Life's Building Block Found in Comet
A fundamental ingredient for life has been discovered in a comet sample, supporting the idea that such icy objects seeded early Earth with the stuff needed to whip up living organisms.
New research firms up past suggestions of glycine, the simplest amino acid used to make proteins, inside samples from the comet Wild 2 (pronounced "Vilt 2").
"This is the first time an amino acid has been found in a comet," said lead researcher Jamie Elsila of NASA's Goddard Space Flight Center in Greenbelt, Md. "Our discovery supports the theory that some of life's ingredients formed in space and were delivered to Earth long ago by meteorite and comet impacts."
How life arose on Earth has long puzzled scientists and philosophers alike, with possible evidence for such building blocks showing up floating about in the cosmos and even inside the mouths of volcanoes.
The new finding, which has been accepted for publication in the journal Meteoritics and Planetary Science, also has implications for finding alien life.
"The discovery of glycine in a comet supports the idea that the fundamental building blocks of life are prevalent in space, and strengthens the argument that life in the universe may be common rather than rare," said Carl Pilcher, director of the NASA Astrobiology Institute, which co-funded the research.
NASA's Stardust spacecraft captured samples of gas and dust from Wild 2 in 2004. The material parachuted to Earth in 2006. Since then, scientists around the world have been analyzing the samples to learn the secrets of comet formation and our solar system's history.
Preliminary testing had suggested glycine was present in the samples. But since glycine is used by terrestrial life, the team couldn't rule out contamination from Earthly sources, according to a NASA statement released today.
Does sugar feed cancer?
Public release date: 17-Aug-2009
Contact: Linda Aagard
linda.aagard@hci.utah.edu
801-587-7639
University of Utah Health Sciences
Does sugar feed cancer?
New research sheds light on old saying
SALT LAKE CITY, Aug. 17, 2009 — Researchers at Huntsman Cancer Institute at the University of Utah have uncovered new information on the notion that sugar "feeds" tumors. The findings may also have implications for other diseases such as diabetes. The research is published in the journal Proceedings of the National Academy of Sciences.
"It's been known since 1923 that tumor cells use a lot more glucose than normal cells. Our research helps show how this process takes place, and how it might be stopped to control tumor growth," says Don Ayer, Ph.D., a Huntsman Cancer Institute investigator and professor in the Department of Oncological Sciences at the University of Utah.
During both normal and cancerous cell growth, a cellular process takes place that involves both glucose (sugar) and glutamine (an amino acid). Glucose and glutamine are both essential for cell growth, and it was long assumed they operated independently, but Ayer's research shows they are inter-dependent. He discovered that by restricting glutamine availability, glucose utilization is also stopped. "Essentially, if you don't have glutamine, the cell is short circuited due to a lack of glucose, which halts the growth of the tumor cell" Ayer says.
The research, spearheaded by Mohan Kaadige, Ph.D., a postdoctoral fellow in Ayer's lab, focused on MondoA, a protein that is responsible for turning genes on and off. In the presence of glutamine, MondoA blocks the expression of a gene called TXNIP. TXNIP is thought to be a tumor suppressor, but when it's blocked by MondoA , it allows cells to take up glucose, which in turn drives tumor growth. Ayer's research could lead to new drugs that would target glutamine utilization, or target MondoA or TXNIP.
Ayer says the next step in his research is to develop animal models to test his ideas about how MondoA and TXNIP control cell growth. "If we can understand that, we can break the cycle of glucose utilization which could be beneficial in the treatment of cancer," Ayer says.
Public release date: 17-Aug-2009
Contact: Linda Aagard
linda.aagard@hci.utah.edu
801-587-7639
University of Utah Health Sciences
Does sugar feed cancer?
New research sheds light on old saying
SALT LAKE CITY, Aug. 17, 2009 — Researchers at Huntsman Cancer Institute at the University of Utah have uncovered new information on the notion that sugar "feeds" tumors. The findings may also have implications for other diseases such as diabetes. The research is published in the journal Proceedings of the National Academy of Sciences.
"It's been known since 1923 that tumor cells use a lot more glucose than normal cells. Our research helps show how this process takes place, and how it might be stopped to control tumor growth," says Don Ayer, Ph.D., a Huntsman Cancer Institute investigator and professor in the Department of Oncological Sciences at the University of Utah.
During both normal and cancerous cell growth, a cellular process takes place that involves both glucose (sugar) and glutamine (an amino acid). Glucose and glutamine are both essential for cell growth, and it was long assumed they operated independently, but Ayer's research shows they are inter-dependent. He discovered that by restricting glutamine availability, glucose utilization is also stopped. "Essentially, if you don't have glutamine, the cell is short circuited due to a lack of glucose, which halts the growth of the tumor cell" Ayer says.
The research, spearheaded by Mohan Kaadige, Ph.D., a postdoctoral fellow in Ayer's lab, focused on MondoA, a protein that is responsible for turning genes on and off. In the presence of glutamine, MondoA blocks the expression of a gene called TXNIP. TXNIP is thought to be a tumor suppressor, but when it's blocked by MondoA , it allows cells to take up glucose, which in turn drives tumor growth. Ayer's research could lead to new drugs that would target glutamine utilization, or target MondoA or TXNIP.
Ayer says the next step in his research is to develop animal models to test his ideas about how MondoA and TXNIP control cell growth. "If we can understand that, we can break the cycle of glucose utilization which could be beneficial in the treatment of cancer," Ayer says.
Unlocking the body's defenses against cancer.
Public release date: 25-Aug-2009
University of Manchester
Scientists have discovered a way of allowing healthy cells to take charge of cancerous cells and stop them developing into tumours in what could provide a new approach to treating early-stage cancers.
University of Manchester researchers found that a special type of the chemicals known as 'kinase inhibitors' opened up communication channels on the surface of cells that enabled healthy cells to 'talk' to the cancer cells.
"When we added the chemicals to a mixture of healthy and cancerous cells in a flask the diseased cells stopped multiplying and began acting like normal cells again," said Dr Ian Hampson, who carried out the research with wife Dr Lynne Hampson.
"Further tests revealed that the chemicals helped the cancer cells form connections with surrounding healthy cells that allowed these normal cells to take charge of the mechanism by which cancer cells divide and grow out of control."
Cell division occurs naturally and continuously in human organs and tissue as part of the body's normal repair processes to combat wear and tear but in cancer the cells divide in an uncontrolled way.
Dr Hampson says the findings, published in the British Journal of Cancer, are all the more exciting because the chemicals, which were developed with colleagues at the University of Salford, appear to be relatively non-toxic and the positive effect on the cancer cells persists even when the chemicals are withdrawn.
"When the chemicals were added to a culture containing just cancer cells they had little effect," said Dr Hampson, who is based in Manchester's School of Cancer and Imaging Sciences. "It was only when we added the chemicals to a mixture of cancer cells and normal cells – similar to how you would find them in the body – that growth was suppressed.
"Intriguingly, the connections that allowed the healthy cells to communicate with the cancer cells stayed open even when the kinase inhibitors were removed indicating that a potential drug based on these chemicals could be given as a short course of treatment.
"Furthermore, the chemicals are non-poisonous and do not actually kill cells like conventional cancer therapies, such as chemotherapy and radiotherapy, so if we were able to develop a drug it is likely to have far fewer side-effects."
The team say the next stage of their research will be to find out exactly how the chemicals are able to increase the number of connections between cancer and normal cells. Once this is known, it should be possible to produce a drug based on these chemicals that could hopefully be used in humans.
Dr Lynne Hampson added: "We are currently applying for funding to carry out further research into the biochemistry of how these chemicals cause the effect we have observed. We also intend to investigate the use of different types of cell cultures to assess the potency and range of activity of these agents."
The research was funded by the Association for International Cancer Research, The Humane Research Trust, The Caring Cancer Research Trust, Kidscan and the Cancer Prevention Research Trust.
Public release date: 25-Aug-2009
University of Manchester
Scientists have discovered a way of allowing healthy cells to take charge of cancerous cells and stop them developing into tumours in what could provide a new approach to treating early-stage cancers.
University of Manchester researchers found that a special type of the chemicals known as 'kinase inhibitors' opened up communication channels on the surface of cells that enabled healthy cells to 'talk' to the cancer cells.
"When we added the chemicals to a mixture of healthy and cancerous cells in a flask the diseased cells stopped multiplying and began acting like normal cells again," said Dr Ian Hampson, who carried out the research with wife Dr Lynne Hampson.
"Further tests revealed that the chemicals helped the cancer cells form connections with surrounding healthy cells that allowed these normal cells to take charge of the mechanism by which cancer cells divide and grow out of control."
Cell division occurs naturally and continuously in human organs and tissue as part of the body's normal repair processes to combat wear and tear but in cancer the cells divide in an uncontrolled way.
Dr Hampson says the findings, published in the British Journal of Cancer, are all the more exciting because the chemicals, which were developed with colleagues at the University of Salford, appear to be relatively non-toxic and the positive effect on the cancer cells persists even when the chemicals are withdrawn.
"When the chemicals were added to a culture containing just cancer cells they had little effect," said Dr Hampson, who is based in Manchester's School of Cancer and Imaging Sciences. "It was only when we added the chemicals to a mixture of cancer cells and normal cells – similar to how you would find them in the body – that growth was suppressed.
"Intriguingly, the connections that allowed the healthy cells to communicate with the cancer cells stayed open even when the kinase inhibitors were removed indicating that a potential drug based on these chemicals could be given as a short course of treatment.
"Furthermore, the chemicals are non-poisonous and do not actually kill cells like conventional cancer therapies, such as chemotherapy and radiotherapy, so if we were able to develop a drug it is likely to have far fewer side-effects."
The team say the next stage of their research will be to find out exactly how the chemicals are able to increase the number of connections between cancer and normal cells. Once this is known, it should be possible to produce a drug based on these chemicals that could hopefully be used in humans.
Dr Lynne Hampson added: "We are currently applying for funding to carry out further research into the biochemistry of how these chemicals cause the effect we have observed. We also intend to investigate the use of different types of cell cultures to assess the potency and range of activity of these agents."
The research was funded by the Association for International Cancer Research, The Humane Research Trust, The Caring Cancer Research Trust, Kidscan and the Cancer Prevention Research Trust.
University of Utah Health Sciences
Public release date: 31-Aug-2009
New hope for deadly childhood bone cancer.
Surprising discovery made by studying so-called 'junk DNA'
SALT LAKE CITY, Aug. 31, 2009 — Researchers at Huntsman Cancer Institute (HCI) at the University of Utah have shed new light on Ewing's sarcoma, an often deadly bone cancer that typically afflicts children and young adults. Their research shows that patients with poor outcomes have tumors with high levels of a protein known as GSTM4, which may suppress the effects of chemotherapy. The research is published online today in the journal Oncogene.
"Doctors and researchers have long known that certain Ewing's sarcoma patients respond to chemotherapy, but others don't even though they have the same form of cancer," says HCI Investigator Stephen Lessnick, M.D., Ph.D. "Our research shows that GSTM4 is found in high levels among those patients where chemotherapy doesn't seem to work. It's found in low levels in patients where chemotherapy is having a more positive effect."
The research could lead to drugs that can suppress GSTM4 in certain patients. It also could lead to a screening test that could reveal which therapies will be most effective for patients. "GSTM4 doesn't seem to suppress the benefits of all chemotherapy drugs, just certain ones. A GSTM4-based test could help to identify the best therapy for each individual patient," Lessnick says.
Ewing's sarcoma is the second most common bone cancer in children and adolescents. The five-year survival rate is considered poor at about 30 percent if the cancer has spread by the time it is diagnosed, and there is an even poorer prognosis for patients who have suffered a relapse.
For this study, researchers focused on an abnormal protein known as EWS-FLI, which is found in most Ewing's sarcoma tumors. What they discovered is that EWS-FLI causes increased amounts of the GSTM4 gene – and the protein it produces – to be expressed in tumors, a previously unknown effect that led them to make the connection between poor outcomes and high levels of GSTM4. The discovery was made by focusing on repetitive DNA sequences called microsatellites. Microsatellites are sometimes referred to as "junk DNA" because they are not thought to have a normal role in the genome. By examining how EWS-FLI interacts with certain microsatellites, Lessnick and his team were able to identify GSTM4.
Lessnick says the next step in research is to focus on testing and treatments that may lead to better survival rates in patients. "Personalized medicine is the next frontier in the battle against cancer," he says. "We now know all cancers are not the same. By focusing on how these proteins are expressed in individual tumors, we may soon be able to offer the treatment that will work best for each patient, and that could lead to higher cure rates," he says.
Public release date: 31-Aug-2009
New hope for deadly childhood bone cancer.
Surprising discovery made by studying so-called 'junk DNA'
SALT LAKE CITY, Aug. 31, 2009 — Researchers at Huntsman Cancer Institute (HCI) at the University of Utah have shed new light on Ewing's sarcoma, an often deadly bone cancer that typically afflicts children and young adults. Their research shows that patients with poor outcomes have tumors with high levels of a protein known as GSTM4, which may suppress the effects of chemotherapy. The research is published online today in the journal Oncogene.
"Doctors and researchers have long known that certain Ewing's sarcoma patients respond to chemotherapy, but others don't even though they have the same form of cancer," says HCI Investigator Stephen Lessnick, M.D., Ph.D. "Our research shows that GSTM4 is found in high levels among those patients where chemotherapy doesn't seem to work. It's found in low levels in patients where chemotherapy is having a more positive effect."
The research could lead to drugs that can suppress GSTM4 in certain patients. It also could lead to a screening test that could reveal which therapies will be most effective for patients. "GSTM4 doesn't seem to suppress the benefits of all chemotherapy drugs, just certain ones. A GSTM4-based test could help to identify the best therapy for each individual patient," Lessnick says.
Ewing's sarcoma is the second most common bone cancer in children and adolescents. The five-year survival rate is considered poor at about 30 percent if the cancer has spread by the time it is diagnosed, and there is an even poorer prognosis for patients who have suffered a relapse.
For this study, researchers focused on an abnormal protein known as EWS-FLI, which is found in most Ewing's sarcoma tumors. What they discovered is that EWS-FLI causes increased amounts of the GSTM4 gene – and the protein it produces – to be expressed in tumors, a previously unknown effect that led them to make the connection between poor outcomes and high levels of GSTM4. The discovery was made by focusing on repetitive DNA sequences called microsatellites. Microsatellites are sometimes referred to as "junk DNA" because they are not thought to have a normal role in the genome. By examining how EWS-FLI interacts with certain microsatellites, Lessnick and his team were able to identify GSTM4.
Lessnick says the next step in research is to focus on testing and treatments that may lead to better survival rates in patients. "Personalized medicine is the next frontier in the battle against cancer," he says. "We now know all cancers are not the same. By focusing on how these proteins are expressed in individual tumors, we may soon be able to offer the treatment that will work best for each patient, and that could lead to higher cure rates," he says.