Search Results - "Heiniger, Cale L"

Abstract B129: Preclinical studies with DCC-3116, an ULK kinase inhibitor designed to inhibit autophagy as a potential strategy to address mutant RAS cancers by Smith, Bryan D, Vogeti, Lakshminarayana, Gupta, Anu, Singh, Jarnail, Al-Ani, Gada, Bulfer, Stacie L, Caldwell, Timothy M, Timson, Mary J, Vogeti, Subha, Ahn, Yu Mi, Al-Hashimi, Hikmat, Crawley, Chase K, Heiniger, Cale L, Leary, Cynthia B, Proto, Justin T, Shen, Quanrong, Telikepalli, Hanumaiah, Yates, Karen, Lu, Wei-Ping, Flynn, Daniel L

“…Abstract Background: Cancer cells activate autophagy, a catabolic process to resupply nutrients and recycle damaged organelles, in order to survive stresses…”
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Abstract 1640: DP-9024, an investigational small molecule modulator of the Integrated Stress Response kinase PERK, causes B-cell cancer growth inhibition as single agent and in combination with standard-of-care agents by Al-Ani, Gada, Groer, Qi, Rudeen, Aaron J., Elliott, Kristin M., Kearney, Patrick C., Zwicker, Jeffery D., Ahn, Yu Mi, Bulfer, Stacie L., Heiniger, Cale L., Hood, Molly M., Javed, Salim, Large, Joshua W., Petty, Max D., Stoltz, Kristen L., Bourdonnec, Bertrand Le, Smith, Bryan D., Flynn, Daniel L.

“…Abstract Background: The Integrated Stress Response (ISR) is a major adaptive stress response pathway in cancer cell maintenance. The ISR kinase family member…”
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Abstract 4033: Pan-exon mutant KIT inhibitor DCC-3009 demonstrates tumor regressions in preclinical gastrointestinal stromal tumor models by Smith, Bryan D., Vogeti, Subha, Caldwell, Timothy M., Telikepalli, Hanumaiah, Ahn, Yu Mi, Al-Ani, Gada, Bulfer, Stacie L., Greenwood, Andrew, Heiniger, Cale L., Large, Joshua W., Leary, Cynthia B., Lu, Wei-Ping, Luther, Kylie, Patt, William C., Petty, Max D., Romero, Yeni K., Stanley, Forrest A., Stoltz, Kristen L., Tanner, Daniel C., Yang, Sihyung, Zhan, Yu, Bourdonnec, Bertrand Le, Flynn, Daniel L.

“…Abstract Introduction: Gastrointestinal stromal tumors (GISTs) are typically driven by primary mutations in KIT exons 9 or 11. Heterogeneous drug-resistant…”
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Abstract 1639: DP-9149, an investigational small molecule modulator of the Integrated Stress Response kinase GCN2, pre-clinically causes solid tumor growth inhibition as a single agent and regression in combination with standard of care agents by Al-Ani, Gada, Groer, Qi, Elliott, Kristin M., Rudeen, Aaron J., Kearney, Patrick C., Zwicker, Jeffery D., Ahn, Yu Mi, Bulfer, Stacie L., Heiniger, Cale L., Hood, Molly M., Javid, Salim, Large, Joshua W., Petty, Max D., Stoltz, Kristen L., Bourdonnec, Bertrand Le, Smith, Bryan D., Flynn, Daniel L.

“…Abstract Background: The Integrated Stress Response (ISR) is one of the major adaptive stress response pathways in cancer and plays an important role in cell…”
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Abstract 1613: Dimerization-induced activation of the integrated stress response kinase PERK by an investigational small molecule modulator, DP-9024 by Al-Ani, Gada, Rudeen, Aaron J., Groer, Qi, Elliott, Kristin M., Kearney, Patrick C., Zwicker, Jeffery D., Ahn, Yu Mi, Bulfer, Stacie L., Heiniger, Cale L., Hood, Molly M., Javid, Salim, Large, Joshua W., Petty, Max D., Stoltz, Kristen L., Bourdonnec, Bertrand Le, Smith, Bryan D., Flynn, Daniel L.

“…Abstract Background: The Integrated Stress Response (ISR) is a major adaptive stress response pathway in cancers. The ISR kinase family member PERK controls…”
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Abstract 4938: DP-9024, an investigational small molecule modulator of the integrated stress response kinase GCN2, synergizes with asparaginase therapy in leukemic tumors by Al-Ani, Gada, Elliott, Kristin M., Groer, Qi, Rudeen, Aaron J., Kearney, Patrick C., Zwicker, Jeffery D., Ahn, Yu Mi, Bulfer, Stacie L., Heiniger, Cale L., Hood, Molly M., Javed, Salim, Large, Joshua W., Petty, Max D., Stoltz, Kristen L., Bourdonnec, Bertrand Le, Smith, Bryan D., Flynn, Daniel L.

“…Abstract Background: The integrated stress response (ISR) is a major adaptive pathway stress response pathway and plays an important role in cell fate…”
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Abstract 4045: DCC-3084, a RAF dimer inhibitor, broadly inhibits BRAF class I, II, III, BRAF fusions, and RAS-driven solid tumors leading to tumor regression in preclinical models by Bulfer, Stacie L., Bourdonnec, Bertrand Le, Zwicker, Jeffery D., Ahn, Yu Mi, Al-Ani, Gada, Al-Hashimi, Hikmat, Crawley, Chase, Elliott, Kristin M., Faisal, Saqib, Harned, Andrew M., Heiniger, Cale L., Hood, Molly M., Javed, Salim, Kennedy, Michael, Large, Joshua W., Leary, Cynthia B., Lu, Wei-Ping, Luther, Kylie, Petty, Max D., Picard, Hunter R., Proto, Justin T., Romero, Yeni K., Stanley, Forrest A., Stoltz, Kristen L., Tanner, Daniel C., Telikepalli, Hanumaiah, Timson, Mary J., Vogeti, Lakshminarayana, Vogeti, Subha, Yang, Sihyung, Zhong, Lexy H., Smith, Bryan D., Flynn, Daniel L.

“…Abstract Background: Mutations in the RAS/MAPK pathway are a frequent driver of cancer, with oncogenic RAS or RAF mutations occurring in >30% of all cancers…”
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