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Gender inequities in organ donation and transplantation
Published in Wendy A. Rogers, Jackie Leach Scully, Stacy M. Carter, Vikki A. Entwistle, Catherine Mills, The Routledge Handbook of Feminist Bioethics, 2022
This detailed examination of sex and gender differences in organ donation and transplantation illustrates the complex factors affecting who gets ill, who becomes a donor, who receives an organ and how they fare post transplantation. The level of detail points to the need for careful analysis to identify gender-related inequities and how these might be addressed. To some extent, these analyses are already taking place in the transplantation literature (see e.g. Puoti et al. 2016; Teegen et al. 2016; Melk et al. 2019). What I hope to show in the remainder of the chapter is how feminist bioethics can bring novel conceptual insights to the analysis of gender inequities and other ethical issues in organ donation and transplantation.
Forensic Application of Telomere Shortening in Age-at-Death Estimation
Published in Sara C. Zapico, Mechanisms Linking Aging, Diseases and Biological Age Estimation, 2017
Terminal Restriction Fragment length of telomeres and age are inversely correlated, which can be used to determine the age of an individual (Ren et al. 2009). Telomere shortening during the aging process occurs and has been tested in different populations and in many cells and tissues, such as fibroblasts (Harley et al. 1990), peripheral blood cells (Iwama et al. 1998), colonic mucosa (Hastie et al. 1990), kidneys (Melk et al. 2000), dental pulp (Takasaki et al. 2003) and buccal cells (Hewakapuge et al. 2008).
Paediatric oncology
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2014
Stephen Lowis, Rachel Cox, John Moppett, Antony Ng
Faury et al.371 reported a series of 32 children and identified two groups of patients. Those with activation of the Akt and Ras pathways had a worse outcome than those without. Active Ras was associated with survival in only 1 patient of 21, compared to 5 of the 11 without. Ras/Akt activation was associated with overexpression of markers associated with neural stem cells such as CD133, nestin, MELK and D1x2. Other factors, such as age, sex or p53 expression, were not associated with outcome.
CRISPR-Directed Gene Editing in a Community Cancer Center
Published in Oncology Issues, 2019
CRISPR has already helped to re-identify the targets for certain well-known drugs. For example, a recent CRISPR/Cas9 screen for the essential genes involved in tumor growth led to the discovery that the MELK protein, known to be an essential for tumor growth, does not in fact drive cell proliferation in cancer cells as previously thought.14 As the era of personalized medicine begins, it will be critical to validate potential (and now previously identified) drug targets by using screening methodologies that act at the level of gene by these more robust genetic techniques.
Emerging alternatives to tyrosine kinase inhibitors for treating chronic myeloid leukemia
Published in Expert Opinion on Emerging Drugs, 2018
Simon Kavanagh, Aisling Nee, Jeffrey H. Lipton
MELK is a cell cycle-dependent protein kinase that is barely detectable in most normal adult tissues but has been found to be upregulated in various types of cancer including breast cancer and glioblastoma [97,98]. It has been found to be expressed in AML cell lines and in AML primary blasts. Expression is significantly higher in the stem cell-enriched population of blast cells obtained from AML patients than that in the more differentiated cell population [99].
Targeting PRAS40: a novel therapeutic strategy for human diseases
Published in Journal of Drug Targeting, 2021
Qun Zhou, Shengsong Tang, Xianhui Zhang, Linxi Chen
In addition, maternal embryonic leucine zipper kinase (Melk) plays an important role in the occurrence and development of tumours. Some studies have pointed out that Melk promoted the occurrence of clear cell renal cell carcinoma (ccRCC) by dissociating PRAS40 from raptor, thus promoting PRAS40 phosphorylation and over-activating mTORC1. In other words, the phosphorylation of PRAS40 mediates the tumorigenesis of Melk [85].