M. Haughton

发表

Dissociation of telomere dynamics from telomerase activity in human thyroid cancer cells.

M. Schlumberger, F. Wyllie, D. Wynford‐Thomas, 1998, Experimental cell research.

Opposing effects of mutant ras oncoprotein on human fibroblast and epithelial cell proliferation: implications for models of human tumorigenesis

A. Bounacer, J. Bond, D. Wynford‐Thomas, 2004, Oncogene.

Mutant p53 rescues human diploid cells from senescence without inhibiting the induction of SDI1/WAF1.

J. R. Smith, J. Blaydes, J. Bond, 1995, Cancer research.

Control of Replicative Life Span in Human Cells: Barriers to Clonal Expansion Intermediate Between M1 Senescence and M2 Crisis

P. Smith, J. Bond, F. Wyllie, 1999, Molecular and Cellular Biology.

Telomere erosion triggers growth arrest but not cell death in human cancer cells retaining wild-type p53: implications for antitelomerase therapy

Christopher J. Jones, D. Wynford‐Thomas, M. Haughton, 2004, Oncogene.

Evidence that transcriptional activation by p53 plays a direct role in the induction of cellular senescence.

J. Blaydes, J. Bond, F. Wyllie, 1996, Oncogene.

Mutant p53 can delay growth arrest and loss of CDK2 activity in senescing human fibroblasts without reducing p21(WAF1) expression.

J. Bartek, F. Wyllie, D. Wynford‐Thomas, 2003, Experimental cell research.

The nature of telomere fusion and a definition of the critical telomere length in human cells.

M. Haughton, D. Baird, M. Tankimanova, 2007, Genes & development.

length in human cells The nature of telomere fusion and a definition of the critical telomere Material

M. Haughton, D. Baird, M. Tankimanova, 2007 .

Telomerase activity and telomere length in thyroid neoplasia: biological and clinical implications

Christopher J. Jones, D. Wynford‐Thomas, J. Skinner, 2001, The Journal of pathology.

Direct evidence from siRNA-directed "knock down" that p16(INK4a) is required for human fibroblast senescence and for limiting ras-induced epithelial cell proliferation.

J. Bond, Christopher J. Jones, D. Wynford‐Thomas, 2004, Experimental cell research.

S phase cell-cycle arrest following DNA damage is independent of the p53/p21(WAF1) signalling pathway.

J. Bond, F. Wyllie, D. Wynford‐Thomas, 1996, Oncogene.

An analysis of replicative senescence in dermal fibroblasts derived from chronic leg wounds predicts that telomerase therapy would fail to reverse their disease-specific cellular and proteolytic phenotype.

F. Wyllie, Christopher J. Jones, J. Skinner, 2003, Experimental cell research.

Telomerase prevents the accelerated cell ageing of Werner syndrome fibroblasts

R. Faragher, F. Wyllie, Christopher J. Jones, 2000, Nature Genetics.

Telomere-based proliferative lifespan barriers in Werner-syndrome fibroblasts involve both p53-dependent and p53-independent mechanisms

R. Faragher, F. Wyllie, Christopher J. Jones, 2003, Journal of Cell Science.

Human thyroid cancer cells as a source of iso-genic, iso-phenotypic cell lines with or without functional p53

F. Wyllie, D. Wynford‐Thomas, M. Haughton, 1999, British Journal of Cancer.

Prevention of Accelerated Cell Aging in the Werner Syndrome

Christopher J. Jones, M. Haughton, D. Kipling, 2006, Annals of the New York Academy of Sciences.

Prevention of accelerated cell aging in Werner syndrome using a p38 mitogen-activated protein kinase inhibitor.

Christopher J. Jones, M. Haughton, D. Kipling, 2005, The journals of gerontology. Series A, Biological sciences and medical sciences.

Evasion of p53-mediated growth control occurs by three alternative mechanisms in transformed thyroid epithelial cells.

M. Schlumberger, J. Blaydes, F. Wyllie, 1995, Oncogene.