Researchers have discovered a way to reprogram mouse liver cells into precursor pancreatic cells by changing the expression of a single gene. They suggest that the finding is an important step toward showing that reprogramming liver cells might offer a way forward for the treatment of type 1 diabetes in humans.

The team - led by researchers from the Max Delbrck Center for Molecular Medicine in Berlin, Germany - reports the study in the journal Nature Communications.

Diabetes is a chronic disease that develops either when the body cannot make enough insulin, or when it cannot effectively use the insulin that it does make. Insulin is a hormone that regulates blood sugar, or glucose, and it helps to convert glucose from food into energy for cells.

Uncontrolled diabetes leads to high blood sugar, or hyperglycemia, which over time causes serious damage to many parts of the body, including the heart, blood vessels, nerves, eyes, and kidneys.

In the United States, an estimated 29.1 million people have diabetes, including 8.1 million who are undiagnosed.

The most common type of diabetes is type 2, in which the body cannot use insulin effectively. Type 1 diabetes, in which the body does not make enough insulin, accounts for around 5 percent of diabetes cases in adults.

The new study is likely to interest researchers developing treatments for type 1 diabetes. In people with type 1 diabetes, the immune system attacks the insulin-producing beta cells of the pancreas.

Researchers in regenerative medicine are exploring ways to generate new populations of pancreatic beta cells as a possible avenue for the treatment of type 1 diabetes.

Fast facts about type 1 diabetes

Learn more about type 1 diabetes

The new study concerns a method called cell reprogramming, in which it is possible to convert one type of cell into another type of cell, by tweaking genes.

An obvious source of cells for reprogramming into insulin-producing beta cells might be other types of cell in the pancreas.

In their study paper, the researchers mention other research that shows such pancreatic cells display a high degree of the necessary "cellular plasticity."

However, the researchers chose to focus on liver cells because, from a clinical perspective, they offer important advantages over pancreatic cells; for example, they are more accessible and abundant.

They also cite studies that have partially corrected hyperglycemia in diabetic mice by reprogramming liver cells into pancreatic beta cells.

The new study shows how just by changing the expression of a single gene called TGIF2, the team was able to coax mouse liver cells to take on a less specialized state and then stimulate them to develop into cells with pancreatic features.

When the researchers transplanted the modified cells into diabetic mice, the animals' blood sugar levels improved, suggesting the cells were behaving in a way similar to pancreatic beta cells.

The researchers identified TGIF2 (Three-Amino-acid-Loop-Extension homeobox TG-interacting factor 2) by running gene expression profiling tests on immature liver and pancreas cells isolated from mouse embryos as the cells differentiated toward their particular cell fates.

They found that at a particular differentiation branchpoint, the expression of TGIF2 changes in opposite directions as the cells commit to either liver or pancreatic fates.

The authors note that their study shows that "TGIF2 is a developmental regulator of pancreas versus liver fate decision," and when expressed in adult mouse liver cells, it suppresses the transcription program for liver cells and induces a subset of pancreatic genes.

There is still a lot of work to do to investigate whether the results with mice translate to humans. The team has already started working on human liver cells.

"There are differences between mice and humans, which we still have to overcome. But we are well on the path to developing a 'proof of concept' for future therapies."

Senior author Dr. Francesca M. Spagnoli, Max Delbrck Center

Learn how type 1 diabetes kills some insulin-producing cells but not others.

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Type 1 diabetes: Reprogramming liver cells may lead to new treatments - Medical News Today

February 15, 2017 Ebolavirus Protein VP24. Credit: University of Kent

Kent researchers have identified how few mutations it can take for Ebolaviruses to adapt to affect previously resistant species.

Ebola is one of the world's most virulent diseases, though rodent species such as guinea pigs, rats and mice are not normally susceptible to it. However, through repeated infection of a host animal, Ebola virus strains can be generated that replicate and cause disease within new host rodent species.

Scientists in the University of Kent's School of Biosciences examined the changes associated with Ebolavirus adaptation to rodents including guinea pigs and mice across four different studies. They found that only very few mutations, probably fewer than five, are required for the virus to adapt.

In particular, a change in the Ebolavirus protein VP24 seems to be critical for Ebola viruses to infect a new animal species. Ebolaviruses infecting domestic species, including pigs and dogs, may also result in virus changes that may increase the risk to humans. Reston viruses, Ebolaviruses that have not been shown to cause disease in humans, so far, are known to circulate in domestic pigs in Asia.

The research was performed by Dr Mark Wass (Senior Lecturer in Computational Biology), Professor Martin Michaelis (Professor of Molecular Medicine), and Dr Jeremy Rossman (Senior Lecturer in Virology) and members of their research groups.

The research, entitled Changes associated with Ebola virus adaptation to novel species, was published in the journal Bioinformatics.

Explore further: Research shows potential for emergence of new Ebola virus that causes disease in humans

More information: Bioinformatics (2017). DOI: 10.1093/bioinformatics/btx065

Journal reference: Bioinformatics

Provided by: University of Kent

New research at the University of Kent has highlighted the potential for the emergence of a new form of Ebolavirus.

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SAN DIEGO, CA--(Marketwired - Feb 14, 2017) - Invivoscribe Technologies Inc., an international company with decades of experience providing clonality and biomarker test solutions for the fields of oncology, personalized molecular diagnostics and personalized molecular medicine, announces today its long-term collaboration agreement with Illumina Inc., to develop and commercialize in vitro diagnostic (IVD) assays for the next-generation sequencing (NGS) MiSeqDx platform. This agreement allows Invivoscribe to bring IVD assays through the FDA, together with the associated bioinformatics software, for sale and distribution in the US.

Under the terms of the agreement, Invivoscribe will work with Illumina to seek FDA clearance or approval of a number of biomarker and immuno-oncology assay kits for use on the MiSeqDx instrument. Invivoscribe has already developed and commercialized a number of RUO and CE-marked IVD assays for the MiSeq instrument. These assays include a FLT3 mutation assay, a series of B- and T-cell clonality assays used to detect IGH, IGK, and TRG rearrangements, and an IGHV somatic hypermutation assay. A TRB assay kit will be released later this year. All Invivoscribe B- and T-cell clonality RUO assay kits were developed with accompanying design-controlled bioinformatics software, so customers can easily detect and track minimal residual disease (MRD) in a research setting.

Additional tests that have been developed and validated by Invivoscribe include MyAML, MyHEME, and MyMRD gene panels, as well as assays targeting other biomarker mutations. For example, the Invivoscribe FLT3 MRD mutation assay, coupled with its proprietary bioinformatics software, detects and tracks both FLT3 internal tandem duplication (ITD) and tyrosine kinase domain (TKD) mutations in case samples of acute myeloid leukemia (AML) to levels as sensitive as 10-6. A related assay targeting NPM1 is available as a service through Invivoscribe clinical laboratories, LabPMM, to track mutations and residual disease in AML samples.

"This agreement allows us to move forward with the opportunity to offer more than just RUO assays here in the US; it allows us to provide laboratories with internationally-standardized, FDA-approved and -cleared kits that will be of huge benefit to patients and to the field of personalized molecular diagnostics and precision medicine," said Dr. Jeffrey Miller, Founder, CSO & CEO of Invivoscribe. "A number of these assays and associated bioinformatics software have already been validated for use at LabPMM, our CLIA/CAP, ISO 15189 accredited, New York State Licensed laboratory in San Diego. They are currently being used by leading cancer treatment centers to optimize treatment for their patients, and by pharmaceutical partners to stratify, select, and track residual disease in subjects in international phase II and phase III clinical studies. We want to make these powerful tools accessible to all of our partners and customers."

This collaboration agreement is consistent with Invivoscribe's ongoing global initiative to develop and provide standardized molecular diagnostic assays to support precision medicine in the oncology field. Invivoscribe's tests and reagents include a menu of more than 40 CE-marked IVDs for use on a number of capillary electrophoresis and NGS platforms used across the world in 65 countries and in more than 650 clinical and research laboratories. Invivoscribe has long embraced the value of quality systems and develops all products, including bioinformatics software, to be compliant with ISO 13485 design control. The company has companion diagnostics development partnerships with Novartis and Astellas Pharma, Inc., and expects to announce additional collaborations in 2017.

About Invivoscribe Invivoscribe Technologies Inc. is a privately held biotechnology company dedicated to improving the quality of healthcare worldwide by providing high quality, reliable, cutting-edge reagents, tests, and bioinformatics tools to advance the fields of personalized molecular diagnostics and personalized molecular medicine. Invivoscribe provides ISO 13485 certified, cGMP manufactured, PCR- and NGS-based reagents; RUO test kits; CE-marked IVDs, including IdentiClone and LymphoTrack Dx Assays and MyInformatics Software; for clonality, MRD, and somatic hypermutation testing. Invivoscribe's clinical laboratories in the USA, Europe, and Japan provide international access to harmonized CLIA, CAP, and ISO 15189 accredited clinical testing and contract research organization (CRO) services. Additional information can be found at http://www.invivoscribe.com.

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Invivoscribe Announces Long-Term Collaboration Agreement with ... - Yahoo Finance

Estrogen explains the exosome-carried messenger profile in the circulation among postmenopausal women Science Daily ... the Institute of Biomedicine, University of Turku and the Turku Clinical Sequencing Laboratory. In addition, researchers from the University of Oulu and The Finnish Institute for Molecular Medicine were involved. The study has been published in the ...

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Estrogen explains the exosome-carried messenger profile in the circulation among postmenopausal women - Science Daily

Kent researchers have identified how few mutations it can take for Ebolaviruses to adapt to affect previously resistant species.

Ebola is one of the worlds most virulent diseases, though rodent species such as guinea pigs, rats and mice are not normally susceptible to it. However, through repeated infection of a host animal, Ebola virus strains can be generated that replicate and cause disease within new host rodent species.

Scientists in the University of Kents School of Biosciences examined the changes associated with Ebolavirus adaptation to rodents including guinea pigs and mice across four different studies. They found that only very few mutations, probably fewer than five, are required for the virus to adapt.

In particular, a change in the Ebolavirus protein VP24 seems to be critical for Ebola viruses to infect a new animal species. Ebolaviruses infecting domestic species, including pigs and dogs, may also result in virus changes that may increase the risk to humans. Reston viruses, Ebolaviruses that have not been shown to cause disease in humans, so far, are known to circulate in domestic pigs in Asia.

The research was performed by Dr Mark Wass (Senior Lecturer in Computational Biology), Professor Martin Michaelis (Professor of Molecular Medicine), and Dr Jeremy Rossman (Senior Lecturer in Virology) and members of their research groups.

The research, entitled Changes associated with Ebola virus adaptation to novel species, was published in the journal Bioinformatics. See here: https://doi.org/10.1093/bioinformatics/btx065

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Ebolaviruses need very few mutations to cause disease in new host species - Outbreak News Today

Intensive bisphosphonate therapy no better than symptomatic therapy in Pagets disease Healio ... maximally suppress bone turnover in Paget's disease is of no benefit and probably is harmful, Stuart H. Ralston, MD, FRCP, FMedSci, FRSE, professor of rheumatology at the MRC Institute of Genetics and Molecular Medicine at the University of ...

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Intensive bisphosphonate therapy no better than symptomatic therapy in Pagets disease - Healio

Joseph Bass, MD, PhD, is the chief and Charles F. Kettering Professor of Endocrinology in the Department of Medicine at Feinberg.

This story originally appeared in the Breakthroughs Newsletter.

Timing is everything may be an old clich, but for Joseph Bass, MD, PhD, its also a reflection of an emerging discovery in physiology: that the bodys circadian clocks are in fact critical to driving a host of behaviors, processes and pathways including those associated with several diseases and pathologies.

Bass, chief of Endocrinology, Metabolism and Molecular Medicine in the Department of Medicine, focuses his research on illuminating how the bodys clocks regulate feeding behavior and glucose metabolism, and identifies how disruptions in that overarching circadian system play a role in metabolic disease. The goal of the research is to develop a deeper understanding of the clock and its mechanisms, which may eventually lead to novel therapies for widespread disorders like obesity and diabetes.

The field of circadian time has been an area of excellence at Northwestern for more than 20 years, said Bass, also the Charles F. Kettering Professorship of Medicine and a member of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University. What were trying to do now is take advantage of our know-how to identify new pathways and drugs for those pathways that could, for example, augment insulin secretion and improve diabetes.

Its long been known that the body possesses a master circadian clock, located in the brain, in the suprachiasmatic nucleus of the hypothalamus. But it wasnt until more recently, as the field of circadian time rapidly advanced, that it was discovered there are also distinct clocks residing in nearly every cell of the body.

The master clock cued by internal factors and environmental signals like light holds the rhythm across all the bodys peripheral clocks, regulating behavior and biological processes throughout the 24-hour light-dark cycle. But when individual clocks fall out of tune with the master timekeeper, the breakdown in synchronization can contribute to a range of disorders, including diabetes.

My focus has increasingly been drawn toward understanding the perspective of time as a variable in biochemical processes that determine our drive to eat in turn affecting bodyweight and regulate blood sugar control, Bass said.

Bass, who joined Northwestern in 2000, arrived at an opportune time in the history of circadian clock discovery. Seminal work in the late 1990s by Fred Turek, PhD, professor of Neurology and Psychiatry and Behavioral Sciences, and Joseph Takahashi, PhD, a former professor of Neurology, for the first time pinpointed and cloned the genes that drive circadian function in mammals.

There was this intersection of critical developments at Northwestern that really opened the field, Bass said. The collaborative environment then enabled me to join together my background in endocrine, metabolic and medical physiology with these powerful strategies from genetics to try to understand how the clock regulates behaviors and physiologic systems.

In a landmark paper published in Science in 2005, Bass, together with Turek and Takahashi, demonstrated that a misaligned biological clock impaired metabolism, increasing the prevalence of obesity and metabolic syndrome. In the study, mutant mice with a dysfunctional clock gene experienced a 35 percent increase in fat mass compared to wild-type mice.

The paper was the first to provide genetic evidence that the clock system regulates both body weight and glucose metabolism; that was key, said Bass, who is also co-director of the Center for Diabetes and Metabolism and of the Comprehensive Metabolic Core.

Numerous breakthroughs in the metabolism-clock connection followed over the next 15 years of Bass tenure at Northwestern. In Nature in 2010, Bass and his team first reported that beta-cells in the pancreas require a clock in order to produce insulin. In a subsequent study building upon those findings, Bass laboratory, together with co-investigator Grant Barish, MD, used next-generation genome sequencing to pinpoint the precise set of genes in the pancreas that are controlled by the clock transcription factors. The findings were published in Science in 2015.

Joe has really been a leader in establishing a very direct connection between the circadian clock and diabetes, said Barish, assistant professor of Medicine in the Division of Endocrinology, Metabolism, and Molecular Medicine. Particularly in this most recent study, the discovery of the underlying regulatory mechanism by which the circadian clock controls the secretion of insulin the principal hormone responsible for glucose homeostasis really cements a link between the clock and aspects of insulin, diabetes and related physiology.

The anticipation is that such fundamental discoveries may eventually inform the development of novel therapeutics for diabetes and other diseases. While were still very early in this, we know that some features of these circadian transcription factors are targetable and, to some extent, are amenable to pharmacologic manipulation, Barish said.

Bass findings also have applications for the treatment of a wider range of disorders, as the bodys metabolism of drugs is in part influenced by the circadian system, an area of study called chronopharmacology. For example, statins are largely administrated at night because the clock coordinates the synthesis of cholesterol to occur at night. Its likely that this is just the tip of the iceberg, and that there are many other processes targeted with drugs that are controlled by the same clock mechanism, Bass said.

In ongoing research, Bass laboratory is also striving to uncover how the clock helps regulate production of a key molecule called NAD+. The connection was first reported in a pair of papers Bass published in Science in 2009 and 2013, with first author Kathryn Ramsey, PhD, and first author Clara Peek, PhD, respectively, both research assistant professors of Medicine in the Division of Endocrinology, Metabolism, and Molecular Medicine.

NAD+ has been shown to be central to the mechanism that connects life span and aging to nutrition. Were now trying to understand how it is that nutrition and clocks influence aging, and we think one of the ways this comes about is through the control of NAD+, Bass said. He is collaborating with colleagues in chemistry, including Milan Mrksich, PhD, professor of Cell and Molecular Biology, and Navdeep Chandel, PhD, David W. Cugell Professor of Medicine and of Cell and Molecular Biology, to address such questions.

Interactions with other groups at Northwestern have enabled us to make key advances in our understanding of the clock and in how its controlling other physiologic systems, Bass said. Because of the history of discoveries here, were now in a position to be on the ground floor in using genetic approaches to get at questions that have been asked for a long time in a more descriptive way.

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Uncovering Metabolism's Clockwork - Northwestern University NewsCenter

Gene discovery sheds light on growth defects linked to dwarfism Science Daily Professor Andrew Jackson, of the University of Edinburgh's Institute for Genetics and Molecular Medicine, says: 'Identification of DONSON as a microcephaly gene has given us new insights into how the genome is protected during DNA replication, and has ... and more »

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Gene discovery sheds light on growth defects linked to dwarfism - Science Daily

The Qatar University College of Medicine (QU-CMED) focuses on four pillars of medical research molecular medicine, clinical research, medical education and public health, a top official of the university told Gulf Times. One of our main goals is to unite CMED researchers, faculty and students with all departments and stakeholders in Qatar to conduct world-class research in medical health, and contribute to the growing healthcare sector. For this, we have identified molecular medicine, clinical research, medical education and public health as the major areas of research, said Dr Egon Toft, QU vice president for Medical and Health Sciences and CMED founding dean. The Colleges molecular medicine research aims to improve patient care by combining basic research excellence with innovations in clinical practice. The research strategy of the college is to shift to translational medicine in addressing major diseases such as diabetes, cancer, inflammatory, metabolic and neurodegenerative diseases, as well as clinical infections such as enteric pathogens causing diarrhoea, ulcer forming bacteria and several respiratory infections, explained Dr Toft. According to the official, in clinical research, researchers and biomedical scientists from QU Health are working closely with researchers across QU health programmes and from HMC to combine basic research excellence with innovations in clinical practice. Medical education research is another focus for us with a special interest in developing agreed standards of professional competence and ethics, and also the use of technology to enhance learning and teaching especially simulation technology in medical education. In public health research, the college is focusing on five inter-disciplinary themes epidemiological studies on chronic diseases, health promotion and healthy lifestyle, healthcare delivery systems, evidence-based healthcare and health informatics, continued the dean. The official maintained that the college focuses on research in areas of national priority. Our research covers the full translational pathway from basic science to applied health research with the aim to advance the healthcare sector in Qatar. CMEDs research agenda is within the broader university-wide health research strategy, and aligns with both the QU 5-year research roadmap and the National Health Strategy. The college has established partnerships with healthcare providers in Qatar especially those under HMC and PHCC, covering the area of research collaboration and aiming to further contribute to enhancing Qatars health research, he noted. The college has enrolled 93 new students to its Class of 2022 in Fall 2016. This is an increase of 16% of the number of students who enrolled the previous year. At 62%, the majority (58) of the new admits are Qatari nationals. The college has also adopted an interactive and engaging pedagogy, incorporating technology-based learning, which contributes to preparing students for the future and to shaping doctors for tomorrow. The college is also registered in the WHOs international directory for medical schools, this registration strengthens its reputation and credibility, added the official.

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College of Medicine focuses on four areas of research - Gulf Times

Fantastic news for Dubrovnik as the city is set to play host to the largest cathering of Nobel Prize laureates in Europe this summer.

Dubrovnik has recently made quite a name for itself as a congress destination, and with continuing talks about gradually increasing the length of the currently accepted summer season, Dubrovnik's tourism spectrum seems to only grow wider.

As DuList reported on the 10th of February 2017, following the announcement of Tourism Minister Gari Cappelli and prof. dr. Dragan Primorac, that the City of Dubrovnik will proudly host the 10th ISABS Conference on Forensic and Anthropologic Genetics and Mayo Clinic Lectures and Individualised Medicine this summer, from the 19th of June to the 24th of June 2017. The truly exceptional scientific event, which is dedicated to advances in the fields of medicine, forensics and anthropological genetics is expected to gather more than 500 participants from approximately 40 countries.

In addition to lectures from the world's leading experts in the field of clinical and molecular medicine and the field of forensic and anthropological genetics, lectures will be held by no less than five Nobel Prize winners in chemistry and medicine.

''This conference is one of the most important international scientific events in 2017 and I was especially glad for it to be held in Croatia, and in Dubrovnik. Croatia has the potential to become one of the most recognisable destinations for business tourism, and the gathering of such a large number of experts from around the world certainly contributes to that strengthening and recognition. Soon, we will open the conference office as part of the Croatian Tourist Board and I believe that in the future, we will witness many such global events that will make Croatia a more competitive tourist destination'' stated Tourism Minister Gari Cappelli.

Prof. dr. Dragan Primorac echoed Minister Cappelli's remarks, pointing out that the position of Croatia as a state of knowledge in this manner is priceless, and that this year's congress signifies a tremendous step forward for Croatia. It is the largest gathering of Nobel laureates in Europe this year.

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Dubrovnik to Host Largest Group of Nobel Prize Winners in Europe - Total Croatia News

Washington - American and Japanese researchers said on Thursday that they had found a genetic mutation that causes obsessive-compulsive disorder and other mental illnesses and said some patients had a second mutation that made their conditions worse.

The rare finding could make it easier to discover better treatments for the disorder, one of the top 10 leading causes of disability worldwide.

Dr Norio Ozaki of Fujita Health University School of Medicine in Japan and colleagues at several American institutions - including the University of Pittsburgh and Yale University - worked on the study, which was published in the journal Molecular Psychiatry.

The gene is called the human serotonin transporter gene, hSERT, and helps control how the body uses serotonin, a message-carrying chemical or neurotransmitter linked with mood.

Some anxiety drugs and antidepressants target serotonin, but the researchers said patients with the mutations are not helped by these drugs.

"In all of molecular medicine, there are few known instances where two variants within one gene have been found to alter the expression and regulation of the gene in a way that appears associated with symptoms of a disorder," said Dr Dennis Murphy of the National Institute of Mental Health, who worked on the study.

The researchers analysed DNA from 170 people, including 30 patients with obsessive-compulsive disorder (OCD), 30 with eating disorders such as anorexia and 30 with seasonal affective disorder - which can cause depression and other symptoms in dark winter months.

They also looked at the DNA of 80 healthy people.

A specific mutation in the hSERT gene was seen in two patients with OCD and their families, but not in other patients.

With such a rare mutation showing up, the researchers believe it is likely to be found in other families with OCD and related disorders.

They interviewed relatives of the patients and found six of the seven people with the mutation had an obsessive-compulsive disorder, and some also had anorexia, Asperger's syndrome, which is a form of autism, social phobia or were abusers of alcohol.

A second mutation was found in hSERT in two patients, giving them a "double dose." The patients and their siblings had especially difficult to treat versions of OCD, the researchers said.

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You're hardwired to go mad - Independent Online

February 10, 2017

A new study from Karolinska Institutet shows that short-course preoperative radiotherapy combined with delayed surgery reduces the adverse side-effects of rectal cancer surgery without compromising its efficacy. The results are presented in the journal The Lancet Oncology.

Rectal cancer affects some 2,000 men and women in Sweden every year. Preoperative radiotherapy was gradually introduced in the early 1990s, with a consequent improvement in prognosis for people with rectal cancer and reduction in the risk of local recurrence.

"Back then we showed that preoperative radiotherapy reduces the risk of local recurrence by over 50 per cent for patients with rectal cancer," says principal investigator Anna Martling, senior consultant surgeon and professor at Karolinska Institutet's Department of Molecular Medicine and Surgery. "Thanks to our results, radiotherapy is recommended to many rectal cancer patients."

However, radiotherapy can cause adverse reactions and the optimal radiotherapeutic method and the interval between it and the ensuing surgery have been mooted.

The study now presented in The Lancet Oncology is based on the claim that the adverse effects of rectal cancer treatment can be reduced by administering more but lower doses of radiation for a longer time, or by increasing the interval between radiotherapy and surgery. These hypotheses have now been tested in a study in which rectal cancer patients were randomly assigned to three different treatment arms:

The results of the study show that patients with delayed surgery develop fewer complications with equally good oncological outcomes. It also showed that there is no difference between long-course and short-course radiotherapy other than that the former considerably lengthens the time for treatment.

"The results of the study will give rise to improved therapeutic strategies, fewer complications with a sustained low incidence of local recurrence, and better survival rates for rectal cancer patients," says Professor Martling. "The results can now be immediately put to clinical use to the considerable benefit of the patients."

Explore further: Specialists make breakthrough for bowel cancer patients

More information: Johan Erlandsson et al. Optimal fractionation of preoperative radiotherapy and timing to surgery for rectal cancer (Stockholm III): a multicentre, randomised, non-blinded, phase 3, non-inferiority trial, The Lancet Oncology (2017). DOI: 10.1016/S1470-2045(17)30086-4

Specialists at The Christie and The University of Manchester have made a breakthrough which will spare patients with cancer of the lower bowel, rectal cancer, from major surgery.

(HealthDay)There are no statistically significant differences in the rates of local recurrence (LR), distant recurrence, relapse-free survival, overall survival, or late toxicity in patients treated with short-course (SC) ...

Appearing in Lancet Oncology, long term results of EORTC trial 22921 with 10.4 years median follow-up show that 5-FU (fluorouracil) based adjuvant chemotherapy after preoperative (chemo)-radiotherapy for patients with cT3-resectable ...

Some older women with breast cancer could safely avoid radiotherapy, without harming their chances of survival, a study has shown.

(HealthDay)Patients with localized rectal cancer may achieve similar survival rates by having minimally invasive laparoscopic surgery, instead of more invasive open surgery, according to new research published in the April ...

A drug first designed to prevent cancer cells from multiplying has a second effect: it switches immune cells that turn down the body's attack on tumors back into the kind that amplify it. This is the finding of a study led ...

Colorectal carcinomas arise in different forms, so all treatments do not work for all patients. OncoTrack, a public-private consortium supported by the Innovative Medicines Initiative Joint Undertaking, has conducted one ...

(Medical Xpress)A team of researchers affiliated with multiple institutions in Korea has found that genetically altering a type of bacteria and injecting it into cancerous mice resulted in the disappearance of tumors in ...

Researchers have identified a gatekeeper protein that prevents pancreatic cancer cells from transitioning into a particularly aggressive cell type and also found therapies capable of thwarting those cells when the gatekeeper ...

A single blood test and basic information about a patient's medical status can indicate which patients with myelodysplastic syndrome (MDS) are likely to benefit from a stem cell transplant, and the intensity of pre-transplant ...

Studies abound that point to a role for plain old aspirin in keeping deadly cancers at bay. While aspirin is not yet part of mainstream treatment for any cancer, it is recommended by the U.S. Preventive Services Task Force ...

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New method reduces adverse effects of rectal cancer treatment - Medical Xpress

CAMBRIDGE, Mass.--(BUSINESS WIRE)--

Foundation Medicine, Inc. (FMI) today announced that financial results for the company's fourth quarter and year ended December 31, 2016 will be released on Wednesday, February 22, 2017. The management team will host a conference call on Wednesday, February 22, 2017, at 4:30 p.m. ET to discuss the company's financial results and recent developments. The call can be accessed by dialing 1-855-420-0652 (domestic) or 1-484-365-2939 (international) five minutes prior to the start of the call and providing the passcode 61272791.

The live, listen-only webcast of the conference call may be accessed by visiting the investors section of the company's website at investors.foundationmedicine.com. A replay of the webcast will be available shortly after the conclusion of the call and will be archived on the company's website for two weeks following the call.

About Foundation Medicine Foundation Medicine (FMI) is a molecular information company dedicated to a transformation in cancer care in which treatment is informed by a deep understanding of the genomic changes that contribute to each patients unique cancer. The company offers a full suite of comprehensive genomic profiling assays to identify the molecular alterations in a patients cancer and match them with relevant targeted therapies, immunotherapies and clinical trials. Foundation Medicine's molecular information platform aims to improve day-to-day care for patients by serving the needs of clinicians, academic researchers and drug developers to help advance the science of molecular medicine in cancer. For more information, please visit http://www.FoundationMedicine.com or follow Foundation Medicine on Twitter (@FoundationATCG).

Foundation Medicineis a registered trademark of Foundation Medicine, Inc.

View source version on businesswire.com: http://www.businesswire.com/news/home/20170206005255/en/

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Foundation Medicine Announces Timing for Fourth Quarter and ... - Yahoo Finance

New method reduces adverse effects of rectal cancer treatment ... Science Daily Short-course preoperative radiotherapy combined with delayed surgery reduces the adverse side-effects of rectal cancer surgery without compromising its ... and more »

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New method reduces adverse effects of rectal cancer treatment ... - Science Daily

High TMAO level predicts CV events in patients with ACS Healio ... a nutrient found in meat and eggs, is known to predict incident CV event risk in stable patients, but its effect on patients with ACS was unknown, Stanley L. Hazen, MD, PhD, chair of the department of cellular and molecular medicine in the Lerner ...

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High TMAO level predicts CV events in patients with ACS - Healio

This weeks features include: Genetic and epigenetic diversity in cancer; epigenetics is the new buzzword in beauty; and the long-lasting impact of chemotherapy.

Im not suggesting that you shouldnt use chemo. In fact, I would suggest that you probably should use the chemo. Im just saying that there are some preventative things that may need to be put in place before you use the chemo if possible.

Michael Skinner, a professor in the WSU School of Biological Sciences and Center for Reproductive Biology

Genetic mutations are a root cause of cancer. But your cells dont just pick up a mutation and turncancerous. In fact, a cell can rack up numerous mutations and not pose adanger. There is no set number of mutations that must be registered, but ratherthe trigger point depends on what genes are affected and in what cell type (among other factors). From person to person, tumors can show a wide range of genetic diversity, even among people with the same affected tissue type and stage.

Overall childhood cancers seem to have a much lower level of genetic diversity, puzzling researchers. One example is Ewing sarcoma (EWS), a bone cancer found mainly in teenagers. Asingle genetic defectthe EWS-ETS fusiondefines most tumors, and overall they are similar genetically, which is perplexing because progression and prognosis can vary drastically from patient to patient. A recent study, published inNature Medicine,found that EWS tumors have a striking level of epigenetic diversity, which may explain theses observed differences.

Researchers at CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences found that EWS tumors have a striking amount of hypomethylation (a process that generally leads to the product of a gene, generally a protein, being produced in an excessive amount) on the disease-defining genetic defect. Furthermore, patients with metastatic EWS show even more alterations in methylation. This finding could help physicians identify which patients are at risk for poorer outcomes.

Maybe shes born with it, maybe itsMaybellineor maybe its epigenetics? Thecosmetics industry is beset by faddish claims that various products and tests can help make your skin younger and restore itsnatural tautness by harnessing the power of epigenetics. One company, Mibellebiochemistry group, claims that a protein calledroyalactin, derived from bees, can induce epigenetic changes in human skin cells that accelerate epidermal regeneration for smoother skin, activates the cellular cleaning process and reveals a more evenly toned skin. Another, Geneu,says they can make a customized serum by looking at your unique epigenetic and genetic profile that will enhance your skins beauty.

Thescience behind these claims is shaky at best. Epigenetic changes are made onto DNA and change the activity of certain genes. But skin cells dont have active DNA. They slowly fill up with keratin, lose their DNA and die. So a cream thattargets geneexpression in the skin is highly unlikely to affect your skins age. Unless you grow crows feet from worrying about your bank account as one of Genus tests can run you $2,200.

Chemotherapy is not perfect. Anyone who has gone through it can tell you it is a miserable process. There are a number of adverse effects that can be severely debilitating: Nausea, fatigue, pain, GI distress, hair loss, vomiting, fever, chills and rashes, and the list goes on. Most of these side effects are short-lived and if the drugs works, the results are pretty fantastic.

But for a number of chemical critics, these adverse demonstratea far-reaching conspiracy by the pharmaceutical industry to keep us sick so they can bleed us of every last dime. (I wont link to any activist sites, but the links are easy to find.)

These baseless and outrageous claims cloud chemotherapy and make it difficult for doctors and scientists to seriously discussions with patients its long-lasting impact for fear a patient will elect an alternative (and ineffective) treatment.

A recent study published inPLOS Oneby Washington State University epigeneticist Michael Skinner highlights this struggle. Skinner found that chemotherapy changed methylation patterns in the sperm of men, which could affect gene expression during any of theiroffsprings development. The study is backed up by previous research onrodents, and Skinner saidhis results are very reproducible. But hismain concern seems to be how his findings might be misrepresentedby activists:

Im not suggesting that you shouldnt use chemo. In fact, I would suggest that you probably should use the chemo. Im just saying that there are some preventative things that may need to be put in place before you use the chemo if possible.

If alterations on the genomes of sperm are found to affect a mans children, it is not proof of a conspiracy by industry to harm patients; nor is it a reason not to undergo chemotherapy. Theymerely indicate that young males with cancer may need to discuss with their physicians about taking precautionary steps to ensure that, after they receive this life-saving medicine, they can still have a healthy family. One example would befreezing their sperm before receiving their first round of treatment.

This weekly roundup of the latest studies and news in the field of epigenetics originated on our GLP sister site, the Epigenetics Literacy Project

Nicholas Staropoli is thedirector of the Epigenetics Literacy Project.He has an M.A. in biology from DePaul University and a B.S. in biomedical sciences from Marist College. Follow him on Twitter@NickfrmBoston.

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Epigenetics Around the Web: Chemo affects sperm? Cancer causes. Younger looking skin? - Genetic Literacy Project

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The Medical College of Wisconsin (MCW) appointed Raul A. Urrutia as director of the Human and Molecular Genetics Center and professor of the Department of Surgery, effective July 1.

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Wauwatosa 4:17 p.m. CT Feb. 9, 2017

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The Medical College of Wisconsin (MCW) appointed Raul A. Urrutia as director of the Human and Molecular Genetics Center and professor of the Department of Surgery, effective July 1.

Urrutia currently serves as professor in the departments of biochemistry and molecular biology, biophysics and medicine at the Mayo Clinic College of Medicine in Rochester, Minnesotaand director of epigenomics education and academic relationships in the epigenomics program, Mayo Clinic Center for Individualized Medicine.

Urrutia will relocatefrom Rochester, Minnesota, with his wifeGwen Lomberk, who will serve as associate professor, chief of the division of research, and director of basic research in the MCW Department of Surgery.

Read or Share this story: http://www.wauwatosanow.com/story/news/local/2017/02/09/medical-college-wisconsin-names-director-human-and-molecular-genetics-center/97714872/

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Medical College of Wisconsin names director of Human and Molecular Genetics Center - Wauwatosa Now

WINDBER An international cancer research effort involving the Windber hospital and research center has been renamed to reduce confusion and better reflect its success, its founder announced.

We are renaming and branding Cancer MoonShot 2020 to Cancer Breakthroughs 2020, a name that elevates the importance and progress of our work to what it truly is breakthroughs, Dr. Patrick Soon-Shiong said in a press release.

Soon-Shiongs nonprofit, Chan Soon-Shiong NantHealth Foundation, is the parent of Chan Soon-Shiong Medical Center at Windber and Chan Soon-Shiong Institute of Molecular Medicine at Windber.

Both are participating in the Cancer Breakthroughs 2020 collaboration of research organizations, hospitals and businesses.

We are extremely proud to play a role in Cancer Breakthroughs 2020, said Tom Kurtz, president and CEO of both Windber facilities.

The name is an accurate description of this action-oriented initiative.

The change will address confusion with other cancer moonshot programs Soon-Shiong said.

It may also help settle a lawsuit filed by the University of Texas MD Anderson Cancer Center, which has been using the Cancer Moon Shotstagline since 2012, the federal lawsuit says.

In addition to the MD Anderson Moon Shots, the federal government has its ownCancer Moonshot.

Two days after Soon-Shiong unveiled his former Cancer MoonShot 2020 in January 2016, then-President Barack Obamacredited his vice president, Joe Biden, with suggesting with a new moonshot, America can cure cancer.

In his State of the Union Address, Obama went on to announce a national Cancer Moonshot effort, putting Biden in charge of Mission Control.

Windbers research program is involved in the national Cancer Moonshot through its partnership with Walter Reed National Military Medical Centers John Murtha Cancer Center in Bethesda, Maryland.

Soon-Shiong says the Cancer Breakthroughs 2020 name is more appropriate.

With recent discoveries in molecular science and rapid advancements in supercomputing technology, we are now on the path that will forever change the way cancer is diagnosed and treated, he said in a press release.

It is no longer a dream no longer just an aspiration. It is the forging of real breakthroughs, long overdue in the fight against cancer, that are giving millions hope that will subdue cancer by harnessing the most powerful defense against this deadly disease ones own immune system.

Randy Griffith is a multimedia reporter for The Tribune-Democrat. He can be reached at 532-5057. Follow him on Twitter@PhotoGriffer57.

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Cancer Breakthroughs 2020: Soon-Shiong's research program gets new name - TribDem.com

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ust under a year ago, Veritas Genetics announced it would be launching the firstwhole genome sequencing test with a price tag under $1,000. Now, the company isbringing on board a new vice president of clinical affairs to help lower the cost of that sequencing and improve the process of interpreting the results.

Birgit Funke has worked extensively on the genetic underpinnings of inherited heart diseases, including cardiomyopathies, and has also written about the racial disparities in genetic testing and research. As of February 1, Funke hassplit her time between theDanvers, Mass.-based spinoff of the non-profit Personal Genome Project and her work as an associate professor at Harvard Medical School and a researcher at Partners Personalized Medicines Laboratory of Molecular Medicine.

This is a STAT Plus article and is only available to STAT Plus subscribers. To read the full story, subscribe to STAT Plus or log in to your account. Good news: your first 30 days are on us.

Kate Sheridan can be reached at kate.sheridan@statnews.com Follow Kate on Twitter @sheridan_kate

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Startup Spotlight: Seeking to improve the $999 genome for consumers - STAT

According to a UNM Health Sciences Centerrelease,Tudor Oprea, a professor of Internal Medicine and chief of UNMs Translational Informatics Division, and a teamcollaborators, have pulled back the curtain onan open-source archive for drug discovery, development and safety that is 20 years in the making.

According to the release, the group recently published their work in the journal "Nature Reviews Drug Discovery."

This is a landmark paper, David Schade, a distinguished professor in the UNM School of Medicine who oversees clinical research in the Department of Internal Medicine, was quoted as saying in the release. Diseases that were not treatable 10 years ago are now treatable thats because of new medications that have been developed and approved by the Food and Drug Administration.

While new drugs have saved lives, they can also complicate treatment. According to the release,doctors often use a combination of drugs to treat diabetes, for example, but they must make sure those drugs compliment one another and no dangerous side appear when combined.

What we want to do, Schade is quoted as saying in the release, is hit multiple targets that are causing the disease.

According to the release, Opreas archive will help doctors to do just that. Olivier Rixe, who oversees all clinical research at the UNM Comprehensive Cancer Center, agrees and plans to use Opreas archive to speed the process of drug discovery and development.

Oprea, now a professor at thecenter, started the drug database 20 years ago when he was a drug developer, according to the release. He archived drug targetsmolecules that drugs act on to make the cell change its behaviorlater expanded his list to include properties of the drugs themselves along with any information about how they acted on their targets.

According to the release, in order to develop the information, Oprea and his international collaborators had to mine data from all over the world, then correctly map the drugs molecular structures and search for data on the diseases the drugs helped to treat.

They collected data on the drugs effects on humans and animals and listed what scientists had learned about how the drugs reacted with the proteins in cells, according to the release.

In total, they cataloged 893 drug targets linked to their mode of action, a term that describes how drugs exert their therapeutic effect at the molecular level, along with 1,578 drugs approved by the FDA.

According to the release, the information is now publicly available through DrugCentral, a system that Opreas research team at UNM developed. DrugCentral resides at UNM and Oprea is building his team to be experts in drug discovery.

This type of expertise is rare, Oprea is quoted as saying in the release. We are one of the teams that has it.

Matthew Reisen is the news editor at theDaily Lobo. He can bereached at news@dailylobo.com or on Twitter @MReisen88.

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New archive developed by UNM doctor to advance precision medicine and drug development - UNM Daily Lobo