GeneNews Limited, Canada, has announced the launch of ColonSentryTM, the world’s first blood-based molecular test for screening colorectal cancer. ColonSentry is a blood test that assesses a patient’s current risk of having colorectal cancer, identifying those with increased risk so that they might benefit from more invasive diagnostic tests such as colonoscopy. This risk stratification approach allows for a more targeted application of colonoscopy, which could increase the detection rate of colorectal cancer by as much as three-fold in an asymptomatic general population. The test requires a simple blood sample. The mRNA expression of a panel of seven specific genes is measured at the molecular level by quantitative RT-PCR, which results in an assessment of the patient’s current risk.

Source: www.prnewswire.com

Malaria parasites (plasmodia), once inside their human hosts, first set up shop in liver cells, then move into red blood cells (RBCs) to replicate and wait for the next mosquito to help continue the cycle. After plasmodia infect a blood cell, they send out clusters of sticky proteins to the cell surface, enabling them to attach to blood vessels and escape destruction by the host’s spleen while they replicate. This can be especially problematic during pregnancy as malaria-infected RBCs congregate in the placenta (the source of food and oxygen for the foetus), creating health problems such as anaemia, low birth-weight, fever and more.

Targeting the sticky proteins with drugs is difficult, as plasmodia contain many different varieties, which they employ to evade the human immune system. However, certain parts of the protein have to remain constant for proper function. A study by Dr. Matthew Higgins from the Department of Biochemistry, University of Cambridge, the United Kingdom, created high-resolution 3-D structures of the malarial sticky protein, PfEMP1, to detail how plasmodia protect these conserved areas.

Dr. Higgins found that a variable region of this protein covers a section that is important for docking up with the placental wall. When the infected RBC gets close to chondroitin sulphate, a structural molecule on blood vessels, the variable region moves aside and ever so briefly exposes the binding region, just enough to allow anchoring to take place. Dr. Higgins suggests that targeting this conserved binding domain of PfEMP1 protein with pharmaceuticals that mimic chondroitin sulphate and expose this region might be a worthwhile approach to develop or hasten immunity.

Source: www.sciencedaily.com

Researchers from the European Union-funded EuroStemCell project have shown that mouse embryonic stem (ES) cells are able to self-renew without the natural culture materials – such as feeder cells, conditioned media, hormones and serum extracts – that scientists have so far used to maintain them and grow stem cell lines. This discovery contradicts previously-held view that these materials provided the signals and instructions to stem cells keep to their undifferentiated ‘blank’ state, and could have wide-ranging implications for stem cell research.

Cells still need to be grown in a culture giving them the sugars and proteins needed to stay alive. However, the scientists were able to show that ES cells produce their own signalling molecules and that these signals are the key driving force behind differentiation. When one of these signalling molecules, Fibroblast Growth Factor (FGF) 4, is eliminated or blocked, the cells can remain in their undifferentiated state indefinitely.

“The new culture conditions will help us to understand the nature of the pluripotent state and how it might be manipulated to produce specialized cells in the laboratory,” explains, Dr. Jason Wray of the Wellcome Trust Centre for Stem Cell Research, and one of the authors on the paper. The research is expected to help the derivation of ES cells from other animals. The discovery is also tipped to have major implications for large scale production of specialized cells, such as brain, heart muscle and insulin producing cells, for future therapeutic use.

Source: www.ec.europa.eu

Researchers at Karolinska Institute in Sweden and the Royal Veterinary College in London have jointly developed a system that eliminates the need for antibiotics and resistance genes in the engineering of industrial and medical products. The method involves safer, less costly alternatives and is well suited for the industrial production of many types of biofuels and biopharmaceuticals. The wide use of antibiotic resistance genes for the selection of recombinant bacteria could contribute to the spread of antibiotic resistance. The practice is particularly inappropriate for some intrinsically resistant bacteria and in vaccine production, and costly for industrial-scale production. The non-antibiotic systems available require mutant host strains, defined media or expensive reagents.

While working on gene targeting in bacteria, the researchers discovered that a well-known interaction between a cell membrane synthesis gene and the biocide triclosan could be exploited for strain selection. Surprisingly, triclosan selection performs better than conventional antibiotic selection. The new cloning vector, pFab, enabled selection by triclosan at 1 ìM. Interestingly, pFab out-performed the parent pUC19-ampicillin system in cell growth, plasmid stability and plasmid yield. In addition, while pFab and triclosan are toxic to host cells when used alone, in combination they enhance growth and plasmid production through a gene-inhibitor interaction. The model thus offers an alternative plasmid selection method based on essential gene over-expression, without the use of antibiotic-resistance genes and conventional antibiotics.

Source: www.greenbio.checkbiotech.org

A scientist at MIT’s Picower Institute for Learning and Memory, the United States, has pinpointed stem cells within the spinal cord that, if coaxed to differentiate into more healing cells and fewer scarring cells following an injury, may lead to a non-surgical treatment for debilitating spinal cord injuries. The results of the work carried out by Dr. Konstantinos Meletis, a post-doctoral fellow at the Picower Institute, and colleagues at the Karolinska Institute in Sweden, could help provide some degree of mobility to the 30,000 people worldwide afflicted each year with spinal-cord injuries.

The stem cells in the adult spinal cord proliferate slowly or rarely, and fail to promote regeneration on their own. But recent experiments show that these same cells, grown in the lab and returned to the injury site, can restore some function in paralysed rodents and primates. In the current study, the researchers found that neural stem cells in the adult spinal cord are limited to a layer of cube- or column-shaped, cilia-covered cells called ependymal cells. These cells form the thin membrane lining the inner-brain ventricles and the connecting central column of the spinal cord.

The study, by identifying for the first time where ependymal cells are found, paves a path towards manipulating them with drugs to boost their ability to repair damaged nerve cells. Upon injury, ependymal cells proliferate and migrate to the injured area, producing a mass of scar-forming cells, plus fewer cells called oligodendrocytes. The oligodendrocytes restore the myelin (coating) on nerve cells’ electrical impulse-carrying projections called axons. The failure of severed axons to regrow and reconnect with their target cells in the peripheral nervous system is one of the reasons for the limited functional recovery typically associated with central nervous system injuries.

Source: www.web.mit.edu

Researchers at the Yokohama City University in Japan have gained a better understanding how influenza viruses replicate, possibly opening the way for the development of drugs to hamper their reproduction. The researchers zeroed in on an enzyme that flu viruses need to replicate and managed, for the first time, to capture a snapshot of the enzyme. Enzymes in influenza viruses are made up of three proteins bound tightly together.

The researchers crystallized the proteins and got a peek at part of the structure, which involves the tip of one of the proteins coming into contact with another protein. “This gives us some hope that we can interrupt this interface,” said Dr. Jeremy Tame, a member of the research team. Such an interruption would “kill the virus, or slow it down sufficiently,” he added. All influenza-A viruses, including the H5N1 bird flu virus, are believed to have similar structures. Theoretically, one drug could fight all of them.

Source: www.reuters.com

A team of scientists at Cold Spring Harbour Laboratory (CSHL), the United States, has identified an enzyme called Brk that may serve as a target for future drugs developed to fight ErbB2-positive tumours. Researchers claim that Brk helps these tumours become virulent and is also implicated in the process through which the tumours develop drug resistance. “The limited success of existing therapy suggested that factors besides ErbB2, or proteins that collude with ErbB2, might nullify the effects of Herceptin and Lapatinib,” explained CSHL Professor, Dr. Senthil Muthuswamy, leader of the research team and corresponding author of the paper. Herceptin and Lapatinib are tumour suppressors.

A detailed analysis of changes that occurred in the genomes of a sample of breast cancer patients helped the researchers confirm that the expression of ErbB2 and Brk was directly linked. By forcing the production of both ErbB2 and Brk within the same cell, they determined how Brk enhances ErbB2 activity and fortifies tumour cells against ErbB2-targeting drugs. The findings may suggest a way to treat patients with advanced ErbB2-positive tumours and those who have developed resistance to ErbB2 inhibitors.

According to the scientists, targeting Brk is a safe strategy because “Brk does not promote the proliferation of normal cells, and its expression in normal tissues is restricted to non-proliferating cells.” Inhibiting this protein might thus “produce fewer unwanted side effects than (targeting) other cancer-promoting proteins” that may be present in larger numbers.

Source: www.biospectrumasia.com

Prof. Eliezer Flescher and his colleagues of The Sackler Faculty of Medicine, Tel Aviv University, Israel, have developed an anti-cancer drug based on a decade of research into the commercial applications of the compound jasmonate, a synthetic compound derived from jasmine flower itself. Both blood cancers and solid tumours have been found to be responsive to the jasmonate compound, known also as methyl jasmonate. Prof. Flescher refers to this as the “jasmonate scaffold”, a basis for developing a series of chemical derivatives.

In terms of bioavailability and safety, early first-in-man studies have been proved successful, and Prof. Flescher is hopeful that an anti-cancer drug based on jasmonate could be on the shelf soon. “The jasmonate compound is used widely in agriculture and in cosmetics,” observes Prof. Flescher. “Proven to be non-toxic, it has the same regulatory status as table salt. That and the fact we are working on a natural chemical gives us a good starting point for launching a new drug.”

Source: www.sciencedaily.com