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Malcolm R. Alison

Researcher at Queen Mary University of London

Publications -  175
Citations -  12218

Malcolm R. Alison is an academic researcher from Queen Mary University of London. The author has contributed to research in topics: Stem cell & Progenitor cell. The author has an hindex of 53, co-authored 158 publications receiving 11695 citations. Previous affiliations of Malcolm R. Alison include London Research Institute & Cancer Research UK.

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Hepatocytes from non-hepatic adult stem cells

TL;DR: This paper showed that adult human liver cells can be derived from stem cells originating in the bone marrow or circulating outside the liver, raising the possibility that blood-system stem cells could be used clinically to generate hepatocytes for replacing damaged tissue.
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Mesenchymal Stem Cells Are Renotropic, Helping to Repair the Kidney and Improve Function in Acute Renal Failure

TL;DR: The results offer a strong case for exploring the possibility that mesenchymal stem cells by virtue of their renotropic property and tubular regenerative potential may have a role in the treatment of acute renal failure in humans.
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Bone marrow contributes to renal parenchymal turnover and regeneration

TL;DR: The presence of bone marrow‐derived cells was noted in both histologically normal mouse kidneys and in human transplanted kidneys suffering damage from a variety of causes, indicating that bone marrow cells contribute to both normal turnover of renal epithelia and regeneration after damage, and is suggested that this could be exploited therapeutically.
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CD133: molecule of the moment.

TL;DR: The utility of CD133 as a marker of haematopoietic stem cells for human allogeneic transplantation is confirmed, and it may be possible to develop future therapies towards targeting cancer stem cells via this marker.
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Bone marrow contribution to tumor-associated myofibroblasts and fibroblasts.

TL;DR: It is shown that the bone marrow can contribute to myofibroblast and fibroblast populations in tumor stroma in a mouse model of pancreatic insulinoma, and this development is at least in part a systemic response that may ultimately yield methods of targeting new therapy.