R E Gale|D C Linch - JoVE Visualize

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Leukemia|March 31, 1998

Clonality studies in acute myeloid leukemiaR E Gale, D C Linch

Leukemia|January 1, 1994

Investigation of methylation at Hha I sites using the hypervariable probe M27 beta allows improved clonal analysis in myeloid leukaemia and demonstrates differences in methylation between leukaemic and remission samplesR E Gale, D C Linch

British Journal of Haematology|October 1, 1991

X-chromosome inactivation patterns using HPRT and PGK polymorphisms in haematologically normal and post-chemotherapy femalesR E Gale, H Wheadon, D C Linch

Leukemia|July 1, 1992

Assessment of X-chromosome inactivation patterns using the hypervariable probe M27 beta in normal hemopoietic cells and acute myeloid leukemic blastsR E Gale, H Wheadon, D C Linch

British Journal of Haematology|June 1, 1996

Analysis of granulocyte colony stimulating factor receptor isoforms, polymorphisms and mutations in normal haemopoietic cells and acute myeloid leukaemia blastsT Bernard, R E Gale, D C Linch

Leukemia|February 1, 1996

Quantification of X-chromosome inactivation patterns in haematological samples using the DNA PCR-based HUMARA assayR E Gale, C A Mein, D C Linch

Leukemia|November 21, 1998

Quantification of X-chromosome inactivation patterns using RT-PCR of the polymorphic iduronate-2-sulphatase gene and correlation of the results obtained with DNA-based techniquesC N Harrison, R E Gale, D C Linch

British Journal of Haematology|October 29, 1998

Activating point mutations in the betaC chain of the GM-CSF, IL-3 and IL-5 receptors are not a major contributory factor in the pathogenesis of acute myeloid leukaemiaR W Freeburn, R E Gale, D C Linch

Blood|May 15, 1994

Tissue specificity of X-chromosome inactivation patternsR E Gale, H Wheadon, P Boulos, et al.

Leukemia|February 11, 2005

PI3-kinase/Akt is constitutively active in primary acute myeloid leukaemia cells and regulates survival and chemoresistance via NF-kappaB, Mapkinase and p53 pathwaysV L Grandage, R E Gale, D C Linch, et al.

Pageof 25

Showing results (1-10 of 244) with videos related to

Sort By:

Pageof 25

Leukemia|March 31, 1998

Clonality studies in acute myeloid leukemiaR E Gale, D C Linch

Leukemia|January 1, 1994

Investigation of methylation at Hha I sites using the hypervariable probe M27 beta allows improved clonal analysis in myeloid leukaemia and demonstrates differences in methylation between leukaemic and remission samplesR E Gale, D C Linch

British Journal of Haematology|October 1, 1991

X-chromosome inactivation patterns using HPRT and PGK polymorphisms in haematologically normal and post-chemotherapy femalesR E Gale, H Wheadon, D C Linch

Leukemia|July 1, 1992

Assessment of X-chromosome inactivation patterns using the hypervariable probe M27 beta in normal hemopoietic cells and acute myeloid leukemic blastsR E Gale, H Wheadon, D C Linch

British Journal of Haematology|June 1, 1996

Analysis of granulocyte colony stimulating factor receptor isoforms, polymorphisms and mutations in normal haemopoietic cells and acute myeloid leukaemia blastsT Bernard, R E Gale, D C Linch

Leukemia|February 1, 1996

Quantification of X-chromosome inactivation patterns in haematological samples using the DNA PCR-based HUMARA assayR E Gale, C A Mein, D C Linch

Leukemia|November 21, 1998

Quantification of X-chromosome inactivation patterns using RT-PCR of the polymorphic iduronate-2-sulphatase gene and correlation of the results obtained with DNA-based techniquesC N Harrison, R E Gale, D C Linch

British Journal of Haematology|October 29, 1998

Activating point mutations in the betaC chain of the GM-CSF, IL-3 and IL-5 receptors are not a major contributory factor in the pathogenesis of acute myeloid leukaemiaR W Freeburn, R E Gale, D C Linch

Blood|May 15, 1994

Tissue specificity of X-chromosome inactivation patternsR E Gale, H Wheadon, P Boulos, et al.

Leukemia|February 11, 2005

PI3-kinase/Akt is constitutively active in primary acute myeloid leukaemia cells and regulates survival and chemoresistance via NF-kappaB, Mapkinase and p53 pathwaysV L Grandage, R E Gale, D C Linch, et al.

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