In August of 2011, Carl June and his team published a landmark paper showing their CART treatment had cleared a patient of cancer. A year-to-the-month later, Jennifer Doudna made an even bigger splash when she published the first major CRISPR paper, setting off a decade of intense research and sometimes even more intense public debate over the ethics of what the gene-editing tool could do.

Last week, June, whose CART work was eventually developed by Novartis into Kymriah, published in Sciencethe first US paper showing how the two could be brought together. It was not only one of the first time scientists have combined the groundbreaking tools, but the first peer-reviewed American paper showing how CRISPR could be used in patients.

June used CRISPR to edit the cells of three patients with advanced blood cancer, deleting the traditional T cell receptor and then erasing the PD1 gene, a move designed to unleash the immune cells. The therapy didnt cure the patients, but the cells remained in the body for a median of 9 months, a major hurdle for the therapy.

Endpoints caught up with June about the long road both he and the field took to get here, if the treatment will ever scale up, and where CRISPR and other advancements can lead it.

The interview has been condensed and edited.

Youve spoken in the past about howyou started working in this field in the mid-90s after your wife passed away from cancer. What were some of those early efforts? How did you start?

Well, I graduated from high school and had a low draft number [for the Vietnam War] and was going to go to study engineering at Stanford, but I was drafted and went into the Naval Academy in 1971, and I did that so I wouldnt have to go to the rice fields.

The war ended in 73, 74, so when I graduated in 1975, I was allowed to go to medical school, and then I had a long term commitment to the Navy because they paid for the Acadamy and Medical school. And I was interested in research and at the time, what the Navy cared about was a small scale nuclear disaster like in a submarine, and like what happened at Chernobyl and Fukushima. So they sent me to the Fred Hutchinson Cancer Center where I got trained in cancer, as a medical oncologist. I was going to open a bone marrow transplant center in Bethesda because the Navy wanted one in the event of a nuclear catastrophe.

And then in 1989, the Berlin Wall came down and there was no more Cold War. I had gone back to the Navy in 86 for the transplant center, which never happened, so then I had to work in the lab full time. But in the Navy, all the research has to be about combat and casualty. They care about HIV, so my first papers were on malaria and infectious disease. And the first CAR-T trials were on HIV in the mid-90s.

In 96, my wife got diagnosed with ovarian cancer and she was in remission for 3-4 years. I moved to the University of Pennsylvania in 1999 and started working on cancer because I wasnt allowed to do that with the Navy. My wife was obviously a lot of motivation to do that. She passed away in 2001. Then I started working with David Porter on adoptive transfer T cells.

I got my first grant to do CAR-T cells on HIV in 2004, and I learned a whole lot. I was lucky to have worked on HIV because we did the first trials using lentiviruses, which is an engineered HIV virus.

I was trained in oncology, and then because of the Navy forced to work on HIV. It was actually a blessing in disguise.

So if you hadnt been drafted, you wouldve become an engineer?

Yes. Thats what I was fully intending. My dad was a chemical engineer, my brother is an engineer. Thats what I thought I was going to do. No one in my family was ever a physician. Its one of those many quirks of fate.

Back then, we didnt have these aptitude tests. It was just haphazard. I applied to three schools Berkeley, Stanford and Caltech and I got into all three. It was just luck, fate.

And it turned out when I went to the Naval Academy, they had added a pre-med thing onto the curriculum the year before, so thats what I did when I started, I did chemistry.

I wouldve [otherwise] been in nuclear submarines. The most interesting thing in the Navy then was the nuclear sub technology.

You talked about doing the first CAR-T trials on HIV patients because thats where the funding was. Was it always in your head that this was eventually going to be something for cancer?

So I got out of the Navy in 99 and moved to Penn. I started in 98 working on treating leukemia, and then once I got to Penn, I continued working one day a week on HIV.

Its kind of a Back-to-the-Future thing because now cancer has paved out a path to show that CART cells can work and put down the manufacturing and its going to be a lot cheaper making it for HIV. I still think thats going to happen.

Jim Riley, who used to be a postdoc in my lab, has some spectacular results in monkeys with HIV models. They have a large NIH and NIAID research program.

So were going to see more and more of that. The CAR technology is going to move outside of cancer, and into autoimmune and chronic infections.

I want to jump over to cytotoxic release syndrome (CRS)because a big part of the CRISPR study was that it didnt provoke this potentially deadly adverse effect. When did you first become aware that CRS was going to be a problem?

I mean we saw it in the very first patient we treated but in all honesty, we missed it. Im an MD, but I dont see the patient and David Porter tookcare of the first three patients and our first pediatric patient,Emily Whitehead.

In our first patients, 2 out of 3, had complete remission and there were fevers and it was CRS but we thought it was just an infection, and we treated with antibiotics for 3 weeks and[eventually] it went away. And sort of miraculously he was in remission and is still in remission, 9 years later.

And then when we treated Emily. She was at a 106-degree fever over three days, and there was no infection.

Ive told this story before. My daughter has rheumatoid arthritis, and I had been president of the Clinical Immunologists Society from 2009 to 2010, and the first good drug for juvenile rheumatoid arthritisthat came out. I was invited to give the Japanese scientist Tadamitsu Kishimoto the presidential award for inventing the drug.

Then in 2012, Emily Whitehead was literally dying from CRS, she had multiple organ failures. And her labs came back and IL-6 levels were 1000x normal. It turns out the drug I was looking at for my daughter, it blocks IL-6 levels. I called the physician and I said, listen theres something actionable here, since its in your formulary to give it to her off-label.

And she gave her the appropriate dose for rheumatoid arthritis. It was miraculous. She woke up very rapidly.

Now its co-labeled. When the FDA approvedKymriah, it was co-labeled. It kind of saved the field.

How were you feeling during this time? Did you have any idea what was happening to her?

No, not until we got the cytokine levels, and then it was really clear. The cytokine levels go up and it exactly coincided. Then we retroactively checked out adults and they had adverse reactions and it easy to see. We hadnt been on the lookout because it wasnt in our mouse models.

And it appeared with those who got cured. Its one of the first on-target toxicities seen in cancer, a toxicity that happens when you get better. All the toxicities from chemotherapy are off-target: like leukopenia or hair loss.

I had a physician who had a fever of 106, I saw him on a fever when he was starting to get CRS. When the nurse came in and it said 106, they thought the thermometer must be broken. On Monday, I saw him, and said how are you feeling and he said fine. And I looked at the thermometer and histemperature was still 102.

People will willingly tolerate on-target toxicity thats very different from chemotherapy if they know it helps get them better. Thats a new principle in cancer therapy.

You had these early CART results almost at the same time that Doudna publishes the first CRISPR papers, then still in bacteria. When did you first start thinking about combining the two?

Yeah, it was published inSciencein 2012 and thats when Emily Whitehead got treated. Its an amazing thing.

Thats something so orthogonal. You think how in the heck can that ever benefit CART cells? but my lab had done the first edited cells in patients, published in 2012. And we used zinc-fingered nucleases, which were the predecessors to CRISPR. It knocked out one gene at a time, but we showed it was safe.

I was already into gene editing because it could make T cells resistant to HIV. So it was pretty obvious that there were candidates in T cells that you can knock out. And almost every lab started working on some with CRISPR, cause it was much easier.

We were the first to get full approval by the FDA, so we worked on it from 2012, had all the preclinical data by 2016, and then it takes a while to develop a lot of new assays for this as we were very cautious to optimize safety and it took longer than we wanted, but in the end, we learned a tremendous amount.

So what did we learn?

First of all our patients had advanced metastatic cancer and had had a lot of chemotherapy. The first patient had had 3 bone marrow transplants.

One thing is feasibility: could you really do all the complex engineering? So we found out we could. feasibility was passed.

Another was the fact that cas9 came out of bacteria, forms of strep and staph. Everyone has pre-existing immunity to Cas9 and we had experience from the first trial with Sangamo[with zinc-finger nucleases] where some patients had a very high fever. In that case, we had used adenoviruses, and it turned out our patients had very high levels of baseline immune response to adenoviruses, so we were worried that would happen with CRISPR, and it did not happen.

It did not have any toxicity. If it had, it would have really set the field back. If there was animmune response to cas9 and CRISPR, there couldve been a real barrier to the field.

And then, the cells survived in the patients. The furthest on, it was 9 months. The cells had a very high level of survival. In the previous trials, the cells survived less than 7 days. In our case, the half-life was 85 days. We dont know the mechanism yet.

And we found very big precision in the molecular scissors, and that was a good thing for the field. You could cut 3 different genes on 3 different chromosomes and have such high fidelity.

It [CRISPR] is living up to the hype. Its going to fix all these diseases.

Whats the potential in CAR-T, specifically?

Well theres many many genes that you can add. There are many genes that knocking outwill make the cells work better. We started with the cell receptor. There are many, I think, academics and biotechs doing this now and it should make the cells more potent and less toxic.

And more broadly, what else are you looking at for the future of CART? The week before your paper, there were the results from MD Anderson on natural killer cells.

Different cell types, natural killer cells, stem cells putting CAR molecules into stem cells, macrophages. One of my graduate students started a company to do CAR macrophages and macrophages actually eat tumor cells, as opposed to T cells that punch holes in them.

There will be different cell types and there will be many more ways to edit cells. The prime editing and base editing. All different new variations.

Youve talked about how people used to think the immuno-oncology, if it ever worked, would nevertheless be a boutique treatment. Despite all the advancements, Novartis and Gilead still have not met the sales they once hoped to grab from their CART treatments. Are you confident CART will ever be widely accessible?

Oh yeah, Novartis sales are going up. They had a hiccup launching.

Back in 96 or 97, when Genentech launched Herceptin, their commercial antibody, they couldnt meet the demand either and then they scaled up and learned how to do better cultures. So right now Novartis is using tech invented in my lab in the 1990s culture tech thats complex and requires a lot of labor, so the most expensive part is human labor. A lot can be made robotic. The scale problem will be much easier.

Thats an engineering problem that will become a thing of the past. The manufacturing problem will get a lot cheaper. Here in the US, we have a huge problem with how drugs are priced. We have a problem with pricing. Thats a political issue.

But in cell therapy, its just kind of the growth things you see in a new industry. Itll get worked out.

This article has been updated to reflect that Jim Riley conducted work on CAR in HIV.

See the original post here:
Carl June on CRISPR, CART and how the Vietnam War dropped him into medicine - Endpoints News

PARP inhibitors interfere with cancers ability to repair damage to its DNA. They are becoming increasingly useful in treating ovarian cancer.

Valencia Halls oncologist wanted to give her the best possible chance of staying in remission, so in June 2017, she prescribed Zejula (niraparib), a once-daily oral treatment thats part of an emerging class of medicines known as poly (ADP-ribose) polymerase (PARP) inhibitors. Just a few months before Valencia Halls disease returned, Zejula had become the first PARP inhibitor approved by the Food and Drug Administration (FDA) to treat women with recurrent ovarian cancer who do not have a genetic abnormality but previously responded well to platinum-based chemotherapy. Valencia Hall was a perfect candidate for the drug, which is referred to as a maintenance treatment because its prescribed with the goal of preventing ovarian cancer from returning.

She has been free of the disease since starting Zejula and has experienced no side effects, aside from a temporary drop in platelet counts that her oncologist corrected by dialing down Valencia Halls daily dose. Zejula has allowed me to live my life as I see fit, says Valencia Hall, 51, a freelance graphic artist in Phoenix. Its an oral medication, so I dont have to go in for infusions. The opportunity to have this as a maintenance therapy is exciting its hope.

Zejula is one of three PARP inhibitors that are taking an increasingly prominent role in ovarian cancer treatment and improving patients prognosis. With dozens of clinical trials underway, including some that seek to combine PARP inhibitors with other cancer treatments, that role could expand even more.

Drugs in this class work by inhibiting the PARP enzyme, which normally helps damaged DNA repair itself. Preventing this repair causes cancer cells to die, especially those that already have DNA repair defects due to a mutated BRCA 1 or 2 gene or other abnormalities. So far, clinical trials have shown that these drugs can lengthen the time until the disease progresses; their impact on the length of life is still being investigated. For women using a PARP inhibitor for maintenance, the drugs can help increase the time between courses of chemotherapy for recurrent disease.

In the past, we would take patients who had a high risk of recurrence and just watch them until cancer came back because we didnt have maintenance therapies that were effective, tolerable or convenient, says Dr. Bradley Monk, a professor and director of the division of gynecologic oncology at Creighton University School of Medicine at St. Josephs Hospital and Medical Center in Phoenix, Arizona, and also medical director of gynecologic oncology research for the U.S. Oncology Research Network. PARP inhibitors have been significant because theyre expanding the treatment opportunity for many patients, he adds.

Each year, more than 22,000 women in the U.S., about half of whom are over age 63, receive a diagnosis of ovarian cancer, according to the American Cancer Society. A small proportion of women have inherited mutations in BRCA1, BRCA2 or other cancer-related genes that raise their risk of ovarian cancer and can take steps to fend off the disease, including surgery to remove their ovaries. But most cases occur out of the blue, and because the symptoms can be vague and easily overlooked, like bloating or stomach pain, many women do not receive a diagnosis until the disease has advanced to the point where it can be hard to treat. The disease will recur in about 85% of women who initially respond to chemotherapy.

For women with ovarian cancer, PARP inhibitors have been an option since 2014, when the FDA approved Lynparza (olaparib) as a maintenance therapy for patients with BRCA mutations who had received three or more chemotherapy treatments. Rubraca (rucaparib) followed in 2016 and Zejula in 2017.

PARP INHIBITORS REACH MORE PATIENTS

Over the past two years, the FDA approved more uses of PARP inhibitors so that many more patients can benefit from these medicines and access the drugs earlier in treatment. In April 2018, Rubraca was approved as a maintenance therapy to treat recurrent ovarian cancer in women who responded at least partially to platinum-based chemotherapy, whether or not they had a genetic mutation. That December, Lynparza was approved as a first-line maintenance treatment for BRCA-mutated ovarian cancer, meaning patients can be given the drug after successfully completing just one round of platinum-based chemotherapy.

That was based on a clinical trial showing the drug reduced the rate of disease progression or death by 70%.

Most recently, in October 2019, the FDA approved Zejula for use in patients with advanced ovarian cancer associated with a cellular abnormality called homologous recombination deficiency. BRCA1 and BRCA2 are two of these types, but in ovarian cancer, about 17 other such genetic abnormalities can drive the disease. Between 41% and 50% of ovarian tumors are thought to have homologous recombination deficiency, which can be detected with a tumor test, Myriad myChoice CDx, that the FDA also approved last October.

In a clinical trial leading to the approval, 24% of participants with homologous recombination deficiency-positive ovarian cancer responded well to Zejula, experiencing some tumor shrinkage. That may not sound like a high response rate, but it surpasses the overall response rate to PARP inhibitors among all patients with ovarian cancer either with or without mutations, says lead clinical trial investigator Dr. Kathleen Moore, associate professor of gynecologic oncology at Stephenson Cancer Center at the University of Oklahoma.

These are heavily pretreated patients in which the response rate has typically been 12%, so this was double what we normally see, Moore says. The clinical benefit here was quite high. She adds that patients with BRCA mutations did particularly well: Nearly 40% of those who previously responded well to platinum-based chemotherapy responded to Zejula. The most common side effects include gastric upset, mouth sores, rash, headache and dizziness. The drug can also cause anemia and abnormal blood counts, which, in rare cases, can lead to myelodysplastic syndrome, a bone marrow problem, or the blood cancer acute myeloid leukemia.

As PARP inhibitors continue to help a widening population of patients with ovarian cancer, a push is underway to use them earlier in the treatment process. Several trials presented at the 2019 European Society for Medical Oncology conference demonstrated the potential value of that strategy.

One study found an 84% survival rate among patients who took Zejula for two years following chemotherapy, regardless of their homologous recombination deficiency status, compared with 77% who got a placebo. The median progression-free survival period (time from treatment to disease progression) for patients taking the drug was 14 months compared with eight months for those on placebo.

Another study evaluated an investigational PARP inhibitor, veliparib, combined with chemotherapy as a first-line treatment followed by veliparib alone for maintenance. Median progression-free survival among patients on that regimen was 23.5 months versus 17.3 months for those taking a placebo.

The third trial presented at the conference involved Avastin (bevacizumab), a drug that cuts off the blood supply to tumors. The FDA approved Avastin in 2018 to treat advanced ovarian cancer in conjunction with chemotherapy.

During the more recent trial, patients with newly diagnosed advanced ovarian cancer took Avastin plus chemotherapy, followed by Avastin with Lynparza for maintenance. Those who took Lynparza along with Avastin had a median progression-free survival of 22 months compared with 17 months for those who received Avastin and a placebo.

In all three studies, progression-free survival rates were the highest among homologous recombination deficiency-positive patients, but the fact that PARP inhibitors extended survival even among those without those mutations was encouraging to oncologists who treat ovarian cancer.

These were all positive studies that undoubtedly show that PARP inhibitor maintenance following chemotherapy will extend beyond BRCA-associated ovarian cancer, Moore says. Its highly likely that a much larger proportion of women with ovarian cancer who are diagnosed in 2020 will receive a PARP inhibitor (than in previous years). Women will be able to live longer with their cancer because were developing effective therapies that push out progression-free survival.

COMBINATIONS GAIN STEAM

A clinical trial investigating a novel PARP combination proved a lifesaver for Diane Sarver, who first received a diagnosis of ovarian cancer in 2010. Chemotherapy put her cancer in remission three times, but when she relapsed again in 2015, she decided to search for a novel treatment strategy and traveled from her home in Lake Oswego, Oregon, to The University of Texas MD Anderson Cancer Center in Houston.

Sarver was entered into an early-phase trial combining Lynparza with the investigational drug AZD2014, which interferes with a cellular pathway (called phosphatidylino-sitol-3 [PI3] kinase) that drives resistance to PARP inhibitors. Within seven weeks of starting the combination therapy which consists of two oral drugs taken twice a day , Sarvers ovarian cancer came under control. As part of the ongoing trial, she continues to take the two drugs, which, she says, have caused no side effects and shes still disease-free.

Whats notable about Sarvers case is that she didnt inherit any genetic mutations that would predict such a long-lasting response to PARP inhibitors. Although her tumor tested positive for a rare BRCA mutation, it was considered nonactionable scientists did not yet know whether or not the mutation produced an aberrant protein that would make it likely to respond to the drug combination being studied. The theory behind the trial is that blocking PI3 kinase may transform tumors that would not normally respond to PARP inhibition into responders.

Im amazed that Ive had such a good outcome, says Sarver, 69, a retired clinical technologist and mother of two grown children. Her only limitation is that she has to fast two hours before and after taking the drugs, she says, but the lack of side effects has given her the freedom to travel, speak to medical students about her experiences and spend time with her family.

Ive seen both children through their college graduations, Sarver says. I feel completely functional and am grateful to have never experienced any fatigue or other physical restriction.

MD Anderson is now planning several midstage clinical trials combining PARP and PI3 kinase inhibition, including one that pairs Lynparza with Piqray (alpelisib), a drug currently used to treat some patients with breast cancer. In an early trial of the combination that was reported in April 2019, 36% of patients had a partial response of some tumor shrinkage and half achieved stable disease, meaning their cancer didnt get worse. That was impressive, considering the bulk of the patients had become resistant to platinum chemotherapy, says Dr. Shannon Westin, a clinical investigator in the department of gynecologic oncology and reproductive medicine at MD Anderson. And there was a similar response rate regardless of mutation status, which was very exciting.

RESEARCHERS PURSUE MORE USES

Pairing PARP inhibitors with drugs that boost the immune systems ability to fight cancer is another idea being investigated in the treatment of ovarian cancer, because tumors with unstable DNA repair abilities might also be easier for the immune system to recognize. For example, Keytruda (pembrolizumab) inhibits programmed cell death protein 1 (PD-1), an immune checkpoint responsible for keeping the immune system under control.

The drug essentially takes the brakes off the immune system so it can better recognize and attack cancer. In an early trial combining Keytruda with Zejula, 65% of patients with ovarian cancer saw their disease come under control, either with total or partial tumor shrinkage or with stable disease.

Several other ongoing studies are combining PARP inhibition with immunotherapy, including a trial of Zejula with Tecentriq (atezolizumab), an inhibitor of a protein called programmed death-ligand 1 (PD-L1), and Cotellic (cobimetinib), which inhibits the cancer-associated mitogen-activated (MEK) protein. Another study combines Zejula with TSR-042, an investigational PD-1 blocker.

Could PARP inhibitors be useful for some women even earlier in the treatment process? MD Anderson recently started a small trial designed to investigate the potential of using the agents in place of chemotherapy in women with newly diagnosed cancer who have BRCA mutations. During the trial, patients will receive Lynparza for up to three months before moving on to surgery and chemotherapy. A similar trial is ongoing using the PARP inhibitor Talzenna (talazoparib) for BRCA-mutated breast cancer.

There could be many advantages of starting treatment with a PARP inhibitor rather than chemotherapy, Westin says. Patients can take the drugs at home instead of going to a facility for chemotherapy infusions. And PARP inhibitors dont cause many of the uncomfortable side effects common with chemotherapy, like neuropathy (numbness and tingling in the extremities) and hair loss. Some patients could potentially avoid that toxicity, Westin says.

The question is: Do we even need chemotherapy? Westin adds. Can we utilize a more targeted therapy to get better results? This is the next step.

The rest is here:
An Expanding Role For PARP Inhibitors Shows Promise In Treating Ovarian Cancer - Curetoday.com

This report focuses on the global Gene Editing status, future forecast, growth opportunity, key market and key players. The study objectives are to present the Gene Editing development in United States, Europe and China.

Gemstones are elements of minerals which when polished and cut are used for making jewelry and other ornaments, as well as for decoration purposes.

Key drivers attributing to the expansion include early applications of DNA editing to therapeutics. Use of the technology for the disease eradication through direct correction of disturbances in normal physiology, engineering the immune response, and alteration of pathogen targets in the host is anticipated to drive the market with substantial opportunities.

Based on end user, the global gene editing technologies market has been segmented into biotechnology industry, horticulture industry, animal breeding and academic & research institutes. Academic and research institutes are expected to contribute maximum share in the global gene editing technologies market over the f recast period as majority of the therapeutic applications of gene editing are not yet commercialized.

United States is expected to lead the global market due to increasing number academic and research institutes. Market in APAC region is expected to witness significant growth rate over the forecast period owing to expansion activities by key market players in the region.

In 2017, the global Gene Editing market size was xx million US$ and it is expected to reach xx million US$ by the end of 2025, with a CAGR of xx% during 2018-2025.

The key players covered in this study

Thermo Fisher Scientific

Merck

Horizo??n Discovery

Sangamo BioSciences

Integrated DNA Technologies

Lonza

New England Biolabs

OriGene Technologies

Transposagen Biopharmaceuticals

Editas Medicine

CRISPR Therapeutics

RGen Solutions

Sigma-Aldrich

GeneCopoeia

Genscript Biotech

OriGene Technologies

Agilent Technologies

Market analysis by product type

Crispr

Talen

Zfn

Market analysis by market

Biotechnology & Pharmaceutical Companies

Academic & Government Research Institutes

Contract Research Organizations

Market analysis by Region

United States

Europe

China

Japan

Southeast Asia

India

Central & South America

The study objectives of this report are:

To analyze global Gene Editing status, future forecast, growth opportunity, key market and key players.

To present the Gene Editing development in United States, Europe and China.

To strategically profile the key players and comprehensively analyze their development plan and strategies.

To define, describe and forecast the market by product type, market and key regions.

In this study, the years considered to estimate the market size of Gene Editing are as follows:

History Year: 2017-2018

Base Year: 2017

Estimated Year: 2018

Forecast Year 2018 to 2025

For the data information by region, company, type and application, 2017 is considered as the base year. Whenever data information was unavailable for the base year, the prior year has been considered.

Table of Contents

Chapter One: Report Overview

1.1 Study Scope

1.2 Key Market Segments

1.3 Players Covered

1.4 Market Analysis by Type

1.4.1 Global Gene Editing Market Size Growth Rate by Type (2018-2025)

1.4.2 Crispr

1.4.3 Talen

1.4.4 Zfn

1.5 Market by Application

1.5.1 Global Gene Editing Market Share by Application (2017-2025)

1.5.2 Biotechnology & Pharmaceutical Companies

1.5.3 Academic & Government Research Institutes

1.5.4 Contract Research Organizations

1.6 Study Objectives

1.7 Years Considered

Chapter Two: Executive Summary

2.1 Gene Editing Market Size

2.2 Gene Editing Growth Trends by Regions

2.2.1 Gene Editing Market Size by Regions (2017-2025)

2.2.2 Gene Editing Market Share by Regions (2017-2025)

2.3 Industry Trends

2.3.1 Market Top Trends

2.3.2 Market Use Cases

Chapter Three: Key Players

3.1 Gene Editing Revenue by Manufacturers (2017-2018)

3.2 Gene Editing Key Players Head office and Area Served

3.3 Key Players Gene Editing Product/Solution/Service

3.4 Date of Enter into Gene Editing Market

3.5 Key Players Gene Editing Funding/Investment Analysis

3.6 Global Key Players Gene Editing Valuation & Market Capitalization

3.7 Mergers & Acquisitions, Expansion Plans

Chapter Four: Breakdown Data by Type and Application

4.1 Global Gene Editing Market Size by Type (2017-2025)

4.2 Global Gene Editing Market Size by Application (2017-2025)

Chapter Five: United States

5.1 United States Gene Editing Market Size (2017-2025)

5.2 Gene Editing Key Players in United States

5.3 United States Gene Editing Market Size by Type

5.4 United States Gene Editing Market Size by Application

Chapter Six: Europe

6.1 Europe Gene Editing Market Size (2017-2025)

6.2 Gene Editing Key Players in Europe

6.3 Europe Gene Editing Market Size by Type

6.4 Europe Gene Editing Market Size by Application

Chapter Seven: China

7.1 China Gene Editing Market Size (2017-2025)

7.2 Gene Editing Key Players in China

Read more:
Global Gene Editing Market 2020: Drivers, Restraints, Opportunities, Threats, Trends, Applications, Growth Analysis and Forecast To 2025 - Nyse Nasdaq...