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Innovations

  • Our Mission

    To actively accelerate innovations to benefit patients, society, and the Dana-Farber Cancer Institute. We team with investigators to identify new discoveries and generate alliances to move science from bench to clinic for maximum impact.

    Our Vision

    To spark and fuel a spirit of innovation across the organization by providing effective tools to continuously question, create, and imagine what else might be possible.

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    In collaborating with Dana-Farber, your organization will have access to the Institute's specialized expertise, and to the unique array of core facilities needed to explore new areas of research. Learn more about Dana-Farber Centers that are interested in partnering with industry. Explore Dana-Farber's extensive Core Facilities. And discover more opportunities to collaborate.

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  • In partnership with the Innovation Office, Dana-Farber makes publicly available a list of FDA-approved therapeutics and diagnostics in which the Institute has a financial interest.
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  • Technology News

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    Dana-Farber Researchers Presented >30 Research Studies at AACR Virtual Meeting Week 1

    Dana-Farber researchers presented more than 30 research studies during Week 1 of the virtual American Association for Cancer Research (AACR) Annual Meeting 2021, April 10-15. AACR is the world’s first and largest professional organization dedicated to advancing cancer research and its mission to prevent and cure cancer. Presentations by, and awards to, Dana-Farber researchers included:

    * Mechanisms of acquired resistance to KRAS G12C inhibition in cancer (Mark Awad, MD, PhD)

    * PATHFINDER: Interim analysis of avapritinib (ava) in patients with advanced systemic mastocytosis (AdvSM) (Daniel DeAngelo, MD, PhD)

    * Plenary by William G. Kaelin Jr., MD, highlighting important physiologic constraints a cancer tissue must operate within, focusing on the critical role hypoxia plays in both tumor growth and progression, and how modulating the hypoxia machinery will limit tumor progression

    * Andrew Aguirre, MD, PhD, named a 2021 AACR NextGen Star

    * Sarah Hill, MD, PhD, received 2021 Cancer Research Early Career Award   

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    Oral NF-κB Inhibitor Dimethylaminoparthenolide Delays Prostate Cancer Resistance to Androgen Receptor Inhibition (Molecular Cancer Research)

    NF-κB activation has been linked to prostate cancer (PCa) progression and is commonly observed in castrate-resistant disease. NF-κB-driven resistance to androgen deprivation therapy (ADT) in PCa cells is suggested to be mediated by aberrant androgen receptor (AR) activation and AR splice variant production. Thus, preventing resistance to ADT may be achieved by utilizing NF-κB inhibitors. Dimethylaminoparthlide (DMAPT) is an oral NF-κB inhibitor in clinical development and has already shown favorable pharmacokinetic and pharmacodyanamic profiles in patients with heme malignancies including decrease of NF-κB in circulating leuchemic blasts. In a recent study in Molecular Cancer Research, first author Katherine Morel, PhD, and senior author Christopher Sweeney, MBBS, report that activation of NF-κB/p65 by castration in mouse and human PCa models resulted in a significant increase in AR variant-7 (AR-V7) expression and modest upregulation of AR. DMAPT inhibits phosphorylated-p65 dependent upregulation of AR-V7 and delays PCa castration resistance ... 

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    miR-15a/16-1 Deletion in Activated B-Cells Promotes Plasma Cell and Mature B-cell Neoplasms (Blood)

    Chromosome 13q deletion [del(13q)], harboring the miR-15a/16-1 cluster, is one of the most common genetic alterations in mature B-cell malignancies, which originate from germinal center (GC) and post-GC B cells. However, the role of miR-15a/16-1 in B-cell activation and initiation of mature B-cell neoplasms remains elusive. As highlighted in a recent study in the American Society of Hematology's Blood, first author Tomasz Sewastianik, PhD, and senior author Ruben Carrasco, MD, PhD, present their findings that loss of miR-15a/16-1 in mice models induces widespread alterations in GC B-cells and promotes plasma and mature B-cell neoplasms. Over time, this leads to the development of mature B-cell neoplasms resembling human extramedullary plasmacytoma (EP), as well as follicular and diffuse large B-cell lymphomas ... 


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