Linch DC - Search Results

1

Two novel activating mutations in the Wiskott-Aldrich syndrome protein result in congenital neutropenia.

Ancliff PJ, Blundell MP, Cory GO, Calle Y, Worth A, Kempski H, Burns S, Jones GE, Sinclair J, Kinnon C, Hann IM, Gale RE, Linch DC, Thrasher AJ. Ancliff PJ, et al. Among authors: linch dc. Blood. 2006 Oct 1;108(7):2182-9. doi: 10.1182/blood-2006-01-010249. Epub 2006 Jun 27. Blood. 2006. PMID: 16804117 Free article.

2

Long-term follow-up of granulocyte colony-stimulating factor receptor mutations in patients with severe congenital neutropenia: implications for leukaemogenesis and therapy.

Ancliff PJ, Gale RE, Liesner R, Hann I, Linch DC. Ancliff PJ, et al. Among authors: linch dc. Br J Haematol. 2003 Feb;120(4):685-90. doi: 10.1046/j.1365-2141.2003.04160.x. Br J Haematol. 2003. PMID: 12588357 Free article.

3

Neutrophil elastase mutations in congenital neutropenia.

Ancliff PJ, Gale RE, Linch DC. Ancliff PJ, et al. Among authors: linch dc. Hematology. 2003 Jun;8(3):165-71. doi: 10.1080/1024533031000107497. Hematology. 2003. PMID: 12745650 Free article. Review.

4

Homozygous HAX1 mutations in severe congenital neutropenia patients with sporadic disease: a novel mutation in two unrelated British kindreds.

Smith BN, Ancliff PJ, Pizzey A, Khwaja A, Linch DC, Gale RE. Smith BN, et al. Among authors: linch dc. Br J Haematol. 2009 Mar;144(5):762-70. doi: 10.1111/j.1365-2141.2008.07493.x. Epub 2008 Nov 22. Br J Haematol. 2009. PMID: 19036076 Free article.

5

Paternal mosaicism proves the pathogenic nature of mutations in neutrophil elastase in severe congenital neutropenia.

Ancliff PJ, Gale RE, Watts MJ, Liesner R, Hann IM, Strobel S, Linch DC. Ancliff PJ, et al. Among authors: linch dc. Blood. 2002 Jul 15;100(2):707-9. doi: 10.1182/blood-2002-01-0060. Blood. 2002. PMID: 12091371 Free article.

6

Mutations in the ELA2 gene encoding neutrophil elastase are present in most patients with sporadic severe congenital neutropenia but only in some patients with the familial form of the disease.

Ancliff PJ, Gale RE, Liesner R, Hann IM, Linch DC. Ancliff PJ, et al. Among authors: linch dc. Blood. 2001 Nov 1;98(9):2645-50. doi: 10.1182/blood.v98.9.2645. Blood. 2001. PMID: 11675333 Free article.

7

Studies of FLT3 mutations in paired presentation and relapse samples from patients with acute myeloid leukemia: implications for the role of FLT3 mutations in leukemogenesis, minimal residual disease detection, and possible therapy with FLT3 inhibitors.

Kottaridis PD, Gale RE, Langabeer SE, Frew ME, Bowen DT, Linch DC. Kottaridis PD, et al. Among authors: linch dc. Blood. 2002 Oct 1;100(7):2393-8. doi: 10.1182/blood-2002-02-0420. Blood. 2002. PMID: 12239147 Free article.

8

Impaired bone marrow homing of cytokine-activated CD34+ cells in the NOD/SCID model.

Ahmed F, Ings SJ, Pizzey AR, Blundell MP, Thrasher AJ, Ye HT, Fahey A, Linch DC, Yong KL. Ahmed F, et al. Among authors: linch dc. Blood. 2004 Mar 15;103(6):2079-87. doi: 10.1182/blood-2003-06-1770. Epub 2003 Nov 20. Blood. 2004. PMID: 14630817 Free article.

9

Long-term serial analysis of X-chromosome inactivation patterns and JAK2 V617F mutant levels in patients with essential thrombocythemia show that minor mutant-positive clones can remain stable for many years.

Gale RE, Allen AJ, Nash MJ, Linch DC. Gale RE, et al. Among authors: linch dc. Blood. 2007 Feb 1;109(3):1241-3. doi: 10.1182/blood-2006-06-029769. Epub 2006 Oct 5. Blood. 2007. PMID: 17023581 Free article.

10

FLT3 tyrosine kinase domain mutations are biologically distinct from and have a significantly more favorable prognosis than FLT3 internal tandem duplications in patients with acute myeloid leukemia.

Mead AJ, Linch DC, Hills RK, Wheatley K, Burnett AK, Gale RE. Mead AJ, et al. Among authors: linch dc. Blood. 2007 Aug 15;110(4):1262-70. doi: 10.1182/blood-2006-04-015826. Epub 2007 Apr 24. Blood. 2007. PMID: 17456725 Free article.

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