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Viral mimic induces melanoma cells to digest themselves
Recent research has uncovered an unexpected vulnerability in deadly
melanoma cells that, when exploited, can cause the cancer cells to turn
against themselves. The study, published by Cell Press in the August issue
of the journal Cancer Cell, identifies a new target for development of
future therapeutics aimed at selectively eliminating this aggressive skin
cancer which is characterized by a notoriously high rate of metastasis and
treatment-resistance.
"Although considerable effort has been devoted to the search for
molecular mechanisms that contribute to the chemo- and immunoresistance of
melanoma, the average survival of patients with inoperable metastases
remains less than 10 months," explains senior study author Dr. Maria S.
Soengas from the Melanoma Laboratory at the Spanish National Cancer
Research Centre in Madrid, Spain. Melanoma has multiple complex genetic
aberrations that make the cells difficult to destroy with current
treatments.
One process that has not been studied in great detail with regards to
melanoma is a type of autophagy (literally, self-eating) that involves
sequestration of components within the cell for eventual degradation.
Previous work has linked autophagy with both cancer cell death and survival
and it is not clear whether this process might be a viable target for
future drug development. Dr. Soengas and colleagues designed a series of
studies to examine the interplay between autophagy and cell death in the
context of tumor cell-selective elimination of melanoma cells.
The researchers discovered that melanoma cells retain the ability to
recognize and respond to double-stranded RNA (dsRNA) located inside the
cell cytoplasm. Most animal cells contain single-stranded RNA and see
dsRNA, which is associated with viruses, as a threat. The melanoma cells
responded to administration of the dsRNA mimic polyinosine-polycytidylic
acid (pIC) by inducing an immune response that led to autophagy. However,
the method of delivering the pIC to the melanoma cells was critical and
required a carrier called polyethyleneimine (PEI) to ensure delivery of pIC
to the cell cytoplasm.
The researchers went on to show that pIC links autophagy to apoptosis, a
well studied cell death pathway. Significantly, the cell autonomous anti-
tumor activity of pIC was observed even in animals with a suppressed immune
system, a condition common to melanoma patients. "Altogether, our results
provide the proof of principle for dsRNA sensors as therapeutic targets to
overcome the inherent resistance of melanoma cells to current anticancer
treatments," says Dr. Soengas.
Importantly, the pIC-PEI complex has two exciting advantages over other
anticancer agents. "First, pIC-PEI can induce both autophagy and apoptosis
in an efficient manner while other compounds are just partial inducers of
one of the two processes. Second, pIC-PEI has a significant anti-melanoma
activity in experimental mouse models without noticeable side effects." The
researchers caution that further research is required before these results
can be translated to the clinic.
The researchers include Damia` Tormo, Spanish National Cancer Research
Centre (CNIO), Madrid, Spain; Agnieszka Checinska, Spanish National Cancer
Research Centre (CNIO), Madrid, Spain; Direna Alonso-Curbelo, Spanish
National Cancer Research Centre (CNIO), Madrid, Spain; Eva Perez-Guijarro,
Spanish National Cancer Research Centre (CNIO), Madrid, Spain; Estela
Canon, Spanish National Cancer Research Centre (CNIO), Madrid, Spain; Erica
Riveiro-Falkenbach, Spanish National Cancer Research Centre (CNIO), Madrid,
Spain; Tonantzin G. Calvo, Spanish National Cancer Research Centre (CNIO),
Madrid, Spain; Lionel Larribere, Spanish National Cancer Research Centre
(CNIO), Madrid, Spain' Diego Megias, Spanish National Cancer Research
Centre (CNIO), Madrid, Spain; Francisca Mulero, Spanish National Cancer
Research Centre (CNIO), Madrid, Spain; Miguel A. Piris, Spanish National
Cancer Research Centre (CNIO), Madrid, Spain; Rupesh Dash, Virginia
Commonwealth University, School of Medicine, Richmond, VA; Paola M. Barral,
Virginia Commonwealth University, School of Medicine, Richmond, VA; Jose´
L. Rodriguez-Peralto, Hospital Universitario, Madrid, Spain; Pablo Ortiz-
Romero, Hospital Universitario, Madrid, Spain; Thomas Tuting, University of
Bonn, Bonn, Germany; Paul B. Fisher, Virginia Commonwealth University,
School of Medicine, Richmond, VA; and Maria S. Soengas, Spanish National
Cancer Research Centre (CNIO), Madrid, Spain.
Groundbreaking study shows exercise benefits leukemia patients
CHAPEL HILL, N.C. - One of the most bothersome symptoms of leukemia is
extreme fatigue, and asking these patients to exercise doesn't sound like a
way to help them feel better.
A new study from the University of North Carolina at Chapel Hill
indicates that exercise may be a great way to do just that, combating the
debilitating fatigue that these patients experience.
In a first-of-its-kind clinical trial, a team of researchers from the
Department of Exercise and Sport Science and UNC Lineberger Comprehensive
Cancer Center have shown that physical activity can significantly improve
symptoms of fatigue and depression, increase cardiovascular endurance and
maintain quality of life for adult patients undergoing treatment for
leukemia.
A total of 10 patients undergoing treatment participated in the EQUAL
(Exercise and Quality of Life in Leukemia/ Lymphoma Patients) study. Each
patient was provided with specially-treated exercise equipment to minimize
the risk of infection. They participated in an individualized exercise
session while in the hospital for the 3-5 weeks of the induction phase of
leukemia treatment. The exercise prescription comprised of aerobic and
resistance exercises, core exercises, and light stretches tailored to the
patient's level of fitness and leukemia symptoms. Upon their discharge from
the hospital, each patient received an aerobic- based exercise prescription
to use during their 2-week home recovery period.
Before and after the exercise program, the researchers tested key
physiological measurements including resting heart rate, blood pressure and
hemoglobin, body weight and height, body composition, cardiorespiratory
fitness and muscular endurance. Psychological measures were tested using
standard scales for assessing fatigue, depression and quality of life in
cancer patients. Blood samples were also taken at baseline, mid, and at the
conclusion of the study, and analyzed for cytokines, biomarkers of
inflammation. The results of the study were recently published in the
journal Integrative Cancer Therapies.
"We found that the patients experienced significant reduction in total
fatigue and depression scores, as well as improved cardiorespiratory
endurance and maintenance of muscular endurance," said Claudio Battaglini,
Ph.D., assistant professor of exercise and sport science and UNC Lineberger
member.
"This is important because of the numerous side-effects related to
cancer treatment, and particularly leukemia treatment, which requires
confinement to a hospital room for 4-6 weeks to avoid the risk of
infection. We have demonstrated that these patients not only can complete
an exercise program in the hospital but that they may receive both
physiological and psychological benefits that could assist in their
recovery," he added.
EQUAL phase II is in development. The follow-up study will consisted of
a randomized clinical-controlled trial to assess the effects on an
individualized exercise prescription in acute leukemia patients vs. a group
of leukemia patients receiving the usual treatment. If the results prove to
be beneficial to patients, the goal of the research team will be to expand
the trial by developing a multi-site research program involving other
cancer centers throughout North Carolina and around the United States.
Along with Battaglini, study co-authors include professor Anthony Hackney,
Ph.D., associate professor Diane Groff, Ed.D., and graduate student
Elizabeth Evans from the Department of Exercise and Sport Science. Hackney
and Groff are also members of UNC Lineberger Comprehensive Cancer Center,
along with nurse consultant Rey Garcia and Thomas Shea, M.D., professor of
hematology/oncology and director of the UNC bone marrow transplant program.
This research was supported by a UNC Lineberger Internal Grants Award, a
UNC Junior Faculty Development Award, and a UNC Institute of Aging,
Stimulus Grant in Aging and made possible due to cooperation by UNC
Hospitals.
Stanford scientists discover bladder cancer stem cell
STANFORD, Calif. - Researchers at Stanford's School of Medicine have
identified the first human bladder cancer stem cell and revealed how it
works to escape the body's natural defenses.
"This is first time we've found this 'don't eat me signal' in a stem
cell of a solid cancer," said Irving Weissman, MD, the Virginia & D.K.
Ludwig Professor for Clinical Investigation in Cancer Research at the
medical school. "We're now moving as fast as we can to look at other tumors
to see if this is a universal strategy of all or most cancer stem cells."
If so, the signal may be a valuable therapeutic target for many types of
cancers.
Weissman, who directs Stanford's Stem Cell Biology and Regenerative
Medicine Institute, is also a member of Stanford's Cancer Center. He is the
senior author of the work, which will be published in the Proceedings of
the National Academy of Sciences on Aug. 3. His laboratory recently
published two studies in the journal Cell showing that human leukemia stem
cells use the same protective molecular signature on their surface to evade
cells called macrophages that engulf and destroy sick or cancerous cells.
Like queen bees, cancer stem cells are constantly replenishing their
"hive" of tumor cells. Therapies that kill off the workers might