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Pancreatic cancer protein discovered | |
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HEALTH TIPS - Wednesday, March 21, 2007
"News That Keeps You Healthy"
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Health Tips and Info From EVTV1.com Health Related Videos
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Pancreatic cancer protein discovered
HOUSTON, -- U.S. scientists have found an overexpressed
protein protects pancreatic cancer cells from self-
destructing, negating one of the body's natural defenses.
University of Texas M. D. Anderson Cancer Center researchers
said the protein tissue transglutaminase, or TG2,
previously was found to be overexpressed in a variety of
drug-resistant cancer cells and in metastasized cancer.
"In general, you rarely see overexpression of TG2 in a
normal cell," said Kapil Mehta, an experimental therapeutics
professor who has been studying TG2 for 10 years. Mehta and
colleagues have linked TG2 overexpression to drug-resistant
and metastatic breast cancer, pancreatic cancer and
melanoma. Up to now, the mechanisms by which TG2 promoted
drug resistance and metastasis have been unknown. But Mehta
and colleagues have shown inhibiting the protein in
pancreatic cancer cells leads to a form of programmed cell
suicide called autophyagy. "Targeting TG2, or its
activating protein PKC, or both, presents a novel and
potentially effective approach to treating patients with
pancreatic cancer," study co-author Dr. Gabriel Lopez-
Berestein said, cautioning research in the mouse model
remains in the early stages. The study is reported in the
March issue of Molecular Cancer Research.
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Preeclampsia proteins identified
-- A U.S.-led team of scientists has identified proteins
released by the placenta that might damage blood vessels
in women with preeclampsia. Preeclampsia is a complication
of pregnancy linked with life-threatening increases in high
blood pressure after 20 weeks gestation. It has long been
recognized that substances called "microparticles" released
by the placenta in preeclampsia damage maternal blood
vessels. Yale University researchers, led by Seth Guller,
sought to detect whether specific proteins were found in
microparticles. The team, including researchers from Berne,
Switzerland, studied placentas obtained from patients with
preeclampsia who had uncomplicated pregnancies delivered at
term by Caesarean section. "In this study, we demonstrate
for the first time that microparticles released by the
placenta may contain factors that damage maternal blood
vessels in preeclampsia," said Guller, an associate
professor. Guller said his team only detected whether
specific proteins were found in microparticles. "In the
future, we will determine whether they are biologically
active -- promote damage in vessel culture models -- and
whether they are present in the blood of women with
preeclampsia," said Guller. The study was presented
Saturday in Reno, Nev., during a meeting of the Society for
Gynecologic Investigation.
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Gene identified as schizophrenia risk
MANHASSET, -- U.S. psychiatric researchers have determined a
specific gene appears to increase the risk of developing
schizophrenia. The researchers at the Feinstein Institute
for Medical Research in Manhasset, N.Y., in collaboration
with the Harvard Medical School, used whole genome
association to search the entire human genome in 178
schizophrenic patients and 144 healthy individuals. The WGA
technology was used to examine more than 500,000 genetic
markers in each individual -- the largest number of such
markers examined to date, and the first published study to
utilize WGA technology in a psychiatric illness. The
researchers observed multiple gene abnormalities in patients
with schizophrenia that were not found, or were found much
less commonly, in healthy individuals. "WGA technology
allowed us to shine a light across virtually the entire
genome, rather than looking at just one gene at a time,"
said Todd Lencz, the first author of the study. "Using WGA,
we found genes that had not been previously considered in
studies of schizophrenia. The critical next step is confirm-
ing these results in independent datasets." The study
results are detailed online in the journal Molecular
Psychiatry.
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