Search Results - "Montano, Ryan"

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  1. 1

    The Mre11 nuclease is critical for the sensitivity of cells to Chk1 inhibition by Thompson, Ruth, Montano, Ryan, Eastman, Alan

    Published in PloS one (24-08-2012)
    “…The Chk1 kinase is required for the arrest of cell cycle progression when DNA is damaged, and for stabilizing stalled replication forks. As a consequence, many…”
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    Journal Article
  2. 2

    Sensitization of human cancer cells to gemcitabine by the Chk1 inhibitor MK-8776: cell cycle perturbation and impact of administration schedule in vitro and in vivo by Montano, Ryan, Thompson, Ruth, Chung, Injae, Hou, Huagang, Khan, Nadeem, Eastman, Alan

    Published in BMC cancer (21-12-2013)
    “…Chk1 inhibitors have emerged as promising anticancer therapeutic agents particularly when combined with antimetabolites such as gemcitabine, cytarabine or…”
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    Journal Article
  3. 3

    Monitoring oxygen levels in orthotopic human glioma xenograft following carbogen inhalation and chemotherapy by implantable resonator‐based oximetry by Hou, Huagang, Krishnamurthy Nemani, Venkata, Du, Gaixin, Montano, Ryan, Song, Rui, Gimi, Barjor, Swartz, Harold M., Eastman, Alan, Khan, Nadeem

    Published in International journal of cancer (01-04-2015)
    “…Hypoxia is a critical hallmark of glioma, and significantly compromises treatment efficacy. Unfortunately, techniques for monitoring glioma pO2 to facilitate…”
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  4. 4

    A subset of cancer cell lines is acutely sensitive to the Chk1 inhibitor MK-8776 as monotherapy due to CDK2 activation in S phase by Sakurikar, Nandini, Thompson, Ruth, Montano, Ryan, Eastman, Alan

    Published in Oncotarget (12-01-2016)
    “…DNA damage activates Checkpoint kinase 1 (Chk1) to halt cell cycle progression thereby preventing further DNA replication and mitosis until the damage has been…”
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  5. 5

    Preclinical development of the novel Chk1 inhibitor SCH900776 in combination with DNA-damaging agents and antimetabolites by Montano, Ryan, Chung, Injae, Garner, Kristen M, Parry, David, Eastman, Alan

    Published in Molecular cancer therapeutics (01-02-2012)
    “…Many anticancer agents damage DNA and arrest cell-cycle progression primarily in S or G(2) phase of the cell cycle. Previous studies with the topoisomerase I…”
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  6. 6

    Cell cycle perturbation induced by gemcitabine in human tumor cells in cell culture, xenografts and bladder cancer patients: implications for clinical trial designs combining gemcitabine with a Chk1 inhibitor by Montano, Ryan, Khan, Nadeem, Hou, Huagang, Seigne, John, Ernstoff, Marc S, Lewis, Lionel D, Eastman, Alan

    Published in Oncotarget (15-09-2017)
    “…Gemcitabine irreversibly inhibits ribonucleotide reductase and induces S phase arrest but whether this occurs in tumors in mice or patients has not been…”
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  7. 7

    Abstract 943: The critical role of CDK2 activation in determining the differential sensitivity of cell lines to Chk1 and Wee1 inhibitors by Sakurikar, Nandini, Thompson, Ruth, Montano, Ryan, Eastman, Alan

    Published in Cancer research (Chicago, Ill.) (01-08-2015)
    “…Abstract Anticancer DNA damaging agents activate checkpoints that halt the cell cycle to prevent further DNA replication and mitosis until the damage has been…”
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  8. 8

    Abstract 2040: The Mre11 nuclease is critical for sensitivity of cells to Chk1 inhibition by Thompson, Ruth H., Montano, Ryan E., Eastman, Alan R.

    Published in Cancer research (Chicago, Ill.) (15-04-2012)
    “…Abstract The Chk1 kinase is required for the arrest of cell cycle progression when DNA is damaged, thereby providing time for cells to repair their DNA and…”
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  9. 9
  10. 10

    Abstract 2510: Efficacy of the Chk1 inhibitor SCH900776 at abrogating cell cycle arrest and enhancing DNA damage-induced cytotoxicity: Comparison with UCN-01 by Eastman, Alan, Montano, Ryan E., Garner, Kristen M., Chung, Injae, Parry, David A.

    Published in Cancer research (Chicago, Ill.) (15-04-2010)
    “…Abstract Many anticancer agents damage DNA and arrest cell cycle progression primarily in S or G2 phase of the cell cycle depending on drug concentration…”
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    Journal Article