Category Archives: Gene Medicine

Researchers strive to address societal health issues through gene editing

In October, three researchers at UC Davis were awarded a $1.5 million grant to fund their project which attempts to demonstrate the effectiveness of gene editing through use of CRISPR, a powerful technology that allows alteration of DNA sequences to change gene function.

This kind of design can help enhance personalized medicine, said R. Holland Cheng, a professor of molecular and cellular biology in the College of Biological Sciences. Specific patients with specific illnesses can be treated in specific ways.

Cheng, along with Kit Lam, a distinguished professor and chair of the Department of Biochemistry and Molecular Medicine in the School of Medicine, and David Segal, a professor in the Department of Biochemistry and Molecular Medicine, were awarded this highly competitive and sought-after grant from the National Institute of Health (NIH).

UC Davis is part of the NIHs Somatic Cell Genome Editing (SCGE) consortium which has awarded grants to 45 other research institutes across the nation so they can begin groundbreaking work on gene editing. Through this consortium, the NIH hopes to find an efficient and safe way to conduct gene editing. Research programs are investigating the best delivery mechanism as well as the most dynamic gene editing tool.

The major problem with gene editing currently is the inability of cells to be edited within a living organism. It has become fairly easy and efficient to edit genes in a cell culture outside of the body but extremely difficult to do the same processes inside the body. Cheng, Lam and Segal are focused on changing this.

The question is how to do it inside of an animal and eventually a human, Lam said.

They are answering this question by utilizing Chengs work in engineering a non-toxic nanoparticle that they hope can transport the gene editing tool CRISPR into the cells of a living organism. Cheng has been able to create a Hepatitis E viral nanoparticle (HEVNP) that when manipulated could be a delivery system for CRISPR. They plan to take this nanoparticle and encase CRISPR inside of it, producing a mechanism for delivery of CRISPR.

The Hepatitis E nanoparticle has the capacity to be a highly efficient way to deliver gene editing to cells in the body due to its unique nature. HEVNP is resistant to the gastric acid environment of the intestines and stomach, enabling it to survive once its entered the body. Given its resistant abilities, HEVNP can be taken orally, making it a useful form of medicine. If able to successfully get HEVNP to the target cells in the body and deploy CRISPR, gene editing abilities could drastically change.

The addition of a cell-type specific targeting ligand to the HEVNP would code the nanoparticle to deliver CRISPR to a specific cell. The abilities of this method to be precise and safe will determine its success.

With five years of funding from the NIH, these three researchers are eager to begin work on this project and see the strides that can be made in gene editing. They have impressive goals for this research, as it has the capacity to reshape medicine.

This will redefine precision medicine as currently there is broad medicine that can cause side effects to people and not be effective, yet by making it specialized it is becoming more precise and effective, Cheng said.

As more effective and safe tools to cure illnesses are being tested and created, the benefits to society could be expansive. With so much potential to help improve the health of society, the NIH is dedicated to coming to new solutions at a quick rate. All programs that received grants will be required to share and utilize the research occurring at other funded programs. The NIH is hoping to eliminate the private nature of research through enforcing the sharing of ideas, as scientists are often constrained by the institutions they work for. It is their hope that by having communication between the programs, positive results will arise faster.

I think this is great because scientists inherently want to work with each other but have real world concerns especially with money, Segal said.

The research results, when groundbreaking, can provide incredible monetary gains and credibility to the institutions that made the discovery. Ultimately, scientists collaborating with one another will serve society as people are able to benefit earlier from this innovative research.

We want the public to know that we are working in their best interest, Segal said.

The NIH grant is competitive and still the third research program to join the consortium at UC Davis. Innovation has never been more prevalent than in this field at UC Davis. With three different programs researching gene editing, UC Davis stands out as a hotspot for this field of research.

Written by: Alma Meckler-Pacheco science@theaggie.org

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UC Davis leads in innovative gene editing research with NIH grants - The Aggie

Serendipity, love, change. These are just some of the forces that brought Weining Lu first to Boston, and then to Boston University, where he and members of his lab collaborated with Pfizer to develop a potential new drug that could offer new hope to the hundreds of millions of people around the world struggling with chronic kidney disease.

Academia and industry scientists working togetherthats a completely different research model than being funded by the National Institutes of Health or a foundation grant, says Lu, BU School of Medicine associate professor of medicine.

Lus hypothesis that a gene called ROBO2 could play a key role in moderating kidney function earned him an opportunity to collaborate with and receive funding from Pfizers Centers for Therapeutic Innovation (CTI) in November 2012, the first BU faculty member to do so. Now, with a promising new compound borne from the research collaboration in phase 2 clinical trials, Lu has been named BUs Innovator of the Year, an award bestowed annually on a faculty member who translates his/her world-class research into inventions and innovations that benefit humankind.

Translating basic research into real-world products, especially in the medical domain, is exceptionally difficult and not an area that many of our faculty are engaged in, says Gloria Waters, BU vice president and associate provost for research. It is very exciting to see one of our faculty members working to translate their basic research into a potential therapeutic that could have a tremendous impact on patients.

The novel drug candidate has made it through a phase 1 clinical trial and is currently in a phase 2 clinical trial.

Dr. Lus creativity and drive has made a [successful collaboration] with Pfizer that could serve as a blueprint for future [joint research programs] with biopharma, David Salant, BU School of Medicine vice-chair of research and professor of medicine, said in his letter nominating Lu for the award.

Lus path toward becoming a BU faculty member and developing a promising new kidney disease drug was full of obstacles. Born in China, Lu says hes fortunate that Chinas Cultural Revolution ended by the time he was 10 years old. Otherwise, [I] likely would have become a member of Chinas lost generationpeople who forewent the opportunity to attend university as most of Chinas institutions of higher education were closed during the [revolution].

At Zhejiang University, Lu earned a medical degree and then went on to complete his residency. I had a good life over there, he says. Lu was working as a hospital clinician until he discovered that a Chinese regulation called Hukou would prevent him from living with his future wife, whom he had met at medical school. Today its better, people in China have much more freedom. But then, this household registration system was in place, Lu says. It was difficult to move freely from one city to another.

Lu found himself at a crossroad. His brother, who had decided to move to the United States to pursue a new life, had immigrated to Boston, where hes the chief acupuncturist at Dana Farber Cancer Institute. Similarly, Lu and his wife thought, why not just go to Boston to start a new life, too?

And so they did. After moving to Boston, Lu was pursuing a PhD at Northeastern University when he was surprised one day to be invited to interview for a research position in the division of nephrology at Brigham and Womens Hospital. Id never applied for any position, though, Lu says. My wife, who was planning to have our first child, had submitted the application for me. And thats how I got into kidney research.

The job change turned out to be a catalyst for his path to BU. Serendipity is a fundamental part of scientific discovery, Lu says. After 10 years doing kidney and genetics-related research at Brigham, BU invited Lu to establish his own lab on the Boston University Medical Campus.

In my lab, we study patients with genetic defects related to their kidney and urinary tracts, Lu says. In his research, he noticed something special about the gene ROBO2 as it relates to a kidneys filtering ability. The observation led to a research collaboration with Pfizer, focused on ROBO2 as a potential drug target. ROBO2 is highly expressed in the developing kidney and urinary tract. We thought that lacking this protein or gene would cause kidney and urinary defects at birth and also adult kidney disease, so we studied this for several years. But our initial hypothesis was wrong, which was okay. Instead, we found that if you block or delete ROBO2 after birth, it could potentially help kidney function.

Although he wanted to publish the results of his findings, Lu took a gamble and held off in order to protect any potential patent rights that could be jeopardized by public disclosure. Over the course of seven years working in collaboration with Pfizer, Lu says hes experienced many challenges. Theres a different culture between academia and industry. The reward systems are completely different, and the habits and behaviors we have are different. In academia, to be promoted you need to stay funded and produce high-impact publications and grant funding.

In contrast, Pfizer says its focused on developing a molecule that can ultimately be translated into a potential therapy.

Deciding to take a chance on a non-traditional research route in collaboration with industry, which works at a different pace, plays by a different set of rules, and communicates progress in a different waythats a really hard choice for an academic researcher to make, says Michael Pratt, BU managing director of technology development. But it really accelerated the project. Lu took a risk and it paid off with the science.

Weining was focused on birth defects of urinary tract and kidney, but he followed the data he was getting [in the lab]. He said, I think I have a potential drug target for adults with kidney disease. So he changed his way of thinking, which is what being innovative is all about, says Steve Berasi, a senior director at Pfizer CTI whos been working with Lu since he first proposed collaborating on ROBO2.

Lu says it helps to keep the end goal in mind. In the case of ROBO2, it could be a significant game changer for the 37 million people in the US and 850 million people worldwide with chronic kidney disease.

Says Lu: I would say to persist and believe in your science.

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Weining Lu, Kidney Researcher, Named BU Innovator of the Year - BU Today

Its hard to watch a loved one get sick. Their eyes go glassy. Their breathing is punctuated by body-wracking coughs. Feverish and aching, they struggle to get out of bed.

Hard as these symptoms are to witness, theyre so familiar you dont need a medical degree to know its probably a bad cold and maybe the flu. Get some rest, hydrate, pop some ibuprofen, see a doctor if the symptoms significantly worsenand wash your hands, for heavens sake.

For most of history, however, even the finest physicians only slowly advanced beyond the basics of biology and medicine we take for granted. There have long been forms of diagnosis, treatment, and prevention, but these were rudimentary at best and superstitious at worst.

The history of innovation is not that excitinguntil you get to the 20th century, Jane Metcalfe, cofounder of Wired and founder of Neo.Life, told the audience at Singularity Universitys Exponential Medicine in San Diego this week.

Since then, biology and medicine have been on a tear, Metcalfe said. Early last century, doctors mastered blood transfusions and complex surgeries. They began controlling and eradicating infectious disease with sterilization, antibiotics, and vaccines and found drugs to manage pain.

Then, around the middle of the century, scientists began amassing a deep body of biological knowledgeknowledge were now using to manipulate the fundamental processes of living things.

Its a familiar story, but one that suggests something radical. Just as physics and chemistry have given humans power over the world of the inanimate, biology is giving us the ability to engineer living systems, from viruses and bacteria to animals and people.

Which is why Metcalfe thinks design could be the next big thing in medicine.

Well combat disease and improve human health by designing biological systems from the ground up. We can design embryos. We can edit genes in humans. We have synthetic biology. And so we really are looking at designing future humans, Metcalfe said.

The best known bio-design tool to date is undoubtedly CRISPR genome editing. With CRISPR, scientists are closer than ever to manipulating genes down to the letter.

There are now a number of increasingly refined CRISPR-based systems, the latest of which, CRISPR prime editing, has been described as a word processor for gene editing. Meanwhile, the first approved gene therapies are making their way (at times painfully) into cancer treatment.

Just last year, Metcalfe said, the world was shocked to learn a scientist in China, Dr. He Jiankui, had used CRISPR to edit human embryos and confer immunity to HIV (and potentially other unintended traits in the process). He went even further by implanting the embryos, and the first genetically modified babies were born in China in 2018. Hes work was universally condemned by the scientific community as sloppy and unethical. Yet, another scientist, this time in Russia, has since made public his intentions to use CRISPR to edit human embryos too.

The ethics quite clearly havent caught up to the science, and the tools themselves are still being sharpened, but its likely only a matter of time before scientists, researchers, and doctors begin more responsibly snipping out disease-causing genes and, perhaps, even splicing in beneficial ones.

George Church is anticipating that day.

George is probably the most prolific bioengineer of our time, Metcalfe said. [There] are fifty different alleles that hes tracking that are beneficial to humans. These variants include genes that help protect against cardiovascular disease and Alzheimers disease. Others may improve memory and learning and extend your telomeres.

But our design abilities wont be limited to existing genes, Metcalfe said. Scientists are assembling entirely new synthetic biological systems from scratch too.

Were writing DNA codeand weve been doing this for a whilebut were starting to get good at it, said Andrew Hessel, Humane Genomics CEO and nanotechnology/biotechnology faculty at Singularity University, in a talk following Metcalfes.

Hessel pointed to Twist Bioscience a synthetic biology company that went public in late 2018. Twist manufactures short custom sequences of DNA (oligos) at scale. Customers can design and order sequences and have them delivered by Fedex. With tools like this, synthetic biologists have begun creating synthetic enzymes and proteins, some of which have even proven themselves functionallike their natural siblingsin bacteria.

Scientists are thinking bigger too.

Craig Venter, already famed for his work sequencing the first human genome, announced the first reproducing synthetic bacteria back in 2010. He followed up with a streamlined minimal synthetic cell in 2016. Boasting the smallest known genome, it has no natural counterpart. Then this year, another group announced theyd made synthetic E. coli bacteria with a four million base-pair genomefour times longer than Venters 2010 achievementand using just 61 codons instead of 64. Currently, scientists are working with yeast to make the first synthetic eukaryotic cells.

The ultimate goal is writing whole human genomes from scratch, and Hessel cofounded Genome Project-write (GP-write) to convene the worlds top synthetic biologists to do just that.

There are obviously big hurdles that still need clearingincluding software that can make design more accurate and efficient and DNA synthesis tools that assemble longer base-pair sequencesand Hessels group recently published a paper outlining the challenges. Nonetheless, Hessel said the group doesnt think any of these will take more than a decade to solve.

Literally in 10 years weve gone from making proteins synthetically to making a eukaryote, he said. As soon as we can start making whole chromosomes, well, weve only got 23 of them. Its not going to take very long until you end up bumping up against the human genome.

The pace of change in biology and medicine has been swift, Metcalfe said.

Researchers discovered DNAs structure in 1953, the first IVF baby was born in 1978, and we met Dolly the sheep, the first cloned animal, in 1996.

In just the last two decades, scientists went from sequencing the human genome at great cost and effort to sequencing it for under $1,000 in a day. Now there are an estimated million-plus complete human genomes on the books.

Weve graduated from complex and costly gene editing tools to tools that can be sold in a kit for a few hundred bucks. Scientists are building genomes from scratch and booting them up.

The question is no longer whether well be able to design our own biologythe tools are already herethe question is can we handle the responsibility?

This technology is going to touch every business, every sector, every government, every person, Hessel said. This isnt a presentation for now, its the start of a conversation with all of you for the future.

Image Credit:gustavo centurion /Unsplash

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Why Designing Our Own Biology Will Be the Next Big Thing in Medicine - Singularity Hub

If certain vegetables have always made you gag, you may be more than a picky eater. Instead, you might be what scientists call a super-taster: a person with a genetic predisposition to taste food differently.

Unfortunately, being a super-taster doesnt make everything taste better. In fact, it can do the opposite.

Super-tasters are extremely sensitive to bitterness, a common characteristic of many dark green, leafy veggies such as broccoli, cauliflower, cabbage and Brussels sprouts, to name a few.

The person who has that genetic propensity gets more of the sulfur flavor of, say, Brussels sprouts, especially if theyve been overcooked, said University of Connecticut professor Valerie Duffy, an expert in the study of food taste, preference and consumption.

So that [bitter] vegetable is disliked, and because people generalize, soon all vegetables are disliked, Duffy said. If you ask people, Do you like vegetables? They dont usually say, Oh yeah, I dont like this, but I like these others. People tend to either like vegetables or not.

In fact, people with the bitter gene are2.6 times more likely to eat fewer vegetables than people who donot have that gene, according to a new study presented Monday at the annual meeting of the American Heart Association.

We wanted to know if genetics affected the ability of people who need to eat heart-healthy foods from eating them, said study author Jennifer Smith, a registered nurse who is a postdoc in cardiovascular science at the University of Kentucky School of Medicine.

While we didnt see results in gene type for sodium, sugar or saturated fat, we did see a difference in vegetables, Smith said, adding that people with the gene tasted a ruin-your-day level of bitterness.

Our sense of taste relies on much more than a gene or two. Receptors on our taste buds are primed to respond to five basic flavors: salty, sweet, sour, bitter and umami, which is a savory flavor created by an amino acid called glutamate (think of mushrooms, soy sauce, broth and aged cheeses).

But its also smelling through the mouth and the touch, texture and temperature of the food, Duffy said. Its very difficult to separate out taste from the rest. So when any of us say the food tastes good, its a composite sensation that were reacting to.

Even our saliva can enter the mix, creating unique ways to experience food.

When we come to the table, we dont perceive the food flavor or the taste of food equally, Duffy said. Some people live in a pastel food world versus others who might live in a more vibrant, neon food world. It could explain some of the differences in our food preference.

While there are more than 25 different taste receptors in our mouth, one in particular has been highly researched: the TAS2R38, which has two variants called AVI and PAV.

About 50% of us inherit one of each, and while we can taste bitter and sweet, we are not especially sensitive to bitter foods.

Another 25% of us are called non-tasters because we received two copies of AVI. Non-tasters arent at all sensitive to bitterness; in fact food might actually be perceived as a bit sweeter.

The last 25% of us have two copies of PAV, which creates the extreme sensitivity to the bitterness some plants develop to keep animals from eating them.

When it comes to bitterness in the veggie family, the worst offenders tend to be cruciferous vegetables, such as broccoli, kale, bok choy, arugula, watercress, collards and cauliflower.

Thats too bad, because they are also full of fiber, low in calories and are nutrient powerhouses. Theyre packed with vitamins A and C and whats called phytonutrients, which are compounds that may help to lower inflammation.

Rejecting cruciferous or any type of vegetable is a problem for the growing waistline and health of America.

As we age as a population, vegetables are very important for helping us maintain our weight, providing all those wonderful nutrients to help us maintain our immune system and lower inflammation to prevent cancer, heart disease and more, Duffy said.

Food scientists are trying to develop ways to reduce the bitterness in veggies, in the hopes we can keep another generation of super-tasters from rejecting vegetables.

Theres been some success. In fact, the Brussels sprouts we eat today are much sweeter than those our parents or grandparents ate. Dutch growers in the 90s searched their seed archives for older, less bitter varieties, then cross-pollinated them with todays higher yielding varieties.

People who already reject vegetables might try to use various cooking methods that can mask the bitter taste.

Just because somebody carries the two copies of the bitter gene doesnt mean that they cant enjoy vegetables, Duffy said. Cooking techniques such as adding a little fat, a little bit of sweetness, strong flavors like garlic or roasting them in the oven, which brings out natural sweetness, can all enhance the overall flavor or taste of the vegetable and block the bitterness.

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Your hatred of heart-healthy veggies could be genetic - WPMT FOX 43

Amended Celgene collaboration to focus on engineered alpha-beta T cell medicines with a $70 million payment to Editas Medicine

Appointed Judith R. Abrams, M.D., as Chief Medical Officer

EDIT-101 (AGN-151587) for LCA10 first patient dosing expected by early 2020

EDIT-301 for hemoglobinopathies in vivo pre-clinical data to be presented at ASH

CAMBRIDGE, Mass., Nov. 12, 2019 (GLOBE NEWSWIRE) -- Editas Medicine, Inc. (Nasdaq: EDIT), a leading genome editing company, today reported business highlights and financial results for the third quarter of 2019.

"Our momentum in 2019 remains strong in advancing our pipeline of in vivo CRISPR and engineered cell medicines," said Cynthia Collins, Chief Executive Officer of Editas Medicine. We announced this morning an amended agreement with Celgene to further expand and accelerate our oncology pipeline. In hemoglobinopathies, we look forward to presenting in vivo pre-clinical data for EDIT-301 at ASH that supports its potential as a best-in-class medicine. Finally, we eagerly anticipate first patient dosing with EDIT-101 for LCA10 in the coming months.

Recent Achievements and OutlookIn VivoCRISPR Medicines

Engineered Cell Medicines

Corporate

Upcoming Events

Editas Medicine will participate in the following investor events:

Editas Medicine will present pre-clinical data for EDIT-301 to address sickle cell disease and beta-thalassemia in at the 61st American Society of Hematology Annual Meeting & Exposition. Details are as follows:

Abstract Number: 4636Title: EDIT-301: An Experimental Autologous Cell Therapy Comprising Cas12a-RNP Modified mPB-CD34+ Cells for the Potential Treatment of SCDPresenter: Edouard De Dreuzy, Ph.D.Session: 801. Gene Therapy and Transfer: Poster III Time: Monday, December 9, 2019: 6:00 PM-8:00 PMLocation: Hall B, Orange County Convention Center, Orlando, FL

Third Quarter 2019 Financial Results

Cash, cash equivalents, and marketable securities at September 30, 2019, were $332.6 million, compared to $369.0 million at December 31, 2018. The $36.4 million decrease was primarily attributable to operating and capital expenses related to our on-going preclinical and clinical activities, patent costs and license fees, and employee-related costs, partially offset by $42.1 million in proceeds from financing activities.

For the three months ended September 30, 2019, net loss was $32.9 million, or $0.66 per share, compared to $15.2 million, or $0.32 per share, for the same period in 2018.

Conference Call

The Editas Medicine management team will host a conference call and webcast today at 8:00 a.m. ET to provide and discuss a corporate update and financial results for the third quarter of 2019. To access the call, please dial 844-348-3801 (domestic) or 213-358-0955 (international) and provide the passcode 6577216. A live webcast of the call will be available on the Investors & Media section of the Editas Medicine website at http://www.editasmedicine.com and a replay will be available approximately two hours after its completion.

About Editas MedicineAs a leading genome editing company, Editas Medicine is focused on translating the power and potential of the CRISPR/Cas9 and CRISPR/Cpf1 (also known as Cas12a) genome editing systems into a robust pipeline of treatments for people living with serious diseases around the world. Editas Medicine aims to discover, develop, manufacture, and commercialize transformative, durable, precision genomic medicines for a broad class of diseases. For the latest information and scientific presentations, please visit http://www.editasmedicine.com.

About EDIT-101 (AGN-151587)EDIT-101 is a CRISPR-based experimental medicine under investigation for the treatment of Leber congenital amaurosis 10 (LCA10). EDIT-101 is administered via a subretinal injection to reach and deliver the gene editing machinery directly to photoreceptor cells.

About Leber Congenital AmaurosisLeber congenital amaurosis, or LCA, is a group of inherited retinal degenerative disorders caused by mutations in at least 18 different genes. It is the most common cause of inherited childhood blindness, with an incidence of two to three per 100,000 live births worldwide. Symptoms of LCA appear within the first years of life, resulting in significant vision loss and potentially blindness. The most common form of the disease, LCA10, is a monogenic disorder caused by mutations in the CEP290 gene and is the cause of disease in approximately 2030 percent of all LCA patients.

About the Editas Medicine-Allergan AllianceIn March 2017, Editas Medicine and Allergan Pharmaceuticals International Limited (Allergan) entered a strategic alliance and option agreement under which Allergan received exclusive access and the option to license up to five of Editas Medicines genome editing programs for ocular diseases, including EDIT-101 (AGN-151587). Under the terms of the agreement, Allergan is responsible for development and commercialization of optioned products, subject to Editas Medicines option to co-develop and share equally in the profits and losses of two optioned products in the United States. In August 2018, Allergan exercised its option to develop and commercialize EDIT-101 globally for the treatment of LCA10. Additionally, Editas Medicine exercised its option to co-develop and share equally in the profits and losses from EDIT-101 in the United States. Editas Medicine is also eligible to receive development and commercial milestones, as well as royalty payments on a per-program basis. The agreement covers a range of first-in-class ocular programs targeting serious, vision-threatening diseases based on Editas Medicines unparalleled CRISPR genome editing platform, including CRISPR/Cas9 and CRISPR/Cpf1 (also known as Cas12a).

Forward-Looking StatementsThis press release contains forward-looking statements and information within the meaning of The Private Securities Litigation Reform Act of 1995. The words anticipate, believe, continue, could, estimate, expect, intend, may, plan, potential, predict, project, target, should, would, and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. Forward-looking statements in this press release include statements regarding the Companys plans with respect to the Brilliance Phase 1/2 clinical trial for EDIT-101 (AGN-151587), including the Companys expectations regarding the timing of dosing a patient by early 2020. The Company may not actually achieve the plans, intentions, or expectations disclosed in these forward-looking statements, and you should not place undue reliance on these forward-looking statements. Actual results or events could differ materially from the plans, intentions and expectations disclosed in these forward-looking statements as a result of various factors, including: uncertainties inherent in the initiation and completion of pre-clinical studies and clinical trials and clinical development of the Companys product candidates; availability and timing of results from pre-clinical studies and clinical trials; whether interim results from a clinical trial will be predictive of the final results of the trial or the results of future trials; expectations for regulatory approvals to conduct trials or to market products and availability of funding sufficient for the Companys foreseeable and unforeseeable operating expenses and capital expenditure requirements. These and other risks are described in greater detail under the caption Risk Factors included in the Companys most recent Quarterly Report on Form 10-Q, which is on file with the Securities and Exchange Commission, and in other filings that the Company may make with the Securities and Exchange Commission in the future. Any forward-looking statements contained in this press release speak only as of the date hereof, and the Company expressly disclaims any obligation to update any forward-looking statements, whether because of new information, future events or otherwise.

Investor ContactMark Mullikin(617) 401-9083mark.mullikin@editasmed.com

Media ContactCristi Barnett(617) 401-0113cristi.barnett@editasmed.com

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Editas Medicine Announces Third Quarter 2019 Results and Update - GlobeNewswire

Heres a batch of fresh news and announcements from across Imperial.

From a study showing a genetic link for obesity, to a new centre for wildfire research, here is some quick-read news from across the College.

An international team has discovered a new genetic link for a type of obesity which affects pathways in the brain as well as in the pancreas.

Caused by mutations in a single gene called MRAP2, the condition is associated with excessive hunger and linked to early onset diabetes and high blood pressure.

Professor Philippe Froguel, who worked with French researchers in Lille on the discovery, hopes the findings could lead to new treatments targeting the MRAP2 protein. He said: Discoveries such as these could help to tackle genetic forms of obesity. Finding the genetic basis is the key to targeting excessive hunger.

Froguels team previously identified the MC4R gene and a treatment to activate the protein and affect appetite. The treatment is expected to become available from next year.

Read more in Nature Medicine: Loss-of-function mutations in MRAP2 are pathogenic in hyperphagic obesity with hyperglycemia and hypertension

When it comes to asthma, neutrophilsmay not be the bad guys people thought they were.

Severe asthma is caused, in part, by inflammation of the branching airways inside the lungs which makes it hard to breathe. White blood cells called neutrophils are a major component of this inflammation, and researchers previously thought these cells were driving much of the lung damage and ensuing symptoms.

But new research fromDr Robert SnelgroveandDr Dhiren Patel, from Imperials National Heart and Lung Institute,hasfound that neutrophils are not all bad in the context of asthma. They show targeting neutrophils can also have a negative effect, as they have a regulatory role over other inflammatory cells in the lung.

Read the full paper in Science Immunology: Neutrophils restrain allergic airway inflammation by limiting ILC2 function and monocytedendritic cell antigen presentation

Professor Ricardo Martinez-Botas, from the Department of Mechanical Engineering, has received an Honorary Doctorate in Engineering from Universiti Teknologi Malaysia (UTM).

Professor Martinez-Botas is the co-Director of UTMs Centre for Low Carbon Transport (LoCARtic) and has supervised more than ten PhD students from UTM and other institutions in Malaysia.

In 2018, the Prime Minister of Malaysia Tun Dr Mahathir bin Mohamad visited Imperial and toured Professor Martinez-Botass Turbo Group lab, learning about the latest developments in low-carbon transport and electric motors, as well as major collaborations with UTM.

Matoha Instrumentation, founded by Imperial scientists and entrepreneurs, has won an Institute of Physics Business Start-Up Award.

The company make technologies that quickly and cheaply analyse the chemical composition of materials that visually look the same, allowing them to be more easily sorted for recycling. They have made two platforms: one that identifies and analyses plastics, and one that works with fabrics.

The technology uses a combination of near-infrared spectroscopy and machine-learning algorithms to continuously improve performance. The small and low-cost nature of the technology means it can also be used where larger, automatic detectors are not feasible, instead providing a better pair of eyes to manual sorters. The team behind Matoha Instrumentation previously won the Faculty of Natural Sciences Make-A-Difference competition.

Read more on the Institute of Physics website

The Equality, Diversity and Inclusion Centre marked the end of Black History Month and six years of the IMPACT talent development programme for Black, Asian and Minority Ethnic (BAME) staff with a special reunion event. Delegates and mentors, old and new, gathered at the event to reflect on and celebrate their time on the programme.

Gabriella Gordon-Kerr, Equality, Diversity and Inclusion Coordinator, has been at the helm of the IMPACT programme since it started in 2014. She said: It was great to gather our delegates and mentors in one room, and to reflect on the success of the IMPACT programme. At our reunion event, we looked at the history of the programme and heard stories of progression from delegates.

We asked delegates to sign a guest book on the day, and one of the quotes that resonated with us said: IMPACT has left an ever-lasting impact on my life in more ways than one. Heres hoping to another great six years.

BBC Security Correspondent Gordon Corera presented the 10th Vincent Briscoe Lecture of Imperials Institute for Security Science and Technology this week.

He spoke of the intertwining history of technology and espionage over the last century, from the most classified heart of the national security state. From Bletchley Park through the Cold War to Google and Huawei he explored how data, encryption and computers transformed what we think of as secret and what this means for us.

This marks the tenth anniversary of the lecture, which was named in honour of Professor Vincent Briscoe, a distinguished inorganic chemist at Imperials Department of Chemistry.

Dr Jackie Bell has won the Rising Star Award from WISE a campaign that promotes the work of women in STEM.

The annual awards recognise inspiring individuals who actively promote these subjects to girls and women. Dedicated to raising aspirations and changing peoples beliefs that science isnt for them, Dr Bell has given talks to schools and community groups across the UK, and helps Imperial and other institutions develop inclusive community outreach approaches.

Jackie is currently developing the Department of Computings outreach strategy, committing to at least 50 per cent female participation for all activities. Jackie said: Im a strong supporter of the WISE Campaign and all that is being done to achieve gender balance. To have my work recognised like this is an honour and winning the Rising Star award has given me a greater platform to bring about positive change.

Imperial held the launch of a new research centre studying the science and impact of wildfires. Speakers from the Leverhulme Centre for Wildfires, Environment and Society were joined by Marc Castellnou, a Strategic Fire Analyst working with Bombers de Catalunya (Firefighters of Catalonia), who warned that warm and wet winters, followed by extremely hot summers are a perfect storm for the most dangerous wildfires.

Historically common in Mediterranean countries, evidence shows these conditions have arrived in the United Kingdom, Ireland and Scandinavia as a result of climate change. The Centres new Director, Imperials Professor Colin Prentice, said, We need a better understanding of how and why wildfires occur, knowledge to make seasonal forecasts, and an urgent need to understand how to live with wildfires.

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Gene targets for obesity and wildfire research: News from the College | Imperial News - Imperial College London