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  1. Article ; Online: Believe the miracles: of biomedical science and human suffering.

    Garraway, Levi A

    The Journal of clinical investigation

    2016  Volume 126, Issue 12, Page(s) 4716–4722

    MeSH term(s) Biomedical Research/methods ; Biomedical Research/standards ; Biomedical Research/trends ; Humans
    Language English
    Publishing date 2016-12-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI90893
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  2. Article ; Online: A Notch for noncoding RNA in melanoma.

    Garraway, Levi A

    The New England journal of medicine

    2014  Volume 370, Issue 20, Page(s) 1950–1951

    MeSH term(s) Gene Expression Regulation, Neoplastic ; Humans ; Melanoma/genetics ; Melanoma/metabolism ; MicroRNAs/metabolism ; Mutation ; Polymorphism, Single Nucleotide ; Proto-Oncogene Proteins B-raf/genetics ; Proto-Oncogene Proteins B-raf/metabolism ; Receptors, Notch/metabolism ; Up-Regulation
    Chemical Substances MIRN146 microRNA, human ; MicroRNAs ; Receptors, Notch ; BRAF protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1)
    Language English
    Publishing date 2014-05-15
    Publishing country United States
    Document type Journal Article
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMcibr1402173
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  3. Article ; Online: Genomics-driven oncology: framework for an emerging paradigm.

    Garraway, Levi A

    Journal of clinical oncology : official journal of the American Society of Clinical Oncology

    2013  Volume 31, Issue 15, Page(s) 1806–1814

    Abstract: A majority of cancers are driven by genomic alterations that dysregulate key oncogenic pathways influencing cell growth and survival. However, the ability to harness tumor genetic information for its full clinical potential has only recently become ... ...

    Abstract A majority of cancers are driven by genomic alterations that dysregulate key oncogenic pathways influencing cell growth and survival. However, the ability to harness tumor genetic information for its full clinical potential has only recently become manifest. Over the past several years, the convergence of discovery, technology, and therapeutic development has created an unparalleled opportunity to test the hypothesis that systematic knowledge of genomic information from individual tumors can improve clinical outcomes for many patients with cancer. Rigorous evaluation of this genomics-driven cancer medicine hypothesis will require many logistic innovations that are guided by overarching conceptual advances in tumor genomic profiling, data interpretation, clinical trial design, and the ethical return of genetic results to oncologists and their patients. The results of these efforts and the rigor with which they are implemented will determine whether and how comprehensive tumor genomic information may become incorporated into the routine care of patients with cancer.
    MeSH term(s) Chromosome Aberrations ; Gene Regulatory Networks ; Genetic Predisposition to Disease/genetics ; Genomics/methods ; Genomics/trends ; Humans ; Medical Oncology/methods ; Medical Oncology/trends ; Models, Genetic ; Mutation ; Neoplasms/drug therapy ; Neoplasms/genetics
    Language English
    Publishing date 2013-05-20
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 604914-x
    ISSN 1527-7755 ; 0732-183X
    ISSN (online) 1527-7755
    ISSN 0732-183X
    DOI 10.1200/JCO.2012.46.8934
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Making cancer research more inclusive.

    Carpten, John D / Fashoyin-Aje, Lola / Garraway, Levi A / Winn, Robert

    Nature reviews. Cancer

    2021  Volume 21, Issue 10, Page(s) 613–618

    MeSH term(s) Biomedical Research/trends ; Blacks ; Health Status Disparities ; Healthcare Disparities ; Humans ; Neoplasms/genetics ; Neoplasms/therapy ; Racism/prevention & control ; Social Inclusion
    Language English
    Publishing date 2021-06-29
    Publishing country England
    Document type Journal Article
    ZDB-ID 2062767-1
    ISSN 1474-1768 ; 1474-175X
    ISSN (online) 1474-1768
    ISSN 1474-175X
    DOI 10.1038/s41568-021-00369-7
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  5. Article ; Online: Concordance and discordance in tumor genomic profiling.

    Garraway, Levi A

    Journal of clinical oncology : official journal of the American Society of Clinical Oncology

    2012  Volume 30, Issue 24, Page(s) 2937–2939

    MeSH term(s) Colorectal Neoplasms/genetics ; Colorectal Neoplasms/secondary ; DNA Copy Number Variations ; Female ; Humans ; Male ; Mutation
    Language English
    Publishing date 2012-08-20
    Publishing country United States
    Document type Comment ; Editorial ; Research Support, Non-U.S. Gov't
    ZDB-ID 604914-x
    ISSN 1527-7755 ; 0732-183X
    ISSN (online) 1527-7755
    ISSN 0732-183X
    DOI 10.1200/JCO.2011.41.3138
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  6. Book: Principles of drug resistance and cancer precision medicine

    Garraway, Levi A

    (NCI Center for Cancer Research eminent lecture)

    2015  

    Title variant Principles of cancer drug resistance and precision medicine
    Institution National Institutes of Health (U.S.),
    Author's details Levi A. Garraway
    Series title NCI Center for Cancer Research eminent lecture
    MeSH term(s) Drug Resistance, Neoplasm ; Neoplasms/drug therapy
    Language English
    Size 1 online resource (1 streaming video file (1 hr., 7 min.)) :, color, sound.
    Document type Book
    Note Closed-captioned. ; Access restricted to HHS only.
    Database Catalogue of the US National Library of Medicine (NLM)

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  7. Article ; Online: A Convergence-Based Framework for Cancer Drug Resistance.

    Konieczkowski, David J / Johannessen, Cory M / Garraway, Levi A

    Cancer cell

    2018  Volume 33, Issue 5, Page(s) 801–815

    Abstract: Despite advances in cancer biology and therapeutics, drug resistance remains problematic. Resistance is often multifactorial, heterogeneous, and prone to undersampling. Nonetheless, many individual mechanisms of targeted therapy resistance may coalesce ... ...

    Abstract Despite advances in cancer biology and therapeutics, drug resistance remains problematic. Resistance is often multifactorial, heterogeneous, and prone to undersampling. Nonetheless, many individual mechanisms of targeted therapy resistance may coalesce into a smaller number of convergences, including pathway reactivation (downstream re-engagement of original effectors), pathway bypass (recruitment of a parallel pathway converging on the same downstream output), and pathway indifference (development of a cellular state independent of the initial therapeutic target). Similar convergences may also underpin immunotherapy resistance. Such parsimonious, convergence-based frameworks may help explain resistance across tumor types and therapeutic categories and may also suggest strategies to overcome it.
    MeSH term(s) Biomarkers, Tumor/metabolism ; Drug Resistance, Neoplasm ; Humans ; Immunotherapy ; Molecular Targeted Therapy ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Precision Medicine
    Chemical Substances Biomarkers, Tumor
    Language English
    Publishing date 2018-05-10
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2078448-X
    ISSN 1878-3686 ; 1535-6108
    ISSN (online) 1878-3686
    ISSN 1535-6108
    DOI 10.1016/j.ccell.2018.03.025
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  8. Article ; Online: Synthetic lethality as an engine for cancer drug target discovery.

    Huang, Alan / Garraway, Levi A / Ashworth, Alan / Weber, Barbara

    Nature reviews. Drug discovery

    2019  Volume 19, Issue 1, Page(s) 23–38

    Abstract: The first wave of genetically targeted therapies for cancer focused on drugging gene products that are recurrently mutated in specific cancer types. However, mutational analysis of tumours has largely been exhausted as a strategy for the identification ... ...

    Abstract The first wave of genetically targeted therapies for cancer focused on drugging gene products that are recurrently mutated in specific cancer types. However, mutational analysis of tumours has largely been exhausted as a strategy for the identification of new cancer targets that are druggable with conventional approaches. Furthermore, some known genetic drivers of cancer have not been directly targeted yet owing to their molecular structure (undruggable oncogenes) or because they result in functional loss (tumour suppressor genes). Functional genomic screening based on the genetic concept of synthetic lethality provides an avenue to discover drug targets in all these areas. Although synthetic lethality is not a new idea, recent advances, including CRISPR-based gene editing, have made possible systematic screens for synthetic lethal drug targets in human cancers. Such approaches have broad potential to drive the discovery of the next wave of genetic cancer targets and ultimately the introduction of effective medicines that are still needed for most cancers.
    MeSH term(s) Antineoplastic Agents/therapeutic use ; Drug Discovery ; Gene Editing ; Genetic Therapy ; Humans ; Molecular Targeted Therapy ; Neoplasm Proteins/antagonists & inhibitors ; Neoplasm Proteins/genetics ; Neoplasms/drug therapy ; Neoplasms/genetics ; Synthetic Lethal Mutations/drug effects
    Chemical Substances Antineoplastic Agents ; Neoplasm Proteins
    Language English
    Publishing date 2019-11-11
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2062954-0
    ISSN 1474-1784 ; 1474-1776
    ISSN (online) 1474-1784
    ISSN 1474-1776
    DOI 10.1038/s41573-019-0046-z
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    Zs.MO 334: Show issues
    Zs.MG 63: Show issues

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  9. Article: Mechanisms of Resistance to Mitogen-Activated Protein Kinase Pathway Inhibition in BRAF-Mutant Melanoma.

    Goetz, Eva M / Garraway, Levi A

    American Society of Clinical Oncology educational book. American Society of Clinical Oncology. Annual Meeting

    2014  , Page(s) 680–684

    Abstract: Anticancer drug resistance remains a crucial impediment to the care of many patients with cancer. Although the exact mechanisms of resistance may differ for each therapy, common mechanisms of resistance predominate, including drug inactivation or ... ...

    Abstract Anticancer drug resistance remains a crucial impediment to the care of many patients with cancer. Although the exact mechanisms of resistance may differ for each therapy, common mechanisms of resistance predominate, including drug inactivation or modification, mutation of the target protein, reduced drug accumulation, or bypass of target inhibition. With the discovery and use of targeted therapies (such as small-molecule kinase inhibitors), resistance has received renewed attention-especially in light of the dramatic responses that may emerge from such therapeutics in particular genetic or molecular contexts. Recently, the mitogen-activated protein kinase (MAPK) pathway has become exemplary in this regard, since it is activated in many different cancers. Drugs targeting RAF and MAPK kinase (MEK) are currently in clinical trials for the treatment of several types of cancer. Vemurafenib, a selective RAF kinase inhibitor recently approved for the treatment of BRAF(V600E) melanoma, shows strong efficacy initially; however, the development of resistance is nearly ubiquitous. In vitro testing and analysis of patient samples have uncovered several mechanisms of resistance to RAF inhibition. Surprisingly, mutations in the drug-binding pocket have not thus far been observed; however, other alterations at the level of RAF, as well as downstream activation of MEK and bypass of MEK/extracellular signal-regulated kinase (ERK) signaling altogether, confer resistance to vemurafenib. Looking forward, combined RAF and MEK inhibitor treatments may improve efficacy-yet we must anticipate mechanisms of resistance to this combination as well. Therefore, understanding and/or determining the mechanism of resistance are paramount to effective cancer treatment.
    Language English
    Publishing date 2014-01-09
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2431126-1
    ISSN 1548-8756 ; 1548-8748
    ISSN (online) 1548-8756
    ISSN 1548-8748
    DOI 10.14694/EdBook_AM.2012.32.680
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Book: Defining the spectrum of resistance to be targeted anti-cancer therapeutics

    Garraway, Levi A

    (NIH Wednesday afternoon lecture)

    2012  

    Abstract: CIT): Dr. Levi Garraway has made seminal research contributions in cancer genomics, drug resistance, and genomics-driven (or "personalized") cancer medicine. He published the first genome sequencing studies of aggressive primary prostate cancer, and has ...

    Institution National Institutes of Health (U.S.)
    Author's details Levi A. Garraway
    Series title NIH Wednesday afternoon lecture
    Abstract (CIT): Dr. Levi Garraway has made seminal research contributions in cancer genomics, drug resistance, and genomics-driven (or "personalized") cancer medicine. He published the first genome sequencing studies of aggressive primary prostate cancer, and has led other major sequencing initiatives in prostate cancer, melanoma and head/neck cancers. This work identified multiple new cancer genes and uncovered mechanisms by which complex rearrangements arise. At the Broad Institute, he leads the Cancer Cell Line Encyclopedia, a collaboration with Novartis that involves a genomic and pharmacological study of ~1000 human cancer cell lines to characterize sensitivity and resistance to anticancer agents. Dr. Garraway is perhaps best known for his contributions to precision cancer medicine. He described the first high-throughput adaptation of a genomic technology to profile human tumors for hundreds of "actionable" cancer gene mutations. This provided a basis for tumor mutation profiling as a means to stratify cancer patients for clinical trial enrollment and, in the future, optimal therapeutic choices. He also demonstrated the promise of massive parallel sequencing as a clinical tumor genomic profiling approach.
    MeSH term(s) Neoplasms/drug therapy ; Molecular Targeted Therapy ; Drug Resistance, Neoplasm
    Language English
    Size 1 online resource (1 streaming video file (1 hr., 3 min.) :, sd., col.)
    Publisher National Institutes of Health
    Publishing place Bethesda, Md
    Document type Book
    Note Closed-captioned.
    Database Catalogue of the US National Library of Medicine (NLM)

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