Immunohistochemical characterization of p57Kip2 expression in tetraploid hydropic placentas.
BACKGROUND
Because there are differences in the origin, morphology, and natural history of hydropic placental villous issues, it is important to identify and document rare specimens that deviate from the diploid complete hydatidiform mole (CM), triploid partial hydatidiform mole (PM), or diploid hydropic abortion (HA). Tetraploid hydropic placentas have rarely been studied.


OBJECTIVE
To evaluate the frequency of p57Kip2 protein (p57) expression in tetraploid hydropic placentas and to determine its clinicopathologic significance.


METHODS
Forty hydropic DNA tetraploid placental specimens were evaluated by immunohistochemistry of formalin-fixed tissues, using a monoclonal antibody against p57, a putative paternally imprinted inhibitor gene. DNA ploidy in all cases was analyzed by flow cytometry.


RESULTS
Thirty cases were histologically diagnosed as CMs, 10 were HAs, and none were PMs. In all HAs, nuclear p57 was strongly expressed in cytotrophoblasts, intermediate trophoblasts, and villous stromal cells. In contrast, in CMs, p57 expression in cytotrophoblasts and villous stromal cells was either absent (26 cases) or very low (4 cases). Assuming that the degree of molar change roughly correlates with the proportion of paternal chromosomes present, all chromosomes might be paternally derived in all tetraploid CMs and the 10 HAs, including 2 that were karyotyped as 92,XXYY or 90,XXYY,-13,-14, which were presumably due to 2 sets of chromosomes each from paternal and maternal origin.


CONCLUSIONS
Expression of p57 is aberrant in tetraploid CMs. This finding is in line with the hypothesis that the loss of p57 is involved in the abnormal development of androgenetic CMs. For the evaluation of a patient with trophoblastic disease, p57 immunostaining is an ancillary diagnostic method that may be used in concert with flow cytometry.
Department of Pathology, Jikei Daisan Hospital, Komae-shi, Tokyo, Japan. maasafu@jikei.ac.jp
Masaharu
M
Fukunaga
D000022:Abortion, Spontaneous / Q000235:genetics* / Q000473:pathology; D000293:Adolescent; D000328:Adult; D000782:Aneuploidy; D002822:Choriocarcinoma / Q000737:chemistry / Q000235:genetics / Q000473:pathology; D002824:Chorionic Villi / Q000737:chemistry / Q000473:pathology; D002877:Chromosomes, Human / Q000648:ultrastructure; D050761:Cyclin-Dependent Kinase Inhibitor p57; D003656:Decidua / Q000737:chemistry / Q000473:pathology; D004487:Edema / Q000473:pathology; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D018392:Genomic Imprinting; D005865:Gestational Age; D006801:Humans; D006828:Hydatidiform Mole / Q000737:chemistry / Q000235:genetics* / Q000473:pathology; D007124:Immunoenzyme Techniques; D007621:Karyotyping; D008875:Middle Aged; D009006:Monosomy; D009363:Neoplasm Proteins / Q000032:analysis* / Q000235:genetics; D009687:Nuclear Proteins; D010920:Placenta / Q000737:chemistry* / Q000473:pathology; D011123:Polyploidy; D011247:Pregnancy; D012189:Retrospective Studies; D017154:Stromal Cells / Q000737:chemistry / Q000473:pathology; D014327:Trophoblasts / Q000737:chemistry / Q000473:pathology; D014594:Uterine Neoplasms / Q000737:chemistry / Q000235:genetics* / Q000473:pathology
C493964:CDKN1C protein, human; D050761:Cyclin-Dependent Kinase Inhibitor p57; D009363:Neoplasm Proteins; D009687:Nuclear Proteins