Senior Medical Director, Oncology, Eli Lilly and Company

Oncology

Robert Ilaria works in the field of Oncology. He went to University of Texas Southwestern Medical School. Robert Ilaria is a published MD. He has 33 papers published. The most current publication "Transformation of hematopoietic cell lines to growth-factor independence and induction of a fatal myelo- and lymphoproliferative disease in mice by retrovirally transd..."

Publications

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• An innovative, multi-arm, complete phase 1b study of the novel anti-Cancer agent tasisulam in patients with advanced solid tumors.
• A randomized, open-label clinical trial of tasisulam sodium versus paclitaxel as second-line treatment in patients with metastatic melanoma.
• A phase II study of tasisulam sodium (LY573636 sodium) as second-line or third-line treatment for patients with unresectable or metastatic Soft tissue sarcoma.
• A phase I study of tasisulam sodium (LY573636 sodium), a novel antiCancer compound, administered as a 24-h continuous infusion in patients with advanced solid tumors.
• A phase 2 study of tasisulam sodium (LY573636 sodium) as second-line treatment for patients with unresectable or metastatic melanoma.
• Tasisulam Sodium (LY573636 Sodium) as Third-Line Treatment in Patients With Unresectable, Metastatic Non-Small-Cell Lung Cancer: A Phase-II Study.
• A phase I study of tasisulam sodium (LY573636 sodium), a novel antiCancer compound in patients with refractory solid tumors.
• Imatinib mesylate inhibits antigen-specific memory CD8 T cell responses in vivo.
• AML: many new tools for discovery, not enough answers (yet).
• STAT5 signaling is required for the efficient induction and maintenance of CML in mice.
• Pathobiology of lymphoid and myeloid blast crisis and management issues.
• Expression of the EWS/FLI-1 oncogene in murine primary bone-derived cells Results in EWS/FLI-1-dependent, ewing Sarcoma-like tumors.
• PD166326, a novel tyrosine kinase inhibitor, has greater antileukemic activity than imatinib mesylate in a murine model of chronic myeloid leukemia.
• Animal models of chronic myelogenous leukemia.
• Imatinib mesylate efficiently achieves therapeutic intratumor concentrations in vivo but has limited activity in a xenograft model of small cell lung Cancer.
• Tyrosine kinases in AML: where do they fit in?
• The epidermal growth factor receptor HER2 is not a major therapeutic target in Ewing Sarcoma.
• The CNS is a sanctuary for leukemic cells in mice receiving imatinib mesylate for Bcr/Abl-induced leukemia.
• Alteration of mesodermal cell differentiation by EWS/FLI-1, the oncogene implicated in Ewing's Sarcoma.
• Bcr/Abl, leukemogenesis, and genomic instability: a complex partnership.
• Establishment of a murine model for therapy-treated chronic myelogenous leukemia using the tyrosine kinase inhibitor STI571.
• STAT isoforms: mediators of STAT specificity or leukemogenesis?
• The src homology 2 domain of Bcr/Abl is required for efficient induction of chronic myeloid leukemia-like disease in mice but not for lymphoid leukemogenesis or activa...
• Interference with the constitutive activation of ERK1 and ERK2 impairs EWS/FLI-1-dependent transformation.
• Regulation of microtubule dynamics and myogenic differentiation by MURF, a striated muscle RING-finger protein.
• Fatal myeloproliferation, induced in mice by TEL/PDGFbetaR expression, depends on PDGFbetaR tyrosines 579/581.
• Dominant negative mutants implicate STAT5 in myeloid cell proliferation and neutrophil differentiation.
• The P190, P210, and P230 forms of the BCR/ABL oncogene induce a similar chronic myeloid leukemia-like syndrome in mice but have different lymphoid leukemogenic activity.
• A novel ubiquitin-specific protease, UBP43, cloned from leukemia fusion protein AML1-ETO-expressing mice, functions in hematopoietic cell differentiation.
• Transformation of hematopoietic cell lines to growth-factor independence and induction of a fatal myelo- and lymphoproliferative disease in mice by retrovirally transd...
• P210 and P190(BCR/ABL) induce the tyrosine phosphorylation and DNA binding activity of multiple specific STAT family members.
• The SH2 domain of P210BCR/ABL is not required for the transformation of hematopoietic factor-dependent cells.

Schools

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• University of Texas Southwestern Medical Center At Dallas

Conditions Treated

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• Anal and Rectal Cancer
• Anemia
• Colorectal Cancer
• Liver Cancer
• View All

Doctors Specialties

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• Hematology
• Medical Oncology
• Oncology

Accepted Insurances

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Education

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• Brigham and Women's Hospital
• University of Texas Southwestern Medical School

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