Surgeons Use Microwave Technology To Destroy Tumors

A new minimally-invasive option for treating liver tumors, called microwave ablation, is now available at UC San Diego Medical Center and Moores UCSD Cancer Center, the only hospitals in the region to offer this technology to patients.“A liver tumor can be removed in many ways,” said Marquis Hart, MD, transplant surgeon at UC San Diego Medical Center. “Now, patients at UC San Diego have a new option called ‘microwave ablation.’ Simply put, we zap and destroy liver tumors with heat derived from microwave energy. This is an important alternative, especially since the majority of liver cancers cannot be partially removed and not all patients are transplant candidates.”

Liver cancer is on the rise in the United States, linked closely with the epidemic of hepatitis and other conditions causing cirrhosis, a degenerative disease of the liver. Current treatment options for liver cancer include transplantation, partial surgical removal of the liver, chemotherapy, radiation, or ablation—the destruction of abnormal tissue with heat from radiofrequency waves, high frequency ultrasound, freezing, or alcohol injection. Now, microwave technology, offered by Covidien, removes the tumor with intense heat.

To perform the procedure, Hart accesses the tumor through the skin, or through a small laparoscopic port or open incision. With ultrasound guidance or a computed tomography (CT) scan, the tumor is located and then pierced with a thin antenna which emits microwaves. This energy spins the water molecules in the tumor producing friction which causes heat. Temperatures above 60 degrees Celsius (140 degrees Fahrenheit) cause cellular death, usually within 10 minutes.

“Microwave ablation causes the tumor to be quickly and precisely removed. If necessary, multiple tumors can be treated at the same time,” said Hart. “This method appears to be more efficient than other ablation techniques which translates to better tumor destruction and less time for the patient under general anesthesia.”

In addition to liver disease, microwave ablation has promising potential in the treatment of lung, kidney, and bone cancer.

“The incidence of liver cancer in the United States has more than doubled in the last 20 years,” said Hart. “Conditions that cause chronic liver damage increase the risk of liver cancer. Fortunately the treatment options at UC San Diego Medical Center and Moores UCSD Cancer Center are numerous. No where else in the region will you find a multidisciplinary team of surgeons, hepatologists, radiologists, and oncologists offering the latest in cancer care. With a team dedicated specifically to the liver, our patients receive cutting–edge care from a diverse team of experts.”

According to the National Cancer Institute, primary liver and bile duct cancers are the fifth most common cause of cancer death in men and the ninth most common cause of cancer death in women. More than 90 percent of all cases occur in men and women age 45 or older. Liver cancer is closely associated with hepatitis virus infections. The incidence and mortality rates for these cancers have increased in all races and both sexes in the past two decades.

Single Gene Lets Bacteria Jump From Host To Host

All life — plants, animals, people — depends on peaceful coexistence with a swarm of microbial life that performs vital services from helping to convert food to energy to protection from disease.Now, with the help of a squid that uses a luminescent bacterium to create a predator-fooling light organ and a fish that uses a different strain of the same species of bacteria like a flashlight to illuminate the dark nooks of the reefs where it lives, scientists have found that gaining a single gene is enough for the microbe to switch host animals.

The finding, reported this week (Feb. 1) in the journal Nature by a team of scientists from the University of Wisconsin-Madison, is important not only because it peels back some of the mystery of how bacteria evolved to colonize different animals, but also because it reveals a genetic pressure point that could be manipulated to thwart the germs that make us sick.

"It seems that every animal we know about has microbes associated with it," says Mark J. Mandel, the lead author of the study and a postdoctoral fellow in the UW-Madison School of Medicine and Public Health. "We pick up our microbial partners from the environment and they provide us with a raft of services from helping digestion to protection from disease."

In the Pacific, a species of bacteria known as Vibrio fischeri lives in luminescent harmony with two distinct hosts: the diminutive nocturnal bobtail squid and the reef-dwelling pinecone fish. In the squid, which feeds at night near the ocean surface, one strain of the bacterium forms a light organ that mimics moonlight and acts like a cloaking device to shield the squid from hungry predators below. In the pinecone fish, another strain of the bacterium colonizes a light organ within the animal's jaw and helps illuminate the dark reefs in which it forages at night. The fish light organ may also play a role in attracting the zooplankton that make up the pinecone fish's menu.

But how did a single species of bacteria come to terms with such different hosts?

Working in the UW-Madison laboratory of microbiologist Ned Ruby, Mandel and his colleagues scoured the genomes of the two different strains of V. fischeri and found that most of the bacterium's genetic architecture was conserved over the course of millions of years of evolutionary history, but with a key difference: The strain that colonizes the squid has a regulatory gene that controls other genes that lay down a biofilm that allows the microbe to colonize the animal's light organ.

"During squid colonization, this regulatory gene turns on a suite of genes that allow bacteria to colonize the squid through mucus produced by the animal," Mandel explains. "The mucus is the pathway to the light organ, but it also helps keep out the bad guys."

Both strains of bacteria, Mandel explains, have the same genes that produce the biofilms the bacterium needs to get established in its host. But the regulatory gene that sets the other biofilm genes in motion is absent in the strain that lives in the pinecone fish, the animal scientists believe was first colonized by V. fischeri before it moved in to the squid light organ when the squid family came onto the scene in the Pacific Ocean at least 30 million years ago.

"The regulatory gene entered the bacterium's lineage and allowed it to expand its host range into the squid," according to Mandel. "The bottom-line message of the paper is that bacteria can shift host range by modifying their capabilities with small regulatory changes."

The regulatory gene acquired by the bacterium, notes Ruby, is essentially a switch the organism uses to activate a set of genes that had been residing quietly in the V. fischeri genome. Such mechanisms, he says, are very likely at play in many other species of bacteria, including those that infect humans and cause illness.

"This is going to inform a question that has been around a long time in the area of pathogenesis," says Ruby. One line of thought is that "in order to become a pathogen, a whole suite of genes needs to be imported to a bacterium."

The new finding by his group, however, suggests that nature is far more parsimonious: Instead of requiring organisms to acquire many new genes to occupy a new host, the combination of a new regulatory gene and genes that already reside in a bacterium is enough to do the trick.

"Together, they can do something neither of them could do before. They can mix and match and open up new niches," says Ruby.

Knowing that a regulatory gene plays a key role in allowing an organism to fit a new host may prove useful in human medicine as many bacterial pathogens arose first in other animals before infecting humans. A single gene can be a much easier target for a drug or other intervention to prevent or mitigate infection, the Wisconsin scientists say.

In addition to Ruby and Mandel, authors of the new Nature report include Michael S. Wollenberg, also of UW-Madison; Eric V. Stabb of the University of Georgia; and Karen L. Visick of Loyola University Chicago. The study was supported by grants from the Betty and Gordon Moore Foundation, the National Institutes of Health and the National Science Foundation.

DNA Component Can Stimulate And Suppress Immune Response

A component of DNA that can both stimulate and suppress the immune system, depending on the dosage, may hold hope for treating cancer and infection, Medical College of Georgia researchers say.Low levels of CpG increase inflammation, part of the body's way of eliminating invaders. But high doses block inflammation by increasing expression of the enzyme indoleamine 2,3 dioxygenase, or IDO, an immunosuppressor, the researchers say.

"The same therapy can have two different effects," says Rusty Johnson, a fifth-year M.D./Ph.D. student in the MCG Schools of Medicine and Graduate Studies. "It was assumed that giving this treatment at higher doses would cause more stimulation, but it has the opposite effect."

The researchers hope that manipulating the dosage can help them optimize the role of inflammation in fighting invaders such as tumors and harmful bacteria. Mr. Johnson presented the findings at the Midwinter Conference of Immunologists this month in Asilomar, Calif. He is working with Drs. Andrew Mellor and David Munn, co-directors of the School of Medicine Immuno Discovery Institute, who discovered IDO's immunosuppressive capabilities more than a decade ago.

With the help of Drs. Babak Baban and Phillip Chandler, scientists in MCG's Immunotherapy Center, they've also learned IDO inhibits inflammation by blocking production of interleukin 6, a secreted factor that causes inflammation.

"This suggests that IDO is a counter-regulatory mechanism that serves as a balance to prevent too much inflammation," Mr. Johnson says. "Too much inflammation leads to destruction of normal body tissue, and this shows IDO's importance in preventing this from occurring."

The researchers already knew that IDO protects tumors from the immune system. While working with collaborators Drs. Alex Muller and George Prendergast at the Lankenau Institute in Philadelphia, they learned its role in tumor formation.

"Without it, a mouse becomes resistant to skin tumor formation, and tumors that do form are smaller and less malignant," Mr. Johnson says.

They've also learned that the cells IDO uses to suppress the immune system – IDO-competent dendritic cells – originate from B cells, which produce antibodies to fight infection.

Mr. Johnson was in his second year of medical school when he heard Dr. Munn lecture about his and Dr. Mellor's groundbreaking discovery of IDO's role in protecting a fetus from the mother's immune system. It was at that point that the Augusta native decided to pursue a career in immunology. Mr. Johnson earned a bachelor's degree in chemistry from the Georgia Institute of Technology and studied piano and voice at Augusta State University prior to coming to MCG.