June 22, 2007, 4:46 AM CT

Treatment Slows The Growth Of Cancers Of The Colon And Liver

Leire García Navarro, a researcher at the School of Pharmacy of the University of Navarra, has developed a new therapy which slows the growth of colon and liver cancers.

This discovery is the principal result of her doctoral dissertation, entitled "Lipo-Polymeric Vectors for the Transfer of DNA in Cancer Cells of the Colon", which was subsidized by the Basque Government. In order to carry out the study, this scientist of the Department of Pharmacy and Pharmaceutical Technology used genetic treatment with non-viral vectors for transferring genetic material to the malignant cells. With this technique, we can assure the therapeutic function of the drug in a wide variety of tissues. In addition, we can apply the therapy repeatedly, since it does not generate immunity, as occurs with viral vectors.

With the objective of improving the effectiveness of this methodology, the specialist worked on designing non-viral systems which act directly upon the liver and the colon. In this manner, she prepared, optimized and reviewed, in vitro and in vivo, a new pharmaceutical format called 'lipopolyplex.' This compound aids the genetic material in penetrating into the damaged cells, and allows drug release in tumorous organs.

500,000 deaths per year

Experimentation with the new drug in mice has shown that it slows tumor growth with respect to those animals subjected to other procedures. This diminishing of the cancerogenous area is possible, as per the scientist, thanks to the stimulation of the immune system, since the introduction of the correct gene in the diseased body can cause it to repair itself and destroy the tumor......... Posted by: Andria      Read more         Source

June 20, 2007, 10:14 AM CT

FISH on a chip offers quicker, less costly cancer diagnosis

For the first time an important diagnostic test for cancer has been miniaturized and automated onto a microfluidic chip by a team of University of Alberta scientists in Edmonton, Canada.

This new technology opens up the possibility of better, faster cancer therapy and greater accessibility to the test, thanks to quicker and more cost-efficient diagnosis.

Chris Backhouse, professor of electrical engineering and cancer scientist Dr. Linda Pilarski have developed a microfluidic chip the size of a microscope slide that can perform fluorescent in situ hybridization (FISH) on a handheld diagnostic device.

FISH is an important and complex test that detects mutations in chromosomes for many different types of cancer. The test involves attaching coloured dyes to chromosomes as a way to visualize and count them as well as to detect cancer-promoting breaks and rejoinings of chromosomes. These abnormalities provide clinically valuable information about disease outcomes and response to treatment. This new system will allow FISH to be rapidly performed for a fraction of the cost of current analysis methods. In comparison to conventional methods for FISH, which can take days to perform, the on-chip FISH test can be done in less than a day with a ten-fold higher rate of processing and a reduction in costs from hundreds to tens of dollars......... Posted by: Andria      Read more         Source

June 15, 2007, 12:24 AM CT

Target tumor microenvironment to stop cancer growth

Cold Spring Harbor Laboratory (CSHL) scientists led by Daniel Nolan and Assistant Professor Vivek Mittal have observed that bone marrow (BM) derived endothelial progenitor cells (EPCs) play a critical role in the early stages of tumor progression and that eliminating EPCs stops cancer growth. Using sophisticated high-resolution microscopy and flow cytometry, they zeroed in on the earliest stages of cancer progression and identified the role of EPCs in generating blood vessels that allow cancers to grow. If we selectively blocked the EPCs, tumors were unable to make blood vessels and could not sustain their own growth, said Vivek Mittal, CSHL Assistant Professor.

The findings open an entirely new field of research on how vascular progenitor cells control tumor growth and underscore their potential for cancer therapeutics. Published on June 15, 2007 in Genes & Development, the CSHL study settles a dispute in the field of angiogenesis that has resulted from years of inconsistent findings about the existence of EPCs in cancer tumors. Until now, this field of research that focuses on new blood vessel development has been split between scientists who have suggested the existence of EPCs and those who have vehemently disputed their presence.

The CSHL research posits that those who did not find evidence of EPCs in tumors were probably looking for them in later stages of tumor progression when EPCs are diluted by host endothelial cells. The new results show that EPCs are only present in the earliest stages of tumor progression, before the formation of blood vessels. We observed that the role of EPCs is to direct the formation and organization of the vascular structure that ultimately feeds the tumor as it grows, said CSHL researcher Daniel Nolan......... Posted by: Andria      Read more         Source

June 13, 2007, 1:22 PM CT

Advanced cancer patients prone to poor sleep quality

Patients with advanced-stage cancer experience very poor sleep quality and often have troubling staying awake, says Emory University researcher Kathy Parker, PhD, RN.

Preliminary findings from the cancer sleep study will be presented June 12 at the annual meeting of the Associated Professional Sleep Societies (APSS) convened in Minneapolis.

The study provides the first comprehensive description of sleep and wake patterns of cancer patients using continuous polysomnography (PSG) data, deemed the gold standard in objective physiological measurement of sleep. It involved 114 advanced cancer patients with an average age of 51.1 years. Study patients underwent continuous sleep monitoring, or PSG, for approximately 42 hours in their home environments.

Results showed that study participants experienced severe difficulty with "state maintenance," or the ability to maintain both the sleep and waking states. Overall they had reduced quantity and quality of nocturnal sleep and episodes of sleep scattered throughout the day. Increased amounts of daytime sleep significantly and adversely affected several key parameters of nocturnal sleep quantity and quality.

However, women, Caucasians, and those who were married/partnered and had more education fared better in nocturnal sleep than other study participants. In addition, relative to breast cancer, lung cancer also may be a risk factor for poor sleep......... Posted by: Andria      Read more         Source

June 13, 2007, 1:13 PM CT

Progress Toward an Antitumor Vaccine

How can we induce the body to use its own weapon, the immune system, to battle cancer? In principle, by the same means used against infectious diseases: immunization. The production of a selective vaccine is not a trivial task, however. A team led by Horst Kunst at the University of Mainz has now found a way to bind a molecule that is typical for tumors to a carrier protein without irritating the immune system. As they report in the journal Angewandte Chemie, their method is based on an immunocompatible connection by way of a sulfur atom, namely, a thioether.

Epithelial tumor cells have uncommonly large amounts of mucin MUC1 on their surface. This MUC1, in comparison with its "normal" cousins, is also modified in a very characteristic manner. Mucins are mucilaginous substances that protect the surfaces of mucus membranes. They are glycoproteins-macromolecules with a central protein chain and long side chains made of polysaccharides. The modified MUC1 would be a good target molecule (antigen) for antibodies in immunological antitumor treatment.

The difficulty with this approach is that such sugar-containing compounds are completely ineffective at stimulating the immune system to form antibodies. "Immunization is only successful if the vaccine is anchored to an immunizing carrier protein by means of a spacer," explains Kunz. This would be very easy to accomplish with polysaccharides, but turns out to be very complicated with glycoproteins, because the protein portion of the molecule has a number of reactive groups that are attacked in the coupling reaction. "In addition," says Kunz, "a number of of the structures that make suitable anchors are themselves highly immunogenic, which can suppress the immune response against the true target, the glycoprotein"......... Posted by: Andria      Read more         Source

June 12, 2007, 5:04 AM CT

Sensitivity to diverse range of chemotherapeutic drugs

Using a functional genomic screen, scientists have defined elements that impact the responsiveness of cancer cells to drugs commonly used as anticancer therapeutics. The research, published in the recent issue of the journal Cancer Cell, published by Cell Press, identifies individual genes that are associated with resistance to chemotherapeutic drugs and sets the stage for future studies that may significantly enhance the ability to predict whether or not a particular tumor will respond to treatment.

Resistance to chemotherapeutic drugs is the primary cause of treatment failure in patients with metastatic cancer. Dr. Julian Downward from the Cancer Research UK London Research Institute and colleagues used RNA interference to directly examine the contribution of over 800 candidate proteins to the sensitivity or resistance of cancer cells to several drugs that are commonly used to treat cancer.

Using this technique, the researchers found that resistance to the chemotherapeutic agent paclitaxel, a member of the taxane family, as expected, involves genes that impair drug-induced mitotic arrest following knockdown. Silencing of these genes in many cases also induces polyploidy and multinucleation in the absence of drug treatment. The researchers conclude that specific disruption of the mitotic checkpoint promotes paclitaxel resistance and that chromosomal numerical heterogeneity may be a useful predictor of paclitaxel resistance in some cancers......... Posted by: Andria      Read more         Source

June 10, 2007, 8:50 PM CT

Sun exposure early in life and skin cancer

Skin cancers often contain different gene mutations, but just how these mutations contribute to the cause of melanomas has been a mystery.

A new clue comes from scientists at the University of North Carolina at Chapel Hill Schools of Medicine and Public Health. Their research indicates that early life sun exposure, from birth to 20 years old, may specifically increase the risk of melanomas with BRAF gene mutations. A different mutation, on the NRAS gene, was found in patients who had sun exposure later in life (between ages 50 to 60 years old). The results indicate that different subtypes of melanoma are associated with different risk factors.

"The findings suggest that melanoma subtypes have different causes. This is important for learning more about how to prevent and treat skin cancer," said Dr. Nancy Thomas, associate professor of dermatology in the UNC School of Medicine, a member of the UNC Lineberger Comprehensive Cancer Center and lead author of the study. This finding is expected to strengthen current recommendations to protect children from sun exposure in order to prevent melanoma, Thomas said.

The study, published in the May 2007 edition of the journal Cancer Epidemiology Biomarkers and Prevention, presents some of the first data to link early life sunlight exposure to a specific mutation in melanomas......... Posted by: Andria      Read more         Source

June 6, 2007, 9:24 PM CT

Big power of small RNAs, in halting cancer

Cold Spring Harbor Laboratory (CSHL) scientists led by Lin He, Xingyue He, and Professor and Howard Hughes Medical Investigator (HHMI) Greg Hannon have identified a family of micro RNAs (miRNAs) that enable a critical tumor suppressor network, called the p53 pathway, to fight cancer growth. At CSHL, we are moving simultaneously on several fronts to understand the p53 pathway because damage to this pathway is something that almost all cancers have in common, said CSHL Cancer Center Deputy Director and HHMI Scott Lowe.

Collaboration among different CSHL research laboratories has not only observed that p53 can arrest the growth and even eradicate cancers, but weve revealed something very surprising about what makes this pathway so powerful, said Hannon. CSHL research published by Nature earlier this year, concluded that even in the latest stages of cancer, reactivation of a previously damaged p53 pathway caused cancer tumors to stop growing and even eliminate themselves by activating an immune response in surrounding healthy cells. Most suspected that proteins would be revealed as key to the power of p53, but this latest research published June 6 by Nature now identifies miRNAs as a critical force behind the anti-proliferation potential of p53.

Expression of most miRNAs is reduced in tumors, suggesting that some miRNAs act to prevent tumor formation. By comparing levels of miRNAs in cells with a variety of pre-malignant genetic lesions, CSHL scientists found a correlation between changes in the p53 pathway and the loss of a specific family of miRNAs, known as miR-34. The fact that p53 uses miRNAs to stop tumor cell growth reveals a completely new dimension of this critical cancer fighting pathway and its ability to trigger the genetic death of cancer cells. Our findings certainly lead to a deeper understanding of a critical tumor suppression mechanism but also may provide insight into how to best engage the p53 pathway to treat cancer by killing tumor cells, said He......... Posted by: Andria      Read more         Source

June 1, 2007, 9:39 PM CT

Cells re-energize to come back from the brink of death

The discovery of how some abnormal cells can avoid a biochemical program of self-destruction by increasing their energy level and repairing the damage, is giving researchers at St. Jude Children's Research Hospital insights into a key strategy cancer cells use to survive and thrive.

The finding offers an explanation of how abnormal cells that have cheated death once by disabling the main suicide pathway called apoptosis can also foil a backup self-destruct program, which allows them to survive and become malignant.

The St. Jude study also suggests that a drug that disrupts a cancer cells ability to block this backup program would allow that program to kill the cell. Such a specifically targeted drug might be more effective and less toxic than standard chemotherapy. A report on this work is in the June 1 issue of Cell.

Apoptosis is triggered by a variety of factors, including gene mutations that can make the cell become malignant. During apoptosis, the membrane covering the cells mitochondria develop holes and leak a molecule called cytochrome c, which triggers the activity of enzymes called caspases. In turn, caspases trigger a series of events that kills the cell. Mitochondria are tiny structures that act as power plants to supply the cell with energy, but also hold the keys to the cells life and death......... Posted by: Andria      Read more         Source

May 25, 2007, 7:17 PM CT

Most pediatric chemotherapy mistakes reach patients

The vast majority of chemotherapy errors identified in children reach patients, as per one of the first epidemiological studies of cancer drug errors in children. Reported in the July 1, 2007 issue of CANCER, a peer-evaluated journal of the American Cancer Society, the study concluded that the antimetabolite class of chemotherapeutic agents are most likely linked to errors, and that errors in drug administration and errors in drug dosing and frequency were the most common mistakes made and consequently, the most potentially harmful.

Chemotherapeutic drugs have been credited with significant gains in survival from pediatric cancers. However, they are among the most toxic medications used today. Calculating dose, route, and frequency, which are often based on a childs weight, are critical to ensure that the drug concentration in the blood is within its narrow safety margins.

Medication errors are common during pediatric hospitalizations, occurring in almost 6 percent of all medicine orders for pediatric inpatients. One of the only comprehensive studies of pediatric chemotherapy errors observed that 13 percent of such errors reached children and 2 percent were serious and mandatory intervention.

Dr. Marlene Miller of Johns Hopkins University and his colleagues conducted a comprehensive review of a nationwide medicine error database of inpatient facilities and outpatient clinics to characterize the patterns of errors and their causes for children receiving chemotherapy. Between 1999 and 2004, 829,492 errors were reported, of which 29,802 involved patients under 18 years old and 310 of these involved a chemotherapeutic drug......... Posted by: Andria      Read more         Source