J. Howard Pringle
University of Leicester
27 Papers
232 Citations
J. Howard Pringle is an academic researcher from University of Leicester. The author has contributed to research in topics: Biology & Tenascin C. The author has an hindex of 17, co-authored 27 publications. Previous affiliations of J. Howard Pringle include Leicester Royal Infirmary.
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Papers
A switch in the expression of embryonic EMT-inducers drives the development of malignant melanoma.
Julie Caramel,Eftychios Papadogeorgakis,Louise Hill,Gareth J. Browne,Geoffrey Richard,Anne Wierinckx,Gerald Saldanha,J.E. Osborne,Peter E. Hutchinson,Gina Tse,Joël Lachuer,Alain Puisieux,J. Howard Pringle,Stéphane Ansieau,Eugene Tulchinsky +14 more
TL;DR: It is found that regulation and functions of EMT-TFs are different in malignant melanoma and this switch results in E-cadherin loss, enhanced invasion, and constitutes an independent factor of poor prognosis in melanoma patients.
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Influence of Plasma Processing on Recovery and Analysis of Circulating Nucleic Acids
Karen Page,David S. Guttery,Nathalie Zahra,L Primrose,Shona R. Elshaw,J. Howard Pringle,Kevin Blighe,Stephanie D. Marchese,Allison Hills,Laura Woodley,Justin Stebbing,R. Charles Coombes,Jacqueline A Shaw +12 more
TL;DR: This work compares the extraction efficiency and reproducibility of 4 commercially available kits for cfDNA and 3 for miRNA using spike-in of reference templates, and successfully generated miRNA profiles for plasma samples stored > 12 years, highlighting the potential for analysis of stored sample biobanks.
Noninvasive Detection of Activating Estrogen Receptor 1 (ESR1) Mutations in Estrogen Receptor–Positive Metastatic Breast Cancer
David S. Guttery,Karen Page,Allison Hills,Laura Woodley,Stephanie D. Marchese,Basma Rghebi,Robert K. Hastings,Jin-Li Luo,J. Howard Pringle,Justin Stebbing,R. Charles Coombes,Simak Ali,Jacqueline A Shaw +12 more
TL;DR: Early identification of ESR1 mutations by liquid biopsy might allow for cessation of ineffective endocrine therapies and switching to other treatments, without the need for tissue biopsy and before the emergence of metastatic disease.
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High BRAF mutation frequency does not characterize all melanocytic tumor types.
Gerald Saldanha,David Purnell,Alan Fletcher,Linda Potter,Angela K. Gillies,J. Howard Pringle +5 more
TL;DR: It is concluded that BRAF and NRAS mutations are not necessary for melanocytic tumor development and that some types of tumor must arise by alternative mechanisms.
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Cutaneous melanoma subtypes show different BRAF and NRAS mutation frequencies.
TL;DR: The combined analysis of BRAF exon 15 and NRAS exon 2 showed that there were no significant differences in the overall mutation frequency between subtypes, and data show that mitogen-activated protein kinase pathway activation may be important in all major subtypes of cutaneous melanoma, although the mechanism by which this is achieved varies.
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