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Good Guy or Bad Guy? The Duality of Wild-Type p53 in Hormone-Dependent Breast Cancer Origin, Treatment, and Recurrence

1
Central Laboratory, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou 510080, China
2
School of Life Sciences, University of Technology Sydney, Sydney 2007, Australia
*
Author to whom correspondence should be addressed.
Cancers 2018, 10(6), 172; https://doi.org/10.3390/cancers10060172
Received: 3 May 2018 / Revised: 26 May 2018 / Accepted: 29 May 2018 / Published: 31 May 2018
(This article belongs to the Special Issue p53 Signaling in Cancers)
Lactation is at one point perilously near becoming a cancerous process if it is at all arrested”, Beatson, 1896. Most breast cancers arise from the milk-producing cells that are characterized by aberrant cellular, molecular, and epigenetic translation. By understanding the underlying molecular disruptions leading to the origin of cancer, we might be able to design novel strategies for more efficacious treatments or, ambitiously, divert the cancerous process. It is an established reality that full-term pregnancy in a young woman provides a lifetime reduction in breast cancer risk, whereas delay in full-term pregnancy increases short-term breast cancer risk and the probability of latent breast cancer development. Hormonal activation of the p53 protein (encode by the TP53 gene) in the mammary gland at a critical time in pregnancy has been identified as one of the most important determinants of whether the mammary gland develops latent breast cancer. This review discusses what is known about the protective influence of female hormones in young parous women, with a specific focus on the opportune role of wild-type p53 reprogramming in mammary cell differentiation. The importance of p53 as a protector or perpetrator in hormone-dependent breast cancer, resistance to treatment, and recurrence is also explored. View Full-Text
Keywords: breast cancer origin; p53 tumor suppressor; latency; treatment; estrogen receptor; pregnancy breast cancer origin; p53 tumor suppressor; latency; treatment; estrogen receptor; pregnancy
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MDPI and ACS Style

McGowan, E.M.; Lin, Y.; Hatoum, D. Good Guy or Bad Guy? The Duality of Wild-Type p53 in Hormone-Dependent Breast Cancer Origin, Treatment, and Recurrence. Cancers 2018, 10, 172. https://doi.org/10.3390/cancers10060172

AMA Style

McGowan EM, Lin Y, Hatoum D. Good Guy or Bad Guy? The Duality of Wild-Type p53 in Hormone-Dependent Breast Cancer Origin, Treatment, and Recurrence. Cancers. 2018; 10(6):172. https://doi.org/10.3390/cancers10060172

Chicago/Turabian Style

McGowan, Eileen M., Yiguang Lin, and Diana Hatoum. 2018. "Good Guy or Bad Guy? The Duality of Wild-Type p53 in Hormone-Dependent Breast Cancer Origin, Treatment, and Recurrence" Cancers 10, no. 6: 172. https://doi.org/10.3390/cancers10060172

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