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Catherine Whibley
Researcher at University of Leeds
Publications - 7
Citations - 1033
Catherine Whibley is an academic researcher from University of Leeds. The author has contributed to research in topics: Gene & Infant mortality. The author has an hindex of 7, co-authored 7 publications receiving 973 citations.
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Journal ArticleDOI
p53 polymorphisms: cancer implications
TL;DR: Polymorphic variants of other genes in the p53 pathway, such as MDM2, which might have biological consequences either individually or in combination with p53 variants are discussed.
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Risk factors for congenital anomaly in a multiethnic birth cohort: an analysis of the Born in Bradford study
Eamonn Sheridan,Eamonn Sheridan,John Wright,Neil Small,Peter Corry,Sam Oddie,Catherine Whibley,Emily S. Petherick,Teena Malik,Nicole Pawson,Patricia McKinney,Roger C Parslow +11 more
TL;DR: The causes of the excess of congenital anomalies in a large multiethnic birth cohort are identified and sensitive advice about the risks is provided to communities at increased risk, and to couples in consanguineous unions, to assist in reproductive decision making.
Journal ArticleDOI
Risk Factors for Congenital Anomaly in a Multiethnic Birth Cohort: An Analysis of the Born in Bradford Study
Eamonn Sheridan,John Wright,Neil Small,Peter Corry,Sam Oddie,Catherine Whibley,Emily S. Petherick,Teena Malik,Nicole Pawson,Patricia McKinney,Roger C Parslow +10 more
TL;DR: The Born in Bradford study as discussed by the authors showed that consanguinity is a major risk factor for congenital anomalies in children of Pakistani origin, and that the risk remains even after adjustment for deprivation, and accounts for almost a third of anomalies in babies of Pakistan origin.
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Common tumour p53 mutations in immortalized cells from Hupki mice heterozygous at codon 72
Reinbold M,Jun-Li Luo,Tatiana Nedelko,Jerchow B,Maureen E. Murphy,Catherine Whibley,Wei Q,Monica Hollstein,Monica Hollstein +8 more
TL;DR: In cell lines ensuing from benzo(a)pyrene-treated cultures the combined p53 mutation pattern showed a predominance of strand-biased G to T transversions, and mutations recurring at smokers' lung tumour hotspot codons 157 and 273, supporting involvement of tobacco carcinogens in shaping the mutation signature in lung cancers of smokers.
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How to become immortal: let MEFs count the ways.
TL;DR: Various routes to p53/ARF disruption in senescence bypass are considered, and dysfunction of other tumour suppressor networks that may contribute to release from tenacious cell cycle arrest in senescent cultures are considered.