41 results on '"Hodgson, Graeme"'
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2. Barriers to the implementation of Flexible Demand services within the GB electricity generation and supply system
3. AML-108 SELECT-AML-1 Trial in Progress: A Phase 2 Study of Tamibarotene in Combination With Venetoclax and Azacitidine in Previously Untreated Adult Patients Selected for RARA-Positive AML who are Ineligible for Standard Induction Therapy
4. Targeting RARA Overexpression with Tamibarotene, a Potent and Selective RARα Agonist, is a Novel Approach in AML
5. Initial Results from SELECT-AML-1, a Phase 2 Study of Tamibarotene in Combination with Venetoclax and Azacitidine in RARA-Positive Newly Diagnosed AML Patients Ineligible for Standard Induction Chemotherapy
6. Poster: AML-108 SELECT-AML-1 Trial in Progress: A Phase 2 Study of Tamibarotene in Combination With Venetoclax and Azacitidine in Previously Untreated Adult Patients Selected for RARA-Positive AML who are Ineligible for Standard Induction Therapy
7. Trial in progress: Phase I study of SY-5609, a potent, selective CDK7 inhibitor, with initial expansion in adults with metastatic pancreatic cancer.
8. SY5609, a Potent and Selective CDK7 Inhibitor, Potentiates BTK Inhibitor Activity in Mantle Cell Lymphoma Preclinical Models
9. Targeting RARAoverexpression with tamibarotene, a potent and selective RARα agonist, is a novel approach in AML
10. Selection of RARA-Positive Newly Diagnosed Unfit AML Patients with Elevated RARA Gene Expression Enriches for Features Associated with Primary Resistance to Venetoclax and Clinical Response to SY-1425, a Potent and Selective RARα Agonist, Plus Azacitidine
11. First-in-human phase I study of SY-5609, an oral, potent, and selective noncovalent CDK7 inhibitor, in adult patients with select advanced solid tumors.
12. Activity of SY-5609, an oral, noncovalent, potent, and selective CDK7 inhibitor, in preclinical models of colorectal cancer.
13. Early evidence of dose-dependent pharmacodynamic activity following treatment with SY-5609, a highly selective and potent oral CDK7 inhibitor, in patients with advanced solid tumors
14. Abstract C091: Preclinical evaluation of PK, PD, and antitumor activity of the oral, non-covalent, potent and highly selective CDK7 inhibitor, SY-5609, provides rationale for clinical development in multiple solid tumor indications
15. Abstract 4409: Prospective identification of RB pathway alterations predict response to SY-1365, a selective CDK7 inhibitor, in a panel of high-grade serous ovarian cancer (HGSOC) patient derived xenograft (PDX) models
16. Abstract 1525: SY-1365, a selective CDK7 inhibitor, exhibits potent antitumor activity against ovarian cancer models in vitro and in vivo
17. Trial design of a first-in-human phase 1 evaluation of SY-1365, a first-in-class selective CDK7 inhibitor, with initial expansions in ovarian and breast cancer.
18. Abstract B171: PK/PD modeling of the first-in-class, potent and selective covalent CDK7 inhibitor, SY-1365, provides mechanistic basis for intermittent dosing regimens in preclinical efficacy models of hematologic and solid tumors
19. Progressive Genomic Instability in the FVB/Kras[superscript LA2] Mouse Model of Lung Cancer
20. Emergence of Sub-Clonal Drug Resistance Mutations during CML Therapy
21. High-Resolution Analysis of the Relationship Between Ponatinib Dose and Molecular Response in CP-CML Patients in the PACE Trial
22. Sy-1365, a Potent and Selective CDK7 Inhibitor, Exhibits Anti-Tumor Activity in Preclinical Models of Hematologic Malignancies, and Demonstrates Interactions with the BCL-XL/BCL2 Mitochondrial Apoptosis Signaling Pathway in Leukemia
23. Tolerability and preliminary activity of the potent, selective, oral CDK7 inhibitor SY-5609 in combination with fulvestrant in patients with advanced hormone receptor-positive (HR+), HER2- breast cancer (BC).
24. Phase 1/1b study of SY-5609, a selective and potent CDK7 inhibitor, in advanced solid tumors and in 2L/3L pancreatic ductal adenocarcinoma (PDAC) in combination with gemcitabine +/- nab-paclitaxel.
25. Progressive Genomic Instability in the FVB/Kras[superscript LA2] Mouse Model of Lung Cancer
26. Comparative TKI Profiling Analyses to Explore Potential Mechanisms of Ponatinib-Associated Arterial Thrombotic Events
27. Detection of BCR-ABL1 Compound and Polyclonal Mutants in Chronic Myeloid Leukemia Patients Using a Novel Next Generation Sequencing Approach That Minimises PCR and Sequencing Errors
28. High-Resolution Analysis of the Relationship Between Dose and Molecular Response in CP-CML Patients Treated with Ponatinib or Imatinib
29. Impact Of Baseline (BL) Mutations, Including Low-Level and Compound Mutations, On Ponatinib Response and End Of Treatment (EOT) Mutation Analysis In Patients (Pts) With Chronic Phase Chronic Myeloid Leukemia (CP-CML)
30. Additional BCR-ABL1 Mutations Identified By Sensitive Mass Spectrometry In Chronic Phase CML Patients With T315I Treated With Ponatinib Are Associated With Relatively Inferior Responses and Outcome
31. Identification of a Poor-Prognosis BRAF-Mutant–Like Population of Patients With Colon Cancer
32. Progressive Genomic Instability in the FVB/KrasLA2 Mouse Model of Lung Cancer
33. A systems engineering approach to resolving structural barriers to the implementation of demand response
34. Abstract 4722: A BRAF-mutated gene expression signature identifies BRAF wild type colon cancer patients with poor prognosis
35. Genome scanning with array CGH delineates regional alterations in mouse islet carcinomas
36. Genomics of islet cell carcinogenesis
37. High-resolution assessment of DNA loss in RIP-Tag mouse pancreatic carcinomas using comparative genomic hybridization to microarrays
38. Genomic DNA Copy Number Alterations Present in AML Bone Marrow Samples with Normal Cytogenetics.
39. Living together
40. Night and water
41. Detection of BCR-ABL1Compound and Polyclonal Mutants in Chronic Myeloid Leukemia Patients Using a Novel Next Generation Sequencing Approach That Minimises PCR and Sequencing Errors
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