Portable Breast Scanner Allows Cancer Detection in the Blink of an Eye

A new portable scanner based on radio frequency technology can show in a second the presence of tumors -- malignant and benign -- in the breast on a computer. The red dot indicates the presence of a tumor.

Women could have a fast test for breast cancer and instantly identify the presence of a tumor in the comfort of their own home thanks to groundbreaking new research from the University of Manchester.
Professor Zhipeng Wu has invented a portable scanner based on radio frequency technology, which is able to show in a second the presence of tumours -- malignant and benign -- in the breast on a computer.
Using radio frequency or microwave technology for breast cancer detection has been proven by researchers in the US, Canada and UK. However, up to now, it can take a few minutes for an image to be produced, and this had to be done in a hospital or specialist care centre.
Now Professor Wu, from the University's School of Electrical and Electronic Engineering, says concerned patients can receive real-time video images in using the radio frequency scanner which would clearly and simply show the presence of a tumour.
Not only is this a quicker and less-intrusive means of testing, it also means women can be tested at GP surgeries, which could help dramatically reduce waiting times and in some cases avoid unnecessary X-ray mammography. The scanner could also be used at home for continuous monitoring of breast health.
The patented real-time radio frequency scanner uses computer tomography and works by using the same technology as a mobile phone, but with only a tiny fraction of its power.
This makes it both safe and low-cost and the electronics can be housed in a case the size of a lunch box for compactness and portability. Other existing systems are much larger.
Breast cancer is the second biggest killer in women, accounting for 8.2% of all cancer deaths. October is National Breast Cancer Awareness month.
The usual way of detecting breast cancer up to now is mammography, which works well for women over the age of 50 and can give results of up to 95% accuracy.
But it is far less effective for younger women. The detection rate could be as low as 60% for women under the age of 50, which accounts for 20% of all breast cancer cases.
At that stage it is even more important get accurate diagnosis. Early diagnosis and treatment could save thousands of lives.
The main difference between the two methods is that mammography works on density, while radio frequency technique works on dielectric contrasts between normal and diseased breast tissues.
In Professor Wu's design, as soon as the breast enters the cup an image appears on screen.
The presence of a tumour or other abnormality will show up in red as the sensor detects the difference in tissue contrasts at radio frequencies. Malignant tissues have higher permittivity and conductivity and therefore appear differently than normal ones to a screen.
Up to 30 images are generated every second, meaning a breast scan could be over in a far shorter time than they are currently.
Professor Wu said: "The system we have is portable and as soon as you lie down you can get a scan -- it's real-time.
"The real-time imaging minimises the chance of missing a breast tumour during scanning.
"Other systems also need to use a liquid or gel as a matching substance, such as in an ultrasound, to work but with our system you don't need that -- it can be done simply in oil, milk, water or even with a bra on.
"Although there is still research to be done, the system has great potential to bring a new way for breast cancer diagnosis.
"This will benefit millions of women in both developed and developing countries bearing in mind that one in nine women may develop breast cancer in their lifetime."
Professor Wu submitted his innovation of the sensor system to the IET Innovation Awards. The technology has been shortlisted in both Electronics and Measurement in Action categories. The winners will be announced in November.

Potential Prostate Cancer Marker Discovered

Images from the desorption electrospray ionization mass spectrometry analysis of prostate tissue samples are shown next to stained slides of the same samples. The images show that cholesterol sulfate is present in cancerous tissue and precancerous legions called high grade prostatic intraepithelial neoplasia, or PIN. A Purdue University-led research team discovered that cholesterol sulfate is a potential marker for prostate cancer. (Credit: Demian Ifa/Purdue Center for Analytical Instrumentation Development)

Studies by a Purdue University-led team have revealed a potential marker for prostate cancer that could be the starting point for less invasive testing and improved diagnosis of the disease.

The team used a new analysis technique to create a profile of the lipids, or fats, found in prostate tissue and discovered a molecular compound that appears to be useful in identifying cancerous and precancerous tissue. The profile revealed that cholesterol sulfate is a compound that is absent in healthy prostate tissue, but is a major fat found in prostate cancer tumors.
Graham Cooks, Purdue's Henry Bohn Hass Distinguished Professor of Chemistry, and Timothy Ratliff, the Robert Wallace Miller Director of the Purdue Center for Cancer Research, led the team.
"It was surprising to find a single compound that is distinctly present in cancerous tissue and not present in healthy tissue," said Cooks, who is co-director of Purdue's Center for Analytical Instrumentation Development. "We've been able to differentiate cancerous from healthy tissue using this new method in the past, but the difference was in the amounts of the same chemical compounds found in healthy tissue. There was no single differentiator of which one could say if it was present there was cancerous tissue."
Ratliff said this characteristic makes the compound a potential marker for the disease, which could lead to new blood or urine tests to screen for prostate cancer.
"Aside from skin cancer, prostate cancer is the most common cancer in men and is the second leading cause of cancer-related deaths," Ratliff said. "Unfortunately, the current screening test has a significant number of false positives because it uses a marker that is present with other non-cancerous conditions. As a result, many men have unnecessary biopsies, which are invasive, expensive and have the potential to cause infection. This new compound appears to be highly specific to prostate cancer cells, which would mean very few false positives."
The current prostate cancer test screens for a protein called prostate-specific antigen, or PSA, that is produced by the cells of the prostate. Elevated levels of PSA in the blood can signify prostate cancer, but non-cancerous conditions such as an enlarged or inflamed prostate also cause an increase in its levels, he said.
The findings of the study, which was funded by the Purdue University Center for Cancer Research and the National Institutes of Health, were published in the journal Analytical Chemistry.
The study was performed in collaboration with physician scientists from Indiana University School of Medicine, who co-authored the paper. They also provided the tissue samples and pathological analysis of the samples to check the new technique's results.
The team used a mass spectrometry analysis technique developed by Cooks and coworkers called desorption electrospray ionization, or DESI, to measure and compare the chemical characteristics of 68 samples of normal and cancerous prostate tissue.
Mass spectrometry works by first turning molecules into ions, or electrically charged versions of themselves, so that they can be identified by their mass. Conventional mass spectrometry requires chemical separations, manipulations of samples and containment in a vacuum chamber for ionization and analysis. The DESI technique eliminates these requirements by performing the ionization step in the air or directly on surfaces outside of the mass spectrometers, making the process much simpler, faster and more applicable to medical examination or surgical settings.
Cooks' research team also has developed software that turns the distribution and intensity of selected ions within a sample into a computer-generated image, much like what would be seen from a stained slide under the microscope. This chemical map of the sample can precisely show the location of cancerous tissue and the borders of tumors, Cooks said.
Livia Eberlin, co-author of the paper and a graduate student in Cooks' group, said the study showed promise in detecting precancerous lesions, as well.
"The DESI examination was able to distinguish a precancerous lesion in a small area of a sample made up of mostly healthy tissue," Eberlin said. "By evaluating the difference in the chemistry of cells, this technique can detect differences in diseased tissue that are otherwise indistinguishable. It could provide a new tool for pathologists to complement microscopic examination."
The team also plans to study differences in the chemistry of different types of prostate cancer tumors to see if there is a way to identify which are aggressive and which are not, she said.
Ratliff said the inability to tell the difference between aggressive and nonaggressive forms of prostate cancer causes problems in its treatment.
"A nonaggressive form of prostate cancer can be very slow to progress, and sometimes it is in the best interest of the patient not to go through rigorous treatments that reduce one's quality of life," he said. "The tests currently used to determine the probability that the cancer is an aggressive form are not very accurate, and about 30 percent of patients are misdiagnosed as having an aggressive form."
Additional co-authors of the paper include graduate students Allison Dill and Anthony Costa, and post doctoral researcher Demian Ifa from Purdue's Department of Chemistry and the Center for Analytical Instrumentation Development; Dr. Liang Cheng from the Indiana University School of Medicine Department of Pathology and Laboratory Medicine; and Dr. Timothy Masterson and Dr. Michael Koch from the Indiana University School of Medicine Department of Urology.
The team is already in the process of performing larger studies and plans to investigate the biological processes responsible for the expression of cholesterol sulfate in cancerous tissue.

Chemotherapy Plus Synthetic Compound Provides Potent Anti-Tumor Effect in Pancreatic Cancers

Human pancreatic cancer cells dramatically regress when treated with chemotherapy in combination with a synthetic compound that mimics the action of a naturally occurring "death-promoting" protein found in cells, researchers at UT Southwestern Medical Center have found.

Researchers led by Dr. Rolf Brekken have shown in mice that pancreatic cancer cells dramatically regress when treated with chemotherapy in combination with a synthetic "death-promoting" compound. 

The research, conducted in mice, appears in the March 23 issue of Cancer Research and could lead to more effective therapies for pancreatic and possibly other cancers, the researchers said.
"This compound enhanced the efficacy of chemotherapy and improved survival in multiple animal models of pancreatic cancer," said Dr. Rolf Brekken, associate professor of surgery and pharmacology and the study's senior author. "We now have multiple lines of evidence in animals showing that this combination is having a potent effect on pancreatic cancer, which is a devastating disease."
In this study, Dr. Brekken and his team transplanted human pancreatic tumors into mice, then allowed the tumors to grow to a significant size. They then administered a synthetic compound called JP1201 in combination with gemcitabine, a chemotherapeutic drug that is considered the standard of care for patients with pancreatic cancer. They found that the drug combination caused regression of the tumors.
"There was a 50 percent regression in tumor size during a two-week treatment of the mice," Dr. Brekken said. "We also looked at survival groups of the animals, which is often depressing in human therapeutic studies for pancreatic cancer because virtually nothing works. We found not only significant decrease in tumor size, but meaningful prolongation of life with the drug combination."
The drug combination was also effective in an aggressive model of spontaneous pancreatic cancer in mice.
The compound JP1201 was created in 2004 by UT Southwestern researchers to mimic the action of a protein called Smac. The researchers discovered Smac in 2000 and found that this protein plays a key role in the normal self-destruction process present in every cell.
Cell death, or apoptosis, is activated when a cell needs to be terminated, such as when a cell is defective or is no longer needed for normal growth and development. In cancer cells, this self-destruct mechanism is faulty and lead to breaks in the cell-death cascade of events. The synthetic Smac, or Smac mimetic, developed at UT Southwestern inhibits these breaks, allowing the cell to die.
"In essence, we're inhibiting an inhibitor," Dr. Brekken said. "And we're allowing the apoptotic cascade to kick off, resulting in the death of cancer cells."
UT Southwestern researchers are using Smac mimetics in breast and lung cancer research, as well. Dr. Brekken said the next step is to develop a compound based on JP1201 that can be tested in humans in clinical trials.
Other UT Southwestern researchers involved in the study included lead author Dr. Sean Dineen, surgery resident; Dr. Christina Roland, surgery resident; Rachel Greer, student research assistant in the Nancy B. and Jake L. Hamon Center for Therapeutic Oncology Research; Juliet Carbon, senior research associate in surgery and in the Hamon Center; Jason Toombs, research assistant in surgery and in the Hamon Center; Dr. Puja Gupta, a pediatric hematology/oncology fellow; Dr. Noelle Williams, associate professor of biochemistry; and Dr. John Minna, director of the W.A. "Tex" and Deborah Moncrief Jr. Center for Cancer Genetics and of the Hamon Center.
The research was supported by Susan G. Komen for the Cure and Joyant Pharmaceuticals, a Dallas-based company and UT Southwestern spinoff that is developing medical applications of Smac-mimetic compounds.

Genetic Variant Offers Protection Against Tuberculosis and Leprosy

When people get exposed to the mycobacterium responsible for tuberculosis (TB), some will become sick with a disease that is a major cause of mortality around the world while others simply don't. Now, researchers reporting in the March 5th issue of the journal Cell, a Cell Press publication, can point to one important reason for this variation in susceptibility or resistance: genetic differences among individuals in levels of an immune enzyme (LTA4H) that is involved in the production of leukotriene B, a pro-inflammatory fatty acid immune signaling molecule.
It turns out individuals who are heterozygous for LTA4H, meaning they carry two versions of the enzyme-encoding gene and produce an average amount of the enzyme (not too little or too much), are less likely to succumb to tuberculosis. They also appear to gain protection against leprosy, a disease which is also caused by mycobacterial infection.
"TB is obviously a big problem," said Lalita Ramakrishnan of the University of Washington. "There isn't a good vaccine, notwithstanding the fact that the TB vaccine has been administered to more people than any other. On top of that, it requires long-term treatment for cure and there is an epidemic of drug-resistant TB. Increasingly, people are becoming infected with strains that are resistant to every antibiotic. On this backdrop, it made sense to go back to the drawing board and try to understand the pathogenesis of the disease."
In the new study, Ramakrishnan and her colleague David Tobin did just that, in an unbiased screen for TB susceptibility genes in the zebrafish. They then collaborated with University of Washington human geneticists Jay Vary, Thomas Hawn and Mary-Claire King and others in Vietnam and Nepal to validate their findings in human populations.
A second study in the same issue of Cell approached the question in another way. Kanury Rao and his colleagues at the International Centre for Genetic Engineering and Biotechnology in India used a genome-wide analysis to produce what now becomes a resource for TB researchers everywhere. They uncovered all of the "cellular machinery" within human macrophages -- the cells primarily targeted by TB -- that interact with the infectious mycobacteria and allow the infection to stably persist.
Rao's team uncovered 275 players within host cells that interact with each other to form a dense network. That picture allowed the researchers to make a detailed molecular-level description of what he refers to as "functional modules" within host cells that are engaged and perturbed by TB infection. Interestingly, they showed that the shape of that interaction varies depending on which isolated strain of TB one considers, suggesting that the different strains rely on somewhat different tactics for successful infection.
Rao's findings offer new leads in the fight against TB, he says. "We identify a core set of molecules which can be targeted through drug development efforts to treat both drug sensitive and multiple drug resistant forms of TB infection. Rather than targeting the pathogen itself, our studies highlight an alternate strategy wherein the host factors required to support pathogen survival can be used as targets for TB therapy."
The discovery of LTA4H as a TB susceptibility gene may have clinical implications too, even if it doesn't offer a direct path to a better vaccine, Ramakrishnan says. For one thing, the finding that medium activity of the immune enzyme is best when it comes to TB might help to explain something that has been known but not well understood in clinical circles: people with hard-to-treat TB sometimes improve when they are given anti-inflammatory, immunosuppressive therapies along with more standard drug treatments alone.
Ramakrishnan also notes that the same polymorphisms in LTA4H they uncovered were earlier linked to heart disease. That suggests that drugs that target this pathway in heart disease might be useful in the context of TB, she says.
The connection between infectious disease and heart disease also has implications for understanding the evolution of the immune system's inflammatory responses. "In general, people have thought that inflammation is a positive when it comes to fighting infection, but then it can cause modern-day disease," Ramakrishnan says. The finding that it is heterozygotes -- with intermediate activity of the immunity enzyme -- who fare best in the context of TB and leprosy suggests that in these infections also, inflammation has to be finely tuned for optimal protection.
The researchers include David M. Tobin, University of Washington, Seattle, WA; Jay C. Vary, Jr., University of Washington, Seattle, WA; John P. Ray, University of Washington, Seattle, WA; Gregory S. Walsh, Howard Hughes Medical Institute and Division of Basic Science, Fred Hutchinson Cancer Research Center, Seattle, WA; Sarah J. Dunstan, Oxford University Clinical Research Unit, Hospital for Tropical Diseases, Ho Chi Minh City, Vietnam, Oxford University, Oxford, UK; Nguyen D. Bang, Pham Ngoc Thach Hospital for Tuberculosis and Lung Disease, Ho Chi Minh City, Vietnam; Deanna A. Hagge, Mycobacterial Research Laboratory, Anandaban Hospital, Kathmandu, Nepal; Saraswoti Khadge, Mycobacterial Research Laboratory, Anandaban Hospital, Kathmandu, Nepal; Mary-Claire King, University of Washington, Seattle, WA; Thomas R. Hawn, University of Washington, Seattle, WA; Cecilia B. Moens, Howard Hughes Medical Institute and Division of Basic Science, Fred Hutchinson Cancer Research Center, Seattle, WA; and Lalita Ramakrishnan, University of Washington, Seattle, WA.

Blocking Inflammation Receptor Kills Breast Cancer Stem Cells, Study Finds

Scientists at the University of Michigan Comprehensive Cancer Center have uncovered an important link between inflammation and breast cancer stem cells that suggests a new way to target cells that are resistant to current treatments.
The researchers identified a receptor, CXCR1, on the cancer stem cells which triggers growth of stem cells in response to inflammation and tissue damage. A drug originally developed to prevent organ transplant rejection blocks this receptor, killing breast cancer stem cells and preventing their metastasis in mice, according to the study.
Cancer stem cells, the small number of cells that fuel a tumor's growth, are believed to be resistant to current chemotherapies and radiation treatment, which researchers say may be the reason cancer so often returns after treatment.
"Developing treatments to effectively target the cancer stem cell population is essential for improving outcomes. This work suggests a new strategy to target cancer stem cells that can be readily translated into the clinic," says senior study author Max S. Wicha, M.D., Distinguished Professor of Oncology and director of the U-M Comprehensive Cancer Center. Wicha was part of the team that first identified stem cells in breast cancer.
Results of the current study appear online Jan. 4 in the Journal of Clinical Investigation and will appear in the journal's February print issue.
CXCR1 is a receptor for Interleukin-8, or IL-8, a protein produced during chronic inflammation and tissue injury. When tumors are exposed to chemotherapy, the dying cells produce IL-8, which stimulates cancer stem cells to replicate. Addition of the drug repertaxin to chemotherapy specifically targets and kills breast cancer stem cells by blocking CXCR1.
Mice treated with repertaxin or the combination of repertaxin and chemotherapy had dramatically fewer cancer stem cells than those treated with chemotherapy alone. In addition, repertaxin-treated mice developed significantly fewer metastases than mice treated with chemotherapy alone.
"These studies suggest that important links between inflammation, tissue damage and breast cancer may be mediated by cancer stem cells. Furthermore, anti-inflammatory drugs such as repertaxin may provide a means of blocking these interactions, thereby targeting breast cancer stem cells," Wicha says.
Repertaxin has been tested in early phase clinical trials to prevent rejection after organ transplantation. In these studies, side effects seem to be minimal. There are no reports of using repertaxin to treat cancer.
Note to patients: This work was done in cell cultures and mice. Repertaxin is not available to patients at this time and no clinical trials are yet planned.
Breast cancer statisitics: 194,280 Americans will be diagnosed with breast cancer this year and 40,610 will die from the disease, according to the American Cancer Society.
Additional authors: Christophe Ginestier, Suling Liu, Mark Diebel, Hasan Korkaya, Ming Luo, Marty Brown, Jun-Lin Guan, Gabriela Dontu, all from U-M; and Julien Wicinski, Olivier Cabaud, Emmanuelle Charafe-Jauffret, Daniel Birnbaum, all from Universite de la Mediterranee, Marseille, France
Funding: National Institutes of Health, Breast Cancer Foundation, Taubman Institute, Department of Defense, Inserm, Institut Paoli-Calmettes, Institut National du Cancer, Ligue Nationale Contre le Cancer
Disclosure: The University of Michigan has filed for patent protection on this technology, and is currently looking for a commercialization partner to help bring the technology to market.

Mango can arrest growth of certain breast and colon cancer cells

ango fruit been found to prevent or stop certain colon and breast cancer cells in the lab.

Mango fruit been found to prevent or stop certain colon and breast cancer cells in the lab.
That's according to a new study by Texas AgriLife Research food scientists, who examined the five varieties most common in the U.S.: Kent, Francine, Ataulfo, Tommy/Atkins and Haden.
Though the mango is an ancient fruit heavily consumed in many parts of the world, little has been known about its health aspects. The National Mango Board commissioned a variety of studies with several U.S. researchers to help determine its nutritional value.
"If you look at what people currently perceive as a superfood, people think of high antioxidant capacity, and mango is not quite there," said Dr. Susanne Talcott, who with her husband, Dr. Steve Talcott, conducted the study on cancer cells. "In comparison with antioxidants in blueberry, acai and pomegranate, it's not even close."
But the team checked mango against cancer cells anyway, and found it prevented or stopped cancer growth in certain breast and colon cell lines, Susanne Talcott noted.
"It has about four to five times less antioxidant capacity than an average wine grape, and it still holds up fairly well in anticancer activity. If you look at it from the physiological and nutritional standpoint, taking everything together, it would be a high-ranking super food," she said. "It would be good to include mangoes as part of the regular diet."
The Talcotts tested mango polyphenol extracts in vitro on colon, breast, lung, leukemia and prostate cancers. Polyphenols are natural substances in plants and are associated with a variety of compounds known to promote good health.
Mango showed some impact on lung, leukemia and prostate cancers but was most effective on the most common breast and colon cancers.
"What we found is that not all cell lines are sensitive to the same extent to an anticancer agent," she said. "But the breast and colon cancer lines underwent apotosis, or programmed cell death. Additionally, we found that when we tested normal colon cells side by side with the colon cancer cells, that the mango polyphenolics did not harm the normal cells."
The duo did further tests on the colon cancer lines because a mango contains both small molecules that are readily absorbed and larger molecules that would not be absorbed and thus remain present in a colon.
"We found the normal cells weren't killed, so mango is not expected to be damaging in the body," she said. "That is a general observation for any natural agent, that they target cancer cells and leave the healthy cells alone, in reasonable concentrations at least."
The Talcotts evaluated polyphenolics, and more specifically gallotannins as being the class of bioactive compounds (responsible for preventing or stopping cancer cells). Tannins are polyphenols that are often bitter or drying and found in such common foods as grape seed, wine and tea.
The study found that the cell cycle, which is the division cells go through, was interrupted. This is crucial information, Suzanne Talcott said, because it indicates a possible mechanism for how the cancer cells are prevented or stopped.
"For cells that may be on the verge of mutating or being damaged, mango polyphenolics prevent this kind of damage," she said.
The Talcotts hope to do a small clinical trial with individuals who have increased inflamation in their intestines with a higher risk for cancer.
"From there, if there is any proven efficacy, then we would do a larger trial to see if there is any clinical relevance," she said.
According to the National Mango Board, based in Winter Park, Fla., most mangoes consumed in the U.S. are produced in Mexico, Ecuador, Peru, Brazil, Guatemala and Haiti. Mangoes are native to southeast Asia and India and are produced in tropical climates. They were introduced to the U.S. in the late 1800s, and a few commercial acres still exist in California and Florida.