Author and MIT researcher Alan J. Fenn has written a book wherein he describes how he adapted the technology he invented for tracking missiles to the treatment of breast cancer.

Treating cancer with heat is not a new idea, but “researchers were having trouble using it to treat tumors deep within the body,” said Fenn. Further, it’s difficult to deliver the heat only to cancer cells without overheating normal tissue.
The microwaves in the new technique heat-and kill-cells containing high amounts of water and ions, or electrically charged atoms. Cancer cells typically have a high content of both, while healthy breast tissue contains much less. The outpatient procedure uses a single tiny needle probe to sense and measure parameters during treatment. Side effects appear to be minimal.
The first clinical study of the treatment involved 75 patients with early-stage breast cancer. Of the 34 patients who received the treatment prior to lumpectomy, none had viable cancer cells remaining at the surgical margins. Of the 41 patients who had a lumpectomy but did not receive the MIT treatment, four had cancer cells at the surgical margins.
This result is important for two reasons. First, additional breast surgery is often recommended for patients with cancer cells close to the edge of the lumpectomy surgical margin. Second, there is a higher risk of local recurrence of the breast cancer when cancer cells are found at the surgical margins. Fenn noted that all patients in both arms of the study received postoperative radiation therapy to reduce the risk of local recurrence.
Also presented in the new book are preliminary results for a study of the treatment in combination with preoperative chemotherapy for breast cancer patients with large tumors. “In this small feasibility study of 28 patients, one of the principal objectives was to increase tumor shrinkage with the combined use of focused microwave thermotherapy and preoperative chemotherapy,” Fenn said.
In this study tumors shrunk by approximately 50 percent more in women treated with both the MIT technique and chemotherapy, versus women treated with chemotherapy alone.

More from MIT…
Available at Amazon.com . . .

Bernhard Palsson and his team of bioengineering researchers at the University of California have spent over a year looking through 50 years of research and text to compile the most comprehensive list of metabolic pathways to date. From that data, they’ve created a ‘virtual model’ that may allow scientists to study how medications may affect the body.

This first-of-its-kind metabolic network builds on the sequencing of the human genome and contains more than 3,300 known human biochemical transformations that have been documented during 50 years of research worldwide.
In a report in the Proceedings of the National Academy of Sciences (PNAS) made available on the journal’s website on Jan. 29, the UCSD researchers led by Bernhard Palsson, a professor of bioengineering in the Jacobs School of Engineering, unveiled the BiGG (biochemically, genetically, and genomically structured) database as the end product of this phase of the research project.
… the UCSD researchers conducted 288 simulations, including the synthesis of testosterone and estrogen, as well as the metabolism of dietary fat. In every case, the behavior of the model matched the published performance of human cells in defined conditions.
Researchers can use the computationally based database to quickly discover the effects on a given cell type of changing the performance of any of the 3,300 known human metabolic reactions operating in that cell. The tool is designed to help scientists explore hundreds of human disorders in the metabolism of amino acids, carbohydrates, lipids, minerals, and other molecules. It also is intended to be used in the future to study metabolic variations between people as a way to individually tailor diet for weight control…
More than two dozen biochemical reactions in human cells are needed to make cholesterol. Cholesterol-lowering drugs called statins affect just one of those reactions, reducing the synthesis of cholesterol as if they were pinching a garden hose, slowing the flow of cholesterol through it. However, metabolic pathways are actually labyrinths of interconnected garden hoses with complicated flow patterns.
“Pinching off one part of the labyrinth can have a good effect, but it can also have unexpected consequences, or even no effect because of redundancy built into metabolic systems,” Palsson said. “The new tool we’ve created allows scientists to tinker with a virtual metabolic system in ways that were, until now, impossible, and to test the modeling predictions in real cells.”
Each type of cell in the human body utilizes only a fraction of all 3,300 metabolic reactions, and scientists can create in silico any type of cell, from a heart cell to a red blood cell, with its particular complement of metabolic enzymes, and adjust their genetic or other properties to compute the cell’s behavior.
“We can analyze abnormal metabolism at the root cause of diseases such as hemolytic anemia, which can result from a deficiency in metabolic reactions,” said Neema Jamshidi, an MD/Ph. D. student at UCSD and co-author of the paper. “We can study both the causes and consequences of this and other diseases, which may lead to novel insights about how new drugs might be designed to treat them.”

Press release at UCSD…
More at the BBC Online . . .
IUBMB-Nicholson: Metabolic Pathways Chart . . .

Teams of investigators, led by biochemists at the University of California, San Diego, hope that they identified the fundamental, long-elusive mechanism:

The study, published in the January 26 issue of the journal Cell, shows that what scientists thought were two distinct processes in cells–the cells’ normal development and the cells’ response to dangers such as invading organisms–are actually linked. The researchers, who were also from the Salk Institute for Biological Studies and the La Jolla Institute for Allergy and Immunology, say that the linkage of these two processes may explain why cancer, which is normal growth and development gone awry, can result from chronic inflammation, which is an out-of-control response to danger.
“Although there is plenty of evidence that chronic inflammation can promote cancer, the cause of this relationship is not understood,” said Alexander Hoffmann, an assistant professor of chemistry and biochemistry at U.C. San Diego, who led the study. “We have identified a basic cellular mechanism that we think may be linking chronic inflammation and cancer…”
Hoffmann referred to the parallel sets of steps in cellular defense and development as “mirror image pathways.” His team showed that these pathways are not distinct from one another because they are linked by a protein called p100. They found that inflammation leads to an increase in p100, but that p100 is also used in certain steps in development. Therefore p100 allows communication between inflammation and development.
A small amount of dialogue between inflammation and development is beneficial, say the researchers, akin to how information from anti-terrorism efforts could be useful to crews building the state’s infrastructure. On the other hand, the constant influence of defense processes on development is detrimental.
“Studies with animals have shown that a little inflammation is necessary for the normal development of the immune system and other organ systems,” explained Hoffmann. “We discovered that the protein p100 provides the cell with a way in which inflammation can influence development. But there can be too much of a good thing. In the case of chronic inflammation, the presence of too much p100 may overactivate the developmental pathway, resulting in cancer.”
In the paper, the researchers propose that thinking of the processes of defense and development as part of a single large system “represents an opportunity for therapeutic intervention.” For example, it might be easier to break the link between inflammation and cancer by targeting the developmental pathway, rather than the inflammation pathway.
“Many of the developmental signals that cells use are sent outside the cell, so they should be easier to block with drugs than inflammation signals, which tend to be confined within cells,” said Hoffmann. “It’s more challenging to design drugs that will enter cells.”
Because the molecules that play a role in the inflammation and development pathways have been extensively studied for many years, the researchers say that it is surprising to find a new molecule that significantly revises scientists’ understanding about the interactions between inflammation and development. They credit their discovery to an approach that combines biochemical techniques and computation.
“Our mathematical model of inflammation and development includes 98 biochemical reactions,” said Soumen Basak, a postdoctoral fellow working with Hoffmann. ” When we ran the model, it predicted that p100 levels would be elevated for a significant period of time when the inflammation pathway was stimulated. We confirmed the prediction using biochemical techniques with cells in the laboratory.”

UCSD’s press release…