May 19, 2008, 6:40 PM CT

Predicting prostate cancer treatment failure

Dynamic contrast-enhanced MRI (DCE-MRI) plus diffusion weighted imaging (DWI) can accurately diagnose residual or recurrent prostate cancer in patients treated with high-intensity focused ultrasonic ablation, a new study shows.

The study included 27 patients who had increased levels of prostate specific antigen after being treated with high-intensity focused ultrasonic (HIFU) ablation; 18 of these patients had local tumor progression seen at biopsy. DCE-MRI and DWI had about a 72% accuracy rate in determining which patients needed additional therapy because they had residual or recurrent cancer, said Chan Kyo Kim, MD, lead author of the study. The study observed that DWI had fewer false positives than DCE-MRI, but DCE-MRI had fewer false negatives.

After HIFU ablation, the normal anatomy of the prostate gland is completely lost or deformed making it difficult to distinguish non-malignant tissue from cancer, said Dr. Kim. The two imaging studies together, which can be done in about seven minutes, can overcome that challenge, he said.

HIFU is becoming more common as a prostate cancer therapy option, especially for those persons who cant or dont want to undergo a radical prostatectomy, said Dr. Kim......... Posted by: Jesmi24      Read more         Source

May 18, 2008, 9:45 PM CT

Drug fends off kidney cancer progression

New data from an international, multicenter Phase III clinical trial has observed that the experimental targeted treatment everolimus (RAD001) significantly delays cancer progression in patients with metastatic kidney cancer whose disease had worsened on other therapys. The study was led by Robert Motzer, MD, an attending doctor at Memorial Sloan-Kettering Cancer Center (MSKCC), who will present the findings on May 31 at the annual meeting of the American Society for Clinical Oncology.

This study has given us a new and clearly useful tool for treating renal cell tumors, and everolimus is an important step forward in terms of disease management and quality of life for patients living with this disease, said Dr. Motzer.

Kidney cancer is among the ten most common cancers in both men and women. The American Cancer Society estimates that there will be about 54,390 new cases of kidney cancer diagnosed in the US in 2008, and that about 13,010 people will die from the disease.

Everolimus, a once-daily oral treatment, targets the mTOR protein, which acts as a central regulator of tumor cell division, cell metabolism, and blood vessel growth. It is currently being reviewed for the therapy of several other cancers including lymphoma and neuroendocrine tumors......... Posted by: Jesmi24      Read more         Source

March 9, 2008, 6:09 PM CT

Researchers control growth rate of blood vessels

Scientists have discovered a way to control the growth rate of replacement tissue and the formation of new blood vessels, which solves one of the vexing problems of growing replacement tissue to treat injuries and trauma in humans.

The procedure could be used in bone grafts, tissue replacement, dental procedures or for diabetics or elderly patients who experience wound healing problems, said William Giannobile, professor at the University of Michigan School of Dentistry and College of Engineering, and corresponding author of the paper. Peter Ma, U-M professor with appointments in engineering and dentistry, is co-author and principal investigator on the National Institutes of Health project.

"If you have such a large defect that your body can't completely heal, this is a way to augment and dose a natural wound healing protein," Giannobile said.

Scientists put platelet-derived growth factor into nanoparticles and then attached them to a lattice-like, biodegradable scaffold. In experiments, the growth factor recruited cells that stimulate the body's own machinery responsible for healing, said Ma, whose lab developed the scaffold and the nanoparticles.

As the tissue grows, it crawls into the scaffold, which eventually dissolves.

"Growth factor is typically dumped in and releases over a period of hours," said Giannobile, who also directs the Michigan Center for Oral Health Research. "With certain wounds you might want a lot (of growth factor) in the beginning, and with others you might want a little released over a longer period of time. We've basically found a way to dial up or dial down the release rate of these growth factors"......... Posted by: Jesmi24      Read more         Source

March 4, 2008, 6:03 PM CT

Cancer risk higher for women in discontinued hormone treatment trial

A follow up study of participants in the Womens Health Initiative (WHI) clinical trial led by a University of North Carolina at Chapel Hill researcher has observed that women who were taking the combined hormone treatment of estrogen plus progestin may have an increased risk of cancer since the intervention was stopped, in comparison to participants in the trials placebo group.

However, the increased risks of heart disease, stroke and blood clots which had been seen in women taking the treatment as part of the WHI trial have diminished in the three years since scientists stopped it, as per a research studyreported in the March 5 issue of the Journal of the American Medical Association.

The studys lead author is Dr. Gerardo Heiss, a Kenan professor of epidemiology in the UNC School of Public Health.

The WHI trial of estrogen plus progestin which included 16,608 healthy postmenopausal women was originally designed to study what effect the hormone therapy would have on cardiovascular disease, cancer risks and bone fractures.

The trial was stopped in July 2002 after participants had been on the treatment for an average of 5.6 years because scientists saw an increased risk of breast cancer and cardiovascular disease in women randomly assigned to hormone treatment, compared with those who received a placebo......... Posted by: Jesmi24      Read more         Source

February 14, 2008, 10:17 PM CT

Oncoproteins destroy vital tumor-suppressor

Two previously unconnected cancer-promoting proteins team up to ambush a critical tumor suppressor by evicting it from the cell's nucleus and then marking it for death by a protein-shredding mechanism, a team led by researchers at The University of Texas M. D. Anderson Cancer Center reports in the Feb. 10 issue of Nature Cell Biology.

The paper is the first to illuminate a mechanism of attack on FOXO3a, a member of the forkhead family of tumor-suppressing proteins, notes senior author Mien-Chie Hung, Ph.D., chair of M. D. Anderson's Department of Molecular and Cellular Oncology.

"We know that FOXO3a is inactivated in about 80 percent of breast tumors, and that it's likely to be inactivated in other solid tumors because three major oncogenic pathways separately target it," Hung said. "The implication is that forkhead activation will be a great therapeutic target because it would be a powerful tumor-suppressor".

Hung and his colleagues focused on the effect of the RAS-ERK signaling pathway, which is known to promote tumor growth and proliferation. FOXO3a and its other forkhead cousins have a specific structure - the forkhead box - that allows them to connect with DNA. They are transcription factors, activating or repressing target genes involved in tumor suppression and DNA damage repair......... Posted by: Jesmi24      Read more         Source

February 4, 2008, 9:24 PM CT

Lnk between cancer, Down syndrome

Theres new hope for breast cancer research, and its coming from a very unlikely place. Scientists at the Texas A&M University College of Veterinary Medicine & Biomedical Sciences recently published articles in the journals Molecular and Cellular Biology and Carcinogenesis indicating that a protein long suspected to play a role in Down Syndrome may also contribute to treating this devastating disease.

It has long been known that Down Syndrome is caused when an individual has an extra copy of the 21st chromosome, giving them a total of three instead of the normal chromosome pair. With improved medical care, people with Down Syndrome are now living longer, healthier lives. With this advance came the observation that individuals with Down Syndrome have a significant decrease in risk for several types of tumors. Most striking is the observation that women with Down Syndrome are 10-25 times less likely to develop breast cancer.

This effect is believed to be due to the presence of one or more tumor suppressor genes on chromosome 21. However, the identity of such genes has not been known, until now.

Years of research into the genetics of Down Syndrome have helped us to discover a very important gene on chromosome 21, said Dr. Weston Porter, associate professor in the Veterinary Integrative Biosciences Department. This gene, called Single-minded 2 or SIM2 is thought to play an important role in Down Syndrome by regulating neuron growth in the developing brain. Based on its developmental role, we hypothesized that SIM2 may also be involved in breast cancer, which is essentially a disease of uncontrolled growth......... Posted by: Jesmi24      Read more         Source

November 12, 2007, 10:08 PM CT

How to switch off cancer cell genes

A new study led by scientists at the University of Southern California (USC) identifies how genes are silenced in cancer cells through distinct changes in the density of nucleosomes within the cells.

The findings, reported in the Nov. 13 issue of the journal Cancer Cell, will enable scientists to explore new therapies to switch the genes back on and may lead to novel therapys for human cancers, says study lead author Peter A. Jones, Ph.D., D.Sc., director of the USC/Norris Comprehensive Cancer Center and Distinguished Professor at the Keck School of Medicine of USC.

"The study shows for the first time exactly how genes get shut down in cancer cells," Jones says. "It identifies what the target looks like so that new therapies can be designed to turn them back on".

The study showed that silencing of transcription start sites in some cancer cells involves distinct changes in nucleosomal occupancy'or the density of nucleosomes'in the cell. Scientists observed that three nucleosomes, almost completely absent from the start site in normal cells, are present in the methylated and silenced promoter, suggesting that epigenetic silencing may be accomplished by the stable placement of nucleosomes into previously vacant positions.

DNA cytosine methylation'the addition of a group of specific chemicals to a stretch of DNA that can lock or silence a gene'may ultimately lead to silencing by enabling the stable presence of nucleosomes at the start sites of cancer-related genes, the study suggests......... Posted by: Jesmi24      Read more         Source

October 2, 2007, 10:28 PM CT

New strategies with greater antitumorous efficacy

One of the biggest problems in the current therapy of cancer is that the agents that are efficacious in the destruction of tumorous cells are, at the same time, extremely toxic for the rest of the healthy cells and tissues of the patient. To address the problem the University of the Basque Country (UPV/EHU) is seeking more specific therapys and studying the differences between tumorous cells and healthy ones.

A research team from the Faculty of Medicine and Odontology is working on identifying pharmacological agents that increase the therapeutic benefit of combinations of chemo-, immune and radiotherapy agents in the therapy of cancer ailments.

The aim of the research team was to identify compounds that act on the metabolic pathways and processes that take place differently depending whether a diseased tissue of a patient or healthy tissue is involved; in this way selective action can be undertaken, increasing the sensitivity of therapys for diseased tissues without damaging healthy cells or tissues at the same time.

With this general goal the scientists tested various biomodulators on many different tumorous modules such as melanoma, sarcoma and cancer of the colon. On the one hand, they studied agents that modulated levels of glutathione (GSH) - key element in the biological processes of cells, both healthy and tumorous. Tumorous cells with high GSH levels have a greater growth and metastatic capacity and a lower sensitivity to antitumorous agents. Conversely, one of the features of tumorous cells is that they lose their normal level of differentiation and, instead of exercising a determined function, they start to proliferate and generate a greater quantity of tumorous cells. This is why the scientists have also used agents that induce differentiation, such as are retinoids......... Posted by: Jesmi24      Read more         Source

August 8, 2007, 8:44 PM CT

Light-activated Molecules To Kill Cancer Cells

A key challenge facing doctors as they treat patients suffering from cancer or other diseases resulting from genetic mutations is that the drugs at their disposal often dont discriminate between healthy cells and dangerous ones -- think of the brute-force approach of chemotherapy, for instance. To address this challenge, Florida State University scientists are investigating techniques for using certain molecules that, when exposed to light, will kill only the harmful cells.

Igor V. Alabugin is an associate professor of chemistry and biochemistry at FSU. He specializes in a branch of chemistry known as photochemistry, in which the interactions between atoms, small molecules and light are analyzed.

When one of the two strands of our cellular DNA is broken, intricate cell machinery is mobilized to repair the damage, he said. Only because this process is efficient can humans function in an environment full of ultraviolet irradiation, heavy metals and other factors that constantly damage our cells.

However, a cell that sustains so much damage that both DNA strands are broken at the same time eventually will commit suicide -- a process known as apoptosis.

In our research, were working on ways to induce apoptosis in cancer cells -- or any cells that have harmful genetic mutations -- by damaging both of their DNA strands, Alabugin said. We have observed that a group of cancer-killing molecules known as lysine conjugates can identify a damaged spot, or cleavage, in a single strand of DNA and then induce cleavage on the DNA strand opposite the damage site. This double cleavage of the DNA is very difficult for the cell to repair and typically leads to apoptosis......... Posted by: Jesmi24      Read more         Source

July 19, 2007, 10:04 PM CT

Nonsmall cell lung cancer: chemotherapy before surgery

Combining pre-operative chemotherapy and surgery increases the average chance of survival at five years by approximately 6% compared with surgery alone.

This conclusion was drawn by a team of Cochrane Researchers from the MRC Clinical Trials Unit in London after they identified 12 eligible randomised controlled trials. Data from seven of these trials were available from trial reports and were combined in a meta-analysis. The seven trials involved a total of 988 patients.

This is currently the best estimate of the effectiveness of this therapy, but is based on a relatively small number of trials and patients, says lead researcher Sarah Burdett.

There was, however, insufficient data to break the patients down into sub-groups and see whether the effectiveness varies for different types of patients or stages of the disease.

This research is important because around the world more than a million new cases of lung cancer are diagnosed each year, around 80% of which are non-small cell lung cancer. In addition, many patients are only diagnosed after the disease has progressed, so survival rates across all stages of disease tend to be fairly low at around 14%, with only a quarter of patients being suitable for surgery.

The Cochrane Systematic Review found that using chemotherapy before surgery can reduce the size of tumours making the surgery simpler, and increasing the number of patients who may be candidates for surgery. The worry is, however, that having a course of chemotherapy delays the operation, and could therefore leave patients at risk of allowing the tumour to spread......... Posted by: Jesmi24      Read more         Source