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C-terminal Tensin-like (CTEN) is an oncogene which alters cell motility possibly through repression of E-cadherin in colorectal cancer (2008)
Journal Article
Albasri, A., Seth, R., Jackson, D., Benhasouna, A., Crook, S., Nateri, A. S., Chapman, R., & Ilyas, M. (2009). C-terminal Tensin-like (CTEN) is an oncogene which alters cell motility possibly through repression of E-cadherin in colorectal cancer. The Journal of Pathology, 218(1), 57-65. https://doi.org/10.1002/path.2508

The Tensin gene family encodes proteins thought to modulate integrin function. C-terminal Tensin-like (CTEN) is a member of the Tensin gene family which lacks the N-terminus actin-binding domain. Cten is reported to have both oncogenic and tumour-sup... Read More about C-terminal Tensin-like (CTEN) is an oncogene which alters cell motility possibly through repression of E-cadherin in colorectal cancer.

Resistance to FLT3 inhibition in an in vitro model of primary AML cells with a stem cell phenotype in a defined microenvironment (2008)
Journal Article
(2008). Resistance to FLT3 inhibition in an in vitro model of primary AML cells with a stem cell phenotype in a defined microenvironment. Leukemia, 22, 1395-1401. https://doi.org/10.1038/leu.2008.125

Relapse in acute myeloid leukaemia (AML) is mediated by survival of leukaemic stem cells following remission-induction chemotherapy. It would therefore be useful to identify therapeutic agents that target leukaemic stem cells. We devised a flow cytom... Read More about Resistance to FLT3 inhibition in an in vitro model of primary AML cells with a stem cell phenotype in a defined microenvironment.

P-glycoprotein is downregulated in KG1a-primitive leukemia cells by LDL cholesterol deprivation and by HMG-CoA reductase inhibitors (2007)
Journal Article
Connelly Smith, L., Pattinson, J., Grundy, M., Shang, S., Seedhouse, C., Russell, N., & Pallis, M. (2007). P-glycoprotein is downregulated in KG1a-primitive leukemia cells by LDL cholesterol deprivation and by HMG-CoA reductase inhibitors. Experimental Hematology, 35(12), 1793-1800. https://doi.org/10.1016/j.exphem.2007.07.017

Objective
P-glycoprotein (pgp) is a membrane transporter encoded by the multidrug resistance (MDR1, ABCB1) gene. Pgp is a poor prognostic factor in elderly patients with acute myeloid leukemia (AML). In addition to its role in drug efflux, pgp has b... Read More about P-glycoprotein is downregulated in KG1a-primitive leukemia cells by LDL cholesterol deprivation and by HMG-CoA reductase inhibitors.

Influence of ursodeoxycholic acid on the mortality and malignancy associated with primary biliary cirrhosis: A population-based cohort study (2007)
Journal Article
Jackson, H., Solaymani-Dodaran, M., Card, T. R., Aithal, G. P., Logan, R., & West, J. (2007). Influence of ursodeoxycholic acid on the mortality and malignancy associated with primary biliary cirrhosis: A population-based cohort study. Hepatology, 46(4), 1131-1137. https://doi.org/10.1002/hep.21795

There is debate over the mortality and malignancy risk in people with primary biliary cirrhosis (PBC) and whether this risk is reduced by use of ursodeoxycholic acid. To investigate this issue, we identified 930 people with PBC and 9,202 control subj... Read More about Influence of ursodeoxycholic acid on the mortality and malignancy associated with primary biliary cirrhosis: A population-based cohort study.

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.

Interaction of phosphorylated c-Jun with TCF4 regulates intestinal cancer development (2005)
Journal Article
Nateri, A. S., Spencer-Dene, B., & Behrens, A. (2005). Interaction of phosphorylated c-Jun with TCF4 regulates intestinal cancer development. Nature, 437(7056), 281-285. https://doi.org/10.1038/nature03914

The proto-oncoprotein c-Jun is a component of the AP-1 transcription factor, the activity of which is augmented in many tumour types. An important mechanism in the stimulation of AP-1 function is amino-terminal phosphorylation of c-Jun by the c-Jun N... Read More about Interaction of phosphorylated c-Jun with TCF4 regulates intestinal cancer development.

The AP-1 transcription factor c-Jun is required for efficient axonal regeneration (2004)
Journal Article
Raivich, G., Bohatschek, M., Da Costa, C., Iwata, O., Galiano, M., Hristova, M., Nateri, A. S., Makwana, M., Riera-Sans, L., Wolfer, D. P., Lipp, H. P., Aguzzi, A., Wagner, E. F., & Behrens, A. (2004). The AP-1 transcription factor c-Jun is required for efficient axonal regeneration. Neuron, 43(1), 57-67. https://doi.org/10.1016/j.neuron.2004.06.005

Nerve injury triggers numerous changes in the injured neurons and surrounding nonneuronal cells that ultimately result in successful target reinnervation or cell death. c-Jun is a component of the heterodimeric AP-1 transcription factor, and c-Jun is... Read More about The AP-1 transcription factor c-Jun is required for efficient axonal regeneration.

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.

The Ubiquitin Ligase SCF Fbw7 Antagonizes Apoptotic JNK Signaling (2004)
Journal Article
Nateri, A. S., Riera-Sans, L., Da Costa, C., & Behrens, A. (2004). The Ubiquitin Ligase SCF Fbw7 Antagonizes Apoptotic JNK Signaling. Science, 303(5662), 1374-1378. https://doi.org/10.1126/science.1092880

Jun N-terminal kinases (JNKs) are essential for neuronal microtubute assembly and apoptosis. Phosphorylation of the activating protein 1 (AP1) transcription factor c-Jun, at multiple sites within its transactivation domain, is required for JNK-induce... Read More about The Ubiquitin Ligase SCF Fbw7 Antagonizes Apoptotic JNK Signaling.

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.