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Research Article Free access | 10.1172/JCI113549

Transient suppression of clonal hemopoiesis associated with pregnancy in a patient with a myeloproliferative disorder.

A G Turhan, R K Humphries, J D Cashman, D A Cuthbert, C J Eaves, and A C Eaves

Terry Fox Laboratory, British Columbia Cancer Research Centre, Vancouver, Canada.

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Terry Fox Laboratory, British Columbia Cancer Research Centre, Vancouver, Canada.

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Terry Fox Laboratory, British Columbia Cancer Research Centre, Vancouver, Canada.

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Terry Fox Laboratory, British Columbia Cancer Research Centre, Vancouver, Canada.

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Terry Fox Laboratory, British Columbia Cancer Research Centre, Vancouver, Canada.

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Terry Fox Laboratory, British Columbia Cancer Research Centre, Vancouver, Canada.

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Published June 1, 1988 - More info

Published in Volume 81, Issue 6 on June 1, 1988
J Clin Invest. 1988;81(6):1999–2003. https://doi.org/10.1172/JCI113549.
© 1988 The American Society for Clinical Investigation
Published June 1, 1988 - Version history
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Abstract

We have used restriction fragment length polymorphism analysis to study the clonal involvement of the blood cells in a woman with myeloproliferative disease, whose initially high platelet count (940,000/microliter) spontaneously decreased during a normal pregnancy but then returned rapidly to the same high level after delivery of her child. Analysis of her erythroid progenitors showed the presence of erythropoietin-independent progenitors before, during, and after her pregnancy, consistent with a diagnosis of myeloproliferative disease, and persistence of the abnormal clone throughout the period of study. Analysis of DNA from her blood granulocytes showed these to be polyclonal at mid-pregnancy, when her platelet count had decreased to normal values, in comparison to the monoclonal pattern exhibited by her blood granulocytes 3 mo postpartum, when her platelet count was again elevated. These results demonstrate a partial conversion to normal, polyclonal hemopoiesis during her pregnancy and suggest a previously unanticipated differential sensitivity of normal and neoplastic hemopoietic cells to physiological changes associated with this state.

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