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  1. Article ; Online: Exploiting RAS Nucleotide Cycling as a Strategy for Drugging RAS-Driven Cancers.

    Mattox, Tyler E / Chen, Xi / Maxuitenko, Yulia Y / Keeton, Adam B / Piazza, Gary A

    International journal of molecular sciences

    2019  Volume 21, Issue 1

    Abstract: Oncogenic mutations ... ...

    Abstract Oncogenic mutations in
    MeSH term(s) Animals ; Antineoplastic Agents/therapeutic use ; Humans ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism ; Signal Transduction/drug effects ; Signal Transduction/genetics ; ras Proteins/genetics
    Chemical Substances Antineoplastic Agents ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; ras Proteins (EC 3.6.5.2)
    Language English
    Publishing date 2019-12-24
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms21010141
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: A Novel Pan-RAS Inhibitor with a Unique Mechanism of Action Blocks Tumor Growth in Mouse Models of GI Cancer.

    Foote, Jeremy B / Mattox, Tyler E / Keeton, Adam B / Chen, Xi / Smith, Forrest T / Berry, Kristy L / Holmes, Thomas / Wang, Junwei / Huang, Chung-Hui / Ward, Antonio B / Hardy, Cherlene / Fleten, Karrianne G / Flatmark, Kjersti / Yoon, Karina J / Sarvesh, Sujith / Ganji, Puranchandra Nagaraju / Maxuitenko, Yulia / Valiyaveettil, Jacob / Carstens, Julienne L /
    Buchsbaum, Donald J / Yang, Jennifer / Zhou, Gang / Nurmemmedov, Elmar / Babic, Ivan / Gaponenko, Vadim / Abdelkarim, Hazem / Mitra, Amit K / Boyd, Michael R / Manne, Upender / Bae, Sejong / El-Rayes, Bassel F / Piazza, Gary A

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Here we characterize a novel pan-RAS inhibitor, ADT-007, that potently and selectively inhibited the growth of histologically diverse cancer cell lines with mutant or activated RAS irrespective of the RAS mutation or isozyme. Growth inhibition was ... ...

    Abstract Here we characterize a novel pan-RAS inhibitor, ADT-007, that potently and selectively inhibited the growth of histologically diverse cancer cell lines with mutant or activated RAS irrespective of the RAS mutation or isozyme. Growth inhibition was dependent on activated RAS and associated with reduced GTP-RAS levels and MAPK/AKT signaling. ADT-007 bound RAS in lysates from sensitive cells with sub-nanomolar EC
    Significance: ADT-007 is a novel pan-RAS inhibitor with a unique mechanism of action having potential to circumvent resistance to mutant-specific KRAS inhibitors and activate antitumor immunity. The findings support further development of ADT-007 analogs and/or prodrugs with oral bioavailability as a generalizable monotherapy or combined with immunotherapy for RAS mutant cancers.
    Background: It is projected that colorectal cancer (CRC) and pancreatic ductal adenocarcinoma (PDA) will cause 52,580 and 49,830 deaths in the US in 2023, respectively (1). The 5-year survival rates for CRC and PDA are 65% and 12%, respectively (1). Over 50% of CRC and 90% of PDA patients harbor mutations in KRAS genes that are associated with poor prognosis, making the development of novel KRAS inhibitors an urgent unmet medical need (2).
    Language English
    Publishing date 2024-01-24
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.05.17.541233
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Enhancing anticancer activity of checkpoint immunotherapy by targeting RAS.

    Ward, Antonio B / Keeton, Adam B / Chen, Xi / Mattox, Tyler E / Coley, Alex B / Maxuitenko, Yulia Y / Buchsbaum, Donald J / Randall, Troy D / Zhou, Gang / Piazza, Gary A

    MedComm

    2020  Volume 1, Issue 2, Page(s) 121–128

    Abstract: Approximately 30% of human cancers harbor a gain-in-function mutation in the RAS gene, resulting in constitutive activation of the RAS protein to stimulate downstream signaling, including the RAS-mitogen activated protein kinase pathway that drives ... ...

    Abstract Approximately 30% of human cancers harbor a gain-in-function mutation in the RAS gene, resulting in constitutive activation of the RAS protein to stimulate downstream signaling, including the RAS-mitogen activated protein kinase pathway that drives cancer cells to proliferate and metastasize. RAS-driven oncogenesis also promotes immune evasion by increasing the expression of programmed cell death ligand-1, reducing the expression of major histocompatibility complex molecules that present antigens to T-lymphocytes and altering the expression of cytokines that promote the differentiation and accumulation of immune suppressive cell types such as myeloid-derived suppressor cells, regulatory T-cells, and cancer-associated fibroblasts. Together, these changes lead to an immune suppressive tumor microenvironment that impedes T-cell activation and infiltration and promotes the outgrowth and metastasis of tumor cells. As a result, despite the growing success of checkpoint immunotherapy, many patients with RAS-driven tumors experience resistance to therapy and poor clinical outcomes. Therefore, RAS inhibitors in development have the potential to weaken cancer cell immune evasion and enhance the antitumor immune response to improve survival of patients with RAS-driven cancers. This review highlights the potential of RAS inhibitors to enhance or broaden the anti-cancer activity of currently available checkpoint immunotherapy.
    Language English
    Publishing date 2020-06-25
    Publishing country China
    Document type Journal Article
    ISSN 2688-2663
    ISSN (online) 2688-2663
    DOI 10.1002/mco2.10
    Database MEDical Literature Analysis and Retrieval System OnLINE

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