Juno Therapeutics Announces Data Presentations at the American Association for Cancer Research Annual Meeting

On April 14, 2016 Juno Therapeutics, Inc. (NASDAQ: JUNO), a biopharmaceutical company focused on re-engaging the body’s immune system to revolutionize the treatment of cancer, reported the Company, in partnership with its collaborators, will present clinical and pre-clinical data from multiple product candidates at the upcoming American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2016 in New Orleans, Louisiana from April 16-20 (Press release, Juno, APR 14, 2016, View Source;p=RssLanding&cat=news&id=2157199 [SID:1234510814]).

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There will be two presentations with clinical updates. On April 18th, Dr. Terry Fry will present the pre-clinical and clinical rationale as well as updated data from the ongoing Phase I trial of JCAR018, a chimeric antigen receptor (CAR) T cell product candidate targeting CD22, in pediatric and young adult patients with relapsed or refractory B-cell acute lymphoblastic leukemia (r/r ALL). On April 20th, Dr. Phil Greenberg will present the pre-clinical rationale as well as the first clinical data in patients with solid organ tumors for JTCR016, a T cell receptor (TCR) cell product candidate targeting Wilms tumor-1 (WT-1).

Dr. Hy Levitsky, Juno’s Executive Vice President, Research and Chief Scientific Officer, will discuss pre-clinical data that informed the rationale and design of the ongoing Phase 1 trial for JCAR024, a CAR T cell product candidate targeting ROR-1, in ROR-expressing tumors. Additionally, two Juno-sponsored posters will be presented and Juno’s investigational CAR T cell product candidates will be featured in three additional presentations.

Clinical and Pre-Clinical Updates

CD22 CAR Update and Novel Mechanisms of Leukemic Resistance
Presenter: Terry J. Fry, M.D., Investigator, Pediatric Oncology Branch and Head of Hematologic Malignancies Section, National Cancer Institute, National Institutes of Health
Date: Monday, April 18, 2016: 12:35 – 12:58 p.m. Eastern Time
Location: Room 243

Targeting Cancer with Engineered T Cells
Presenter: Phil Greenberg, M.D., Head of Program in Immunology at the Fred Hutchinson Cancer Research Center and Professor, Medicine/Oncology and Immunology, University of Washington
Date: Wednesday, April 20, 2016: 10:55 – 11:20 a.m. Eastern Time
Location: New Orleans Theater B

Pre-Clinical Updates
ROR1 Targeted by CAR T Cells
Presenter: Hy Levitsky, M.D., Juno’s Executive Vice President, Research and Chief Scientific Officer
Date: Tuesday, April 19, 2016: 1:05 – 1:30 p.m. Eastern Time
Location: New Orleans Theater C

Toxicity and Efficacy Probability Intervals Design for Phase I Dose-Finding in Oncology Trials
Authors: Daniel Li, Ph.D., et al., Juno Department of Clinical Statistics
Date: Sunday, April 17, 2016: 1:00 – 5:00 p.m. Eastern Time
Location: Section 20, Poster Board #29

Comprehensive TIL Profiling by Simultaneous DNA Barcoding of Proteins, RNA and Natively Paired Immune Receptors from Millions of Single Cells
Authors: Katherine Connor, Ph.D., et al., Juno Department of Research, Receptor Discovery
Date: Monday, April 18, 2016: 8:00 a.m. – 12:00 p.m. Eastern Time
Location: Section 24, Poster Board #3

Educational and Major Symposia Sessions
The New T Cell Engineering Arsenal: CARs, CCRs, iCARs, and More
Presenter: Michel Sadelain, M.D., Ph.D., Director, Center for Cell Engineering & Gene Transfer and Gene Expression Laboratory; Stephen and Barbara Friedman Chair, Memorial Sloan Kettering Cancer Center
Date: Saturday, April 16, 2016: 2:00 – 2:25 p.m. Eastern Time
Location: New Orleans Theater A

Novel Designs and Targets for CAR T Cells
Presenter: Stan Riddell, M.D., Member, Program in Immunology, Clinical Research Division, Fred Hutchinson Cancer Research Center, Professor of Oncology, University of Washington School of Medicine
Date: Tuesday, April 19, 2016: 10:40 – 11:05 a.m. Eastern Time
Location: La Nouvelle Orleans Ballroom

Turbo Charged CAR T Cells
Presenter: Michel Sadelain, M.D., Ph.D., Director, Center for Cell Engineering & Gene Transfer and Gene Expression Laboratory; Stephen and Barbara Friedman Chair, Memorial Sloan Kettering Cancer Center
Date: Tuesday, April 19, 2016: 11:40 a.m. – 12:05 p.m. Eastern Time
Location: La Nouvelle Orleans Ballroom

About Juno’s Chimeric Antigen Receptor (CAR) and T Cell Receptor (TCR) Technologies

Juno’s CAR and TCR technologies genetically engineer T cells to recognize and kill cancer cells. Juno’s CAR T cell technology inserts a gene for a particular CAR into the T cell, enabling it to recognize cancer cells based on the expression of a specific protein located on the cell surface. Juno’s TCR technology provides the T cells with a specific T cell receptor to recognize protein fragments derived from either the surface or inside the cell. When either type of engineered T cell engages the target protein on the cancer cell, it initiates a cell-killing response against the cancer cell. JCAR018, JTCR016, and JCAR024 are investigational product candidates and their safety and efficacy have not been established.

The use of bisphosphonates in the management of bone involvement from solid tumours and haematological malignancies – a European survey.

Bone metastases in patients with solid tumours (ST) and bone lesions in patients with haematological malignancies (HM) are common. Associated skeletal-related events (SREs) cause severe pain, reduced quality of life and place a burden on health care resources. Bone-targeted agents can reduce the risk of SREs. We evaluated the management of bone metastasis/lesions in five European countries (France, Germany, Italy, Spain and the UK) by an observational chart audit. In total, 881 physicians completed brief questionnaires on 17 193 patients during the observation period, and detailed questionnaires for a further 9303 individuals. Patient cases were weighted according to the probability of inclusion. Although a large proportion of patients with bone metastases/lesions were receiving bisphosphonates, many had their treatment stopped (ST, 19%; HM, 36%) or will never be treated (ST, 18%; HM, 13%). The results were generally similar across the countries, although German patients were more likely to have asymptomatic bone lesions detected during routine imaging. In conclusion, many patients who could benefit from bone-targeted agents do not receive bisphosphonates and many have their treatment stopped when they could benefit from continued treatment. Developing treatment guidelines, educating physicians and increasing the availability of new agents could benefit patients and reduce costs.
© 2016 The Authors. European Journal of Cancer Care Published by John Wiley & Sons Ltd.

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Structure-Based Design of a Novel SMYD3 Inhibitor that Bridges the SAM-and MEKK2-Binding Pockets.

SMYD3 is a lysine methyltransferase overexpressed in colorectal, breast, prostate, and hepatocellular tumors, and has been implicated as an oncogene in human malignancies. Methylation of MEKK2 by SMYD3 is important for regulation of the MEK/ERK pathway, suggesting the possibility of selectively targeting SMYD3 in RAS-driven cancers. Structural and kinetic characterization of SMYD3 was undertaken leading to a co-crystal structure of SMYD3 with a MEKK2-peptide substrate bound, and the observation that SMYD3 follows a partially processive mechanism. These insights allowed for the design of GSK2807, a potent and selective, SAM-competitive inhibitor of SMYD3 (Ki = 14 nM). A high-resolution crystal structure reveals that GSK2807 bridges the gap between the SAM-binding pocket and the substrate lysine tunnel of SMYD3. Taken together, our data demonstrate that small-molecule inhibitors of SMYD3 can be designed to prevent methylation of MEKK2 and these could have potential use as anticancer therapeutics.
Copyright © 2016 Elsevier Ltd. All rights reserved.

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Myriad Genetics Announces Presentations at the 2016 American Association for Cancer Research Annual Meeting

On April 14, 2016 Myriad Genetics, Inc. (NASDAQ:MYGN), a leader in molecular diagnostics and personalized medicine, reported that the company and its scientific collaborators will present two studies at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) annual meeting, April 16-20, in New Orleans, La (Press release, Myriad Genetics, APR 14, 2016, View Source [SID:1234510815]). The data will highlight early clinical trials of PARP inhibitors targeting the DNA repair pathway and the use of novel biomarkers to select patients for treatment.

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"Myriad is a leader in developing companion diagnostics for promising new medicines like the PARP inhibitors currently in clinical development," said Richard Wenstrup, M.D., chief medical officer, Myriad Genetics. "Our successful collaborations demonstrate our collective goal of improving patient care through precision medicine. Our growing portfolio of companion diagnostics will achieve that objective by helping physicians select the right treatments for their patients with cancer."

The studies to be presented are described below, and the abstracts are now available at: View Source Follow Myriad on Twitter via @MyriadGenetics to stay informed about news and updates from the Company.

Featured AACR (Free AACR Whitepaper) Mini-Symposia

Title: Safety and efficacy results from a Phase 1 dose-escalation trial of the PARP inhibitor talazoparib (BMN-673) in combination with either temozolomide or irinotecan in patients with advanced malignancies.
Date: Sunday, April 17, 2016: 4:30—4:45 p.m. CDT.
Location: Podium CT011.
Presenter: Zev A. Wainberg, M.D., UCLA Medical Center

Title: Preclinical evaluation of the PARP inhibitor niraparib and cytotoxic chemotherapy alone in combination in a panel of 25 triple-negative breast cancer PDX models: relevance of BRCA mutations, HRD status and other biomarkers.
Date: Tuesday, April 19, 2016: 3:20—3:35 p.m. CDT.
Location: Podium 4353.
Presenter: Olivier Deas, Ph.D., XenTech SAS.

10-Q/A [Amend] – Quarterly report [Sections 13 or 15(d)]

(Filing, 10-K, TapImmune, 2015, APR 14, 2016, View Source [SID:1234510877])

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