All Outputs (507)

Fracture Risk in People With Primary Biliary Cirrhosis: A Population-Based Cohort Study (2006)
Journal Article
Solaymani–Dodaran, M., Card, T. R., Aithal, G. P., & West, J. (2006). Fracture Risk in People With Primary Biliary Cirrhosis: A Population-Based Cohort Study. Gastroenterology, 131(6), 1752-1757. https://doi.org/10.1053/j.gastro.2006.09.012

Background & Aims: Controversy exists as to whether people with primary biliary cirrhosis (PBC) have an increased risk of developing osteoporosis and the extent to which this may translate into an increased risk of fracture. We have performed a coh... Read More about Fracture Risk in People With Primary Biliary Cirrhosis: A Population-Based Cohort Study.

Advances in the understanding of susceptibility to treatment-related acute myeloid leukaemia (2004)
Journal Article
Seedhouse, C., & Russell, N. (2004). Advances in the understanding of susceptibility to treatment-related acute myeloid leukaemia. British Journal of Haematology, 137(6), 513-529. https://doi.org/10.1111/j.1365-2141.2007.06613.x

Treatment-related acute myeloid leukaemia (t-AML) is a devastating complication following exposure to the cytotoxic and genotoxic agents used to treat a primary malignancy. Whilst the incidence of t-AML is rising, it still only occurs in a minority o... Read More about Advances in the understanding of susceptibility to treatment-related acute myeloid leukaemia.

Clonal haemopoiesis may occur after conventional chemotherapy and is associated with accelerated telomere shortening and defects in the NQO1 pathway; possible mechanisms leading to an increased risk of t-AML/MDS (2004)
Journal Article
Fern, L., Pallis, M., Carter, G. I., Seedhouse, C., Russell, N., & Byrne, J. (2004). Clonal haemopoiesis may occur after conventional chemotherapy and is associated with accelerated telomere shortening and defects in the NQO1 pathway; possible mechanisms leading to an increased risk of t-AML/MDS. British Journal of Haematology, 126(1), 63-71. https://doi.org/10.1111/j.1365-2141.2004.05006.x

The molecular pathogenesis of therapy-related acute myeloid leukaemia/myelodysplastic syndrome (t-AML/MDS) remains uncertain. However, clonal haemopoiesis may develop following stem cell transplantation and precede the development of t-AML/MDS. Moreo... Read More about Clonal haemopoiesis may occur after conventional chemotherapy and is associated with accelerated telomere shortening and defects in the NQO1 pathway; possible mechanisms leading to an increased risk of t-AML/MDS.

Polymorphisms in Genes Involved in Homologous Recombination Repair Interact to Increase the Risk of Developing Acute Myeloid Leukemia (2004)
Journal Article
Seedhouse, C., Faulkner, R., Ashraf, N., Das-Gupta, E., & Russell, N. (2004). Polymorphisms in Genes Involved in Homologous Recombination Repair Interact to Increase the Risk of Developing Acute Myeloid Leukemia. Clinical Cancer Research, 10(8), 2675–2680. https://doi.org/10.1158/1078-0432.CCR-03-0372

Purpose: Double-strand break repair via homologous recombination is essential in maintaining genetic integrity. RAD51 and XRCC3 are involved in the repair of DNA by this pathway, and polymorphisms have been identified in both the RAD51 (RAD51-G135C)... Read More about Polymorphisms in Genes Involved in Homologous Recombination Repair Interact to Increase the Risk of Developing Acute Myeloid Leukemia.

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.

The genotype distribution of the XRCC1 gene indicates a role for base excision repair in the development of therapy-related acute myeloblastic leukemia (2002)
Journal Article
Seedhouse, C., Bainton, R., Lewis, M., Harding, A., Russell, N., & Das-Gupta, E. (2002). The genotype distribution of the XRCC1 gene indicates a role for base excision repair in the development of therapy-related acute myeloblastic leukemia. Blood, 100(10), 3761-3766. https://doi.org/10.1182/blood-2002-04-1152

Polymorphisms in several DNA repair genes have been described. These polymorphisms may affect DNA repair capacity and modulate cancer susceptibility by means of gene-environment interactions. We investigated DNA repair capacity and its association wi... Read More about The genotype distribution of the XRCC1 gene indicates a role for base excision repair in the development of therapy-related acute myeloblastic leukemia.