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Joint Session: Clinical Science Intersections between Melanoma and Hematologic Malignancies

Abstract IA12: Preclinical models for targeting oncogenic Ras signaling in cancer

Kevin Shannon
Kevin Shannon
University of California, San Francisco, CA.
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DOI: 10.1158/1538-7445.MEL2014-IA12 Published July 2015
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Abstracts: AACR Special Conference on Advances in Melanoma: From Biology to Therapy; September 20-23, 2014; Philadelphia, PA

Abstract

Somatic RAS mutations occur in 30% of human cancers, and are common in both melanoma and hematopoietic cancers. Importantly, whereas KRAS mutations predominate in epithelial cancers, NRAS is mutated much more often in melanoma and hematopoietic cancers. The most obvious therapeutic strategy for cancers with RAS mutations – developing specific inhibitors of the mutant protein – is extremely challenging due to the very high affinity of Ras for GTP, structural considerations of the Ras/GTPase activating protein (Ras/GAP) molecular switch, and the loss of normal enzymatic activity as a consequence of oncogenic RAS mutations. Given these issues, most recent drug discovery efforts have focused on inhibiting downstream biochemical targets of mutant Ras such as Raf, MEK, and Akt with many compounds undergoing clinical evaluation. We have exploited strains of mice that recapitulate endogenous expression of cancer-associated RAS alleles or NF1 inactivation to model human hematologic cancers and to conduct biologic and preclinical studies. In particular, we have deployed the MOL4070LTR retrovirus as an insertional mutagen to generate genetically heterogeneous transplantable myeloid and lymphoid leukemias characterized by hyperactive Ras signaling. We utilize cohorts of mice that are engrafted with the same primary leukemias for preclinical testing. In this presentation, I will focus on three biologic and therapeutic questions related to NRAS in tumorigenesis: (1) loss of the normal NRAS allele in cancers with oncogenic NRAS mutations; (2) responses of primary Nras mutant leukemias to MEK and PI3 kinase inhibitors; and, (3) potential strategies for selectively targeting oncogenic N-Ras in cancer.

Note: This abstract was presented as part of the Joint Session: Clinical Science Interactions between Melanoma and Hematologic Malignancies with the AACR Special Conference: Hematologic Malignancies: Translating Discoveries to Novel Therapies held September 20-23, 2014 in Philadelphia, PA.

Citation Format: Kevin Shannon. Preclinical models for targeting oncogenic Ras signaling in cancer. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Melanoma: From Biology to Therapy; Sep 20-23, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(14 Suppl):Abstract nr IA12.

  • ©2015 American Association for Cancer Research.
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Cancer Research: 75 (14 Supplement)
July 2015
Volume 75, Issue 14 Supplement
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Abstract IA12: Preclinical models for targeting oncogenic Ras signaling in cancer
Kevin Shannon
Cancer Res July 15 2015 (75) (14 Supplement) IA12; DOI: 10.1158/1538-7445.MEL2014-IA12

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Abstract IA12: Preclinical models for targeting oncogenic Ras signaling in cancer
Kevin Shannon
Cancer Res July 15 2015 (75) (14 Supplement) IA12; DOI: 10.1158/1538-7445.MEL2014-IA12
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Joint Session: Clinical Science Intersections between Melanoma and Hematologic Malignancies

  • Abstract IA13: Treatment of non-V600-mutated BRAF melanoma: A role for combination MEK and CDK4/6 inhibition
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Joint Session: Clinical Science Intersections between Melanoma and Hematologic Malignancies: Oral Presentations - Invited Abstracts

  • Abstract IA13: Treatment of non-V600-mutated BRAF melanoma: A role for combination MEK and CDK4/6 inhibition
  • Abstract IA15: Adoptive T cell therapy with CAR modified T cells: We have a model A Ford, can we build a Ferrari?
  • Abstract IA12: Preclinical models for targeting oncogenic Ras signaling in cancer
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Cancer Research Online ISSN: 1538-7445
Cancer Research Print ISSN: 0008-5472
Journal of Cancer Research ISSN: 0099-7013
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