https://orcid.org/0000-0002-4724-9327
![A 34-year-old pregnant woman presented with increasing leukocytosis (white blood cell count, 58 000 × 109/μL) and severe anemia (hemoglobin, 8 g/dL) during the third trimester. Morphological and immunophenotypic analyses of bone marrow aspirate (panel D; May-Grunwald Giemsa stain, original magnification ×400) were consistent with acute myeloid leukemia (AML; French-American-British M4). Molecular analysis did not show NPM1 and FLT3 mutations. Fluorescence in situ hybridization analysis identified t(11;19)(q23p13) mixed-lineage-leukemia–rearranged AML (2017 European LeukemiaNet adverse-risk category). Delivery was performed. A “7+3” regimen was then administered, but disease remission was not achieved. We carried out a pathologic examination of the placenta, to track this rare route of AML transmission. Unexpectedly, we found a focal nodule of CD34+/−, MPO−/+, CD68/PG-M1+/− leukemic blasts (panel C, arrows; CD68 stain, original magnification ×400). The latter were scattered between maternal cotyledons (panel A, star) with fetal side sparing (panel A, arrowhead and panel B, arrows; hematoxylin and eosin stain, original magnification ×100 [A], ×400 [B]). This finding was consistent with placental myeloid sarcoma. Fortunately, the newborn displayed normal blood counts and was in good clinical condition; however, a close follow-up has been maintained, considering the risk of delayed development of AML.](https://ash.silverchair-cdn.com/ash/content_public/journal/blood/135/16/10.1182_blood.2020004975/4/m_bloodbld2020004975f1.png?Expires=1769786559&Signature=yjcaSMsxqZJEAgSoiQ8jZYm10zXfdNBLZmtZIht3MKtlmgQx~IEmyT3VccymP7TAm1TGy4pLro6aGTt6NvsV66QYDgwnvI8GnWKi5FOnYhbvC2j6xaxusHESJFTIrscmmUHmyVub~1GVJ3H1la04zTE2R6XKHnqHD2e59mDG2z9eCR6r6li8oHDsnJZcF2XRFKn~kFEVo987eB9tONxsLB4PPN1T3gL~iMrXqPmVK0j1zFecCy59UmlCYMWiZVNn8T56BrEiSBDLwHN~7d9qOHL8BiPohcNvkDi0Z73tlRfQN-6d9qYCMUX3koQml0IozVOaMfphXXKgXDVjCOoavg__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)
A 34-year-old pregnant woman presented with increasing leukocytosis (white blood cell count, 58 000 × 109/μL) and severe anemia (hemoglobin, 8 g/dL) during the third trimester. Morphological and immunophenotypic analyses of bone marrow aspirate (panel D; May-Grunwald Giemsa stain, original magnification ×400) were consistent with acute myeloid leukemia (AML; French-American-British M4). Molecular analysis did not show NPM1 and FLT3 mutations. Fluorescence in situ hybridization analysis identified t(11;19)(q23p13) mixed-lineage-leukemia–rearranged AML (2017 European LeukemiaNet adverse-risk category). Delivery was performed. A “7+3” regimen was then administered, but disease remission was not achieved. We carried out a pathologic examination of the placenta, to track this rare route of AML transmission. Unexpectedly, we found a focal nodule of CD34+/−, MPO−/+, CD68/PG-M1+/− leukemic blasts (panel C, arrows; CD68 stain, original magnification ×400). The latter were scattered between maternal cotyledons (panel A, star) with fetal side sparing (panel A, arrowhead and panel B, arrows; hematoxylin and eosin stain, original magnification ×100 [A], ×400 [B]). This finding was consistent with placental myeloid sarcoma. Fortunately, the newborn displayed normal blood counts and was in good clinical condition; however, a close follow-up has been maintained, considering the risk of delayed development of AML.
Reported cases of placental involvement by cancer cells are mostly melanoma or leukemia/lymphoma. Even if it is extremely rare, transplacental transmission may occur, thus representing a life-threatening condition for the newborn. Pathologic examination of the placenta should be recommended for the diagnostic work-up of maternal AML, which has an estimated incidence of ∼1:100 000 pregnancies.
A 34-year-old pregnant woman presented with increasing leukocytosis (white blood cell count, 58 000 × 109/μL) and severe anemia (hemoglobin, 8 g/dL) during the third trimester. Morphological and immunophenotypic analyses of bone marrow aspirate (panel D; May-Grunwald Giemsa stain, original magnification ×400) were consistent with acute myeloid leukemia (AML; French-American-British M4). Molecular analysis did not show NPM1 and FLT3 mutations. Fluorescence in situ hybridization analysis identified t(11;19)(q23p13) mixed-lineage-leukemia–rearranged AML (2017 European LeukemiaNet adverse-risk category). Delivery was performed. A “7+3” regimen was then administered, but disease remission was not achieved. We carried out a pathologic examination of the placenta, to track this rare route of AML transmission. Unexpectedly, we found a focal nodule of CD34+/−, MPO−/+, CD68/PG-M1+/− leukemic blasts (panel C, arrows; CD68 stain, original magnification ×400). The latter were scattered between maternal cotyledons (panel A, star) with fetal side sparing (panel A, arrowhead and panel B, arrows; hematoxylin and eosin stain, original magnification ×100 [A], ×400 [B]). This finding was consistent with placental myeloid sarcoma. Fortunately, the newborn displayed normal blood counts and was in good clinical condition; however, a close follow-up has been maintained, considering the risk of delayed development of AML.
Reported cases of placental involvement by cancer cells are mostly melanoma or leukemia/lymphoma. Even if it is extremely rare, transplacental transmission may occur, thus representing a life-threatening condition for the newborn. Pathologic examination of the placenta should be recommended for the diagnostic work-up of maternal AML, which has an estimated incidence of ∼1:100 000 pregnancies.
For additional images, visit the ASH Image Bank, a reference and teaching tool that is continually updated with new atlas and case study images. For more information, visit http://imagebank.hematology.org.
![A 34-year-old pregnant woman presented with increasing leukocytosis (white blood cell count, 58 000 × 109/μL) and severe anemia (hemoglobin, 8 g/dL) during the third trimester. Morphological and immunophenotypic analyses of bone marrow aspirate (panel D; May-Grunwald Giemsa stain, original magnification ×400) were consistent with acute myeloid leukemia (AML; French-American-British M4). Molecular analysis did not show NPM1 and FLT3 mutations. Fluorescence in situ hybridization analysis identified t(11;19)(q23p13) mixed-lineage-leukemia–rearranged AML (2017 European LeukemiaNet adverse-risk category). Delivery was performed. A “7+3” regimen was then administered, but disease remission was not achieved. We carried out a pathologic examination of the placenta, to track this rare route of AML transmission. Unexpectedly, we found a focal nodule of CD34+/−, MPO−/+, CD68/PG-M1+/− leukemic blasts (panel C, arrows; CD68 stain, original magnification ×400). The latter were scattered between maternal cotyledons (panel A, star) with fetal side sparing (panel A, arrowhead and panel B, arrows; hematoxylin and eosin stain, original magnification ×100 [A], ×400 [B]). This finding was consistent with placental myeloid sarcoma. Fortunately, the newborn displayed normal blood counts and was in good clinical condition; however, a close follow-up has been maintained, considering the risk of delayed development of AML.](https://ash.silverchair-cdn.com/ash/content_public/journal/blood/135/16/10.1182_blood.2020004975/4/m_bloodbld2020004975f1.png?Expires=1769786561&Signature=Sk6WoGXVJjEcvmXcqZVWakHPVCBkYUrdWdXnte7GUPYLNRFcvI9GYP1uf5kSXJoeiJhh-MXraAbrtzG4lWPrrPr2vI45tBgw03b0Xa~xHGH~h6Ud8SAk1FLrty-Xk2FFWhUxfdSm9onDXqfg~kVz8h4Kkb0Jtlx2rp5NnDWyku~6IJvxwL8209dpzxOSW7vimQhaeymHq1~B3GhIyCHan4oj-jQzVb~FvcfZT6LflCUDZ6JpOgvJCHf01l8jO1NzTdBst8bZLVFvlyPdcRzPepyj-Y6Q2hVmrLbqj-YslK8e-fvRWAvHdLdvlwtPhjjzvrIMhW2MwSD0blJZ03VXYg__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)
