Turhan A G, Humphries R K, Cashman J D, Cuthbert D A, Eaves C J, Eaves A C
Terry Fox Laboratory, British Columbia Cancer Research Centre, Vancouver, Canada.
J Clin Invest. 1988 Jun;81(6):1999-2003. doi: 10.1172/JCI113549.
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.