cancers
Sex after cancer? Don't count on it. It's just not happening for thousands of couples, and neither doctors nor their patients like to talk about it. It is a painful phenomenon, and while researchers may understand why it happens, they've only just begun to be able to predict who will - and who won't - have a successful adjustment to sex after treatment.
Researchers have for the first time described a method that Staphylococcus aureus (staph) infection uses to inactivate the body's immune system. A protein produced by the staph bacteria causes previously healthy B cells -- a specialized cell of the immune system -- to commit suicide, a process called apoptosis. "By the targeted elimination of disease-causing B cells, properly dosed injections of SpA may have the potential to control the over-activity of the immune system that causes damage in autoimmune diseases like lupus and in certain cancers," said Gregg Silverman, M.D., UCSD professor of medicine and senior author of the paper.
Scientists at the Comprehensive Cancer Center of Wake Forest University have developed a colony of mice that successfully fight off virulent transplanted cancers. "The mice are healthy, cancer-free and have a normal life span," the 10-member team reported in the Proceedings of the National Academy of Sciences online edition to be published the week of April 28. The transplantation of the cancer cells in these special mice provokes a massive infiltration of white blood cells that destroy the cancer, said Zheng Cui, M.D., Ph.D., associate professor of pathology at Wake Forest University Baptist Medical Center and the lead scientist.
Regular use of ibuprofen and aspirin inhibits the formation and growth of breast cancer, according to data published in the Proceedings for the 94th Annual Meeting of the American Association for Cancer Research (AACR). The data, taken from the National Cancer Institute?s (NCI) Women?s Health Initiative (WHI) Observational Study, concluded that weekly doses of non-steroidal anti-inflammatory drugs (NSAIDs) had a significant effect in reducing the risk of breast cancer.
?These results suggest that even women at high risk for breast cancer may be protected by taking NSAIDs,? explains Randall Harris, M.D., Ph.D., lead investigator of the study, professor of the division of epidemiology and biometrics at the Ohio State University. ?However, before usage guidelines for NSAIDs can be implemented, additional studies are needed.?
Cancer rates could further increase by 50% to 15 million new cases in the year 2020, according to the World Cancer Report, the most comprehensive global examination of the disease to date. However, the report also provides clear evidence that healthy lifestyles and public health action by governments and health practitioners could stem this trend, and prevent as many as one third of cancers worldwide. In the year 2000, malignant tumours were responsible for 12 per cent of the nearly 56 million deaths worldwide from all causes. In many countries, more than a quarter of deaths are attributable to cancer. In 2000, 5.3 million men and 4.7 million women developed a malignant tumour and altogether 6.2 million died from the disease. The report also reveals that cancer has emerged as a major public health problem in developing countries, matching its effect in industrialized nations.
Researchers have developed a new system to improve the delivery of genes, which could have the potential cure for several genetically transmitted diseases. Under the direction of Prashant Kumta, a professor of materials science, engineering and biomedical engineering, researchers are creating nano-particles capable of delivering DNA-based therapies for potential use in a variety of cancers and several genetic diseases. "We have developed a new system that will help physicians deliver their genetic life-saving payloads into enough cells to do some good," said Kumta, who has applied for a patent on the non-viral gene delivery system.
Results of a new study show that breast sonography is more accurate than mammography in symptomatic women 45 years old or younger, and may be an appropriate initial imaging test in investigating these women, says Nehmat Houssami, MD, PhD, and lead author of the study. The study, published in the April 2003 issue of the American Journal of Roentgenology, "is the first published study to examine the comparative sensitivity and specificity of mammography and sonography in relation to age in young women with breast symptoms, where the two tests were interpreted independently of each other and where almost all subjects had undergone both tests," says Dr. Houssami.
Scientists at Tularik Inc. and Cold Spring Harbor Laboratory have discovered a new gene that is expressed at abnormally high levels in nearly 50% of the breast cancer specimens they examined, and is similarly overexpressed in a large proportion of lung cancers (35%).
By analyzing the genes that are active in tumor cells, scientists may be able to predict whether the most common form of liver cancer, hepatocellular carcinoma, is likely to spread from its original site. Researchers at the National Cancer Institute (NCI), in collaboration with surgeons at the Liver Cancer Institute of Fudan University in Shanghai, report in a study published in Nature Medicine* that they have identified a pattern of gene activity that is unique to hepatocellular carcinoma cells that spread, or metastasize. Knowing whether a tumor is likely to metastasize can help physicians decide on the best treatment strategy for a patient.
Of all the neoplastic cells in human breast cancers, only a small minority - perhaps as few as one in 100 - appear to be capable of forming new malignant tumors, according to just-published research by scientists in the University of Michigan Comprehensive Cancer Center. The discovery could help researchers zero in on the most dangerous cancer cells to develop new, more effective treatments.
Researchers have found that a recently discovered gene plays an essential role in mediating apoptosis, or cell death, in colorectal cancer cells. The gene, PUMA, or p53 up-regulated modulator of apoptosis, is controlled by p53 ? a tumor-suppressing gene that prevents normal cells from turning into life-threatening tumor cells. Previous research has determined that damage to p53 is fundamental to the development of a vast majority of cancers, and inactivation of the growth-controlling function of p53 is critical to the growth and spread of most cancers.
Researchers have developed a novel approach to genetically instruct human immune cells to recognize and kill cancer cells in a mouse model. The investigators plan to ultimately apply this strategy in a clinical trial setting for patients with certain forms of leukemias and lymphomas. Scientists at Memorial Sloan-Kettering Cancer Center (MSKCC) genetically engineered an antigen receptor, introduced it into cultured human T cells, and infused the T cells in mice that bear widespread tumor cells. The modified T cells, now able to recognize the targeted antigen present on the tumor cells, eradicated the cancer.
Researchers have produced the first laboratory evidence to show that a cell's possession of an abnormal numbers of chromosomes contributes to the development of cancers. Their report on the role of this chromosomal instability, known as aneuploidy, appears in today's online edition of the Feb. 3 Journal of Cell Biology. Because 85 percent of human cancer cells possess an abnormal number of chromosomes, researchers have long been curious about the role of aneuploidy in the multistep cancer process.
Scientists at St. Jude Children's Research Hospital have discovered a novel biochemical process that plays a critical role in helping cells in the body respond to DNA damage, such as that caused by exposure to radiation, environmental toxins or free radicals. The findings could lead to new approaches to prevent cancer, better ways to treat cancer and to the development of sensitive methods determining whether people have been exposed to radiation or environmental toxins, according to the researchers.
Scientists have found that much of the widespread damage that the rare genetic disease ataxia telangiectasia, or AT, wreaks on the body results from the progressive shortening of telomeres, the structures that cap the ends of a cell's chromosomes. In genetically altered mice, the researchers found that the shortening of telomeres led to a "crisis" that disrupted chromosomes "like a hand grenade thrown into the cell," as one scientist put it. The resulting cellular chaos was manifested throughout the rodents' bodies by the loss of reparative stem cells that different organs normally have in reserve, producing symptoms of premature aging such as hair loss and slow wound healing, and early death.
