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The global generic pharmaceuticals market is likely to witness strong growth in the next few years owing to the patent expiration of key blockbuster drugs and the judicious cost containment efforts…

Source: PATENT EXPIRY DATES


CancerBase.org – The Global HUB for Diagnoses, Genomes, Pathology Images: A Real-time Diagnosis and Therapy Mapping Service for Cancer Patients – Anonymized Medical Records accessible to anyone on Earth

Reporter: Aviva Lev-Ari, PhD, RN

 

July 27, 2016
world map illustration
Illustration by Tricia Seibold and iStock/liuzishan

During his 2016 State of the Union address, President Barack Obama called on Vice President Joe Biden – who had months earlier lost his son Beau to brain cancer – to head a “moonshot” to significantly accelerate research into the disease. The president said he wanted to harness the spirit of American innovation that took us from zero to landing a man on the moon in a decade to similarly find new ways to prevent, diagnose and treat cancer.

One of those intrigued by that call to action was Stanford’s Jan Liphardt, an associate professor of bioengineering who specializes in biophysics, the tumor microenvironment and data analysis. Stanford Engineering talked to Liphardt about how he came to be involved with the moonshot and his approach to using data and the voice of patients to better understand cancer and how it can be treated, and how sharing information can better inform the course of cancer research.

How did you get involved in the National Cancer Moonshot?

In March, after the president’s charge, the vice president challenged scientists, doctors, industry and patients to give their best ideas to the moonshot. The White House also reached out to a few outsiders, myself included. The White House instructions were unusual: “Do something big and different. There is no money and you have 87 days. Go.”

I like a challenge, and this was a chance to serve, even in the face of administrative hurdles. So I looked for advice, teammates and support. Russ Altman, a colleague at Stanford, suggested it was time to give patients a way to volunteer their own health data in order to help find cures. I collaborated with Peter Kuhn, a professor of medicine and engineering at the University of Southern California, who’s known for carefully listening to cancer patients, advocates and their supporters. In short order we had links with advocates like AnneMarie Ciccarella, Sonja Durham, Lori Marx-Rubiner, Jack Whelan and Jack Park. That’s how we got to CancerBase.org.

What’s the idea the team came up with?

We thought for about a week: What would matter to the patients that Stanford and other research institutions serve? What would scale? Well, we’re not going to run a clinical trial, go near protected health information, invent a new drug or write a research proposal. There’s no time for that. Whatever it was, it had to be useful, scalable, legal and different. That pointed to data, the web, patients and decisions.

One thing jumped out: Right now, there’s significant friction in medical data sharing. People all over the world can already effortlessly share other kinds of information – pictures, movies, ideas, stories, tweets. Increasingly, they are using the same tools to share personal medical information. It’s remarkable what cancer patients already share: diagnoses, genomes, pathology images. But that information is not yet widely used to understand where they are with their diseases.

Ideally, everyone, including scientists and doctors, would have as much information as possible at their fingertips. Many patients think when they give data for research, magically scientists all over the world can dig into this information, find patterns and help. The practical reality is that it’s nearly impossible for any one scientist to access the amounts of data they would like.

So that’s the simple idea: A global map and give patients the tools they need to share their data – if they want to. They can donate information for the greater good. In return, we make a simple promise: When you post data, we’ll anonymize them and make them available to anyone on Earth in one second. We plan to display this information like real-time traffic data. HIPAA doesn’t apply to this direct data-sharing. The patients can give us whatever information they want, and they can tell us what they want us to do with it. We’re a conduit. Their data belong to them, not to us.

How does it work?

Today we ask just five basic questions. Over time we will add more. You join, give some information, and we’ll put you on a global map. Right now, some of the things we don’t know about cancer are incredibly simple: Where is everyone on Earth with cancer? How old are they? What is their diagnosis? Did their cancers metastasize? Global, instantaneous data sharing is the story.

In a second phase, we are going to see if we can plot all the information just like Waze does for traffic. Our role is to synthesize the information and plot it in ways that ordinary people can understand. Think of it this way – patients want to be able to chart their treatment path. Who went straight, who went left? People just getting on the highway are curious about what people did who came before them, and what happened to those people. Did they arrive at the destination easily and promptly? We’re a real-time diagnosis and therapy mapping service for cancer.

You say that giving patients a way to share their health data is important to help finding cures. Why?

Let me give you a specific example. At Stanford, I’m part of a team of cancer biologists and clinicians funded by the Stanford Cancer Institute to think about the next generation of screening for breast cancer in the U.S. Every year, the U.S. uses mammography to screen more than 40 million women for breast cancer. In this project, it quickly became clear that there is currently no central, easy-to-access repository of mammograms for research use.

That’s a major lost opportunity – our nation spends billions on screening, but we don’t store, share and analyze this information in a scalable and simple manner. In the traditional approach, our team would spend several hundred thousand dollars, and about three years, to assemble perhaps 1,000 mammograms. We would then use this tiny dataset to try to find something interesting, but since the dataset is so small, we would be blind to rare features of breast cancer and its predictors. It clearly makes a lot more sense to compare and explore 100 million images.

This sounds completely impossible until you realize that Instagram users upload 58 million images every day. Once you start to think about supposedly intractable research problems from a web or social networking perspective, new possibilities open. Imagine, for example, if there were a simple way for every single woman on Earth to upload and share her de-identified mammogram? Or more generally, imagine a world in which patients have the tools to globally share de-identified health data, if they want to. That’s exactly the idea behind CancerBase – let’s just give people those tools and see what happens.

How much data and how many people are needed to make this viable?

We think we are going to need several tens-of-thousands of members. There are approximately 50 million people on Earth with a cancer diagnosed in the last five years, and 200 million more people have an immediate family member with cancer. Almost 2 billion people are active on Twitter and Facebook – a quarter of the world’s population. If just a few percent of those people sign up, we could do something no one on Earth has done before.

Are there hopes to create a “developer community,” people who find ways to use your data that you didn’t even think about or have the time to work on?

Definitely. As much as we think we can predict what these data are useful for, we don’t really know. By making the anonymized data available to everyone within one second, they might start to do things that we never dreamed of. The more eyes look at these data, the better off everyone will be. The dream is to have cancer-relevant medical data flow unimpeded around the world in seconds, so that everyone, wherever they are, can see and use this information.

SOURCE

https://engineering.stanford.edu/news/how-data-can-help-us-understand-cancer-and-its-treatment


A New Potential Target for Pancreatic Cancer Treatment: Rapid Screening Technique finds Gene Defending Tumors from DNA Damage @M. D. Anderson Cancer Center

Reporter: Aviva Lev-Ari, PhD, RN

Novel gene-hunting method implicates new culprit in pancreatic cancer

Researchers develop rapid screening technique; find gene defends tumors from DNA damage

Date:
June 23, 2016
Source:
University of Texas M. D. Anderson Cancer Center
Summary:
Using an innovative approach to identify a cancer’s genetic vulnerabilities by more swiftly analyzing human tumors transplanted into mice, researchers have identified a new potential target for pancreatic cancer treatment.

WDR5 emerges as robust “hit”

WD repeat-containing protein 5 (WDR5), a core part of the COMPASS complex regulating chromatin function, was implicated in multiple screens. Recent research by others had shown WDR5 to be upregulated in prostate and bladder cancers and critical for cancer cell proliferation.

The team confirmed WDR5 was highly expressed in pancreatic cancer compared to normal pancreas tissue and then conducted a series of experiments which showed knocking down the gene impaired cell proliferation and tumor growth and greatly increased survival in mice.

Subsequent experiments showed WDR5 works in concert with Myc to protect pancreatic cancer from DNA damage. There is no known method for targeting either WDR5 or Myc separately, Carugo said, but the team thinks there might be ways to block their interaction.

While the team targeted epigenetic regulators, Carugo noted the technique can be used with other shRNA libraries aimed at different classes of genes.

This technology is being widely adopted by MD Anderson’s moon shot teams to identify genetic vulnerabilities and cancer targets specific to various disease subtypes.


Story Source:

The above post is reprinted from materials provided by University of Texas M. D. Anderson Cancer Center. Note: Materials may be edited for content and length.

SOURCE

University of Texas M. D. Anderson Cancer Center. “Novel gene-hunting method implicates new culprit in pancreatic cancer: Researchers develop rapid screening technique; find gene defends tumors from DNA damage.” ScienceDaily. ScienceDaily, 23 June 2016. www.sciencedaily.com/releases/2016/06/160623115741.htm.

Alessandro Carugo et al. In Vivo Functional Platform Targeting Patient-Derived Xenografts Identifies WDR5-Myc Association as a Critical Determinant of Pancreatic Cancer. Cell Reports, June 2016 DOI:10.1016/j.celrep.2016.05.063

Cell Rep. 2016 Jun 28;16(1):133-47. doi: 10.1016/j.celrep.2016.05.063. Epub 2016 Jun 16.

In Vivo Functional Platform Targeting Patient-Derived Xenografts Identifies WDR5-Myc Association as a Critical Determinant of Pancreatic Cancer.

Author information

  • 1Department of Genomic Medicine, UT MD Anderson Cancer Center, Houston, TX 77030, USA; Department of Molecular and Cellular Oncology, UT MD Anderson Cancer Center, Houston, TX 77030, USA; Department of Experimental Oncology, European Institute of Oncology, Milan 20139, Italy. Electronic address: acarugo@mdanderson.org.
  • 2Department of Genomic Medicine, UT MD Anderson Cancer Center, Houston, TX 77030, USA; Department of Molecular and Cellular Oncology, UT MD Anderson Cancer Center, Houston, TX 77030, USA.
  • 3Institute for Applied Cancer Science, UT MD Anderson Cancer Center, Houston, TX 77030, USA.
  • 4Department of Experimental Oncology, European Institute of Oncology, Milan 20139, Italy.
  • 5Department of Genomic Medicine, UT MD Anderson Cancer Center, Houston, TX 77030, USA.
  • 6Sheikh Ahmed Bin Zayed Al Nahyan Center for Pancreatic Cancer Research, UT MD Anderson Cancer Center, Houston, TX 77030, USA.
  • 7Department of Epigenetics and Molecular Carcinogenesis, UT MD Anderson Cancer Center, Houston, TX 77030, USA.
  • 8Department of Experimental Oncology, European Institute of Oncology, Milan 20139, Italy; Department of Oncology and Hemato-oncology, University of Milan, Milan 20139, Italy.
  • 9Center for Genomic Science of IIT@SEMM, Istituto Italiano di Tecnologia (IIT), Milan 20139, Italy.
  • 10Department of Genomic Medicine, UT MD Anderson Cancer Center, Houston, TX 77030, USA; Institute for Applied Cancer Science, UT MD Anderson Cancer Center, Houston, TX 77030, USA.
  • 11Department of Surgical Oncology, UT MD Anderson Cancer Center, Houston, TX 77030, USA.
  • 12Department of Pathology, UT MD Anderson Cancer Center, Houston, TX 77030, USA.
  • 13Department of Cancer Biology, UT MD Anderson Cancer Center, Houston, TX 77030, USA.
  • 14Department of Experimental Oncology, European Institute of Oncology, Milan 20139, Italy. Electronic address: luisa.lanfrancone@ieo.eu.
  • 15C-4 Therapeutics, Cambridge, MA 02142, USA. Electronic address: theffernan@c4therapeutics.com.
  • 16Department of Genomic Medicine, UT MD Anderson Cancer Center, Houston, TX 77030, USA; Institute for Applied Cancer Science, UT MD Anderson Cancer Center, Houston, TX 77030, USA; Department of Molecular and Cellular Oncology, UT MD Anderson Cancer Center, Houston, TX 77030, USA. Electronic address: gdraetta@mdanderson.org.

Abstract

Current treatment regimens for pancreatic ductal adenocarcinoma (PDAC) yield poor 5-year survival, emphasizing the critical need to identify druggable targets essential for PDAC maintenance. We developed an unbiased and in vivo target discovery approach to identify molecular vulnerabilities in low-passage and patient-derived PDAC xenografts or genetically engineered mouse model-derived allografts. Focusing on epigenetic regulators, we identified WDR5, a core member of the COMPASS histone H3 Lys4 (H3K4) MLL (1-4) methyltransferase complex, as a top tumor maintenance hit required across multiple human and mouse tumors. Mechanistically, WDR5 functions to sustain proper execution of DNA replication in PDAC cells, as previously suggested by replication stress studies involving MLL1, and c-Myc, also found to interact with WDR5. We indeed demonstrate that interaction with c-Myc is critical for this function. By showing that ATR inhibition mimicked the effects of WDR5 suppression, these data provide rationale to test ATR and WDR5 inhibitors for activity in this disease.

Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.


Advances in Gene Editing and Gene Silencing | September 20-21, 2016 | Boston, MA

Kinase Inhibitor Discovery September 21-22, 2016 Boston

KEYNOTE SESSION: GENOME EDITING FOR IN VIVO APPLICATIONS

Part 1 (of a two-part conference) will cover the use of CRISPR/Cas9 and RNAi for identifying new drug targets and therapies. It will bring together experts from all aspects of basic science and clinical research to talk about how and where gene editing and RNAi can be best applied. What are the different tools that can be used and what are their strengths and limitations? How does the CRISPR/Cas system compare to RNAi and other gene editing tools, such as Transcription Activator-like Effector Nucleases (TALENs) and zinc finger nucleases (ZFNs), and do they have any complementary uses? Scientists and clinicians from pharma/biotech as well as from academic and government labs will share their experiences leveraging the utility of gene editing for target discovery, disease modeling, and for creating cell and viral therapies. Learn more atDiscoveryOnTarget.com/RNAi-screens-functional-genomics

Advance Registration Discount Available!
Register by August 12 Week to Save up to $200

Keynote Session: Genome Editing for In Vivo Applications

AAV for Gene Therapy and Genome Editing
James Wilson, M.D., Ph.D., Professor, Department of Pathology and Laboratory Medicine, Perelman School of Medicine; Director, Orphan Disease Center and Director, Gene Therapy Program, University of Pennsylvania
In vivo delivery of nucleic acid therapeutics remains the primary barrier to success. My lab has focused on the use of vectors based on adeno-associated virus (AAV) for achieving success in pre-clinical and clinical applications of gene replacement therapy. Most of the current academic and commercial applications of in vivo gene replacement therapy are based on endogenous AAVs we discovered as latent viral genomes in primates. These vectors are reasonably safe and efficient for application of gene replacement therapy. The emergence of genome editing methods has suggested more precise and effective methods to treat inherited diseases in which genes are silenced or mutations are corrected. AAV vectors have been the most efficient platform for achieving genome editing in vivo. We will review our attempts to achieve therapeutic genome editing in animal models of liver disease using AAV.

Using CRISPR/Cas to Target and Destroy Viral DNA Genomes
Bryan R. Cullen, Ph.D., James B. Duke Professor of Molecular Genetics and Microbiology and Director, Center for Virology, Duke University
A number of pathogenic human DNA viruses, including HBV, HIV-1 and HSV1, cause chronic diseases in humans that remain refractory to cure, though these diseases can be controlled by antivirals. In addition the DNA virus HPV causes tumors that depend on the continued expression of viral genes. Here, I will present data demonstrating that several of these viruses can be efficiently cleaved and destroyed using viral vectors that express Cas9 and virus-specific guide RNAs, thus providing a potential novel approach to treatment.

Targeted Endonucleases as Antiviral Agents: Promises and Pitfalls
Keith R. Jerome, M.D., Ph.D., Member, Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center; Professor and Head, Virology Division, Department of Laboratory Medicine, University of Washington
Genome editing offers the prospect of cure for infections such as HIV, hepatitis B virus, herpes simplex, and human papillomavirus, by disruption of essential viral nucleic acids or the human genes encoding receptors needed for viral entry. This talk will highlight the most recent laboratory data and the challenges still ahead in bringing this technology to the clinic.

Nucleic Acid Delivery Systems for RNA Therapy and Gene Editing
Daniel Anderson, Ph.D., Professor, Department of Chemical Engineering, Institute for Medical Engineering & Science, Harvard-MIT Division of Health Sciences & Technology and David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
High throughput, combinatorial approaches have revolutionized small molecule drug discovery. Here we describe our high throughput methods for developing and characterizing RNA delivery and gene editing systems. Libraries of degradable polymers and lipid-like materials have been synthesized, formulated and screened for their ability to deliver RNA, both in vitro and in vivo. A number of delivery formulations have been developed with in vivo efficacy, and show potential applications for the treatment of genetic diseases, viral infections and cancers.

PANEL DISCUSSION: CRISPR/Cas: A Realistic and Practical Look at What the Future Could Hold
Moderator: Bryan R. Cullen, Ph.D., James B. Duke Professor of Molecular Genetics and Microbiology and Director, Center for Virology, Duke University
Participants: Session Speakers
Each speaker will spend a few minutes sharing their viewpoints and experiences on where things stand with using the CRISPR/Cas system for in vivo applications. Attendees will have an opportunity to ask questions and share their opinions.

About the Conference

Cambridge Healthtech Institute’s 13th annual two-part conference on Advances in Gene Editing and Gene Silencing will cover the latest in the use of CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats)/Cas9-based gene editing and RNA interference (RNAi) for use in drug discovery and for developing novel drug therapies.


For sponsorship and exhibit sales information including podium presentation opportunities, contact:
Jon Stroup | T: +1 781-972-5483 | E: jstroup@healthtech.com


Recommended All Access Package:
Includes access to 1 Symposium and 2 Conferences

September 19 Symposium: 
Understanding CRISPR: Mechanisms and Applications

September 20-21 Conference:
Advances in Gene Editing and Gene Silencing – Part 1

September 21-22 Conference: 
Advances in Gene Editing and Gene Silencing – Part 2


Cambridge Healthtech Institute, 250 First Avenue, Suite 300, Needham, MA, USA

Tel: 781-972-5400 | Fax: 781-972-5425 | www.healthtech.com
This email is being sent to sjwilliamspa@comcast.net for marketing purposes. If it is not of interest to you, please disregard and we apologize for any inconvenience this may have caused.

Topical Solution for Combination Oncology Drug Therapy: Patch that delivers Drug, Gene, and Light-based Therapy to Tumor

Reporter: Aviva Lev-Ari, PhD, RN

 

Self-assembled RNA-triple-helix hydrogel scaffold for microRNA modulation in the tumour microenvironment

Affiliations

  1. Massachusetts Institute of Technology, Institute for Medical Engineering and Science, Harvard-MIT Division for Health Sciences and Technology, Cambridge, Massachusetts 02139, USA
    • João Conde,
    • Nuria Oliva,
    • Mariana Atilano,
    • Hyun Seok Song &
    • Natalie Artzi
  2. School of Engineering and Materials Science, Queen Mary University of London, London E1 4NS, UK
    • João Conde
  3. Grup dEnginyeria de Materials, Institut Químic de Sarrià-Universitat Ramon Llull, Barcelona 08017, Spain
    • Mariana Atilano
  4. Division of Bioconvergence Analysis, Korea Basic Science Institute, Yuseong, Daejeon 169-148, Republic of Korea
    • Hyun Seok Song
  5. Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA
    • Natalie Artzi
  6. Department of Medicine, Biomedical Engineering Division, Brigham and Womens Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    • Natalie Artzi

Contributions

J.C. and N.A. conceived the project and designed the experiments. J.C., N.O., H.S.S. and M.A. performed the experiments, collected and analysed the data. J.C. and N.A. co-wrote the manuscript. All authors discussed the results and reviewed the manuscript.

Nature Materials
15,
353–363
(2016)
doi:10.1038/nmat4497
Received
22 April 2015
Accepted
26 October 2015
Published online
07 December 2015

The therapeutic potential of miRNA (miR) in cancer is limited by the lack of efficient delivery vehicles. Here, we show that a self-assembled dual-colour RNA-triple-helix structure comprising two miRNAs—a miR mimic (tumour suppressor miRNA) and an antagomiR (oncomiR inhibitor)—provides outstanding capability to synergistically abrogate tumours. Conjugation of RNA triple helices to dendrimers allows the formation of stable triplex nanoparticles, which form an RNA-triple-helix adhesive scaffold upon interaction with dextran aldehyde, the latter able to chemically interact and adhere to natural tissue amines in the tumour. We also show that the self-assembled RNA-triple-helix conjugates remain functional in vitro and in vivo, and that they lead to nearly 90% levels of tumour shrinkage two weeks post-gel implantation in a triple-negative breast cancer mouse model. Our findings suggest that the RNA-triple-helix hydrogels can be used as an efficient anticancer platform to locally modulate the expression of endogenous miRs in cancer.

SOURCE

http://www.nature.com/nmat/journal/v15/n3/abs/nmat4497.html#author-information

 

 

Patch that delivers drug, gene, and light-based therapy to tumor sites shows promising results

In mice, device destroyed colorectal tumors and prevented remission after surgery.

Helen Knight | MIT News Office
July 25, 2016

Approximately one in 20 people will develop colorectal cancer in their lifetime, making it the third-most prevalent form of the disease in the U.S. In Europe, it is the second-most common form of cancer.

The most widely used first line of treatment is surgery, but this can result in incomplete removal of the tumor. Cancer cells can be left behind, potentially leading to recurrence and increased risk of metastasis. Indeed, while many patients remain cancer-free for months or even years after surgery, tumors are known to recur in up to 50 percent of cases.

Conventional therapies used to prevent tumors recurring after surgery do not sufficiently differentiate between healthy and cancerous cells, leading to serious side effects.

In a paper published today in the journal Nature Materials, researchers at MIT describe an adhesive patch that can stick to the tumor site, either before or after surgery, to deliver a triple-combination of drug, gene, and photo (light-based) therapy.

Releasing this triple combination therapy locally, at the tumor site, may increase the efficacy of the treatment, according to Natalie Artzi, a principal research scientist at MIT’s Institute for Medical Engineering and Science (IMES) and an assistant professor of medicine at Brigham and Women’s Hospital, who led the research.

The general approach to cancer treatment today is the use of systemic, or whole-body, therapies such as chemotherapy drugs. But the lack of specificity of anticancer drugs means they produce undesired side effects when systemically administered.

What’s more, only a small portion of the drug reaches the tumor site itself, meaning the primary tumor is not treated as effectively as it should be.

Indeed, recent research in mice has found that only 0.7 percent of nanoparticles administered systemically actually found their way to the target tumor.

“This means that we are treating both the source of the cancer — the tumor — and the metastases resulting from that source, in a suboptimal manner,” Artzi says. “That is what prompted us to think a little bit differently, to look at how we can leverage advancements in materials science, and in particular nanotechnology, to treat the primary tumor in a local and sustained manner.”

The researchers have developed a triple-therapy hydrogel patch, which can be used to treat tumors locally. This is particularly effective as it can treat not only the tumor itself but any cells left at the site after surgery, preventing the cancer from recurring or metastasizing in the future.

Firstly, the patch contains gold nanorods, which heat up when near-infrared radiation is applied to the local area. This is used to thermally ablate, or destroy, the tumor.

These nanorods are also equipped with a chemotherapy drug, which is released when they are heated, to target the tumor and its surrounding cells.

Finally, gold nanospheres that do not heat up in response to the near-infrared radiation are used to deliver RNA, or gene therapy to the site, in order to silence an important oncogene in colorectal cancer. Oncogenes are genes that can cause healthy cells to transform into tumor cells.

The researchers envision that a clinician could remove the tumor, and then apply the patch to the inner surface of the colon, to ensure that no cells that are likely to cause cancer recurrence remain at the site. As the patch degrades, it will gradually release the various therapies.

The patch can also serve as a neoadjuvant, a therapy designed to shrink tumors prior to their resection, Artzi says.

When the researchers tested the treatment in mice, they found that in 40 percent of cases where the patch was not applied after tumor removal, the cancer returned.

But when the patch was applied after surgery, the treatment resulted in complete remission.

Indeed, even when the tumor was not removed, the triple-combination therapy alone was enough to destroy it.

The technology is an extraordinary and unprecedented synergy of three concurrent modalities of treatment, according to Mauro Ferrari, president and CEO of the Houston Methodist Research Institute, who was not involved in the research.

“What is particularly intriguing is that by delivering the treatment locally, multimodal therapy may be better than systemic therapy, at least in certain clinical situations,” Ferrari says.

Unlike existing colorectal cancer surgery, this treatment can also be applied in a minimally invasive manner. In the next phase of their work, the researchers hope to move to experiments in larger models, in order to use colonoscopy equipment not only for cancer diagnosis but also to inject the patch to the site of a tumor, when detected.

“This administration modality would enable, at least in early-stage cancer patients, the avoidance of open field surgery and colon resection,” Artzi says. “Local application of the triple therapy could thus improve patients’ quality of life and therapeutic outcome.”

Artzi is joined on the paper by João Conde, Nuria Oliva, and Yi Zhang, of IMES. Conde is also at Queen Mary University in London.

SOURCE

http://news.mit.edu/2016/patch-delivers-drug-gene-light-based-therapy-tumor-0725

Other related articles published in thie Open Access Online Scientific Journal include the following:

The Development of siRNA-Based Therapies for Cancer

Author: Ziv Raviv, PhD

https://pharmaceuticalintelligence.com/2013/05/09/the-development-of-sirna-based-therapies-for-cancer/

 

Targeted Liposome Based Delivery System to Present HLA Class I Antigens to Tumor Cells: Two papers

Reporter: Stephen J. Williams, Ph.D.

https://pharmaceuticalintelligence.com/2016/07/20/targeted-liposome-based-delivery-system-to-present-hla-class-i-antigens-to-tumor-cells-two-papers/

 

Blast Crisis in Myeloid Leukemia and the Activation of a microRNA-editing Enzyme called ADAR1

Curator: Larry H. Bernstein, MD, FCAP

https://pharmaceuticalintelligence.com/2016/06/10/blast-crisis-in-myeloid-leukemia-and-the-activation-of-a-microrna-editing-enzyme-called-adar1/

 

First challenge to make use of the new NCI Cloud Pilots – Somatic Mutation Challenge – RNA: Best algorithms for detecting all of the abnormal RNA molecules in a cancer cell

Reporter: Aviva Lev-Ari, PhD, RN

https://pharmaceuticalintelligence.com/2016/07/17/first-challenge-to-make-use-of-the-new-nci-cloud-pilots-somatic-mutation-challenge-rna-best-algorithms-for-detecting-all-of-the-abnormal-rna-molecules-in-a-cancer-cell/

 

miRNA Therapeutic Promise

Curator: Larry H. Bernstein, MD, FCAP

https://pharmaceuticalintelligence.com/2016/05/01/mirna-therapeutic-promise/


Business Forward Roundtable with John Podesta: Economic Growth and Opportunity

Reporter: Stephen J. Williams, Ph.D.

July 26, 2016 (Philadelphia, PA)

A Round Table and Q&A with the Entrepreneur Group Business Forward and John Podesta,Chairman and Founder of Center for American Progress on Policy, Economic Growth and Opportunity

ABOUT BUSINESS FORWARD

With the help of more than 50 of the world’s most respected companies, Business Forward is making it easier for tens of thousands of business leaders from across America to advise Washington on how to create jobs and accelerate our economy. Business Forward is active in over 100 cities and works with more than 450 senior Administration officials, Members of Congress, mayors, and governors.

Business leaders who have participated in our briefings have seen their suggestions implemented in the Affordable Care Act, the Jobs Act, three trade agreements, and every one of the President’s budgets. Many have also shared their recommendations with their representatives in Congress and through op-eds and interviews with local media. Ninety-eight out of 100 business leaders who have participated in a Business Forward briefing would be interested in participating in another one.

Member Companies

Many of America’s largest and most respected firms – from America’s software, telecommunications, media, hospitality, financial services, manufacturing, apparel, defense and pharmaceutical industries – have already joined Business Forward.

Members include Aetna, American Airlines, AT&T, Comcast, Cheniere Energy, Deloitte, Dow, eBay Inc., Fidelity Investments, Facebook, Ford, Google, Intuit, Lockheed Martin, Microsoft, the National Restaurant Association, Pacific Gas & Electric, POET, Pricewaterhouse Cooper, Qualcomm, SAS, T-Mobile, Time Warner, Time Warner Cable, Verizon, Viacom, Visa, and Walmart.

These corporations work with Business Forward to identify, recruit and brief small business owners, venture capitalists and entrepreneurs of all kinds who are looking for a meaningful way to participate in policy debates.

John Podesta on Economic Policy, Equality and Growth

John Podesta delivered opening remarks at the launch event for the Washington Center for Equitable Growth on November 15, 2013.

Recommendations to Advance Progressive Change

Business Forward Round Table on Economic Strategy and Opportunity Agenda with John Podesta: Policy

John Padesta (JP): We have had an economic bounce back from the recession however it is agreed that wages need to go up in US.  The goal of policy is to return to a more equitable time such as during the 90’s.  The Hillary Clinton campaign is actively reaching out to find out what is happening on all levels of the economy: from small startups to international trade and workers views.

JP: There are five main areas the Clinton campaign is focusing on with regard to economic growth policy

  1.  jobs, investment, create context to spur private-public partnership investments
  2. skills training – human capital
  3. invest in places left behind: promise zones
  4. sustainable growth: allowing workers to share in productivity gains by tax reform, profit sharing
  5. family policy – says they will define this policy later in the week

JP: want to get entrepreneurs more involved with policy decision.  Clear directive from Hillary is that policy requires input from ALL stakeholders in economy in all sectors

There may be a focus on paid leave

Question from audience:  What about the crisis in rural health.

Definitely a problem Ann O’Leary will be heading up the health policy for Clinton campaign

 

 


The Roles of Graduate Students and Postdocs in the Emergence of Gene Editing: CRISPR Science and Technology

Curator: Aviva Lev-Ari, PhD, RN

 

PLAN TO ATTEND

DOT-150x150

Understanding CRISPR: Mechanisms and Applications: CHI, September 19-22, 2016, Westin Boston Waterfront, Boston

https://pharmaceuticalintelligence.com/2016/04/06/understanding-crispr-mechanisms-and-applications-chi-september-19-22-2016-westin-boston-waterfront-boston/

Announcement from LPBI Group: key code LPBI16 for Exclusive Discount to attend Boston’s Discovery on Target (September 19-22, 2016, CRISPR: Mechanisms to Applications on 9/19/2016)

https://pharmaceuticalintelligence.com/2016/05/13/announcement-from-lpbi-group-key-code-lpbi16-for-exclusive-discount-to-attend-bostons-discovery-on-target-september-2016/

 

The emergence of Gene Editing: CRISPR Science and Technology provide evidence that since the NIH effort to sequence the Genome, this endeavor is the second one to follow as an evolving scientific community ecosystem at their best in COMPETITION AND COLLABORATION, as well as in the survival of the fittest struggle that yielded a legal battle on appropriation of the discovery and the rights to its Intellectual Property (IP).

On our Journal we published

70 articles on Gene Editing: CRISPR Science and Technology

See references in

UPDATED – Status “Interference — Initial memorandum” – CRISPR/Cas9 – The Biotech Patent Fight of the Century: UC, Berkeley and Broad Institute @MIT

UPDATED – Status “Interference — Initial memorandum” – CRISPR/Cas9 – The Biotech Patent Fight of the Century

Reporter: Aviva Lev-Ari, PhD, RN

The unsung heroes of CRISPR

The soaring popularity of gene editing has made celebrities of the principal investigators who pioneered the field — but their graduate students and postdocs are often overlooked.

20 July 2016
Nature 535,342–344(21 July 2016)doi:10.1038/535342a
Heidi writes and Wiedenheft is quoted:
Doudna and other principal investigators involved in the seminal work have become scientific celebrities: they are profiled in major newspapers, star in documentaries and are rumoured to be contenders for a Nobel prize. “When I came to the lab, I was the only person studying CRISPR,” Wiedenheft says. “When I left the lab, almost everyone was studying it.”

His work with Doudna yielded a First author place on their 2011 Nature article:

Wiedenheft, B. et al. Nature 477, 486489 (2011).

In January 2016, Eric Lander, president of the Broad Institute of MIT and Harvard in Cambridge, Massachusetts, tossed into this minefield a historical portrait called ‘The Heroes of CRISPR

Lander, E. S. Cell 164, 1828 (2016).

Perspective

The Heroes of CRISPR

Eric S. Landercorrespondence

Editor of Cell received letters questioning the decision to publish Eric Lander’s article due to Broad Institute involvement in a legal dispute and presenting an incomplete picture of the evolution of the discovery and using a title that assigns the Heroism on a matter legally unsettled.

Does the Cell, 2016 article present all attributions due to:

1.The quiet revolutionary: How the co-discovery of CRISPR explosively changed Emmanuelle Charpentier’s life

The microbiologist spent years moving labs and relishing solitude. Then her work on gene-editing thrust her into the scientific spotlight.

27 April 2016

http://www.nature.com/news/the-quiet-revolutionary-how-the-co-discovery-of-crispr-explosively-changed-emmanuelle-charpentier-s-life-1.19814

and

2. Bitter fight over CRISPR patent heats up

Unusual battle among academic institutions holds key to gene-editing tool’s future use.

12 January 2016
Prof. Doudna at UC, Berkeley and Prof. Church at Harvard, both support appropriate credit to students involved in the discovery, yet the reality is that the
credit in science goes to the Leader of the lab, as do any prizes that follow.

BioTech Industry Prospect for Student of Powerhouse Academic Labs: Alternative Careers to Academic Positions

 

 

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