SAN FRANCISCO -- San Francisco Zoo officials are mourning the death of "Gene," a 41-year-old black rhinoceros who's been a popular figure at the zoo since 1978.

Zoo officials, who described Gene as gentle and friendly, said he died of kidney failure on Monday.

The zoo's animal care and veterinary staff had been keeping an eye on Gene because his appetite had dropped and he was lethargic, according to zoo officials.

After a recent blood sample indicated that Gene had kidney failure, zoo staff focused on keeping him comfortable for the remainder of his life.

Gene was named after the late Eugene Friend, who served on the Recreation and Park Commission for 24 years, zoo officials said.

Gene was born in Kenya and came to the San Francisco Zoo in 1978 at the age of seven.

During his time at the zoo, Gene fathered five offspring, three of which are now living at other accredited zoos, zoo officials said.

Gene's animal keeper, Julie McGilvray, said he had a good disposition and was very friendly.

"We nicknamed him Big Dog because he loved to be rubbed, either by hand or with a scrub brush, and oftentimes he would lie down and absorb the soothing experience," McGilvray said in a statement.

Zoo officials said black rhinos are a critically endangered species because they are targeted by poachers who covet their valuable horns.

See the original post here:
41-year-old black rhino 'Gene' dies of kidney failure

Public release date: 1-Mar-2012 [ | E-mail | Share ]

Contact: Stephanie Desmon sdesmon1@jhmi.edu 410-955-8665 Johns Hopkins Medical Institutions

Researchers, led by scientists from Johns Hopkins, have found five previously unknown gene mutations believed to be associated with elevated blood platelet counts in African-Americans, findings they say could someday lead to the development of new drugs to help prevent coronary artery disease.

The study is believed to be the first of its size to focus on platelet genetics in African Americans, who have a higher risk of stroke than other racial groups. They also have relatively higher platelet counts and average platelet volume, and worse outcomes than whites after a heart attack.

"Improving our understanding of the biology and genetics of platelets and how they function will aid us in developing better treatments and more individualized treatments to reduce risk of heart disease associated with platelets," says study leader Rehan Qayyum, M.D., an assistant professor in the division of general internal medicine at the Johns Hopkins University School of Medicine.

Qayyum cautions that there are believed to be many more genes involved in platelet function that remain unknown.

Platelets are cells produced in bone marrow, smaller than red or white blood cells, which foster blood clotting. While clotting is critical to stop bleeding after injuries, it can also cause harm by allowing clumps of blood cells to clog blood vessels leading to the heart, brain and other organs, cutting off blood flow.

Studies have shown that the greater the platelet volume or count in the blood, and the larger platelets are, the greater the risk of dangerous clot formation. Qayyum notes that the number of platelets in a given amount of blood (platelet count) and the size of these platelets (measured as average platelet count) vary from person to person in much the way that height, weight and eye color traits differ. Thus, he said, the search for genes that control this variation is a potentially fruitful line of scientific inquiry.

Qayyum and his colleagues, publishing in the online journal PLoS Genetics, report that they conducted a meta-analysis and genomewide association study, looking at genetic data from 16,000 African-American participants from seven separate studies. They compared information from each study, tracking 2.5 million single possible changes in the human genetic code to see which genes stood out across the entire group as significantly associated with increased or decreased platelet counts.

The researchers found five such alterations, involving the addition or deletion of a single piece of genetic code, across the studied genomes that had not been identified in other populations. When they checked their findings against data from Caucasian and Hispanic groups, they found three of the novel gene mutations in those populations, too. Four of the previously unknown gene mutations were later found in the genetic code of platelet cells, but one was not. That one, however, was found close to a gene that is known to be essential in the formation of normal platelets. The exact role played by each of these mutations still needs to be determined, Qayyum says.

Visit link:
Researchers find 5 novel gene mutations linked to platelet counts in African Americans

SAN FRANCISCO --San Francisco zoo officials are mourning the death of "Gene," a 41-year-old black rhinoceros who's been a popular figure at the zoo since 1978.

Zoo officials, who described Gene as gentle and friendly, said he died of kidney failure on Monday.

The zoo's animal care and veterinary staff had been keeping an eye on Gene because his appetite had dropped and he was lethargic, according to zoo officials.

After a recent blood sample indicated that Gene had kidney failure, zoo staff focused on keeping him comfortable for the remainder of his life.

Gene was named after the late Eugene Friend, who served on the Recreation and Park Commission for 24 years, zoo officials said.

Gene was born in Kenya and came to the San Francisco Zoo in 1978 at the age of seven.

During his time at the zoo, Gene fathered five offspring, three of which are now living at other accredited zoos, zoo officials said.

Gene's animal keeper, Julie McGilvray, said he had a good disposition and was very friendly.

"We nicknamed him Big Dog because he loved to be rubbed, either by hand or with a scrub brush, and oftentimes he would lie down and absorb the soothing experience," McGilvray said in a statement.

Zoo officials said black rhinos are a critically endangered species because they are targeted by poachers who covet their valuable horns.

View post:
San Francisco: 41-year-old black rhino 'Gene' dies zoo

08-02-2012 12:15 Joan shares her family story of bipolar disorder and her journey as a mental health advocate. This workshop is part of a genomics curriculum for practicing healthcare providers developed by the Genomic Medicine Institute at El Camino Hospital, Genetic Alliance, and the National Coalition for Health Professional Education in Genetics. This workshop, the fifth in a 10-part series, covered understanding genetic contribution to schizophrenia, major depression, hypertension, and diabetes; risk assessment for complex conditions; establishing diagnosis; pharmacogenomics; gene-environment interaction; and management.

Original post:
Workshop 5: Genetics of Complex Disease - Joan Esnayra - Video

Editor's Choice Academic Journal Main Category: Urology / Nephrology Article Date: 28 Feb 2012 - 9:00 PST

email to a friend printer friendly opinions

Current Article Ratings:

Interstitial cystitis or bladder pain syndrome is a debilitating urinary bladder disease that can occur with or without bladder ulcers - called Hunner lesions. Researching the disease is difficult, due to limited animal models, because human patients are not ethically permitted to undergo invasive research procedures.

The researchers set out to develop a noninvasive method to evaluate the bladder epithelium as objectively and directly as possible by using microarray technology to examine cells shed into the urine. The alternative would be conducting a bladder biopsy, which requires anesthesia and has a small risk of injuring the bladder.

The findings demonstrated that urine cells, from patients with Hunner lesions had a distinct gene signature for inflammation. The findings were comparable to those from an earlier microarray study of bladder biopsies, which was the first to objectively demonstrate this inflammation without biopsy in Hunner lesion patients.

Eric Blalock, associate professor in the Department of Molecular and Biomedical Pharmacology at the UK College of Medicine, says that providing these preliminary results validate future research, they could potentially lead to a noninvasive biomarker for Hunner lesion-interstitial cystitis/bladder pain syndrome.

He states:

Gene signatures were similar to healthy controls in interstitial cystitis patients without Hunner lesions.

Urologist Deborah Erickson declared:

Excerpt from:
Bladder Pain Syndrome - Gene Expression Analysis Shows Promise

GIA announces the release of a comprehensive global report on Gene Therapy markets. The global market for Gene Therapy is forecast to reach US$794 million by 2017. Key factors driving growth in the market include rising demand for new and effective therapies for cancer treatment, in addition to completion of human genome project, rising incidence and prevalence of cancers and other critical diseases, prospective launch of gene therapies in major global markets.

San Jose, California (PRWEB) February 28, 2012

Follow us on LinkedIn – Gene therapy embarks on rapid advancements in the area of novel drug research. In less than a couple of decades, gene therapy has witnessed significant advances. From conceptual stage, gene therapy progressed to the current clinical trials stage in various disease conditions. Gene Therapy holds a distinctive edge when compared to conventional methods such as radiotherapy and chemotherapy, owing to the fact that they do not repress the immune system. Analysis reveals that gene therapy holds a great potential for treating several diseases, especially cancer. However, with failures of gene therapies continuing worldwide and regulatory authorities being stringent and watchful, and no drug approved until now in major markets like US and Europe, the global gene therapy market has significant ground to cover. Scientists, besides being actively involved in expanding the horizons in gene therapy by research and development, are simultaneously involved in patenting new technologies.

The most important advantage of gene therapy is elimination of chemotherapy, which is a dreaded procedure with several side effects. Another advantage of gene therapy is evasion of several side effects including hearing impairment and kidney damage resulting from platinum-induced chemotherapy. Gendicine is the first gene therapy medicine to be approved for treatment of Head and Neck Squamous Cell Carcinoma (HNSCC), and is currently marketed in China. The drug developed by Shenzhen SiBiono Gene Technologies Co (SiBiono) Ltd., is also called as Recombinant Ad-p53 Anti-cancer Injection. The medicine is formulated with an adenoviral vector and p53 tumor suppressor gene and has emerged as a new treatment for HNSCC. Worldwide, there are about five drugs that have completed clinical trials and are awaiting clearance from the concerned regulatory authorities. These drugs include HGF DNA Plasmid from Sosei and Daiichi Sankyo. The drug investigated for treating peripheral vascular disease was filed for approval in Japan way back in 2008, and is yet to receive approval from the Japanese authorities.

Regulation of gene therapy needs to be harmonized on a global scale for promoting international exchange. This could be achieved by extensive circulation of information. With rapid advancements made in the field of gene therapy, the regulation norms tend to change as storehouse of knowledge increases. Somatic gene therapy encompasses a broad spectrum of therapeutic strategies and procedures; hence, the review process is being conducted in a phased manner. Currently under clinical trials, gene therapy is far from being stabilized. Steps need to be taken for regulation of gene therapy with respect to safety features. Development of gene therapy is hampered due to lack of efficiency and specificity of Gene Transfer Systems. High levels of uncertainty envelop technical, clinical, and commercial development of gene therapy.

Major players profiled in the report include AnGes MG Inc., BioSante Pharmaceuticals, GenVec, Oxford BioMedica, Shenzhen SiBiono GeneTech Co., Ltd, Transgene, Urigen Pharmaceuticals Inc., and Vical, Inc.

The research report titled “Gene Therapy: A Global Strategic Business Report” announced by Global Industry Analysts Inc., provides a comprehensive review of the gene therapy market, current market trends, key growth drivers, recent industry activity, and profiles of major/niche global market participants. The report provides annual sales estimates and projections for global gene therapy market for the years 2008 through 2017.

For more details about this comprehensive market research report, please visit –

http://www.strategyr.com/Gene_Therapy_Market_Report.asp

About Global Industry Analysts, Inc.

Global Industry Analysts, Inc., (GIA) is a leading publisher of off-the-shelf market research. Founded in 1987, the company currently employs over 800 people worldwide. Annually, GIA publishes more than 1300 full-scale research reports and analyzes 40,000+ market and technology trends while monitoring more than 126,000 Companies worldwide. Serving over 9500 clients in 27 countries, GIA is recognized today, as one of the world's largest and reputed market research firms.

Follow us on LinkedIn

Global Industry Analysts, Inc.

Telephone: 408-528-9966

Fax: 408-528-9977

Email: press(at)StrategyR(dot)com

Web Site: http://www.StrategyR.com/

###

Public Relations
Global Industry Analysts, Inc.
(408) 528-9966
Email Information

View original post here:
Global Gene Therapy Market to Reach US$794 Million by 2017, According to New Report by Global Industry Analysts, Inc.

Public release date: 27-Feb-2012
[ | E-mail | Share ]

Contact: Graciela Gutierrez
ggutierr@bcm.edu
713-798-4710
Baylor College of Medicine

HOUSTON (Feb. 27, 2012) ? Antisense oligonucleotides ? short segments of genetic material designed to target specific areas of a gene or chromosome ? that activated an enzyme to "chew up" toxic RNA (ribonucleic acid) could point the way to a treatment for a degenerative muscle disease called myotonic dystrophy, said researchers from Baylor College of Medicine and Isis Pharmaceuticals, Inc., in a report in the journal Proceedings of the National Academy of Sciences.

"This is a proof-of-principle therapy that is very effective in cell culture and mice," said Dr. Thomas A. Cooper, professor of pathology and immunology and molecular and cellular biology at BCM and the report's corresponding author. "The treatment will have to be refined to deliver systemically in people with myotonic dystrophy."

Myotonic dystrophy is the most common muscular disease in adults, affecting mainly the skeletal muscles, heart and central nervous system. It occurs because of a mutation that causes numerous repeats of three letters of the genetic code (CTG) in a gene called DMPK. RNA is made as a step in the cell's production of the protein associated with the gene. The messenger RNA (the chemical blueprint for making a protein) that is produced from the mutated gene also contains the abnormal long repeats that cause the RNA to accumulate in the cell's nucleus. There it sequesters and blocks the function of a protein called Muscleblind-like 1 and activates another protein called CELF1. These proteins antagonize one another and the result is abnormal expression of proteins from many other genes in adult tissues, resulting in disease.

To counteract this, Cooper and his colleagues created antisense oligonucleotides called gapmers, which are simply strands of genetic material that seek out portions of the abnormal RNA repeats and target an enzyme called RNase H to the toxic RNA causing its degradation. They also showed that combining the gapmers with other antisense oligonucleotides that help released the sequestered Muscleblind-like1 can enhance the effect.

"It worked in cultures of cells with the expanded repeats and in mice that model myotonic dystrophy," said Cooper. "We did it in skeletal muscle first because we can inject the material directly into the muscle."

Later, he plans to determine if the material also works in the animals' hearts.

Using the treatment in people will require more fine-tuning, said Cooper. He would like to be able to give the therapy systemically rather than directly into the muscle. They saw some muscle damage and inflammation in the animals they treated.

Antisense oligonucleotide treatments are being tested in Duchenne muscular dystrophy and another disease called spinal muscular atrophy, said Cooper.

###

Others who took part in this research include Johanna E. Lee of BCM and C. Frank Bennett of Isis.

Funding for this work came from the National Institutes of Health, the Muscular Dystrophy Association and the Shanna and Andrew Linbeck Family Charitable Fund.

[ | E-mail | Share ]

AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

Read this article:
Antisense oligonucleotides make sense in myotonic dystrophy

FRIDAY, Feb. 24 (HealthDay News) -- Sudden Infant Death Syndrome (SIDS) may sometimes have a genetic component, a team of German researchers reports.

DNA analysis from a small group of infants who succumbed to SIDS revealed that many of the male children carried a particular enzyme mutation that may have impaired their ability to breath properly. This was not the case for female SIDS patients.

Study author Dr. Michael Klintschar, director of the Institute for Legal Medicine at Medical University Hannover in Germany, said his team tried to build upon previous research suggesting that "abnormalities in the brain stem, the part of the brain that regulates breathing and other basic functions, lead to SIDS."

"The reasons for these abnormalities are unclear," he noted, "but some scientists believe that the genes inherited by the parents might be one of several factors."

Klintschar and his colleagues found indications that SIDS risk might be higher among male infants who carry a mutation of an enzyme -- called MAOA -- that appears to impede key neurotransmitter function.

"Babies that have this variant inherited might have an impaired breathing regulation," he said. "But the risk conveyed by this gene variant is relatively small compared to other factors, like sleeping position [or exposure to] smoking. Moreover, the findings have to be replicated in another population sample."

The study appears online and in the March issue of Pediatrics.

The authors noted that SIDS is one of the great mysteries in pediatric medicine, with efforts to pin down the root cause for the sudden loss of children under the age of 1 year falling short of a definitive answer.

The new study focused on 156 white infants (99 boys and 57 girls) who were born in the Lower Saxony region of Germany and died while sleeping.

The deaths took place between the second and the 51st week of life, and all remained "unexplained" despite full autopsies, clinical history reviews and analyses of the circumstances of death.

DNA samples were taken from all the deceased, as well as from another 260 male adults between the ages of 18 and 30.

The result: MAOA mutations were more commonly found among male SIDS children than among their healthy male counterparts. This did not hold true with female SIDS children.

Most mutations appeared to be clustered within a specific time frame of death that correlated with the majority of SIDS fatalities. That is, infants who had died between the age of 46 days and 154 days -- the most prevalent period of SIDS deaths among the study group -- were significantly more likely to carry MAOA mutations than those children who died at ages above 5 months.

The authors concluded that among at least a subset of male SIDS patients, a genetic brain stem abnormality might be the driving force leading to their sudden loss.

"Our study furthers our understanding of the mechanism of SIDS," Klintschar said. "[But] it does not lead directly to a 'cure' of SIDS. And up to now [it] does not enable a lab test to estimate the individual risk of a baby to die from SIDS. But it emphasizes that measures already recommended to prevent SIDS -- using pacifiers, avoid sleeping in the prone position, no smoking during pregnancy -- make sense. Mothers of families with a prior SIDS case in the family should be more careful than others. But in most cases, obeying these recommendations keeps the baby safe."

However, while also an advocate of such basic preventive measures, Dr. Warren Guntheroth, a professor of pediatrics at the University of Washington School of Medicine in Seattle, holds no stock in a genetic basis for SIDS.

"I think it's nonsense," he said. "There's years and years of research that has shown that SIDS is not inherited. Not genetic. The only genetic link I will admit to is that males are definitely more at risk than females. But apart from that, I think fooling around with laboratory studies of genes and saying that that might cause SIDS is a far reach."

So what can parents do?

"Probably one of the most important things is not to put the baby on its tummy for sleep. That reduces risk by 50 percent," Guntheroth said. "Another is the use of the pacifier. Pacifiers, for reasons nobody understands well, reduces the risk. Also, don't overheat the child, by overdressing or putting the infant in a room that is too hot. Finally, cigarettes increase the risk terribly. Living with a parent that smokes is a definite risk factor, so the parent can do themselves and the child a favor by quitting or at least not smoking in the same area as the child."

More information

For more on SIDS, visit the U.S. National Library of Medicine.

See the original post here:
Gene Might Be a Culprit in Sudden Infant Death for Boys

Next time you take your medicine, consider that mice likely helped in testing it.

The structure of human and mouse DNA is about 96 percent similar, which makes mice excellent subjects for testing products that could be used on humans. As research has progressed, however, a problem arose within the mice population.

There were very few strains of mice bred for testing, which led to a severe lack of genetic diversity in lab mice. Despite the similarities in DNA structure, the diversity of the mouse population did not match the diversity of the human population, and lab test results in mice could not be safely extrapolated to humans.

In 2001, a program called Collaborative Cross sought to fix this problem. David Threadgill, head of the Genetics Department, works with this group to find ways to diversify lab mouse populations.

"When we started this project, at least a third or half of the mouse genome had no diversity in it, so there were blind spots within the genome, and you couldn't interrogate functions of those parts," Threadgill said.

Threadgill and his colleagues randomly bred eight strains of lab and wild mice, creating a library of test mouse strains with sufficient diversity to mirror the human population.

"We use mice as a surrogate for you, to investigate the causation of human disease," Threadgill said.

Collaborative Cross now has about 1,600 strains of mice, housed and curated at a facility in Chapel Hill. Ten representatives of each strain are kept in the facility's 16,000 cages and are made available to researchers around the world. The mice of Collaborative Cross are currently used in various research projects. From cancer research to infertility studies, these mice of a diverse genetic background enable researchers to investigate the genetic basis of human disease more thoroughly.

Human cell division may mutate into the uncontrolled division of cells, resulting in the development of a cancerous tumor, but researchers can now investigate the causative factors in an expendable mouse population that more closely mirrors the human genome. Because the carriers of these genes, the mice, reproduce very quickly, complete investigations of the behavior and function of genes in relation to the disease in question are possible.

Though Collaborative Cross doesn't just offer mice for direct testing, it also maintains a massive library of genes. Each individual bred through the project has its DNA catalogued in an online resource available to the public. This genome browser is a critical aspect of the project.

It is important in consolidating the work of Collaborative Cross, and offers an excellent reference for any scientist doing work with test mice, according to Threadgill. For example, some diseases are caused by unfavorable combinations of specific genes in an organism's DNA.

"What these mice are telling us is that a lot of human diseases are coming about because of genetic disruption of normal feedback systems," Threadgill said. "There are unique combinations of genetic variation that just don't function well together."

With a resource like the mouse genome library, these unfavorable polymorphisms in genes can be identified, isolated and studied through population analysis.

In the future, Collaborative Cross plans to expand their operation, with new distribution centers around the world and more strains of mice. Being able to perform large scale studies on diverse populations will be even more important as we develop a better understanding of the genetic basis of disease.

For complicated problems, complicated models are needed. According to Threadgill, that's just what Collaborative Cross is developing. 

Link:
Researchers diversify lab mouse gene pool

Sudden infant death syndrome (SIDS) may sometimes have a genetic component, a team of German researchers reports.

DNA analysis from a small group of infants who succumbed to SIDS revealed that many of the male children carried a particular enzyme mutation that may have impaired their ability to breath properly. This was not the case for female SIDS patients.

Study author Dr. Michael Klintschar, director of the Institute for Legal Medicine at Medical University Hannover in Germany, said his team tried to build upon previous research suggesting that "abnormalities in the brain stem, the part of the brain that regulates breathing and other basic functions, lead to SIDS."

"The reasons for these abnormalities are unclear," he noted, "but some scientists believe that the genes inherited by the parents might be one of several factors."

Klintschar and his colleagues found indications that SIDS risk might be higher among male infants who carry a mutation of an enzyme -- called MAOA -- that appears to impede key neurotransmitter function.

"Babies that have this variant inherited might have an impaired breathing regulation," he said. "But the risk conveyed by this gene variant is relatively small compared to other factors, like sleeping position (or exposure to) smoking. Moreover, the findings have to be replicated in another population sample."

The study appears online and in the March issue of Pediatrics.

The authors noted that SIDS is one of the great mysteries in pediatric medicine, with efforts to pin down the root cause for the sudden loss of children under the age of 1 year falling short of a definitive answer.

The new study focused on 156 white infants (99 boys and 57 girls) who were born in the Lower Saxony region of Germany and died while sleeping.

The deaths took place between the second and the 51st week of life, and all remained "unexplained" despite full autopsies, clinical history reviews and analyses of the circumstances of death.

DNA samples were taken from all the deceased, as well as from another 260 male adults between the ages of 18 and 30.

The result: MAOA mutations were more commonly found among male SIDS children than among their healthy male counterparts. This did not hold true with female SIDS children.

View post:
Gene may be culprit in SIDS for boys

Scientists have identified a new gene that may increase the risk of breast cancer, according to a new study from Finland.

In the study, mutations in this gene, called Abraxas,were linked to cases of hereditary breast cancer.

Researchers have now identified more than 10 genes that increase breast cancer risk; perhaps the most well-known of these are the BRCA1 and BRCA2 genes. But only about 20 percent of women with a family history of breast cancer have mutations in BRAC1 or BRAC2 — meaning in many cases, it's likely other genes are at work.

The mutation does not appear to be common — it was found in 2.4 percent of families with a history of breast cancer. But importantly, the mutation was not found in anyone without breast cancer in the study.

Because the study was conducted in Finland, future studies will need to investigatehow common the mutation is in other countries, said study researcher Roger Greenberg, an associate professor of cancer biology at the University of Pennsylvania School of Medicine.

In the future, women with a family history of breast cancer might be tested for the Abraxas mutation, Greenbergsaid.

Greenberg and colleagues found the Abraxas mutation in three of 125 breast cancer patients from families with a history of the condition. This gene had been suspected to play a role in breast cancer risk because it interacts with BRCA1.

When the researchers looked at an additional 991 breast cancer patients, they found the Abraxas mutation in one woman, who also turned out to have breast cancer in her family. None of the 868 healthy patients in the study had the Abraxas mutation.

The mutated Abraxas gene prevents cells from fixing damaged DNA, increasing the risk that a cell will become cancerous. The gene may increase the risk of other cancers as well. Indeed, one patient in the study was diagnosed with both breast andendometrial cancer, and some patients with the Abraxas mutation had family members with lung cancer, lip cancer and lymphoma.

More research is needed to know exactly how much of an increase in breast cancer risk the Abraxas mutation brings. But Greenberg noted women in the study with this mutation were diagnosed around the same age as those with BRCA1 and BRCA2 mutations — in their mid-40s.

Women with a mutation in BRCA1 or BRCA2 are about five times more likely to develop breast cancer in their lifetimes compared with women who do not have this mutation, according to the National Cancer Institute.

"Identifying more of these mutations will make it easier for patients to know their risk of developing breast cancer," said Dr. Kristin Byrne, chief of breast imaging at Lenox Hill Hospital in New York City, who was not involved in the study. Such genetic information may even help doctors better diagnose breast cancer. Most patients with the Abraxas mutation in the study had a type of breast cancer called lobular carcinoma, which is harder to detect on a mammogram. Knowing that a patient has this mutation might mean doctors use additional screening methods, such as MRI, Byrne said.

The study is published today (Feb. 22) in the journal Science Translational Medicine.

Pass it on: Some cases of hereditary breast cancer may be caused, in part, by mutations in a gene called Abraxas.

Copyright 2012 MyHealthNewsDaily, a TechMediaNetwork company. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.

Follow this link:
New breast cancer gene found

05-02-2012 04:30 A documentary about Cystic Fibrosis made in 1994. Since this was made a lot of development in treatment has happened. However it is interesting to see how things were and compare them with how things are now. The only thing that hasn't changed is what Cystic Fibrosis is all about and the importance to continue raising much needed funds for the Cystic Fibrosis Research Trust to help find a cure for CF! For more information on CF and how you can help find a cure, visit http://www.cftrust.org.uk

See original here:
The Way To Win With Cystic Fibrosis (filmed in 1994). - Video

Public release date: 22-Feb-2012
[ | E-mail | Share ]

Contact: Karen Kreeger
karen.kreeger@uphs.upenn.edu
215-349-5658
University of Pennsylvania School of Medicine

PHILADELPHIA - The infamous BRCA genes do not act alone in causing cancer; there is a molecular syndicate at work preventing the way cells normally repair breaks in DNA that is at the root of breast cancer. But finding all of the BRCA molecular collaborators has been elusive.

Researchers at the Perelman School of Medicine at the University of Pennsylvania and the University of Oulu, Finland, published their discovery of a mutation in the Abraxas gene, which interacts with the well-known breast-cancer gene BRCA1, in Science Translational Medicine this week.

The mutation affects the ability of the Abraxas protein to enter the nucleus and bind to sites adjacent to damaged DNA. Abraxas organizes a large BRCA1 protein-containing complex that is required to fix DNA-damage. A mutated Abraxas protein impairs the BRCA1 complex's ability to migrate to sites of DNA damage and repair breaks. This results in alterations to the genome that increase breast-cancer risk, notes senior author Roger Greenberg, PhD, associate professor of Cancer Biology.

A Family Affair

Before 1990, breast cancer was generally viewed as a disease resulting from a complex relationship between multiple genes and environmental factors. The discovery that it is linked to mutations in BRCA1 in certain families transformed this view, and since that time, mutations in several genes involved in BRCA1-related pathways have also been associated with breast cancer susceptibility.

About ten percent of all breast cancers are thought to be hereditary - caused by genes passed down family lines. This type of cancer susceptibility represents more than 20,000 new cases of breast cancer annually in the United States. Relatively large numbers of families in which detailed medical records are kept are necessary to make associations about mutations that may cause disease.

To get a clearer picture of the heritable causes of breast cancer, the Penn group, working with Finnish scientists at the University of Oulu, screened 125 Northern Finnish breast cancer families for Abraxas mutations. Greenberg collaborated with Dr. Robert Winqvist, a Finnish breast cancer researcher and co-senior author who maintains a large collection of DNA samples from Finnish families that have multiple cases of breast cancer. The group found women who had the Abraxas mutation, as well as breast cancer, in four families with a history of breast cancer.

This association makes Abraxas the newest candidate for yet-unexplained breast cancer susceptibility.

The mutation they found affects a region on chromosome 4 that governs the signal to guide Abraxas to the site of DNA damage in the nucleus. In addition, the researchers showed that the mutation impairs guiding of the Abraxas protein in cultured cells?the mutant protein in these cultures was also not recruited to sites of DNA damage compared to control cells in culture.

What's more, expression of the Abraxas mutation caused hypersensitivity to ionizing radiation-- a cause of DNA damage -- and reduced BRCA1 localization at sites of DNA damage in several cell lines.

Taken together, these observations suggest that the Abraxas mutation keeps the Abraxas protein from migrating with its binding partners at sites where DNA repair is needed, and establishes Abraxas as a breast cancer susceptibility gene. In time, this mutation may be added to a list of about 14 mutations for which breast cancer?prone families can be tested, say the authors.

###

Funding for the research was obtained in part from the National Cancer Institute (1R01CA138835-01), an American Cancer Society Research Scholar Grant, and the the Abramson Family Cancer Research Institute.

Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $4 billion enterprise.

Penn's Perelman School of Medicine is currently ranked #2 in U.S. News & World Report's survey of research-oriented medical schools and among the top 10 schools for primary care. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $507.6 million awarded in the 2010 fiscal year.

The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania -- recognized as one of the nation's top 10 hospitals by U.S. News & World Report; Penn Presbyterian Medical Center; and Pennsylvania Hospital ? the nation's first hospital, founded in 1751. Penn Medicine also includes additional patient care facilities and services throughout the Philadelphia region.

Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2010, Penn Medicine provided $788 million to benefit our community.

[ | E-mail | Share ]

AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

Read more:
New member of the breast-cancer gene network found by Penn-led team

By a GenomeWeb staff reporter

NEW YORK (GenomeWeb News) – Researchers from the US and Finland have tracked down a new gene contributing to familial breast cancer risk in a DNA damage response pathway that also relies on the well known breast and ovarian cancer gene BRCA1.

Through a candidate gene sequencing and genotyping study involving hundreds of Finnish women with or without breast cancer, including women from more than 100 moderate- or high-risk families, the team found a recurrent mutation in Abraxas, a gene coding for a component in a checkpoint that kicks in when cells face ionizing radiation or other sources of DNA damage.

As they reported online today in Science Translational Medicine, researchers found that the recurrent Abraxas alteration seems to predispose women to inherited breast cancer by interfering with the resulting protein's ability to localize to the nucleus. That compromises the DNA damage pathway, which also contains a protein encoded by BRCA1.

"These findings contribute to the concept of a BRCA-centered tumor suppressor network and provide the identity of Abraxas as a new breast cancer susceptibility gene," co-corresponding authors Robert Winqvist, a clinical geneticist from the University of Oulu, and Roger Greenberg, a University of Pennsylvania cancer biology researcher, and colleagues wrote.

Both BRCA1 and BRCA2 have been linked to hereditary forms of breast and ovarian cancer risk. Despite the importance of these two genes, only around one-fifth of familial breast cancer cases around the world are explained by BRCA1 or BRCA2 germline mutations, authors of the new study explained.

As such, they argued that there may yet be unidentified genes that can significantly influence breast and ovarian cancer risk, along with lower penetrance genes and environmental risk factors.

For the current study, researchers focused on Abraxas, a gene coding for a DNA damage checkpoint component that interacts with BRCA1 and other members of a complex that responds to DNA damage, most often caused by ionizing radiation. Given its central role in this complex, the team speculated that Abraxas mutations might elevate cancer risk.

To test that notion, they screened for alterations in the Abraxas gene in individuals from families enrolled at Oulu University Hospital in northern Finland that had a history of breast cancer or of both breast and ovarian cancer.

Using conformation-sensitive gel electrophoresis and targeted Sanger sequencing of Abraxas exons, the team screened for mutations in one individual each from 125 Finnish families classified as being at high or moderate cancer risk. Of these, 15 individuals had tested positive for mutations in known cancer risk genes such as BRCA1, BRCA2, TP53, or PALB2.

Using this screening approach, the team unearthed several changes to Abraxas in individuals from at-risk families. But just one of these alterations was predicted to produce functional changes to the resulting protein.

That same mutation — a guanine to adenine change at position 1,083 of the Abraxas gene — occurred in individuals from three of the families tested.

And when researchers genotyped 991 more unrelated women with breast cancer and 868 unaffected controls at three informative SNPs in Abraxas, they found another woman with the same mutation. That individual was tested in the unselected group, but also came from a family with a history of breast cancer.

None of the four affected women carried mutations in cancer-related genes such as BRCA1/2, TP53, PALB2 or CDH1. Moreover, the Abraxas mutation appeared to co-segregate with cancer cases in the two families for which additional samples were available.

Because the recurrent mutation leads to an amino acid swap within a predicted nuclear localization signal in the Abraxas protein, researchers suspected that this change might have serious functional consequences.

Indeed, results of their follow-up immunofluorescence experiments in several cell lines suggest that the mutation hinders Abraxas protein localization to the nucleus, affecting its ability to participate in the DNA damage checkpoint.

In addition, they found that cell lines expressing mutant versions of the Abraxas gene showed impaired nuclear localization of BRCA1 and another DNA damage checkpoint component, RAP80, and were more prone to ionizing radiation-induced damage.

The pathway affected by the Abraxas mutation appears to be independent of the DNA repair pathways comprised of BRCA1, BRCA2, PALB2, and other proteins, the study authors noted, suggesting tumors with Abraxas or RAP80 alterations might respond to different treatments than tumors harboring mutations in other BRCA-related pathways.

Excerpt from:
Team IDs Familial Breast Cancer Risk Gene in BRCA1-Containing DNA Damage Response Pathway

OXFORD, England--(BUSINESS WIRE)--

Oxford Gene Technology (OGT), provider of innovative clinical genetics and diagnostic solutions to advance molecular medicine, announced today that it has entered into an exclusive licensing agreement with Inven2, the technology transfer office at Oslo University Hospital (OUS) and University of Oslo (UiO), for 12 highly promising colorectal cancer tissue biomarkers.

The exclusive license allows OGT to commercialise any resulting test developed using these biomarkers and to sublicense the markers to other parties. The DNA methylation biomarkers were developed in the laboratory of Professor Ragnhild A. Lothe, in the department of Cancer Prevention, the Norwegian Radium Hospital, part of the Oslo University Hospital.

OGT has validated the results obtained in Professor Lothe’s laboratory showing sensitivity of 93% and specificity of 90% when using tissue biopsies. Further work investigating the efficacy of these biomarkers in blood and faecal samples is ongoing.

“This licensing agreement gives OGT exclusive access to genetic markers which are associated with colorectal cancer.” stated Mike Evans, CEO, of OGT. “We believe that developing tests that include these genetic markers will permit the earlier identification of patients at risk of this disease and allow for more timely diagnosis and clinical interventions.” He added, “The higher specificity of this new panel of markers could provide a more robust screening tool than the tests currently used, while eventually lowering overall costs, which would be of significant benefit for both patients and the clinicians using them.”

“Biomarkers have the potential to greatly improve the accuracy and impact of colorectal cancer screening.” commented Professor Lothe, from the Norwegian Radium Hospital. “We look forward to continuing our collaborative efforts with OGT to develop and validate a future test which will help screen people early for this treatable form of cancer.”

Benedicte Bakke, Business Development Manager at Inven2 AS, Oslo technology transfer office, concluded: “We fully support the collaboration with Oxford Gene Technology to develop a new method of detecting colorectal cancer using these biomarkers. This deal demonstrates the importance of industry and academic collaboration in turning scientific excellence into products that address medical needs.”

-Ends-

Notes for editors:

About Oxford Gene Technology

Founded by Professor Ed Southern, Oxford Gene Technology (OGT) provides innovative clinical genetics and diagnostic solutions to advance molecular medicine. The company has two trading businesses, Biomarker Discovery and Clinical & Genomic Solutions. Biomarker Discovery: OGT delivers tailored biomarker discovery solutions that optimise drug and diagnostic development programmes. With expertise in genomic and proteomic diagnostic biomarkers, OGT provides highly specific customised biomarker panels for cancer and other diseases, both for direct sale and also for collaboration with partner companies. Clinical & Genomic Solutions: OGT’s Genefficiency™ is a unique combination of world-leading platforms, people, processing power and performance synchronised to deliver rapid, high-quality genomic data to customers worldwide. OGT’s CytoSure™ cytogenetics array, labelling and interpretation software products and services provide a complete solution for the detection of chromosomal abnormalities. Together, Genefficiency and CytoSure offer a unique, standardised and integrated solution for cytogenetics research.

For more information on the Company, please visit our website at: http://www.ogt.co.uk

CytoSure: For research use only. Not for use in diagnostic procedures.

About Inven2

Inven2 is the Technology Transfer Office for the University of Oslo and Oslo University Hospital, Norway's largest and leading university and hospital representing pioneering research. Inven2 is the largest contributor in Norway within the field of commercialization of research within Life Science. For more information on Inven2, please visit our website at: http://www.inven2.com

Colorectal cancer

Colorectal cancer (commonly known as colon or bowel cancer) is the 2nd most common cancer in women (behind breast) and the 3rd most common cancer in men (behind prostate and lung). Worldwide, 1.23 million new cases of bowel cancer were diagnosed in 2008. The chance of cure is much better if this cancer is detected at an early stage rather than at a later stage. In the past decade, there has been unprecedented progress in reducing colorectal cancer incidence and death rates; this progress has come about largely through the prevention and early detection of colorectal cancer through screening. However, it is estimated that there could be further improvement ? up to 20,000 fewer deaths from colorectal cancer over the next 20 years ? if just 60% of those eligible took up the invitation for bowel screening (Cancer research UK).

Colorectal cancer screening

In the UK, the current primary screening tool is the faecal occult blood test in England (FOBt; the Faecal immunochemical test, FIT, is used in Scotland). The test is based on determining the presence/absence of blood within a patients stool. Although the test does not diagnose colorectal cancer it directs patients for further evaluation should a positive test be returned to the health care professional. This could ultimately lead to a further examination entailing a colonoscopy. However, the presence of blood in the faeces can be due to a number of factors and so for every 10 people who undergo a colonoscopy 7 will have a ‘normal’ result. The poor positive predictive value of the FOBt leads to unnecessary concern for the patient and a huge cost implication for the NHS.

Consequently, there is a need for a robust preventive strategy that can stratify patients into appropriate screening or surveillance programmes for the early detection of cancer. Internationally, the chosen modality of colorectal cancer screening varies, with cost and availability of diagnostic resources likely to be leading factors in?uencing programme design. The majority of countries, where a national screening programme exists, employ the FOBt (inclusive of Japan and Taiwan). In North America and other European countries, there is ongoing regional colorectal cancer research initiatives/pilot programmes intended to evaluate the potential of implementing national screening programmes.

Recently, there has been growing interest in investigating biomarkers (aberrant hypermethylation of CpG islands) in patients who suffer from colorectal cancer to develop more accurate and patient-friendly tests.

Follow this link:
OGT Signs Licensing Deal for Colorectal Cancer Biomarkers

WEDNESDAY, Feb. 22 (HealthDay News) -- Scientists have identified a new gene mutation linked to breast cancer.

The mutation is in the Abraxas gene, which interacts with the well-known breast cancer gene BRCA1. Abraxas organizes a large BRCA1 protein-containing complex that is needed to repair DNA damage.

The mutation affects the ability of the Abraxas protein to enter the nucleus and bind to sites adjacent to damaged DNA. This leads to genetic alterations that increase breast cancer risk, Roger Greenberg, an associate professor of cancer biology at the Perelman School of Medicine at the University of Pennsylvania, said in a university news release.

Greenberg and his colleagues screened the members of 125 families in Finland with a history of breast cancer, and found women with both the Abraxas mutation and breast cancer in four families.

The findings, published Feb. 22 in the journal Science Translational Medicine, appears to establish Abraxas as a breast cancer-susceptibility gene, according to the researchers.

It has been known that BRCA genes do not act alone in causing breast cancer, but it has proven difficult for scientists to identify other culprits. In time, this Abraxas mutation may be added to the list of 14 mutations for which women in families with a history of breast cancer can be tested, the researchers said.

More information

The U.S. National Cancer Institute has more about breast-cancer risk.

See original here:
Researchers Spot New Gene Mutation Linked to Breast Cancer

By Rachael Rettner
MyHealthNewsDaily

Scientists have identified a new gene that may increase the risk of breast cancer, according to a new study from Finland.

In the study, mutations in this gene, called Abraxas,were linked to cases of hereditary breast cancer.

Researchers have now identified more than 10 genes that increase breast cancer risk; perhaps the most well-known of these are the BRCA1 and BRCA2 genes. But only about 20 percent of women with a family history of breast cancer have mutations in BRAC1 or BRAC2 — meaning in many cases, it's likely other genes are at work.

The mutation does not appear to be common — it was found in 2.4 percent of families with a history of breast cancer. But importantly, the mutation was not found in anyone without breast cancer in the study.

Because the study was conducted in Finland, future studies will need to investigate how common the mutation is in other countries, said study researcher Roger Greenberg, an associate professor of cancer biology at the University of Pennsylvania School of Medicine.

In the future, women with a family history of breast cancer might be tested for the Abraxas mutation, Greenberg said.

Greenberg and colleagues found the Abraxas mutation in three of 125 breast cancer patients from families with a history of the condition. This gene had been suspected to play a role in breast cancer risk because it interacts with BRCA1.

When the researchers looked at an additional 991 breast cancer patients, they found the Abraxas mutation in one woman, who also turned out to have breast cancer in her family. None of the 868 healthy patients in the study had the Abraxas mutation.

The mutated Abraxas gene prevents cells from fixing damaged DNA, increasing the risk that a cell will become cancerous. The gene may increase the risk of other cancers as well. Indeed, one patient in the study was diagnosed with both breast and endometrial cancer, and some patients with the Abraxas mutation had family members with lung cancer, lip cancer and lymphoma.

More research is needed to know exactly how much of an increase in breast cancer risk the Abraxas mutation brings. But Greenberg noted women in the study with this mutation were diagnosed around the same age as those with BRCA1 and BRCA2 mutations — in their mid-40s.

Women with a mutation in BRCA1 or BRCA2 are about five times more likely to develop breast cancer in their lifetimes compared with women who do not have this mutation, according to the National Cancer Institute.

"Identifying more of these mutations will make it easier for patients to know their risk of developing breast cancer," said Dr. Kristin Byrne, chief of breast imaging at Lenox Hill Hospital in New York City, who was not involved in the study. Such genetic information may even help doctors better diagnose breast cancer. Most patients with the Abraxas mutation in the study had a type of breast cancer called lobular carcinoma, which is harder to detect on a mammogram. Knowing that a patient has this mutation might mean doctors use additional screening methods, such as MRI, Byrne said.

The study is published today (Feb. 22) in the journal Science Translational Medicine.

Follow MyHealthNewsDaily staff writer Rachael Rettner on Twitter@RachaelRettner.

See the original post:
New breast cancer gene discovered

Washington, Feb 22 (ANI): Scientists have discovered that a gene known to control lens development is also vital for the development of neurons responsible for mechanosensory - touch sensation - function.

Neurobiologists of the Max Delbruck Center for Molecular Medicine (MDC) Berlin-Buch found that in mice in which they had removed the c-Maf gene in the nerve cells, touch sensation is impaired.

This similarly applies to human carriers of a mutant c-Maf gene. People with such a mutation suffer already at a young age from cataracts, a clouding of the lens, which typically affects the elderly.

The patients, as demonstrated by Professor Carmen Birchmeier and Dr. Hagen Wende in collaboration with Professor Gary Lewin and Dr. Stefan Lechner, have difficulty holding objects such as a sheet of paper as a consequence of this mutation.

"c-Maf is an important gene for the development of the peripheral nerve cells," Professor Birchmeier, a developmental biologist, commented on the findings of her research group.

The gene controls the development of neurons that detect touch, the mechanosensory neurons. Previously, c-Maf was known as a key regulator of lens development.

Furthermore, the gene is also active in the dorsal root ganglia, an aggregate of nerve cells next to the spinal cord in which the cell bodies of mechanosensory neurons are localized.

The nerve cells form long axons, which terminate in the skin in touch corpuscles or at hair shafts.

These axons detect mechanical stimuli, which in turn are converted into electrical signals and transmitted to the brain. When you stroke your fingers over a surface, its structure triggers high-frequency vibrations in the finger, to which specific touch receptors, the Pacinian corpuscles, respond.

In mice with deactivated c-Maf gene only few Pacinian corpuscles are formed, and moreover these few are not intact.

The mice are therefore unable to recognize high-frequency vibrations. The same is true for a Swiss family with an inherited mutant c-Maf gene.

The consequence is that the affected patients develop cataracts at an early age and have an impaired sense of touch.(ANI)

Read the original post:
'Vision' gene also involved in sensing vibrations

Public release date: 21-Feb-2012
[ | E-mail | Share ]

Contact: Barbara Bachtler
bachtler@mdc-berlin.de
49-309-406-3896
Helmholtz Association of German Research Centres

A gene known to control lens development in mice and humans is also crucial for the development of neurons responsible for mechanosensory function, as neurobiologists of the Max Delbr?ck Center for Molecular Medicine (MDC) Berlin-Buch have now discovered. They found that in mice in which they had removed the c-Maf gene in the nerve cells, touch sensation is impaired. This similarly applies to human carriers of a mutant c-Maf gene. People with such a mutation suffer already at a young age from cataracts, a clouding of the lens which typically affects the elderly. The patients, as demonstrated by Professor Carmen Birchmeier and Dr. Hagen Wende in collaboration with Professor Gary Lewin and Dr. Stefan Lechner, have difficulty holding objects such as a sheet of paper as a consequence of this mutation. (Science Express, 16 February 2012 / Page 1 / 10.1126/science.1214314)*.

Professor Birchmeier, a developmental biologist, commented on the findings of her research group: "c-Maf is an important gene for the development of the peripheral nerve cells." The gene controls the development of neurons that detect touch, the mechanosensory neurons. Previously, c-Maf was known as a key regulator of lens development.

Furthermore, the gene is also active in the dorsal root ganglia, an aggregate of nerve cells next to the spinal cord in which the cell bodies of mechanosensory neurons are localized. The nerve cells form long axons, which terminate in the skin in touch corpuscles or at hair shafts. These axons detect mechanical stimuli, which in turn are converted into electrical signals and transmitted to the brain. When you stroke your fingers over a surface, its structure triggers high-frequency vibrations in the finger, to which specific touch receptors, the Pacinian corpuscles, respond.

In mice with deactivated c-Maf gene only few Pacinian corpuscles are formed, and moreover these few are not intact. The mice are therefore unable to recognize high-frequency vibrations. The same is true for a Swiss family with an inherited mutant c-Maf gene. The consequence is that the affected patients develop cataracts at an early age and have an impaired sense of touch.

###

*The transcription factor c-Maf controls touch receptor development and function
Hagen Wende1, Stefan G. Lechner2, Cyril Cheret1, Steeve Bourane3, Maria E. Kolanczyk1, Alexandre Pattyn4, Katja Reuter1,5, Francis L. Munier6, Patrick Carroll4, Gary R. Lewin2 and Carmen Birchmeier1,*

1Developmental Biology, 2Molecular Physiology, Max-Delbr?ck-Center for Molecular Medicine, Robert-R?ssle-Strasse 10, 13125 Berlin, Germany.
3Molecular Neurobiology Laboratory, Salk Institute, La Jolla, California, USA.
4INSERM U.1051, 80 Rue Augustin Fliche, 34091 Montpellier cedex 05, France.
5New address: University of California, San Francisco, CA 94107.
6Jules Gonin Eye Hospital, Av. de France 15, 1004 Lausanne, Switzerland

A photo can be downloaded from the Internet at: http://www.mdc-berlin.de/de/index.html

Contact:
Barbara Bachtler
Press Department
Max Delbr?ck Center for Molecular Medicine (MDC) Berlin-Buch
in the Helmholtz Association
Robert-R?ssle-Stra?e 10
13125 Berlin
Phone: +49 (0) 30 94 06 - 38 96
Fax: +49 (0) 30 94 06 - 38 33
e-mail: presse@mdc-berlin.de
http://www.mdc-berlin.de/

[ | E-mail | Share ]

AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

Go here to see the original:
The molecular basis of touch sensation

Prospects for a DNA sequencing device that is the size of a USB memory stick sent IP Group hurtling up 12, or 11.9pc, to 113p almost a four-year high.

Small-cap IP, which commercialises intellectual property from universities, has a 21.5pc stake in Oxford Nanopore, a spin-out from the University of Oxford that has developed a portable gene sequencing device allowing people to analyse the building blocks of life on the go.

Monday was the first opportunity for investors to respond to Oxford Nanopore presenting its technology at a conference late on Friday, where it unveiled its “MiniON”, a disposable DNA sequencing device the size of a memory stick. The product could make sequencing which can help identify new targets for medicines and illuminate crop science simpler and cheaper.

Analysts at Peel Hunt described the technology as a “game-changer”, which has the “potential to accelerate delivery of personalised medicine to the masses”. They added that $1bn (£630m) was not a “ridiculous valuation” for Oxford Nanopore, but “with supportive private shareholders with deep pockets”, they thought that a flotation “may never happen”. As such, they tipped IP as the “key way to gain exposure to Oxford Nanopore’s value” and raised their target price to 160p from 112p.

Numis analysts went further on Oxford Nanopore’s value, calculating that it could be worth $2bn, or 69p to IP Group’s valuation. They lifted their target price on IP to 129p from 98p and lifted their rating to “buy”.

Back among the blue-chips, miners were hoisting the index higher. China’s move to spur growth by cutting the amount of cash banks must keep in reserve fuelled the miners as investors counted on the metal-hungry country using more raw materials.

Vedanta Resources (EUREX: VR9F.EX - news) rose 46p to £13.58 and iron ore miner Rio Tinto gained 84p to £37.06.

Weir Group (Other OTC: WEIGF.PK - news) , which makes pumps and valves for the mining sector, climbed 135p to £21.86 thanks to a push from Bank of America (NYSE: IKJ - news) -Merrill Lynch (NYSE: MER - news) .

Among other resource stocks, oil producers were fuelled by a spurt in the price of oil after Iran said it had stopped selling crude to British and French companies. BP put on 10.3 to 499¼p. Also lifting the oil giant was the first government settlement involving the Macondo well at the centre of last year’s Gulf of Mexico oil spill. Mitsui’s Moex unit, a minority partner in the well, agreed a $90m settlement on Friday, spurring hopes that BP could yet settle before a trial into claims relating to the disaster begins next week.

The scent of M&A sparked a rise among some smaller oil companies as Friday’s news that Dragon Oil (Xetra: 877789 - news) was considering a tilt at BowLeven (LSE: BLVN.L - news) fuelled hopes that other explorers could attract a suitor. UBS (NYSEArca: DJCI - news) said it expected M&A read-across, although not necessarily with Dragon as a buyer, to be helpful for among others Premier Oil (LSE: PMO.L - news) , Soco International and Heritage Oil (Frankfurt: A0NG6K - news) . Premier (BSE: PREMIER.BO - news) rose 9 to 431.2p while Soco put on 1.6 to 315p, but Heritage eased 0.1 to 188.5p. BowLeven itself fell 1 to 119p.

With miners and oil giants on the march, the FTSE 100 (Euronext: VFTSE.NX - news) climbed 40.18 points to 5,945.25 its highest level in seven months and the FTSE 250 (FTSE: ^FTMC - news) jumped 108 points to 11,420.21. Lifting the market’s spirits were signs that Greece could be close to finalising its bail-out as finance ministers convened in Brussels.

That put a spring in the step of the banks, with Royal Bank of Scotland (LSE: RBS.L - news) gaining 0.88 to 28.48p and Lloyds Banking Group (LSE: LLOY.L - news) rising 0.89 to 36.35p. However, City scribblers remained circumspect ahead of the lenders’ annual results later this week. Nomura kept its “reduce” rating on both RBS and the Black Horse, while Ian Gordon, banking analyst at Investec (Frankfurt: A0J32R - news) , cut his rating on RBS to “hold”. “The house view is that the FTSE 100 will rally to 6,200 this year, and against this benchmark, following its strong year-to-date recovery, we now expect RBS to underperform,” he said. “As such, it is time to take profits take the money and run!”

As traders bought into riskier stocks, defensives missed out. Shire (Stuttgart: A0MMAG - news) lost 26p to £22.52 while Imperial Tobacco (LSE: IMT.L - news) shed 19p to £25.00.

On the second tier, CSR (LSE: CSR.L - news) was the out-and-out winner. Having unveiled plans to lift its dividend and buy back $50m of shares, the maker of microchips shot up 47.3 to 275p. Not far behind was Misys (Xetra: 944235.DE - news) , up 20½ to 330.1p. The software provider is already in talks about merging with Swiss peer Temenos, but Misys said yesterday that it had received a rival approach said to be worth £1.2bn from Vista Equity Partners.

Gaining ground too were a raft of housebuilders, with Persimmon (LSE: PSN.L - news) up 21 to 609p, Barratt Developments 5.1 higher at 130p and Taylor Wimpey (Dusseldorf: 408518.DU - news) rising 1.8 to 48¾p. Landlord Segro advanced 5.9 to 236.7p after selling five industrial estates to funds owned by Ignis Asset Management for £80.2m.

But traders lost their taste for The Restaurant Group . Having been cut to “reduce” by Numis, the owner of Frankie & Benny’s and Garfunkel’s slipped 5½ to 304.2p. “Trading during the last six weeks will not have been helped by increasing competition and unemployment as well as a 14.6pc decline in cinema box office takings,” said analysts.

Inmarsat (EUREX: ISAF.EX - news) loses ground over US deal payment

Inmarsat lost altitude as the satellite operator said that its American partner, LightSquared, had not paid a $56.3m (£35.5m) instalment due to the British company. Inmarsat, which is building a US mobile broadband service with Inmarsat’s spectrum, said it was scheduled to receive the payment from LightSquared after the completion of the first phase of their agreement. However, LightSquared said it had raised “several matters that require resolution before the first phase comes to a close”, adding that the terms of the agreement allow for additional time to resolve pending questions before the final payment is due. Inmarsat said its core business, which provides communications to shipping, aircraft and remote locations worldwide, was unaffected. But it shed 5.5 to 477.1p.

Here is the original post:
Hopes for gene analysis device lift IP Group