Literature DB >> 1970199

Use of polymerase chain reaction-detected sequence polymorphisms to document engraftment following allogeneic bone marrow transplantation.

M S Roth1, J H Antin, E L Bingham, D Ginsburg.   

Abstract

Distinguishing between host and donor origin of cells after bone marrow transplantation is important in understanding the engraftment process. Restriction fragment-length polymorphism (RFLP) analysis, the most generally applicable approach for this purpose, is limited by a requirement for at least 10(6) cells per assay. The small number of cells available at early time points post-BMT has thus precluded studies of early engraftment kinetics. This report describes the application of the polymerase chain reaction (PCR) to engraftment analysis following allogeneic BMT. We describe a series of PCR polymorphisms (PCRFLP/s) that allows the distinction of most patient-donor pairs (excluding identical twins). Thirteen patient-donor pairs were evaluated using this approach, and engraftment data obtained at time points when leukocyte counts were often too low for conventional analysis. This approach is quantitative and significantly more rapid than conventional techniques. (Analysis can be completed in less than a day). Serial evaluation at early time points post-BMT in five patients demonstrated residual host cells early (days 7-14) followed by their subsequent rapid disappearance. In one patient an apparent resurgence of host elements occurred around days 28-35, followed by a sharp decline by day 42.

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Year:  1990        PMID: 1970199     DOI: 10.1097/00007890-199004000-00012

Source DB:  PubMed          Journal:  Transplantation        ISSN: 0041-1337            Impact factor:   4.939


  6 in total

1.  Severe von Willebrand disease due to a defect at the level of von Willebrand factor mRNA expression: detection by exonic PCR-restriction fragment length polymorphism analysis.

Authors:  W C Nichols; S E Lyons; J S Harrison; R L Cody; D Ginsburg
Journal:  Proc Natl Acad Sci U S A       Date:  1991-05-01       Impact factor: 11.205

2.  The molecular defect in type IIB von Willebrand disease. Identification of four potential missense mutations within the putative GpIb binding domain.

Authors:  K A Cooney; W C Nichols; M E Bruck; W F Bahou; A D Shapiro; E J Bowie; H R Gralnick; D Ginsburg
Journal:  J Clin Invest       Date:  1991-04       Impact factor: 14.808

3.  Conserved linkage of neurotrophin-3 and von Willebrand factor on mouse chromosome 6.

Authors:  L L Barrow; K Simin; K Mohlke; W C Nichols; D Ginsburg; M H Meisler
Journal:  Mamm Genome       Date:  1993       Impact factor: 2.957

4.  Analysis of the relationship of von Willebrand disease (vWD) and hereditary hemorrhagic telangiectasia and identification of a potential type IIA vWD mutation (IIe865 to Thr).

Authors:  M C Iannuzzi; N Hidaka; M Boehnke; M E Bruck; W T Hanna; F S Collins; D Ginsburg
Journal:  Am J Hum Genet       Date:  1991-04       Impact factor: 11.025

5.  Cellular therapy following allogeneic stem-cell transplantation.

Authors:  Alison Rager; David L Porter
Journal:  Ther Adv Hematol       Date:  2011-12

6.  Molecular basis for H blood group deficiency in Bombay (Oh) and para-Bombay individuals.

Authors:  R J Kelly; L K Ernst; R D Larsen; J G Bryant; J S Robinson; J B Lowe
Journal:  Proc Natl Acad Sci U S A       Date:  1994-06-21       Impact factor: 11.205

  6 in total

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