All Outputs (7)

Hydrogel-Based Pre-Clinical Evaluation of Repurposed FDA-Approved Drugs for AML (2023)
Journal Article
James, J. R., Curd, J., Ashworth, J. C., Abuhantash, M., Grundy, M., Seedhouse, C. H., …Thompson, A. (2023). Hydrogel-Based Pre-Clinical Evaluation of Repurposed FDA-Approved Drugs for AML. International Journal of Molecular Sciences, 24(4), Article 4235. https://doi.org/10.3390/ijms24044235

In vivo models of acute myeloid leukemia (AML) are low throughput, and standard liquid culture models fail to recapitulate the mechanical and biochemical properties of the extracellular matrix-rich protective bone marrow niche that contributes to dru... Read More about Hydrogel-Based Pre-Clinical Evaluation of Repurposed FDA-Approved Drugs for AML.

A same?day assay predicts apoptotic response to combined BCL?2 and MCL?1 BH3?mimetic targeting in multiple myeloma cells (2020)
Journal Article
Grundy, M., Al?Kaisi, F., Cull, J., Williams, C., Smith, D., & Seedhouse, C. H. (2021). A same?day assay predicts apoptotic response to combined BCL?2 and MCL?1 BH3?mimetic targeting in multiple myeloma cells. eJHaem, 2(1), 40-47. https://doi.org/10.1002/jha2.133

Recent advances in treatment options for multiple myeloma (MM) have positive impact on patient survival. However, there is a short fall of rapid and reliable assays that can predict patient response to novel agents. The anti-apoptotic proteins B-cell... Read More about A same?day assay predicts apoptotic response to combined BCL?2 and MCL?1 BH3?mimetic targeting in multiple myeloma cells.

The multi-kinase inhibitor TG02 overcomes signalling activation by survival factors to deplete MCL1 and XIAP and induce cell death in primary acute myeloid leukaemia cells (2012)
Journal Article
Pallis, M., Abdul-Aziz, A., Burrows, F., Seedhouse, C., Grundy, M., & Russell, N. (2012). The multi-kinase inhibitor TG02 overcomes signalling activation by survival factors to deplete MCL1 and XIAP and induce cell death in primary acute myeloid leukaemia cells. British Journal of Haematology, 159(2), 191-203. https://doi.org/10.1111/bjh.12018

The novel multi-kinase inhibitor TG02 has selectivity against cell cycle and transcriptional cyclin dependent kinases (CDKs) as well as fms-like tyrosine kinase receptor-3 (FLT3). Inhibition of transcriptional CDKs preferentially depletes short-lived... Read More about The multi-kinase inhibitor TG02 overcomes signalling activation by survival factors to deplete MCL1 and XIAP and induce cell death in primary acute myeloid leukaemia cells.

P-glycoprotein and breast cancer resistance protein in acute myeloid leukaemia cells treated with the Aurora-B Kinase Inhibitor barasertib-hQPA (2011)
Journal Article
Grundy, M., Seedhouse, C., Russell, N. H., & Pallis, M. (2011). P-glycoprotein and breast cancer resistance protein in acute myeloid leukaemia cells treated with the Aurora-B Kinase Inhibitor barasertib-hQPA. BMC Cancer, 11, Article 254. https://doi.org/10.1186/1471-2407-11-254

Background Aurora kinases play an essential role in orchestrating chromosome alignment, segregation and cytokinesis during mitotic progression, with both aurora-A and B frequently over-expressed in a variety of human malignancies. Over-expression of... Read More about P-glycoprotein and breast cancer resistance protein in acute myeloid leukaemia cells treated with the Aurora-B Kinase Inhibitor barasertib-hQPA.

Analysis of factors that affect in vitro chemosensitivity of leukaemic stem and progenitor cells to gemtuzumab ozogamicin (Mylotarg) in acute myeloid leukaemia (2009)
Journal Article
Jawad, M., Seedhouse, C., Mony, U., Grundy, M., Russell, N. H., & Pallis, M. (2010). Analysis of factors that affect in vitro chemosensitivity of leukaemic stem and progenitor cells to gemtuzumab ozogamicin (Mylotarg) in acute myeloid leukaemia. Leukemia, 24, 74-80. https://doi.org/10.1038/leu.2009.199

Relapse in acute myeloid leukaemia (AML) is considered to result from the persistence of drug-resistant leukaemic stem and progenitor cells (LSPC) within a bone marrow ‘niche’ microenvironment. Identifying novel agents that have the potential to targ... Read More about Analysis of factors that affect in vitro chemosensitivity of leukaemic stem and progenitor cells to gemtuzumab ozogamicin (Mylotarg) in acute myeloid leukaemia.

Resistance to spontaneous apoptosis in acute myeloid leukaemia blasts is associated with p-glycoprotein expression and function, but not with the presence of FLT3 internal tandem duplications (2003)
Journal Article
Pallis, M., Turzanski, J., Grundy, M., Seedhouse, C., & Russell, N. (2003). Resistance to spontaneous apoptosis in acute myeloid leukaemia blasts is associated with p-glycoprotein expression and function, but not with the presence of FLT3 internal tandem duplications. British Journal of Haematology, 120(6), 1009-1016. https://doi.org/10.1046/j.1365-2141.2003.04210.x

The ability of acute myeloid leukaemia (AML) blasts to survive in culture has been associated with poor patient response to chemotherapy. Other biological factors predicting an adverse outcome include p-glycoprotein (pgp) expression, which is associa... Read More about Resistance to spontaneous apoptosis in acute myeloid leukaemia blasts is associated with p-glycoprotein expression and function, but not with the presence of FLT3 internal tandem duplications.

Flow cytometric measurement of phosphorylated STAT5 in AML: Lack of specific association with FLT3 internal tandem duplications (2003)
Journal Article
Pallis, M., Seedhouse, C., Grundy, M., & Russell, N. (2003). Flow cytometric measurement of phosphorylated STAT5 in AML: Lack of specific association with FLT3 internal tandem duplications. Leukemia Research, 27(9), 803-805. https://doi.org/10.1016/S0145-2126%2803%2900012-2

STAT5 phosphorylation has been noted in 69–95% of AML cases by Western blotting. We used flow cytometry to measure phosphorylated STAT5 on a semi-quantitative scale. The method was validated on K562 cells, which constitutively express phosphorylated... Read More about Flow cytometric measurement of phosphorylated STAT5 in AML: Lack of specific association with FLT3 internal tandem duplications.