P53 in Head and Neck Squamous Cell Carcinoma

Parameswaran, Janaki; Burtness, Barbara

doi:10.1007/978-3-319-78762-6_9

Cited by 1 publication

(3 citation statements)

References 183 publications

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“…The tumour suppressor gene TP53 is an important anticancer gene because of its frequent mutations in most human solid cancers such as HNSCC (Stewart and Wild, 2014;Parameswaran and Burtness, 2018). The gene TP53 encodes the p53 tumour suppressor protein which initiates cell cycle arrest and apoptosis in response to cellular deoxyribonucleic acid (DNA) damage.…”

Section: Background On the Protein 53 Signalling Pathwaymentioning

confidence: 99%

“…MDM2 and p53 are connected through an autoregulatory feedback loop that maintains low cellular p53 levels in the absence of stress (Moll and Petrenko, 2003). Its amplification frequency in HNSCC is overexpressed in up to 46% of cases (Millon et al, 2001) leading to inhibition of p53 (Parameswaran and Burtness, 2018). CDKN2A produces the protein p14ARF: a tumour suppressor that reduces MDM2 and stabilizes p53 (Parameswaran and Burtness, 2018).…”

Section: Background On the Protein 53 Signalling Pathwaymentioning

confidence: 99%

“…Its amplification frequency in HNSCC is overexpressed in up to 46% of cases (Millon et al ., ) leading to inhibition of p53 (Parameswaran and Burtness, ). CDKN2A produces the protein p14ARF: a tumour suppressor that reduces MDM2 and stabilizes p53 (Parameswaran and Burtness, ).…”

Section: Introductionmentioning

confidence: 99%

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Causal Discovery of Gene Regulation with Incomplete Data

Foraita

Friemel

Günther

et al. 2020

Journal of the Royal Statistical Society Series A: Statistics in Society

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Causal discovery algorithms aim to identify causal relations from observational data and have become a popular tool for analysing genetic regulatory systems. In this work, we applied causal discovery to obtain novel insights into the genetic regulation underlying head-andneck squamous cell carcinoma. Some methodological challenges needed to be resolved first. The available data contained missing values, but most approaches to causal discovery require complete data. Hence, we propose a new procedure combining constraint-based causal discovery with multiple imputation. This is based on using Rubin's rules for pooling tests of conditional independence. A second challenge was that causal discovery relies on strong assumptions and can be rather unstable. To assess the robustness of our results, we supplemented our investigation with sensitivity analyses, including a non-parametric bootstrap to quantify the variability of the estimated causal structures. We applied these methods to investigate how the high mobility group AT-Hook 2 (HMGA2) gene is incorporated in the protein 53 signalling pathway playing an important role in head-and-neck squamous cell carcinoma. Our results were quite stable and found direct associations between HMGA2 and other relevant proteins, but they did not provide clear support for the claim that HMGA2 itself is a key regulator gene.

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Section: Background On the Protein 53 Signalling Pathwaymentioning

confidence: 99%