Mainstream academic debate on the ethics of human gene editing is currently not as inclusive as it should be. For example, it currently does not give due consideration to Indigenous groups and cultures, such as those living in rural and remote areas of Canada. Once such people are given due consideration, then several important points emerge, which have so far gone unnoticed or under-emphasized in the debate. This article focuses on two of those points: (a) Some vulnerable people who are currently being ignored in the debate may not desire to use gene editing, even if it is safe, effective and affordable, and they will have compelling reasons for making this decision; and (b) even if such people do decide to use the technology, the gene editing enterprise itself is unlikely to do much good for them (and may even be harmful to them), as it alarmingly misses the point regarding the underlying contributing causes of the most pressing problems that those people are facing. Therefore, the promise of the gene editing enterprise is a hollow one for some groups of vulnerable people. These considerations should be used more prominently to guide debate on the ethics of human gene editing.
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http://dx.doi.org/10.1111/bioe.12882 | DOI Listing |
Cell Rep
January 2025
Department of Surgery, University of California, San Francisco, San Francisco, CA 94143, USA; Eli & Edythe Broad Center for Regeneration Medicine, University of California, San Francisco, San Francisco, CA 94143, USA; Department of Bioengineering & Therapeutic Sciences, University of California, San Francisco, San Francisco, CA 94158, USA. Electronic address:
The most severe form of α-thalassemia results from loss of all four copies of α-globin. Postnatally, patients face challenges similar to β-thalassemia, including severe anemia and erythrotoxicity due to the imbalance of β-globin and α-globin chains. Despite progress in genome editing treatments for β-thalassemia, there is no analogous curative option for α-thalassemia.
View Article and Find Full Text PDFStem Cell Rev Rep
January 2025
Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati, Guwahati, Assam, India.
Background: Undifferentiated embryonic cell transcription factor 1 (UTF1) is predominantly expressed in pluripotent stem cells and plays a vital role in embryonic development and pluripotency maintenance. Despite its established importance in murine models, the role of UTF1 on human induced pluripotent stem cells (iPSCs) has not been comprehensively studied.
Methods: This study utilized CRISPR/Cas9 gene editing to create UTF1 knockout in human fibroblasts and iPSCs.
Biol Sex Differ
January 2025
Department of Laboratory Medicine and Pathology, School of Medicine, University of Washington, Seattle, WA, 98195, USA.
Background: X chromosome inactivation (XCI) is a female-specific process in which one X chromosome is silenced to balance X-linked gene expression between the sexes. XCI is initiated in early development by upregulation of the lncRNA Xist on the future inactive X (Xi). A subset of X-linked genes escape silencing and thus have higher expression in females, suggesting female-specific functions.
View Article and Find Full Text PDFJ Nanobiotechnology
January 2025
Stomatological Hospital, School of Stomatology, Southern Medical University, Guangzhou, Guangdong, China.
Extracellular vesicles (EVs) are membrane-bound vesicles that are shed or secreted from the cell membrane and enveloped by a lipid bilayer. They possess stability, low immunogenicity, and non-cytotoxicity, exhibiting extensive prospects in regenerative medicine (RM). However, natural EVs pose challenges, such as insufficient targeting capabilities, potential biosafety concerns, and limited acquisition pathways.
View Article and Find Full Text PDFCNS Neurosci Ther
January 2025
Jiujiang Clinical Precision Medicine Research Center, Jiujiang, Jiangxi, China.
Background: Adenosine deaminase action on RNA 1 (ADAR1) can convert the adenosine in double-stranded RNA (dsRNA) molecules into inosine in a process known as A-to-I RNA editing. ADAR1 regulates gene expression output by interacting with RNA and other proteins; plays important roles in development, including growth; and is linked to innate immunity, tumors, and central nervous system (CNS) diseases.
Results: In recent years, the role of ADAR1 in tumors has been widely discussed, but its role in CNS diseases has not been reviewed.
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