Enzyme Controlling Metastasis of Breast Cancer Identified
Researchers at the University of California, San Diego School of Medicine have identified an enzyme that controls the spread of breast cancer.  The findings, reported in the current issue of PNAS, offer hope for the leading cause of breast cancer mortality worldwide. An estimated 40,000 women in America will die of breast cancer in 2014, according to the American Cancer Society.
“The take-home message of the study is that we have found a way to target breast cancer metastasis through a pathway regulated by an enzyme,” said lead author Xuefeng Wu, PhD, a postdoctoral researcher at UC San Diego.
The enzyme, called UBC13, was found to be present in breast cancer cells at two to three times the levels of normal healthy cells. Although the enzyme’s role in regulating normal cell growth and healthy immune system function is well-documented, the study is among the first to show a link to the spread of breast cancer.
Specifically, Wu and colleagues with the UC San Diego Moores Cancer Center found that the enzyme regulates cancer cells’ ability to transmit signals that stimulate cell growth and survival by regulating the activity of a protein called p38 which when “knocked down” prevents metastasis. Of clinical note, the researchers said a compound that inhibits the activation of p38 is already being tested for treatment of rheumatoid arthritis.
In their experiments, scientists took human breast cancer cell lines and used a lentivirus to silence the expression of both the UBC13 and p38 proteins. These altered cancer cells were then injected into the mammary tissues of mice.  Although the primary tumors grew in these mice, their cancers did not spread.
“Primary tumors are not normally lethal,” Wu said. “The real danger is cancer cells that have successfully left the primary site, escaped through the blood vessels and invaded new organs. It may be only a few cells that escape, but they are aggressive. Our study shows we may be able to block these cells and save lives.”
Pictured: A tumor with reduced levels of enzyme UBC13 (top) and a control tumor (bottom) that has spread to the lungs.

Enzyme Controlling Metastasis of Breast Cancer Identified

Researchers at the University of California, San Diego School of Medicine have identified an enzyme that controls the spread of breast cancer.  The findings, reported in the current issue of PNAS, offer hope for the leading cause of breast cancer mortality worldwide. An estimated 40,000 women in America will die of breast cancer in 2014, according to the American Cancer Society.

“The take-home message of the study is that we have found a way to target breast cancer metastasis through a pathway regulated by an enzyme,” said lead author Xuefeng Wu, PhD, a postdoctoral researcher at UC San Diego.

The enzyme, called UBC13, was found to be present in breast cancer cells at two to three times the levels of normal healthy cells. Although the enzyme’s role in regulating normal cell growth and healthy immune system function is well-documented, the study is among the first to show a link to the spread of breast cancer.

Specifically, Wu and colleagues with the UC San Diego Moores Cancer Center found that the enzyme regulates cancer cells’ ability to transmit signals that stimulate cell growth and survival by regulating the activity of a protein called p38 which when “knocked down” prevents metastasis. Of clinical note, the researchers said a compound that inhibits the activation of p38 is already being tested for treatment of rheumatoid arthritis.

In their experiments, scientists took human breast cancer cell lines and used a lentivirus to silence the expression of both the UBC13 and p38 proteins. These altered cancer cells were then injected into the mammary tissues of mice.  Although the primary tumors grew in these mice, their cancers did not spread.

“Primary tumors are not normally lethal,” Wu said. “The real danger is cancer cells that have successfully left the primary site, escaped through the blood vessels and invaded new organs. It may be only a few cells that escape, but they are aggressive. Our study shows we may be able to block these cells and save lives.”

Pictured: A tumor with reduced levels of enzyme UBC13 (top) and a control tumor (bottom) that has spread to the lungs.

Silky Smooth
The image on the left is a scanning electron micrograph of human skin, produced by Thomas Deerinck at the National Center for Microscopic and Imaging Research at UC San Diego. Human epidermis – the outermost layer of skin – contains no blood cells and receives its nutrients solely through diffusion from capillaries in the underlying dermis. Over time, these cells lose their cytoplasm, which is replaced by keratin, a structural protein that forms tough, insoluble fibers (your hair and nails are excellent examples). After roughly a month, the cells die and are sloughed off at a rate of 30,000 to 40,000 per minute!
The comparatively smooth skin surface in the image to the right, courtesy of Carbajo Maria, is that of a spider. It features a few hairs and some random grains of adhering pollen.

Silky Smooth

The image on the left is a scanning electron micrograph of human skin, produced by Thomas Deerinck at the National Center for Microscopic and Imaging Research at UC San Diego. Human epidermis – the outermost layer of skin – contains no blood cells and receives its nutrients solely through diffusion from capillaries in the underlying dermis. Over time, these cells lose their cytoplasm, which is replaced by keratin, a structural protein that forms tough, insoluble fibers (your hair and nails are excellent examples). After roughly a month, the cells die and are sloughed off at a rate of 30,000 to 40,000 per minute!

The comparatively smooth skin surface in the image to the right, courtesy of Carbajo Maria, is that of a spider. It features a few hairs and some random grains of adhering pollen.

See the original piece by NPR’s Jon Hamilton here. Dr. Michael Rafii, director of our Memory Disorders Clinic and Dr. William Mobley, executive director of our Down Syndrome Center for Research and Treatment discuss the links between Down’s Syndrome and Alzheimer’s Disease and why research is looking at this population.
asapscience:

The descent into Alzheimer’s disease. A doctor chronicles the signatures of his patient as the disease took hold of her. Our love goes out to anyone who’s dealt with this awful disease in some way. 
via Reddit

See the original piece by NPR’s Jon Hamilton here. Dr. Michael Rafii, director of our Memory Disorders Clinic and Dr. William Mobley, executive director of our Down Syndrome Center for Research and Treatment discuss the links between Down’s Syndrome and Alzheimer’s Disease and why research is looking at this population.

asapscience:

The descent into Alzheimer’s disease. 

A doctor chronicles the signatures of his patient as the disease took hold of her. Our love goes out to anyone who’s dealt with this awful disease in some way. 

via Reddit

1,000 posts! Not a bad way to start a Tuesday!
Our 1,000th post was about human head lice … coincidence?

1,000 posts! Not a bad way to start a Tuesday!

Our 1,000th post was about human head lice … coincidence?

Close Nit
With Labor Day looming and the beginning of school, many of the academically minded among us turn their thoughts and eyes to topics like classroom supplies, textbooks and the likelihood little Johnny is going to come home with head lice.
It’s hard to know how many people get head lice (Pediculus humanus capitis) each year. The Centers for Disease Control estimates 6 to 12 million infestations annually in the United States among children three to 11 years of age – the most common targets.
Getting head lice is not a matter of cleanliness. The wingless parasitic insect is spread primarily by direct contact with the hair of an infested person. The most common way is head-to-head contact. Some studies suggest girls get head lice more often than boys.
Less common modes of transmission are wearing infested clothing, such as hats or scarves, using infested combs, brushes or towels or lying on a bed, couch, pillow or carpet recently in contact with an infested person.
Head lice are not known to transmit disease, but secondary bacterial skin infections may occur from scratching the infestation site. Some folks argue that beyond their basic harmlessness, head lice might actually promote health by boosting a natural immune response to body lice (Pediculus humanus humanus), which pose a more serious health threat.
Head lice spend their entire lives on human scalps, clamped onto a strand of hair, feeding exclusively on human blood. There are other species of lice that infest other mammals and birds.
Treatment involves the use of pediculicides – medicines that kill lice and their eggs. Supplemental measures include thorough cleaning of all clothes and exposed materials and grooming with a special, fine-toothed comb to extract adults and eggs, called nits.
Above: A colorized scanning electron micrograph of a nit (green) affixed to a strand of human hair, courtesy of Kevin Mackenzie, one of the winners of this year’s Wellcome Image Awards.

Close Nit

With Labor Day looming and the beginning of school, many of the academically minded among us turn their thoughts and eyes to topics like classroom supplies, textbooks and the likelihood little Johnny is going to come home with head lice.

It’s hard to know how many people get head lice (Pediculus humanus capitis) each year. The Centers for Disease Control estimates 6 to 12 million infestations annually in the United States among children three to 11 years of age – the most common targets.

Getting head lice is not a matter of cleanliness. The wingless parasitic insect is spread primarily by direct contact with the hair of an infested person. The most common way is head-to-head contact. Some studies suggest girls get head lice more often than boys.

Less common modes of transmission are wearing infested clothing, such as hats or scarves, using infested combs, brushes or towels or lying on a bed, couch, pillow or carpet recently in contact with an infested person.

Head lice are not known to transmit disease, but secondary bacterial skin infections may occur from scratching the infestation site. Some folks argue that beyond their basic harmlessness, head lice might actually promote health by boosting a natural immune response to body lice (Pediculus humanus humanus), which pose a more serious health threat.

Head lice spend their entire lives on human scalps, clamped onto a strand of hair, feeding exclusively on human blood. There are other species of lice that infest other mammals and birds.

Treatment involves the use of pediculicides – medicines that kill lice and their eggs. Supplemental measures include thorough cleaning of all clothes and exposed materials and grooming with a special, fine-toothed comb to extract adults and eggs, called nits.

Above: A colorized scanning electron micrograph of a nit (green) affixed to a strand of human hair, courtesy of Kevin Mackenzie, one of the winners of this year’s Wellcome Image Awards.

Finding Keys to Glioblastoma Therapeutic Resistance
Researchers at the University of California, San Diego School of Medicine have found one of the keys to why certain glioblastomas – the primary form of a deadly brain cancer – are resistant to drug therapy. The answer lies not in the DNA sequence of the tumor, but in its epigenetic signature. These findings have been published online as a priority report in the journal Oncotarget.
“There is a growing interest to guide cancer therapy by sequencing the DNA of the cancer cell,” said Clark Chen, MD, PhD, vice-chairman of Research and Academic Development, UC San Diego Division of Neurosurgery and the principal investigator of the study. “Our study demonstrates that the sensitivity of glioblastoma to a drug is influenced not only by the content of its DNA sequences, but also by how the DNA sequences are organized and interpreted by the cell.”
The team of scientists, led by Chen, used a method called comparative gene signature analysis to study the genetic profiles of tumor specimens collected from approximately 900 glioblastoma patients. The method allows investigators to discriminate whether specific cellular processes are “turned on” or “turned off” in glioblastomas. “Our study showed that not all glioblastomas are the same. We were able to classify glioblastomas based on the type of cellular processes that the cancer cells used to drive tumor growth,” said Jie Li, PhD, senior postdoctoral researcher in the Center for Theoretical and Applied Neuro-Oncology at UC San Diego and co-first author of the paper.
One of these cellular processes involves Epidermal Growth Factor Receptor (EGFR). The study revealed that EGFR signaling is suppressed in a subset of glioblastomas. Importantly, this suppression is not the result of altered DNA sequences or mutations. Instead, EGFR is turned off as a result of how the DNA encoding the EGFR gene is organized in the cancer cell. This form of regulation is termed “epigenetic.” Because EGFR is turned off in these glioblastomas, they become insensitive to drugs designed to inhibit EGFR signaling.
“Our research suggests that the selection of appropriate therapies for our brain tumor patients will require a meaningful synthesis of genetic and epigenetic information derived from the cancer cell,” said co-first author Zachary J. Taich.

Finding Keys to Glioblastoma Therapeutic Resistance

Researchers at the University of California, San Diego School of Medicine have found one of the keys to why certain glioblastomas – the primary form of a deadly brain cancer – are resistant to drug therapy. The answer lies not in the DNA sequence of the tumor, but in its epigenetic signature. These findings have been published online as a priority report in the journal Oncotarget.

“There is a growing interest to guide cancer therapy by sequencing the DNA of the cancer cell,” said Clark Chen, MD, PhD, vice-chairman of Research and Academic Development, UC San Diego Division of Neurosurgery and the principal investigator of the study. “Our study demonstrates that the sensitivity of glioblastoma to a drug is influenced not only by the content of its DNA sequences, but also by how the DNA sequences are organized and interpreted by the cell.”

The team of scientists, led by Chen, used a method called comparative gene signature analysis to study the genetic profiles of tumor specimens collected from approximately 900 glioblastoma patients. The method allows investigators to discriminate whether specific cellular processes are “turned on” or “turned off” in glioblastomas. “Our study showed that not all glioblastomas are the same. We were able to classify glioblastomas based on the type of cellular processes that the cancer cells used to drive tumor growth,” said Jie Li, PhD, senior postdoctoral researcher in the Center for Theoretical and Applied Neuro-Oncology at UC San Diego and co-first author of the paper.

One of these cellular processes involves Epidermal Growth Factor Receptor (EGFR). The study revealed that EGFR signaling is suppressed in a subset of glioblastomas. Importantly, this suppression is not the result of altered DNA sequences or mutations. Instead, EGFR is turned off as a result of how the DNA encoding the EGFR gene is organized in the cancer cell. This form of regulation is termed “epigenetic.” Because EGFR is turned off in these glioblastomas, they become insensitive to drugs designed to inhibit EGFR signaling.

“Our research suggests that the selection of appropriate therapies for our brain tumor patients will require a meaningful synthesis of genetic and epigenetic information derived from the cancer cell,” said co-first author Zachary J. Taich.

Protein-DNA Interaction Network Yields Surprising Discovery In Regulation Of Gene Expression
Although homeodomain proteins, which control development and execution of the body’s genetic roadmap, were described 30 years ago, scientists still do not fully understand how these proteins affect gene expression.
In a paper published online in Nature, researchers at the University of California, San Diego School of Medicine reveal that homeodomain transcription factors require interaction with subnuclear structures in order to function properly.
The POU-homeodomain protein Pit1 plays an important role in animal and human life by regulating expression of hormone genes in the pituitary gland. But a common mutation in this protein causes it to lose interaction with two other proteins, Satb1 and β-catenin, and in turn disconnects it from what turns out to be a vital subnuclear structure: the matrin-3 network. This naturally occurring mutation leads to a combined pituitary hormone deficiency.
In collaboration with scientists at the Lawrence Berkeley National Laboratory, California, researchers in the M. Geoffrey Rosenfeld laboratory were able for the first time to establish the functional link between this subnuclear structure and gene activation.
“This information allows us to see in even more detail how genes are activated at the exact time and place in the body,” said Dorota Skowronska-Krawczyk, PhD, an UC San Diego School of Medicine assistant project scientist in the Department of Cellular and Molecular Medicine and first author of the paper. “This helps us understand the process of gene expression. Scientists may use this information to investigate the role of matrin-3 subnuclear network in cancer or other diseases and whether the knowledge of its function could be used to improve existing therapies or design new ones.”

Protein-DNA Interaction Network Yields Surprising Discovery In Regulation Of Gene Expression

Although homeodomain proteins, which control development and execution of the body’s genetic roadmap, were described 30 years ago, scientists still do not fully understand how these proteins affect gene expression.

In a paper published online in Nature, researchers at the University of California, San Diego School of Medicine reveal that homeodomain transcription factors require interaction with subnuclear structures in order to function properly.

The POU-homeodomain protein Pit1 plays an important role in animal and human life by regulating expression of hormone genes in the pituitary gland. But a common mutation in this protein causes it to lose interaction with two other proteins, Satb1 and β-catenin, and in turn disconnects it from what turns out to be a vital subnuclear structure: the matrin-3 network. This naturally occurring mutation leads to a combined pituitary hormone deficiency.

In collaboration with scientists at the Lawrence Berkeley National Laboratory, California, researchers in the M. Geoffrey Rosenfeld laboratory were able for the first time to establish the functional link between this subnuclear structure and gene activation.

“This information allows us to see in even more detail how genes are activated at the exact time and place in the body,” said Dorota Skowronska-Krawczyk, PhD, an UC San Diego School of Medicine assistant project scientist in the Department of Cellular and Molecular Medicine and first author of the paper. “This helps us understand the process of gene expression. Scientists may use this information to investigate the role of matrin-3 subnuclear network in cancer or other diseases and whether the knowledge of its function could be used to improve existing therapies or design new ones.”

Memorable pictures
The hippocampus is a major component of the brains of humans and other vertebrates, playing critical roles in the consolidation of information from short-term memory to long-term memory and in spatial navigation. Damage to the hippocampus, whether from oxygen starvation, diseases such as encephalitis or epilepsy or physical trauma can result in memory loss and disorientation, including anterograde amnesia – the inability to form or retain new memories.
The hippocampus is also among the first regions of the brain to be affected by Alzheimer’s disease.
The hippocampus is a many-layered splendor, as these false-color confocal micrographs of a rat hippocampus by Thomas Deerinck of the National Center for Microscopy and Imaging Research at UC San Diego brilliantly show, layer upon lovely layer of pyramidal neurons, support cells and neuronal fibers.

Memorable pictures

The hippocampus is a major component of the brains of humans and other vertebrates, playing critical roles in the consolidation of information from short-term memory to long-term memory and in spatial navigation. Damage to the hippocampus, whether from oxygen starvation, diseases such as encephalitis or epilepsy or physical trauma can result in memory loss and disorientation, including anterograde amnesia – the inability to form or retain new memories.

The hippocampus is also among the first regions of the brain to be affected by Alzheimer’s disease.

The hippocampus is a many-layered splendor, as these false-color confocal micrographs of a rat hippocampus by Thomas Deerinck of the National Center for Microscopy and Imaging Research at UC San Diego brilliantly show, layer upon lovely layer of pyramidal neurons, support cells and neuronal fibers.

Aspirin, Take TwoWhite blood cell research shows how causing and conquering inflammation are inextricably linked
Hugely popular non-steroidal anti-inflammation drugs like aspirin, naproxen (marketed as Aleve) and ibuprofen (Advil, Motrin) all work by inhibiting or killing an enzyme called cyclooxygenase – a key catalyst in production of hormone-like lipid compounds called prostaglandins that are linked to a variety of ailments, from headaches and arthritis to menstrual cramps and wound sepsis.
In a new paper, published this week in the online early edition of PNAS, researchers at the University of California, San Diego School of Medicine conclude that aspirin has a second effect: Not only does it kill cyclooxygenase, thus preventing production of the prostaglandins that cause inflammation and pain, it also prompts the enzyme to generate another compound that hastens the end of inflammation, returning the affected cells to homeostatic health.
“Aspirin causes the cyclooxygenase to make a small amount of a related product called 15-HETE,” said senior author Edward A. Dennis, PhD, Distinguished Professor of Pharmacology, Chemistry and Biochemistry. “During infection and inflammation, the 15-HETE can be converted by a second enzyme into lipoxin, which is known to help reverse inflammation and cause its resolution – a good thing.”
Specifically, Dennis and colleagues looked at the function of a type of white blood cells called macrophages, a major player in the body’s immune response to injury and infection. They found that macrophages contain the biochemical tools to not just initiate inflammation, a natural part of the immune response, but also to promote recovery from inflammation by releasing 15-HETE and converting it into lipoxin as the inflammation progresses.
Dennis said the findings may open new possibilities for anti-inflammatory therapies by developing new drugs based on analogues of lipoxin and other related molecules that promote resolution of inflammation. “If we can find ways to promote more resolution of inflammation, we can promote health,” he said.  
Image: Scanning electron micrograph of macrophage. Image courtesy of National Cancer Institute.

Aspirin, Take Two
White blood cell research shows how causing and conquering inflammation are inextricably linked

Hugely popular non-steroidal anti-inflammation drugs like aspirin, naproxen (marketed as Aleve) and ibuprofen (Advil, Motrin) all work by inhibiting or killing an enzyme called cyclooxygenase – a key catalyst in production of hormone-like lipid compounds called prostaglandins that are linked to a variety of ailments, from headaches and arthritis to menstrual cramps and wound sepsis.

In a new paper, published this week in the online early edition of PNAS, researchers at the University of California, San Diego School of Medicine conclude that aspirin has a second effect: Not only does it kill cyclooxygenase, thus preventing production of the prostaglandins that cause inflammation and pain, it also prompts the enzyme to generate another compound that hastens the end of inflammation, returning the affected cells to homeostatic health.

“Aspirin causes the cyclooxygenase to make a small amount of a related product called 15-HETE,” said senior author Edward A. Dennis, PhD, Distinguished Professor of Pharmacology, Chemistry and Biochemistry. “During infection and inflammation, the 15-HETE can be converted by a second enzyme into lipoxin, which is known to help reverse inflammation and cause its resolution – a good thing.”

Specifically, Dennis and colleagues looked at the function of a type of white blood cells called macrophages, a major player in the body’s immune response to injury and infection. They found that macrophages contain the biochemical tools to not just initiate inflammation, a natural part of the immune response, but also to promote recovery from inflammation by releasing 15-HETE and converting it into lipoxin as the inflammation progresses.

Dennis said the findings may open new possibilities for anti-inflammatory therapies by developing new drugs based on analogues of lipoxin and other related molecules that promote resolution of inflammation. “If we can find ways to promote more resolution of inflammation, we can promote health,” he said.  

Image: Scanning electron micrograph of macrophage. Image courtesy of National Cancer Institute.

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