Study gives promise to new treatment for appendix cancer
Appendix cancer is rare, with approximately 600 to 1,000 new patients diagnosed each year and an estimated 10,000 currently living with the disease. Because it is rare, few studies have been devoted to this cancer and standard treatment for appendix cancers relies upon the same chemotherapy drugs used for colorectal cancer. A new study by researchers at the University of California, San Diego School of Medicine has found that genetic mutations in appendix and colon cancers are, in fact, quite different, suggesting that new and different approaches to appendix cancer treatment should be explored.
The study was published in a recent issue of Genome Medicine.
Cancers are characterized by different gene mutations. Historically, genetic mutations in appendix cancer have been poorly characterized due to its low incidence. The cancer often remains undiagnosed until it is discovered during or after abdominal surgery or when an abnormal mass is detected  during a CT scan for an unrelated condition.
The primary treatment of localized appendix cancer is surgical but treatment for patients with inoperable appendix cancer has been limited to therapies developed for colorectal cancer. Although the chemotherapy drugs used for colorectal cancer dramatically improve patient outcomes, they have not proven to be as successful in patients with appendix cancer.
“We have been treating appendix cancer like colorectal cancer because it was thought to be the most similar tumor type, but this study identifies the signature differences between these two cancers,” said Andrew Lowy, MD, FACS, a senior author of the study and professor of Surgery at UC San Diego School of Medicine. “These findings suggest opportunities to develop novel therapies that specifically target appendix cancer.”  
The study initially evaluated 10 cases, nine with low-grade appendix cancers and one with high-grade cancer. The results from this group were then validated with 19 additional cases.
The results also identified a gene mutation in appendix cancer that is commonly found in a form of pancreatic cancer, which typically spreads rapidly and is seldom detected in its early stages.
“The study’s results are promising for patients. We now have a more in-depth knowledge of the biological make up of appendix cancers, which allow for a more customized approach,” said Lowy, who also serves as chief of the Division of Surgical Oncology at UC San Diego Health System. “The goal is to now conduct more studies that will test specific treatments targeted to these unique genetic mutations.”
To learn more about cancer treatments at UC San Diego Health System, visit cancer.ucsd.edu         Image: A histopathological photomicrograph depicting cancerous cells in the appendix.

Study gives promise to new treatment for appendix cancer

Appendix cancer is rare, with approximately 600 to 1,000 new patients diagnosed each year and an estimated 10,000 currently living with the disease. Because it is rare, few studies have been devoted to this cancer and standard treatment for appendix cancers relies upon the same chemotherapy drugs used for colorectal cancer. A new study by researchers at the University of California, San Diego School of Medicine has found that genetic mutations in appendix and colon cancers are, in fact, quite different, suggesting that new and different approaches to appendix cancer treatment should be explored.

The study was published in a recent issue of Genome Medicine.

Cancers are characterized by different gene mutations. Historically, genetic mutations in appendix cancer have been poorly characterized due to its low incidence. The cancer often remains undiagnosed until it is discovered during or after abdominal surgery or when an abnormal mass is detected  during a CT scan for an unrelated condition.

The primary treatment of localized appendix cancer is surgical but treatment for patients with inoperable appendix cancer has been limited to therapies developed for colorectal cancer. Although the chemotherapy drugs used for colorectal cancer dramatically improve patient outcomes, they have not proven to be as successful in patients with appendix cancer.

“We have been treating appendix cancer like colorectal cancer because it was thought to be the most similar tumor type, but this study identifies the signature differences between these two cancers,” said Andrew Lowy, MD, FACS, a senior author of the study and professor of Surgery at UC San Diego School of Medicine. “These findings suggest opportunities to develop novel therapies that specifically target appendix cancer.”  

The study initially evaluated 10 cases, nine with low-grade appendix cancers and one with high-grade cancer. The results from this group were then validated with 19 additional cases.

The results also identified a gene mutation in appendix cancer that is commonly found in a form of pancreatic cancer, which typically spreads rapidly and is seldom detected in its early stages.

“The study’s results are promising for patients. We now have a more in-depth knowledge of the biological make up of appendix cancers, which allow for a more customized approach,” said Lowy, who also serves as chief of the Division of Surgical Oncology at UC San Diego Health System. “The goal is to now conduct more studies that will test specific treatments targeted to these unique genetic mutations.”

To learn more about cancer treatments at UC San Diego Health System, visit cancer.ucsd.edu        

Image: A histopathological photomicrograph depicting cancerous cells in the appendix.

Novel Technologies Advance Brain Surgery to Benefit Patients
Minimally invasive brain surgery at UC San Diego Health System

In a milestone procedure, neurosurgeons at UC San Diego Health System have integrated advanced 3D imaging, computer simulation and next-generation surgical tools to perform a highly complex brain surgery through a small incision to remove deep-seated tumors. This is the first time this complex choreography of technologies has been brought together in an operating room in California.

“Tumors located at the base of the skull are particularly challenging to treat due to the location of delicate anatomic structures and critical blood vessels,” said neurosurgeon Clark C. Chen, MD, PhD, UC San Diego Health System. “The conventional approach to excising these tumors involves long skin incisions and removal of a large piece of skull. This new minimally invasive approach is far less radical. It decreases the risk of the surgery and shortens the patient’s hospital stay.” 

“A critical part of this surgery involves identifying the neural fibers in the brain, the connections that allow the brain to perform its essential functions. The orientation of these fibers determines the trajectory to the tumor,” said Chen, vice-chairman of Academic Affairs for the Division of Neurosurgery at UC San Diego School of Medicine. “We visualized these fibers with restriction spectrum imaging, a proprietary technology developed at UC San Diego. Color-coded visualization of the tracts allows us to plot the safest path to the tumor.”

After surgery planning, a 2-inch incision was made near the patient’s hairline, followed by a quarter-sized hole in the skull. The surgery was carried out through a thin tube-like retractor that created a narrow path to the tumor.  Aided by a robotic arm and high-resolution cameras, the team was able to safely remove two tumors within millimeter precision.

“What we are seeing is a new wave of advances in minimally invasive surgery for patients with brain cancer,” said Bob Carter, MD, PhD, professor and chief of Neurosurgery, UC San Diego School of Medicine. “These minimally invasive approaches permit smaller incisions and a shorter recovery. In this case, the patient was able to go home the day after the successful removal of multiple brain tumors.”

A Moveable Yeast: modeling shows proteins never sit still
Our body’s proteins – encoded by DNA to do the hard work of building and operating our bodies – are forever on the move. Literally, according to new findings reported by Trey Ideker, PhD, chief of the Division of Genetics in the UC San Diego School of Medicine, and colleagues in a recent issue of the Proceedings of the National Academy of Sciences.
Hemoglobin protein molecules, for example, continuously transit through our blood vessels while other proteins you’ve never heard of bustle about inside cells as they grow, develop, respond to stimuli and succumb to disease.
To better understand the role of proteins in biological systems, Ideker and colleagues developed a computer model that can predict a protein’s intracellular wanderings in response to a variety of stress conditions.
To date, the model has been used to predict the effects of 18 different DNA-damaging stress conditions on the sub-cellular locations and molecular functions of more than 5,800 proteins produced by yeasts. They found, for example, that yeast proteins could move from mitochondria to the cell nucleus and from the endoplasmic reticulum to Golgi apparatus.
Though the model debut involved yeasts, researchers said the coding can be adapted to study changes in protein locations for any biological system in which gene expression sequences have been identified, including stem cell differentiation and drug response in humans.
Image courtesy of Material Mavens

A Moveable Yeast: modeling shows proteins never sit still

Our body’s proteins – encoded by DNA to do the hard work of building and operating our bodies – are forever on the move. Literally, according to new findings reported by Trey Ideker, PhD, chief of the Division of Genetics in the UC San Diego School of Medicine, and colleagues in a recent issue of the Proceedings of the National Academy of Sciences.

Hemoglobin protein molecules, for example, continuously transit through our blood vessels while other proteins you’ve never heard of bustle about inside cells as they grow, develop, respond to stimuli and succumb to disease.

To better understand the role of proteins in biological systems, Ideker and colleagues developed a computer model that can predict a protein’s intracellular wanderings in response to a variety of stress conditions.

To date, the model has been used to predict the effects of 18 different DNA-damaging stress conditions on the sub-cellular locations and molecular functions of more than 5,800 proteins produced by yeasts. They found, for example, that yeast proteins could move from mitochondria to the cell nucleus and from the endoplasmic reticulum to Golgi apparatus.

Though the model debut involved yeasts, researchers said the coding can be adapted to study changes in protein locations for any biological system in which gene expression sequences have been identified, including stem cell differentiation and drug response in humans.

Image courtesy of Material Mavens

Food for thought
Admittedly there’s no known scientific or therapeutic value to the brain image above. It’s not likely to satisfy our hunger for knowledge in, say, the way a tractograph or fMRI might. Instead, it’s just likely to make you hungry – for more.
Feast your eyes on Sara Asnaghi’s similar cerebral takes of the edible brain here.

Food for thought

Admittedly there’s no known scientific or therapeutic value to the brain image above. It’s not likely to satisfy our hunger for knowledge in, say, the way a tractograph or fMRI might. Instead, it’s just likely to make you hungry – for more.

Feast your eyes on Sara Asnaghi’s similar cerebral takes of the edible brain here.

Fighting dead zones of cancer
Almost all high-risk, poor-prognosis cancers have very low levels of oxygen in the primary tumor’s interior. A marker for this oxygen-depleted state is the presence of a protein known as H1FI alpha. 
In healthy cells, HIF1 alpha is degraded into harmless nothingness in the cytoplasm. In low-oxygen cancer cells however, the normal breakdown goes awry and HiFl alpha is able to enter the nucleus, where it may activate genes that further promote aberrant cell growth.
A new study conducted by researchers at the University of California, San Diego School of Medicine shows that an emerging class of anticancer treatments known as PI-3K inhibitors help to degrade the HIF1 alpha protein and thus may offer a potential therapy for treating deadly hypoxic tumors. The study was published in a recent issue of the Journal of Biological Chemistry.
“Our main finding is that, in the absence of PI-3K signaling, MDM2 proteins cannot go inside the nucleus,” said lead author Shweta Joshi, PhD, postdoctoral researcher. “In the cytoplasm, the MDM2 proteins degrade HIF1 alpha. This is good news because it means that some new cancer therapies may help patients in more ways that was initially realized.”
"These HIF1 proteins are major players in driving the cancer state," said co-author Donald Durden, MD, PhD, professor and vice chair for Research in the Department of Pediatrics and research director, Division of Hematology/Oncology at the UC San Diego Moores Cancer Center. “They control degradation of surrounding tissues, induce a change in metabolism and induce the formation of blood vessels. That is why our observation is so important, because it reveals an entirely new way of HIF1 regulation.”
Pictured: A false-color, scanning electron micrograph of two cultured HeLa cancer cells, courtesy of Thomas Deerinck, National Center for Microscopy and Imaging Research at San Diego.

Fighting dead zones of cancer

Almost all high-risk, poor-prognosis cancers have very low levels of oxygen in the primary tumor’s interior. A marker for this oxygen-depleted state is the presence of a protein known as H1FI alpha.

In healthy cells, HIF1 alpha is degraded into harmless nothingness in the cytoplasm. In low-oxygen cancer cells however, the normal breakdown goes awry and HiFl alpha is able to enter the nucleus, where it may activate genes that further promote aberrant cell growth.

A new study conducted by researchers at the University of California, San Diego School of Medicine shows that an emerging class of anticancer treatments known as PI-3K inhibitors help to degrade the HIF1 alpha protein and thus may offer a potential therapy for treating deadly hypoxic tumors. The study was published in a recent issue of the Journal of Biological Chemistry.

“Our main finding is that, in the absence of PI-3K signaling, MDM2 proteins cannot go inside the nucleus,” said lead author Shweta Joshi, PhD, postdoctoral researcher. “In the cytoplasm, the MDM2 proteins degrade HIF1 alpha. This is good news because it means that some new cancer therapies may help patients in more ways that was initially realized.”

"These HIF1 proteins are major players in driving the cancer state," said co-author Donald Durden, MD, PhD, professor and vice chair for Research in the Department of Pediatrics and research director, Division of Hematology/Oncology at the UC San Diego Moores Cancer Center. “They control degradation of surrounding tissues, induce a change in metabolism and induce the formation of blood vessels. That is why our observation is so important, because it reveals an entirely new way of HIF1 regulation.”

Pictured: A false-color, scanning electron micrograph of two cultured HeLa cancer cells, courtesy of Thomas Deerinck, National Center for Microscopy and Imaging Research at San Diego.

Uh oh!
A diagnosis of prostate cancer can be an “uh oh” moment. After skin cancer, it’s the most common cancer in American men, with more than 238,000 new cases diagnosed each year and almost 30,000 deaths.
However, the confocal micrograph above, produced by Xiaochen Lu and C. Chase Bolt at the University of Illinois at Urbana-Champaign, is not an uh-oh moment. Rather, it may be an “ah-hah!”
It depicts the actual prostate and ureter of an embryonic mouse – a winning image from the 2013 Olympus BioScapes competition.
Mouse models of prostate cancer are widely used, in part because the disease is often very slow progressing in humans and typically not detected in men until their 60s or older.

Uh oh!

A diagnosis of prostate cancer can be an “uh oh” moment. After skin cancer, it’s the most common cancer in American men, with more than 238,000 new cases diagnosed each year and almost 30,000 deaths.

However, the confocal micrograph above, produced by Xiaochen Lu and C. Chase Bolt at the University of Illinois at Urbana-Champaign, is not an uh-oh moment. Rather, it may be an “ah-hah!”

It depicts the actual prostate and ureter of an embryonic mouse – a winning image from the 2013 Olympus BioScapes competition.

Mouse models of prostate cancer are widely used, in part because the disease is often very slow progressing in humans and typically not detected in men until their 60s or older.

Charles E. Daniels to be Honored for His Leadership in Health-System Pharmacy
The American Society of Health-System Pharmacists (ASHP) has named Charles E. Daniels, PhD, FASHP, as the recipient of the 2014 John W. Webb Lecture Award. The Webb Award honors health-system pharmacy practitioners or educators who stand apart because of their extraordinary dedication to fostering excellence in pharmacy management and leadership.
“This prestigious award reflects Dr. Daniels international recognition as a leader in expanding pharmacy practices and academic development in health systems to improve patient care,” said James H. McKerrow, MD, PhD, dean of the UC San Diego Skaggs School of Pharmacy and Pharmaceutical Sciences. “Throughout his career, Dr. Daniels has focused on solving issues that regularly confront health system pharmacists, including medication safety, cost-effective use of medications, and increased efficiency of health-system operations.”
Daniels is pharmacist-in-chief for UC San Diego Health System and professor of clinical pharmacy and associate dean at UC San Diego Skaggs School of Pharmacy and Pharmaceutical Sciences. Daniels serves as system-wide pharmacy officer for the university’s hospitals and clinics. His leadership has cultivated an understanding among health system executives and health care providers of the importance of including pharmacists in key leadership and decision-making positions. He also has served as a champion for postgraduate education and training in order to best prepare pharmacists for practice.

Charles E. Daniels to be Honored for His Leadership in Health-System Pharmacy

The American Society of Health-System Pharmacists (ASHP) has named Charles E. Daniels, PhD, FASHP, as the recipient of the 2014 John W. Webb Lecture Award. The Webb Award honors health-system pharmacy practitioners or educators who stand apart because of their extraordinary dedication to fostering excellence in pharmacy management and leadership.

“This prestigious award reflects Dr. Daniels international recognition as a leader in expanding pharmacy practices and academic development in health systems to improve patient care,” said James H. McKerrow, MD, PhD, dean of the UC San Diego Skaggs School of Pharmacy and Pharmaceutical Sciences. “Throughout his career, Dr. Daniels has focused on solving issues that regularly confront health system pharmacists, including medication safety, cost-effective use of medications, and increased efficiency of health-system operations.”

Daniels is pharmacist-in-chief for UC San Diego Health System and professor of clinical pharmacy and associate dean at UC San Diego Skaggs School of Pharmacy and Pharmaceutical Sciences. Daniels serves as system-wide pharmacy officer for the university’s hospitals and clinics. His leadership has cultivated an understanding among health system executives and health care providers of the importance of including pharmacists in key leadership and decision-making positions. He also has served as a champion for postgraduate education and training in order to best prepare pharmacists for practice.

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