Cancer
Cellular fuel gauge may hold the key to restricting cancer growth
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Researchers at McGill University have discovered that a key regulator of energy metabolism in cancer cells known as the AMP-activated protein kinase (AMPK) may play a crucial role in restricting cancer cell growth. AMPK acts as a “fuel gauge” in cells; AMPK is turned on when it senses changes in energy levels, and helps to change metabolism when energy levels are low, such as during exercise or when fasting. The researchers found that AMPK also regulates cancer cell metabolism and can restrict cancer cell growth.
The discovery was made by Russell (Rusty) Jones, an assistant professor at McGill’s Goodman Cancer Research Centre and the Department of Physiology, Faculty of Medicine. Jones along with his team is the first to show that AMPK can act as a tumour suppressor in animals. The research will be published December 27 in the journal Cell Metabolism.
“Cancer is a disease in which cells lose their normal restraints on growth and start to divide uncontrollably. But, in order for cells to grow quickly they need enough energy to complete the task,” Jones explained. “AMPK acts like the fuel gauge in your car – it lets the body know when energy levels are low, and stops cell growth until there is enough gas in the tank. We wanted to see if this fuel gauge could affect the development and progression of cancer. We found that mice lacking AMPK developed tumours faster, suggesting that AMPK is important for keeping tumour development in check, at least for some types of cancer.” For this study, Jones’ team focused specifically on a type of blood cancer known as lymphoma. They discovered that the protein Myc, which is activated in more than half of all cancers, could promote lymphoma more rapidly when mice were deficient for AMPK.
Italy court ruling links mobile phone use to tumor
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Italy’s supreme court has upheld a ruling that said there was a link between a business executive’s brain tumor and his heavy mobile phone usage, potentially opening the door to further legal claims.
The court’s decision flies in the face of much scientific opinion, which generally says there is not enough evidence to declare a link between mobile phone use and diseases such as cancer and some experts said the Italian ruling should not be used to draw wider conclusions about the subject.
“Great caution is needed before we jump to conclusions about mobile phones and brain tumors,” said Malcolm Sperrin, director of medical physics and clinical engineering at Britain’s Royal Berkshire Hospital.
‘Disgusted’ Rats Teaching Scientists About Nausea, Work May Lead to New Cancer Treatments
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Nausea is a common and distressing side effect of many drugs and treatments. Unlike vomiting, nausea is not well understood, but new research by University of Guelph scientists may soon change that.
Guelph PhD student Katharine Tuerke, neuroscience researcher Cheryl Limebeer and Prof. Linda Parker in the Department of Psychology believe they’ve found the mechanism in the brain that is responsible for the sensation of nausea – with the help of some “disgusted” rats.
Their study was published this week in Journal of Neuroscience.
“Although everyone has experienced nausea at some point, its neurobiology is poorly understood due to a lack of animal models,” said Parker, who holds the Canada Research Chair in Behavioural Neuroscience.
Cedars-Sinai study sheds light on bone marrow stem cell therapy for pancreatic recovery
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Researchers at Cedars-Sinai’s Maxine Dunitz Neurosurgical Institute have found that a blood vessel-building gene boosts the ability of human bone marrow stem cells to sustain pancreatic recovery in a laboratory mouse model of insulin-dependent diabetes.
The findings, published in a PLOS ONE article of the Public Library of Science, offer new insights on mechanisms involved in regeneration of insulin-producing cells and provide new evidence that a diabetic’s own bone marrow one day may be a source of treatment.
Scientists began studying bone marrow-derived stem cells for pancreatic regeneration a decade ago. Recent studies involving several pancreas-related genes and delivery methods – transplantation into the organ or injection into the blood – have shown that bone marrow stem cell therapy could reverse or improve diabetes in some laboratory mice. But little has been known about how stem cells affect beta cells – pancreas cells that produce insulin – or how scientists could promote sustained beta cell renewal and insulin production.
Study reveals genomic similarities between breast cancer and ovarian cancers
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One subtype of breast cancer shares many genetic features with high-grade serous ovarian cancer, a cancer that is very difficult to treat, according to researchers supported by the National Institutes of Health. The findings suggest that the two cancers are of similar molecular origin, which may facilitate the comparison of therapeutic data for subtypes of breast and ovarian cancers.
The researchers, using data generated as part of The Cancer Genome Atlas (TCGA), described new insights into the four standard molecular subtypes based on a comprehensive characterization of samples from 825 breast cancer patients.
The study, a collaborative effort funded by the National Cancer Institute (NCI) and the National Human Genome Research Institute (NHGRI), both part of NIH, was published online Sept. 23, 2012, and in print Oct. 4, 2012, in the journal Nature.
“TCGA’s comprehensive characterization of their high-quality samples allows researchers an unprecedented look at these breast cancer subgroups,” said NIH Director Francis S. Collins, M.D., Ph.D.
Could smoking pot raise testicular cancer risk?
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Do men who frequently smoke pot have a higher risk of testicular cancer than those who do not? It’s possible, according to a new study. However, the researchers say the link is currently a “hypothesis” that needs further testing.
Testicular cancer is relatively rare - a man’s lifetime chance of developing the disease is about 1 in 300 (and dying of it is about 1 in 5,000). Frequent or long-term marijuana smokers could have about double the risk of nonusers, according to the report in the February 9 issue of the journal Cancer.
In the study, a team led by Dr. Janet R. Daling of the Fred Hutchinson Cancer Research Center in Seattle, Washington, interviewed 369 men between the ages of 18 and 44 from the Seattle-Puget Sound area whose testicular cancer had been diagnosed. They compared those men with 979 men who lived in the same area, but did not have cancer.
Genome-wide scan maps mutations in deadly lung cancers; reveals embryonic gene link
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Scientists have completed a comprehensive map of genetic mutations linked to an aggressive and lethal type of lung cancer.
Among the errors found in small cell lung cancers, the team of scientists, including those at the Johns Hopkins Kimmel Cancer Center, found an alteration in a gene called SOX2 associated with early embryonic development.
“Small cell lung cancers are very aggressive. Most are found late, when the cancer has spread and typical survival is less than a year after diagnosis,” says Charles Rudin, M.D., Ph.D., professor of oncology at the Johns Hopkins Kimmel Cancer Center. “Our genomic studies may help identify genetic pathways responsible for the disease and give us new ideas on developing drugs to treat it.”
The scientists found an increase in the copy number of the SOX2 gene in about 27 percent of small cell lung cancer samples. The resulting overproduction of proteins made by the SOX2 gene may play a role in igniting or sustaining abnormal cell growth in the lung. SOX2 offers a new target for scientists working to develop new drugs to combat this intractable cancer, say the investigators.
George to begin chemotherapy next week
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Following the advice of his medical team, Chicago’s Cardinal Francis George will begin four months of chemotherapy next week, according to a statement released Tuesday by the Roman Catholic Archdiocese of Chicago.
George, 75, who battled bladder cancer six years ago, learned this month that doctors had discovered cancerous cells on his liver and a kidney.
Tests, including a biopsy last week, confirmed that the removal of a cancerous nodule from the cardinal’s liver left no cancer behind, the archdiocese reported. But doctors also confirmed that the cardinal’s right kidney contained a malignant lesion. Because cancerous cells are impossible to detect in the bloodstream, they could not rule out a presence of the disease elsewhere in the body, according to the statement.
Having consulted with the cardinal’s doctors at Mayo Clinic in Rochester, Minn., physicians at Loyola University Medical Center reportedly recommended Monday that he should undergo chemotherapy.
RA Patients Get Cancer Screens, May Need More
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Patients with rheumatoid arthritis (RA) are receiving the recommended cancer screening tests, but the recommendations may not be adequate for these patients, researchers reported.
Compared with controls, women with RA were more likely to have had a Pap smear (HR 1.21, 95% CI 1.17 to 1.24), a mammogram (HR 1.49, 95% CI 1.45 to 1.53), and a colonoscopy (HR 1.69, 95% CI 1.61 to 1.77), according to Seoyoung C. Kim, MD, and colleagues from Brigham and Women’s Hospital in Boston.
However, “given the increased risk of some cancers in RA and concerns in the association between various types of RA treatment and malignancy, it may be worth investigating the effectiveness of current cancer screening guidelines in patients with RA and in subgroups on specific treatments,” Kim and colleagues wrote online in Arthritis & Rheumatism.
Moderate exercise tied to lower breast cancer risk
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Women who exercise moderately may be less likely than their inactive peers to develop breast cancer after menopause, a study published Monday suggests.
Researchers found that of more than 3,000 women with and without breast cancer, those who’d exercised during their childbearing years were less likely to develop the cancer after menopause.
The same was true when women took up exercise after menopause.
And it did not take a vigorous workout; regular exercise at any intensity level was linked to a lower breast cancer risk, the researchers say.
Doctors try to make sense of cancer’s genetic jumble
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Not too long ago, knowing the organ where a cancer first takes hold was generally all a doctor needed to determine what treatments to use. Not anymore.
Advances in understanding cancer at the molecular level mean doctors can better select the drugs that will most help individual patients. To do so, they must identify which genetic mutations are driving the growth of a patient’s tumor, and that shift is making their work much harder.
“We’ve had this biological revolution that has sliced the pie for these cancers finer and finer as we’ve learned more about the genomics of cancer,” said Dr. George Sledge, co-director of the breast cancer program at Indiana University and a past president of the American Society of Clinical Oncology (ASCO).
Experimental drug shrinks cancer tumors
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An experimental cancer drug successfully shrank tumors in patients with different kinds of cancer, including typically hard-to-treat lung cancers, according to a new study. Oncologists said the research was encouraging, but more study was needed to know whether the drug would prolong life for cancer patients.
The study, led by Dr. Suzanne Topalian, was presented Friday at the Super Bowl of cancer professionals, a meeting of the American Society of Clinical Oncology, and published in the New England Journal of Medicine.
In a small, early phase study, researchers used a drug targeting a portion of the body’s immune system, a pathway called PD-1, which usually works to stop the body from fighting cancerous tumors. By shutting down the pathway, the drug stokes the body’s immune system to fight tumor cells.
Avastin Slows Resistant Ovarian Cancer
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Progression of platinum-resistant ovarian cancer slowed by more than 50% in patients who received bevacizumab (Avastin) plus chemotherapy compared with nonplatinum chemotherapy alone, results of a randomized trial showed.
Median progression-free survival (PFS) increased from 3.4 months with chemotherapy to 6.7 months with chemotherapy and bevacizumab.
The objective response rate more than doubled with the addition of the angiogenesis inhibitor, Eric Pujade-Lauraine, MD, of Hopital Hotel-Dieu in Paris, reported here at the American Society for Clinical Oncology meeting.
Strategy Discovered to Activate Genes that Suppress Tumors and Inhibit Cancer
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A team of scientists has developed a promising new strategy for “reactivating” genes that cause cancer tumors to shrink and die. The researchers hope that their discovery will aid in the development of an innovative anti-cancer drug that effectively targets unhealthy, cancerous tissue without damaging healthy, non-cancerous tissue and vital organs. The research will be published in the Journal of Biological Chemistry.
The team, led by Yanming Wang, a Penn State University associate professor of biochemistry and molecular biology, and Gong Chen, a Penn State assistant professor of chemistry, developed the new strategy after years of earlier research on a gene called PAD4 (peptidylarginine deiminase 4), which produces the PAD4 enzyme. Previous research by Wang and other scientists revealed that the PAD4 enzyme plays an important role in protecting the body from infection. The scientists compared normal mice with a functioning PAD4 gene to other mice that had a defective a PAD4 gene. When infected with bacteria, cells from the normal mice attacked and killed about 30 percent of the harmful bacteria, while cells from the defective mice battled a mere 10 percent. The researchers discovered that cells with a functioning PAD4 enzyme are able to build around themselves a protective, bacteria-killing web that Wang and his colleagues dubbed a NET (neutrophil extracellular trap). This NET is especially effective at fighting off flesh-eating bacteria.
Biomarker predicts response to cancer treatment
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VIB researcher Diether Lambrechts, associated with KU Leuven, has discovered a biomarker that might potentially predict which patients will benefit more from treatment with bevacizumab (Avastin). If validated, this discovery could be an important step towards personalized medicine and patient-tailored use of this important cancer drug.
Diether Lambrechts (VIB - KU Leuven) said “in two large clinical studies with patients with advanced stages of pancreas and kidney cancer a variant in the DNA was discovered that identified patients who did not respond well to the prescribed course of bevacizumab. Further research in the lab showed that this variant, or biomarker, was responsible for increasing the production of a certain protein that is hypothesized to neutralize the effect of bevacizumab in these patients. If this marker would be clinically validated, the marker could be used to distinguish patients that would benefit from the drug from those that would not, and spare them a futile therapy with possible side effects.”
Biomarkers for targeted treatments
Oncologists want to use treatments that target the particular cancer. Every cancer is characterized by a specific set of proteins that is responsible for the abnormal behavior of the tumor. Therapies aimed at blocking these proteins can significantly extend the life of cancer patients, provided that they receive the drug that is right for them. Cancers with a different set of proteins will not respond to a therapy that does not target those proteins. That is why developing biomarkers for all targeted therapies is so important.
