 on
the American Society of Clinical Oncology website in advance of presentation June 2.
"This establishes a new standard of care for a traditionally very difficult cancer in
children," said lead author Alice Yu, MD, PhD, professor of pediatric
hematology/oncology at the University of California, San Diego School of Medicine and the
Moores UCSD Cancer Center. "High-risk neuroblastoma has always been a frustrating
cancer to treat because, despite aggressive therapy, it has a high relapse rate." The
therapy targets a specific glycan (a complex sugar chain found on the surface of cells) on
neuroblastoma cells called GD2, which inhibit the immune system from killing cancer cells.
The antibody – ch14.18 – binds to this glycan, enabling various types of immune
cells to attack the cancer.
Glutamine supplements show promise
in treating stomach ulcers
Nearly 20 years ago, it was discovered that bacteria known as Helicobacter pylori were
responsible for stomach ulcers. Since then, antibiotics have become the primary therapy
used to combat the H. pylori infection, which affects approximately six percent of the
world population and is also a primary cause of stomach cancer. But today the bacteria is
growing increasingly resistant to antibiotics. Now a study led by scientists at Beth
Israel Deaconess Medical Center (BIDMC) and the Massachusetts Institute of Technology
demonstrates that the amino acid glutamine, found in many foods as well as in dietary
supplements, may prove beneficial in offsetting gastric damage caused by H. pylori
infection. Reported in the May 2009 issue of the Journal of Nutrition., the findings offer
the possibility of an alternative to antibiotics for the treatment of stomach ulcers.
"Our findings suggest that extra glutamine in the diet could protect against gastric
damage caused by H. pylori," says senior author Susan Hagen, PhD, Associate Director
of Research in the Department of Surgery at BIDMC and Associate Professor of Surgery at
Harvard Medical School. "Gastric damage develops when the bacteria weakens the
stomach's protective mucous coating, damages cells and elicits a robust immune response
that is ineffective at ridding the infection." Eventually, she notes, years of
infection result in a combination of persistent gastritis, cell damage and an environment
conducive to cancer development. Glutamine is a nonessential amino acid naturally found in
certain foods, including beef, chicken, fish, eggs, dairy products and some fruits and
vegetables. L-glutamine – the biologically active isomer of glutamine – is
widely used as a dietary supplement by body builders to increase muscle mass. Hagen and
her coauthors had previously shown that glutamine protects against cell death from H.
pylori-produced ammonia. "Our work demonstrated that the damaging effects of ammonia
on gastric cells could be reversed completely by the administration of L-glutamine,"
explains Hagen. "The amino acid stimulated ammonia detoxification in the stomach
– as it does in the liver – so that the effective concentration of ammonia was
reduced, thereby blocking cell damage."
Study Indicates High Blood Pressure
Could Be Caused By A Common Virus
A new study suggests for the first time that cytomegalovirus (CMV), a common viral
infection affecting between 60 and 99 percent of adults worldwide, is a cause of high
blood pressure. Led by researchers at Beth Israel Deaconess Medical Center (BIDMC) and
published in the May 15, 2009 issue of PLoS Pathogens, the findings also show that in
conjunction with other risk factors the virus can lead to the development of
atherosclerosis, or hardening of the arteries. “CMV infects humans commonly all over
the world,” explains co-senior author Clyde Crumpacker, MD, an investigator in the
Division of Infectious Diseases at BIDMC and Professor of Medicine at Harvard Medical
School. “This new discovery may eventually provide doctors with a whole new approach
to treating hypertension, with anti-viral therapies or vaccines becoming part of the
prescription.” A member of the herpes virus family, CMV affects all age groups and is
the source of congenital infection, mononucleosis, and severe infection in transplant
patients. By the age of 40, most adults will have contracted the virus, though many will
never exhibit symptoms. Once it enters the body, CMV usually remains latent in the body
until the immune system is compromised.
Researchers identify key proteins
needed for ovulation
Researchers from the National Institutes of Health and other institutions have identified
in mice two proteins essential for ovulation to take place. The finding has implications
for treating infertility resulting from a failure of ovulation to occur as well as for
developing new means to prevent pregnancy by preventing the release of the egg. The
proteins, called ERK1 and ERK2, appear to bring about the maturation and release of the
egg. The study, appearing in the May 15 issue of Science, was funded in part by two NIH
institutes, the Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD) and the National Cancer Institute (NCI). "Ovulation results from
a complex interplay of chemical sequences," said Duane Alexander, M.D., director of
the NICHD. "The researchers have identified a crucial biochemical intermediary
controlling the release of the egg. The finding advances our understanding and may one day
contribute to new treatments for infertility as well as new ways to prevent pregnancy from
occurring." The study's senior author, JoAnne Richards, Ph.D., of Baylor College of
Medicine, worked with Esta Sterneck and Peter Johnson, of the NCI's Center for Cancer
Research; with Heng-Yu Fan and Zhilin Liu of Baylor; Masayuki Shimada, of Hiroshima
University, in Japan; and Stephen Hedrick, of the University of California, San Diego. The
immature egg is contained inside a covering of cells, known as the ovarian follicle. The
follicle is made largely of cells known as granulosa cells. Each month, the pituitary
gland releases follicle-stimulating hormone and luteinizing hormone which cause the egg
and the ovarian granulosa cells surrounding it to grow and develop into a mature follicle.
Midway through the woman's monthly cycle, the pituitary releases a large surge of
luteinizing hormone, which causes the follicle to rupture, releasing the egg cell. The
granulosa cells in the ruptured follicle transform into luteal cells. Previously,
researchers did not know how luteinizing hormone triggered the ovary's release of the egg
and the production of progesterone by the granulosa cells. In the current study, the
researchers discerned that luteinizing hormone appears to signal the release of molecules
known as extracellular-regulated protein kinases 1 and 2 (ERK 1 and ERK 2). In turn, these
molecules trigger a chain of chemical sequences that bring about the release of the egg,
the transformation of granulosa cells into luteal cells, and the production of
progesterone. ERK1 and ERK2 are a critical nexus between the surge in luteinizing hormone
and ovulation, explained the NICHD project officer for the study, Louis V. De Paolo,
Ph.D., chief of the NICHD Reproductive Sciences Branch. "This a key chemical pathway
that affects not only ovulation, but egg cell maturation and granulosa cell
differentiation into luteal cells," Dr. De Paolo said.
Perceived cancer risks may not
reflect actual risks or prevention needs
Working with a population of individuals at risk for gastrointestinal cancers, researchers
at Fox Chase Cancer Center have learned that many people misjudge their actual degree of
cancer risk and, therefore, their true need for prevention support. Strategies for
accurately assessing cancer risk are critical for appropriately targeting educational,
counseling, and diagnostic resources to prevent cancer in as many individuals as possible,
the investigators say. The study, to be presented at the 2009 Annual Meeting of the
American Society of Clinical Oncology, evaluated participants in the Gastrointestinal
Tumor Risk Assessment Program at Fox Chase. With the growth in genetic cancer risk
assessment in recent years, Fox Chase clinicians and scientists have seen increasing
numbers of patients enrolling in the Center's risk assessment programs, including those
for breast, ovarian, melanoma, prostate, and gastrointestinal cancers. Risk for
gastrointestinal cancers, the focus of the current study, is established through family
and personal histories of gastrointestinal cancers and/or colorectal polyps, as well as
genetic testing. "The goal of our study was to improve how we think about and direct
our prevention resources," says Michael Hall, M.D., medical oncologist at Fox Chase
and lead author on the study. "We examined clinical cancer prevention needs among
individuals seeking gastrointestinal risk evaluation, including in our assessment their
estimated personal risk, risk beliefs, and interest in genetic testing." The study
evaluated 398 individuals from 278 families enrolled in the Gastrointestinal Tumor Risk
Assessment Program at Fox Chase over a nine-year period. The program provides risk
assessment to people seeking evaluation for a risk of a gastrointestinal or related
cancer. Participants were required to sign an informed consent and complete a health
history questionnaire prior to counseling, education, and genetic services. Results showed
that more than 17 percent of the individuals were at high-risk; 70 percent were at
moderate-to-high risk; and 12 percent were at low-risk.
Gene Signature May Predict Patient
Response to Therapy for Gastrointestinal Stromal Tumors
Researchers at Fox Chase Cancer Center uncovered a genetic pattern that may help predict
how gastrointestinal stromal tumor (GIST) patients respond to the targeted therapy
imatinib mesylate (Gleevec). Moreover, their findings point to genes that could be
suppressed in order to make these tumors respond more readily to imatinib. Lori Rink, PhD,
a postdoctoral fellow in the laboratory of Andrew K. Godwin, PhD, at Fox Chase, presents
their findings at the 2009 Annual Meeting of the American Society of Clinical Oncology.
The study uses tumor specimens collected as part of a Phase II trial on the use of the
drug before surgical resection for GIST, which is led by the Radiation Therapy Oncology
Group, a national clinical cooperative group funded by the National Cancer Institute.
“Imatinib has been the first drug that has really made a dent in GIST progression
– up to 80 percent response – yet some GIST patients have little or no response
to the drug,” says Rink. “We are looking to see how we can help clinicians make
better decisions in applying imatinib or additional therapies to their GIST patients.”
Rink and her colleagues followed 63 GIST patients in the RTOG trial, who were given
imatinib before surgery for primary or recurrent tumors. Using tumor samples collected
before and after the patients were given the drug, the researchers studied which genes
were active in the tumors and then compared these profiles of gene expression to how well
the tumors responded to short-term imatinib treatment. According to Rink, they found a
selection of 38 genes that were expressed higher in tumors that did not respond well to
imatinib. Of these, they identified 20 KRAB-zinc finger genes that encode for proteins
that typically act as transcriptional repressors of other genes. Ten of these genes, Rink
says, are located to a single section of Chromosome 19.
Should Parents Share the Results of
BRCA1/2 Genetic Testing with Their Children?
If you learned that you were at high risk of cancer because you carry the hereditary
BRCA1/2 gene mutation, would you tell your children? A recent study at Fox Chase Cancer
Center not only considered that question, but also took it to the next level and studied
the parent perceptions of the impact of such a decision on children. The study will be
presented at the 2009 Annual Meeting of the American Society of Clinical Oncology. BRCA1/2
are hereditary gene mutations that indicate an increased risk of developing breast cancer.
"We know that many people who carry the BRCA1/2 gene mutation share their genetic
test results with their children," explained Angela Bradbury, MD, medical oncologist
at Fox Chase and lead author on the study. "What we did not know was the impact this
communication has on their children." In order to learn the impact this has on
children, researchers evaluated results from 163 parents who had BRCA1/2 testing. Of
those, 52 tested positive for BRCA1/2. Just over 100 parents (66 percent) shared their
results with at least one of their children, which totaled 323 children who were between
the ages of 5 – 25. The child's age and parent cancer history had a direct
correlation to whether or not they shared the results. Not surprising, those without a
BRCA1/2 mutation were more likely to communicate test results than parents with a
mutation. Among parents who disclosed their results, few reported negative reactions from
their children (9 percent) or that their child did not understand the information (11
percent). Overall, most parents reported that their children handled the information well,
although negative reactions were more frequent among certain subgroups (younger children
and those of parents with a mutation or a variant of uncertain significance).
Long-term study results validate
efficacy of CT scans for chest pain diagnosis
The first long-term study following a large number of chest pain patients who are screened
with coronary computerized tomographic angiography (CTA) confirms that the test is a safe,
effective way to rule out serious cardiovascular disease in patients who come to hospital
emergency rooms with chest pain, according to new research from the University of
Pennsylvania School of Medicine which will be presented Friday, May 15, 2009 at the
Society for Academic Emergency Medicine's annual conference. Chest pain is a common and
costly health complaint in the United States, bringing 8 million Americans to hospital
emergency departments each year. Although just five to 15 percent of those patients are
found to be suffering from heart attacks or other cardiac diseases, more than half are
admitted to the hospital for observation and further testing. CTA streamlines the process
and provides a faster, and less expensive way to evaluate which patients have an acute
coronary syndrome that require treatment. "The ability to rapidly determine that
there is nothing seriously wrong allows us to provide reassurance to the patient and to
help reduce crowding in the emergency department," says lead author Judd Hollander,
MD, professor and clinical research director in Penn's department of Emergency Medicine.
"The use of this test is a win-win." Among patients enrolled in the trial after
getting a negative scan – a scan showing no evidence of dangerous blockages in the
coronary arteries – no patients in the study had heart attacks or required bypass
surgery or placement of cardiac stents in the year following their test. The authors say
the findings provide a roadmap for how to appropriately and cost-effectively use this
advanced imaging technology, which generates lifelike, three-dimensional photos of the
heart and the matrix of blood vessels that surround it. Investigators followed 481
patients who received negative CTA scans for one year after their hospital visit. The
patients studied had a mean age of 46. While 11 percent of patients were rehospitalized
and 11 percent received additional cardiac testing – stress tests or cardiac
catheterizations – over the following year, none had heart attacks or needed
revascularization procedures to prop open blocked coronary arteries. One patient in the
study died of an unrelated cause during the year.
Genetic marker may predict early
onset of prostate cancer
Fox Chase Cancer Center researchers have identified a genetic marker that is associated
with an earlier onset of prostate cancer in Caucasian men who have a family history of
prostate cancer. If the data are confirmed, the marker may help clinicians personalize
prostate cancer screening. Veda Giri, M.D., a medical oncologist and director of the
Prostate Cancer Risk Assessment Program at Fox Chase, will present the data at the annual
meeting of the American Society of Clinical Oncology on Saturday, May 30. "Genetic
testing for prostate cancer is not yet clinically well characterized as it is for breast,
ovarian cancer and colon cancer," Giri says. "Markers such as this one are
useful because they may help clinicians distinguish between men who are at risk for
earlier onset of disease where intensive screening approaches can be discussed. Men who do
not carry genetic markers of risk may not need such screening measures." More than
half of all prostate tumors carry a fusion gene called, TMPRSS2-ERG, which may have a role
in prostate cancer formation. Recently, scientists reported that a single nucleotide
polymorphism, called the Met160Val SNP (also referred to as rs12329760), is associated
with the gene fusion. Specifically, prostate cancer patients who carry the T allele of
Met160Val are more likely to have a prostate tumor with the gene fusion than patients who
have the C allele. To find out if the T allele is clinically relevant in men who are at
high risk of developing prostate cancer but do not yet have the disease, Giri and
colleagues genotyped 631 men enrolled in the Prostate Cancer Risk Assessment Program at
Fox Chase. Overall, while there were differences in the distribution of the alleles by
race, the risk allele did not have a major contribution to disease in 400 African American
men or in 231 Caucasian men with a family history of prostate cancer. They then evaluated
this marker in 183 Caucasian men who have a family history of prostate cancer undergoing
follow-up in the Prostate Cancer Risk Assessment Program. They found that the high risk
allele was associated with a 2.5-fold increased risk of developing prostate cancer,
relative to the low risk allele. Additionally, more men carrying the high risk allele
developed prostate cancer earlier than men not carrying the risk allele. "We need
longer follow-up to know the precise time frame for cancer development, but we have
learned some information on the difference in time to diagnosis from this study,"
Giri says.
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