Derrick J Rossi
Affiliation: Stanford University
- Stems cells and the pathways to aging and cancerDerrick J Rossi
Immune Disease Institute, Harvard Stem Cell Institute, and the Department of Pathology, Harvard Medical School, Boston, MA 02115, USA
Cell 132:681-96. 2008..Here, we examine evidence linking stem cell dysfunction to the pathophysiological conditions accompanying aging, focusing on the mechanisms underlying stem cell decline and their contribution to disease pathogenesis...
- Hematopoietic stem cell aging: mechanism and consequenceDerrick J Rossi
Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA
Exp Gerontol 42:385-90. 2007....
- Pten, tumorigenesis, and stem cell self-renewalDerrick J Rossi
Department of Pathology, Stanford University School of Medicine, Beckman Center B259, 279 Campus Drive, Stanford, CA 94305, USA
Cell 125:229-31. 2006..2006) report in a recent Nature paper, this may not be the case for the tumor suppressor protein Pten, which drives the self-renewal of normal hematopoietic stem cells and the formation of leukemia cells through different mechanisms...
- Cell intrinsic alterations underlie hematopoietic stem cell agingDerrick J Rossi
Department of Pathology and Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA
Proc Natl Acad Sci U S A 102:9194-9. 2005....
- Hematopoietic stem cell quiescence attenuates DNA damage response and permits DNA damage accumulation during agingDerrick J Rossi
Department of Pathology, Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California 94305, USA
Cell Cycle 6:2371-6. 2007..Moreover, the cytoprotection afforded by stem cell quiescence in stress-free, steady-state conditions suggests a mechanism through which potentially dangerous lesions can accumulate in the stem cell pool with age...
- Deficiencies in DNA damage repair limit the function of haematopoietic stem cells with ageDerrick J Rossi
Department of Pathology, and Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California 94305, USA
Nature 447:725-9. 2007..These data are consistent with DNA damage accrual being a physiological mechanism of stem cell ageing that may contribute to the diminished capacity of aged tissues to return to homeostasis after exposure to acute stress or injury...
- Gene Expression Commons: an open platform for absolute gene expression profilingJun Seita
Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California, United States of America
PLoS ONE 7:e40321. 2012....
- Human bone marrow hematopoietic stem cells are increased in frequency and myeloid-biased with ageWendy W Pang
Institute for Stem Cell Biology and Regenerative Medicine, Ludwig Center for Stem Cell Research, and Department of Pathology, Stanford University, Stanford, CA 94305, USA
Proc Natl Acad Sci U S A 108:20012-7. 2011....
- Rapid lymphocyte reconstitution of unconditioned immunodeficient mice with non-self-renewing multipotent hematopoietic progenitorsDeepta Bhattacharya
Institute of Cancer and Stem Cell Biology and Medicine, Department of Pathology, Stanford University School of Medicine, Stanford, California, USA
Cell Cycle 5:1135-9. 2006..Based on recent evidence, we discuss novel strategies to achieve the replacement of abnormal HSCs without the use of cytotoxic conditioning regimens...
- Niche recycling through division-independent egress of hematopoietic stem cellsDeepta Bhattacharya
Institute of Stem Cell Biology and Regenerative Medicine Stanford University School of Medicine Stanford, CA 94305, USA
J Exp Med 206:2837-50. 2009..These data provide insight as to how HSC replacement can occur despite the residence of endogenous HSCs in niches, and suggest therapeutic interventions that capitalize upon physiological HSC egress...
- Purified hematopoietic stem cell engraftment of rare niches corrects severe lymphoid deficiencies without host conditioningDeepta Bhattacharya
Department of Pathology, Institute of Cancer and Stem Cell Biology and Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA
J Exp Med 203:73-85. 2006..These experiments provide a general mechanism by which transplanted HSCs can correct hematopoietic deficiencies without any host conditioning or with only highly specific and transient lymphoablation...
- Stem cells and aging in the hematopoietic systemLuigi A Warren
Department of Pathology, Harvard Medical School, Harvard University, Boston, MA 02115, USA
Mech Ageing Dev 130:46-53. 2009..Challenges for the future include assessing the significance of 'lineage skewing' to immune dysfunction, and investigating the role of epigenetic dysregulation in HSC aging...
- Hematopoietic stem cells: the paradigmatic tissue-specific stem cellDavid Bryder
Stanford University School of Medicine, B257 Beckman Center, Stanford, CA 94305-5323, USA
Am J Pathol 169:338-46. 2006..In this review we discuss some general concepts regarding stem cell biology learned from the study of HSCs with a highlight on recent work pertaining to emerging topics of interest for stem cell biology...
- Stem cells and the aging hematopoietic systemIsabel Beerman
Department of Pathology, Harvard Medical School, Harvard Stem Cell Institute, Immune Disease Institute, Program in Cellular and Molecular Medicine, Children s Hospital Boston, Boston, MA 02115, USA
Curr Opin Immunol 22:500-6. 2010..Recent developments have shed light on how aging of the hematopoietic stem cell compartment contributes to hematopoietic decline through diverse mechanisms...
- Hematopoietic reconstitution by multipotent adult progenitor cells: precursors to long-term hematopoietic stem cellsMarta Serafini
Stem Cell Institute and Cancer Center and Department of Pediatrics, Division of Hematology, Oncology, Blood and Marrow Transplant Program, University of Minnesota, Minneapolis, MN 55455, USA
J Exp Med 204:129-39. 2007..Because GFP+ host-derived CD45.1+ cells were not observed, fusion is not likely to account for the generation of HSCs by MAPCs...
- Conditional ablation of the Mat1 subunit of TFIIH in Schwann cells provides evidence that Mat1 is not required for general transcriptionNina Korsisaari
Haartman Institute and Helsinki University Central Hospital, Biomedicum Helsinki, PO Box 63, Haartmaninkatu 8, 00014 University of Helsinki, Finland
J Cell Sci 115:4275-84. 2002....
- Transcriptional instability is not a universal attribute of agingLuigi A Warren
Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA
Aging Cell 6:775-82. 2007..We conclude that large-scale regulatory destabilization is not a universal concomitant of aging, and may be of significance as an aging mechanism primarily in nonrenewing tissues...
- Deciphering developmental stages of adult myelopoiesisCornelis J Pronk
Institution for Experimental Medical Science, Immunology Section, Lund University, Lund, Sweden
Cell Cycle 7:706-13. 2008..When functionally evaluated, such early granulocyte/monocyte precursors displayed a latent lymphoid activity, which was pronounced in subsets bearing high expression of the tyrosine kinase receptor FLT3...
- Elucidation of the phenotypic, functional, and molecular topography of a myeloerythroid progenitor cell hierarchyCornelis J H Pronk
Lund Strategic Research Center for Stem Cell Biology and Cell Therapy, Lund University, BMC I13, 221 84 Lund, Sweden Immunology Unit, Institution for Experimental Medical Science, Lund University, BMC I13, 221 84 Lund, Sweden
Cell Stem Cell 1:428-42. 2007....
- SIRT1 acts as a nutrient-sensitive growth suppressor and its loss is associated with increased AMPK and telomerase activitySwami R Narala
Ontario Cancer Institute, Department of Medical Biophysics, University of Toronto, Toronto, ON, M5G 2M9, Canada
Mol Biol Cell 19:1210-9. 2008..Our findings challenge certain models and connect nutrient sensing enzymes to the immortalization process. Furthermore, they show that in certain cell lineages, SIRT1 can act as a growth suppressor gene...
- Ménage-à-trois 1 is critical for the transcriptional function of PPARgamma coactivator 1Motoaki Sano
Center for Cardiovascular Development, Baylor College of Medicine, Houston, TX 77030, USA
Cell Metab 5:129-42. 2007..PGC-1 bound to both MAT1 and Cdk7 in coprecipitation assays. Thus, we demonstrate a requirement for MAT1 in the operation of PGC-1 coactivators that control cell metabolism...
- Suppression of Peutz-Jeghers polyposis by inhibition of cyclooxygenase-2Lina Udd
Molecular Cancer Biology Research Program, Biomedicum Helsinki, Finland
Gastroenterology 127:1030-7. 2004..This study was designed to determine whether COX-2 inhibition would reduce tumor burden in Lkb1(+/-) mice or Peutz-Jeghers patients...
- Ephrin-B2 and EphB1 mediate retinal axon divergence at the optic chiasmScott E Williams
Departments of Pathology, Anatomy and Cell Biology, Center for Neurobiology and Behavior, Columbia University, College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032, USA
Neuron 39:919-35. 2003..EphB1 null mice exhibit a dramatically reduced ipsilateral projection, suggesting that this receptor contributes to the formation of the ipsilateral retinal projection, most likely through its repulsive interaction with ephrin-B2...
- The histidine triad protein Hint is not required for murine development or Cdk7 functionNina Korsisaari
Haartman Institute and Helsinki University Central Hospital, Biomedicum Helsinki, 00014 University of Helsinki, Finland
Mol Cell Biol 23:3929-35. 2003..Finally, Cdk7 kinase activity and cell cycle kinetics were found to be comparable in wild-type and Hint(-/-) mouse embryonic fibroblasts, suggesting that Hint may not be a key regulator of Cdk7 activity...
- Induction of cyclooxygenase-2 in a mouse model of Peutz-Jeghers polyposisDerrick J Rossi
Haartman Institute and Helsinki University Central Hospital, Biomedicum Helsinki, P O Box 63, University of Helsinki, 00014 Helsinki, Finland
Proc Natl Acad Sci U S A 99:12327-32. 2002..These findings thereby identify COX-2 as a potential target for chemoprevention in PJS patients...
- Stem Cell Aging: Functional Decline, DNA damage and Therapeutic TargetsDerrick Rossi; Fiscal Year: 2007....