Results tagged “research” from Cancer

Women who had their tonsils removed in childhood may be at increased risk of developing pre-menopausal breast cancer, according to University at Buffalo researchers.

Study leader Theodore Brasky said an apparent association may be related to the loss of protective function of the tonsils when they are removed.

Alternatively, tonsils that needed to be removed may have been markers for severe or chronic infections in childhood, and that such infections cause inflammation that may contribute to cancer, Brasky said.

Scientists have pinpointed a set of common variations in human DNA that signal a higher risk for prostate cancer in men who carry them. Some of these variations are more common in African-American men, which may help explain why prostate cancer rates are higher in African Americans than in men of other races.

The findings, published in 3 separate studies, may lead to genetic tests that will help identify those most at risk for the disease. The findings may also help unlock the biological mysteries behind prostate cancer, which could speed up the discovery of new treatments.

The 3 studies focus on DNA variations located on chromosome 8 in some men. The variations may be linked to as many as 68% of prostate cancer cases in African Americans, 60% in Japanese Americans, 46% in Latinos, 45% in native Hawaiians and 32% in whites, the authors of 1 of the studies calculate.

CUTTING-edge technology to improve breast cancer detection rates by 30 per cent will be rolled out across the state under a package announced yesterday.

The $26 million hi-tech breast screening process will boost cancer discovery rates by introducing digital intelligence to replace standard X-ray films.

The 21st-century system is particularly useful for picking up breast cancers in younger women, whose breast tissue is usually too dense to be filmed accurately by the old machines.

Breast cancer expert Dr Wendy Vincent said the new equipment would provide instant images for both patient and doctor and would be invaluable in regional NSW.

Scientists surveying the human genome have found that many more gene mutations drive the development of cancer than previously thought.

The survey is reported in the journal Nature.

In the largest survey of its kind, an international team comprising over 60 scientists from the UK, Hong Kong, the Netherlands, Belgium, USA and Australia, working for the Cancer Genome Project, examined more than 500 genes and 200 cancers and sequenced more than 250 million letters of DNA code.

They found about 120 new genes that drive the development of cancer cells.

A gene that prevents cancer also controls the skin's suntanning machinery, researchers report in the March 9, 2007 issue of the journal Cell.

"The p53 tumor suppressor is commonly mutated in human cancer," explained David Fisher, director of the Melanoma Program in Medical Oncology at Dana-Farber Cancer Institute. "Now, we've found that it plays a role in the skin's tanning response."

The researchers also linked the p53-driven process to other instances of skin darkening not associated with the sun

Breast cancer treatment trials supported by the pharmaceutical industry are more likely to report positive results than non-sponsored studies, according to a study to be published in the April 1, 2007 issue of CANCER, a peer-reviewed journal of the American Cancer Society. In addition, there are significant differences in the design of trials and types of questions addressed by pharmaceutical industry sponsored trials compared to non-sponsored trials. The study is the first to examine the impact of the pharmaceutical industry on breast cancer research.

Research and development (R&D) is critical to developing new therapies. The drug industry is a significant contributor to this effort, now with far greater spending than the United States' National Institutes of Health. As collaboration between the for-profit drug industry and academic medical centers has increased, so too have concerns over the potential impact of for-profit sponsorship on the nature and quality of the research and the potential for conflicts of interest. Several studies in other areas of medicine have suggested that pharmaceutical sponsorship leads to a greater chance that a clinical trial will yield positive results. The importance of this association for patients and researchers and the prevalence of this finding in cancer research are not yet clear.

Science Daily — There is an urgent reason to study stem cells: stem cells are at the heart of some, if not all, cancers. Mounting evidence implicates a clutch of rogue stem cells brandishing ‘epigenetic’ marks as the main culprits in cancer. Wiping out tumours for good, some biologists believe, depends on uprooting these wayward stem cells.

A team in the Netherlands has uncovered a key protein that could stop these stem cells from becoming malignant. “This is a hot topic in the cancer field,” Maarten van Lohuizen of The Netherlands Cancer Institute, Amsterdam told participants at a EuroSTELLS workshop, held in Montpellier, France, 23-24 January. “To be successful in cancer therapy you need to target these stem cells: they are intrinsically resistant to chemotherapy.”

Polycomb proteins have emerged as key players in cancer pathogenesis. They are powerful epigenetic regulators that normally silence genes without altering the cell’s DNA. Compounds that regulate polycomb could result in novel anticancer drugs that shrink malignant tissue, and prevent cancer recurrence, a common problem with most chemotherapies.

Researchers in Spain conducted a Phase III clinical trial called GEICAM. They wanted to compare different chemotherapy regimes in women diagnosed with metastatic breast cancer. The trial included 252 women who had already been treated with anthracyclines and taxanes and experienced a recurrence.

One group of women was treated with Gemzar (gemcitabine) and Navelbine (vinorelbine), the other group was treated with Navelbine alone. The results were published in Lancet Oncology that states the combination of the two drugs improves progression free survival. It was also mentioned that this combination however did not improve overall survival.

When cells become cancerous, they also become 100 times more likely to genetically mutate than regular cells, researchers have found. The findings may explain why cells in a tumor have so many genetic mutations, but could also be bad news for cancer treatments that target a particular gene controlling cancer malignancy.

The research was led by Dr. Lawrence Loeb, professor of pathology and biochemistry at the University of Washington School of Medicine in Seattle. Loeb presented his research Feb. 18 at the meeting of the American Association for the Advancement of Science in San Francisco.

AUSTRALIAN researchers have discovered a new way that cancer can be passed down from parents to children that will allow them to diagnose the disease earlier.

Previously researchers believed young cancer sufferers inherited a parent's gene mutation.
However doctors were at a loss to explain why tests showed no sign of genetic mutation in some people with cancer.

Now researchers from St Vincent's Hospital in Sydney and the University of New South Wales have discovered that a chemical which paralyses part of the body's DNA can also be passed down from parents to children and cause cancer.

Aggressive research currently underway brings hope of dramatic advances in breast cancer management, according to a new review. Published in the March 15, 2007 issue of CANCER, a peer-reviewed journal of the American Cancer Society, the review reveals that new approaches in breast cancer imaging, investigations into the timing of chemotherapy, and research on breast cancer vaccines may lead to exciting new nonsurgical tools for the physician treating breast cancer patients. These new tools may significantly alter current screening and treatment paradigms used by surgical oncologists, as well improving the care of patients.

Science Daily — Cancer cells are sick, but they keep growing because they don't react to internal signals urging them to die. Now researchers at Washington University School of Medicine in St. Louis have found an efficient way to get a messenger into cancer cells that forces them to respond to death signals. And they did it using one of the most sinister pathogens around — HIV.

"HIV knows how to insert itself into many different types of cells," says senior author William G. Hawkins, M.D., assistant professor of surgery and a member of the Siteman Cancer Center at the School of Medicine and Barnes-Jewish Hospital. "A portion of the HIV protein called TAT can transport biologically active compounds into cells. TAT is small, but it can move massive molecules. You could almost hook TAT up to a train, and TAT would drag it inside a cell. So we've taken advantage of this ability."

WASHINGTON (Reuters) - Women who switch from the breast cancer pill tamoxifen to a newer class of drugs called aromatase inhibitors live longer, Italian researchers reported on Monday.

Their study, published in the journal Cancer, adds to a growing body of evidence that the new drugs are far safer, preventing cancer with fewer side effects than tamoxifen.

Dr. Lauren Cassell of Lenox Hill Hospital in New York said the research is changing how doctors treat breast cancer patients after their tumors are surgically removed.

"If they have been on tamoxifen we are switching them to an aromatase inhibitor. If they are newly diagnosed we are using an aromatase inhibitor instead of tamoxifen," she said in a statement.

Newswise — In the past couple of years, researchers at Oncolytics Biotech have been developing a harmless virus as a potent cancer killer, but they have also been accumulating data that suggests in addition to directly killing tumor cells, the reovirus may prime the immune system to mount a separate, powerful and long lasting defence against cancer.

Evidence for this theory has been mounting for the past year. On January 10, 2007, Dr. Sheila Fraser of St. James' University Hospital in Leeds, U.K. delivered a paper at the Society of Academic & Research Surgery Conference in Cambridge, U.K., in which she described a test tube experiment further supporting this claim.

Fraser’s presentation, titled “Reovirus as a Potentially Immunogenic as well as Cytotoxic Therapy for Metastatic Colorectal Cancer,” reported how cells taken from a colorectal cancer liver metastases were more susceptible to death many weeks after treatment with reovirus, and long after the virus had cleared the patient’s system. These cells, when cultured in the laboratory, also appeared to be vulnerable to re-infection with reovirus. Moreover, Dr. Fraser noted that dendritic cells, which prime the immune system against cancer, were activated by exposure to the reovirus.

Her carefully cultured cells were dead and Katherine Schaefer was annoyed, but just a few minutes later, the researcher realized she had stumbled onto a potential new cancer treatment.

Schaefer and colleagues at the University of Rochester Medical Center in New York believe they have discovered a new way to attack tumors that have learned how to evade existing drugs.

Tests in mice suggest the compound helps break down the cell walls of tumors, almost like destroying a tumor cell's "skeleton."

The researchers will test the new compound for safety and hope they can develop it to treat cancers such as colon cancer, esophageal cancer, liver and skin cancers.

A promising drug for fighting cancer is found. It has already been proven relatively safe. Laboratory and animal tests have shown it kills cancer cells and shrinks tumors.

You would think the drug companies would fall all over themselves to do the clinical trials necessary for the drug to be prescribed to cancer patients. Right?

Wrong.

This may be the biggest scandal to hit the medical world in years. Yet so far, all the commercial U.S. media have stayed away from reporting on it.

Scientists in the US claim to have discovered a small group of cells in pancreatic cancer that are capable of fuelling tumour growth.

The research at the University of Michigan Comprehensive Cancer Centre (UMCCC) appears to be the first to successfully identify stem cells in pancreatic tumours.

Cancer stem cells are crucial to a tumour's development and it is hoped that successfully identifying them will lead to more effective treatment.

Pancreatic cancer has one of the worst survival rates among cancer types, making a potential breakthrough in this area all the more significant.

WEDNESDAY, Jan. 17 (HealthDay News) -- A genetic "signature" that consists of 186 genes combined together can predict the risk of breast cancer recurrence in women with the disease, a new study found.

And the same set of genes also predicts the recurrence of prostate cancer, lung cancer and medulloblastoma, the most common form of childhood brain cancer, the researchers said.

"This is very impressive data that will hopefully be able to predict which patients can benefit or not benefit from certain types of treatment," said Dr. Jay Brooks, chairman of hematology/oncology at Ochsner Health System in Baton Rouge, La., who was not involved with the study. "Whether this can be taken into the direct clinical arena will remain to be seen."

Researchers at the University of Southern California (USC) recently made significant strides toward settling a decades-old debate centering on the role played by stem cells in cancer development.

According to the study's findings, which appear in an upcoming issue of Nature Genetics and now available online, genes that are reversibly repressed in embryonic stem cells are over-represented among genes that are permanently silenced in cancers; this link lends support to the increasingly discussed theory that cancer is rooted in small populations of stem cells.

USC researchers uncovered this link after observing that of 177 genes repressed by Polycomb group (PcG) proteins, fully 77 showed evidence of cancer-associated enzymatic modification of DNA (known as methylation). "Finding that a Polycomb target in an embryonic stem cell is 12 times more likely to become abnormally methylated in cancer is highly significant," says Peter Laird, Ph.D., one of the lead researchers and associate professor of surgery, biochemistry and molecular biology, and director of basic research for surgery at the Keck School of Medicine of USC.

Liverpool, UK - 8 January 2007: Scientists at the University of Liverpool have found how two molecules fight in the blood to control the spread of cancer cells.

 

Researchers discovered that a large protein, which forms a protective shield around cancer cells and prevents them from causing secondary tumours, is attacked by a small protein that exists in the blood.

In diseases such as breast, lung and colorectal cancer, infected cells lose growth control and eventually form tumours at these sites.  If caught early these tumours can be effectively removed surgically. However, when the cancer cells have invaded the blood, the effectiveness of surgery is reduced.