电子垃圾拆解区新生儿脐带血铬水平

背景与目的:探讨电子垃圾拆解区--贵屿镇新生儿铬污染状况及其影响因素.材料与方法:选择2006年5～9月足月健康新生儿152例,其中来自贵屿镇的100例(暴露组),来自周边乡镇的52例(对照组).采用石墨炉原子吸收光谱法检测新生儿脐带血铬水平,通过调查表对产妇进行问卷调查,分析相关影响因素.结果:贵屿组新生儿脐带血铬几何均值为303.38 μg/L,与对照组20.30 μg/L相比,差别有统计学意义(P＜0.01).孕妇从事电子垃圾处理相关工作等因素与新生儿脐带血铬水平呈正相关.结论:电子垃圾拆解区部分新生儿铬负荷处于较高的水平,新生儿的铬负荷水平与当地的电子垃圾拆解业及所造成的铬污染有关,铬污染可能对当地新生儿的健康构成威胁.     

血管内皮生长因子与膜型基质金属蛋白酶-1在口腔鳞状细胞癌表达及意义

[目的]检测血管内皮生长因子（VEGF）和膜型基质金属蛋白酶-1（MT1-MMP）在口腔鳞状细胞癌（OSCC）中的表达,并探讨其意义。[方法]采用免疫组织化学SP法检测VEGF、MT1-MMP在40例OSCC和10例口腔正常黏膜组织中的表达。[结果]VEGF和MT1-MMP在OSCC组织中的阳性表达率分别为67．50％和75．00％,在正常口腔黏膜组织中均阴性表达．差异有显著性（P〈0．001）。VEGF表达与OSCC的临床分期（P〈0．05）及淋巴结转移显著相关（P〈0．011,与肿瘤的分化程度无关。MT1-MMP表达与OSCC的分化程度（P〈0．05）及淋巴结转移显著相关（P〈0．01）,但与肿瘤的临床分期无相关性。VEGF与MT1-MMP表达呈正相关（rs=0．650,P〈0．001）。[结论]VEGF与MT1-MMP在OSCC发生发展中起重要作用,共同促进OSCC的浸润转移。     

乳腺癌组织中金属硫蛋白（MT）和拓扑异构酶Ⅱ（TopoⅡα）的表达及临床意义

目的：探讨乳腺癌中拓扑异构酶Ⅱ（TopoⅡα）和金属硫蛋白（MT）的表达与乳腺癌预后的关系,并分析两者的相关性。方法：采用SABC免疫组化方法检测72例乳腺癌标本中MT和TopoⅡα的表达。结果：MT和TopoⅡα的阳性率分别为33.33%和48.61%。MT阳性表达率与乳腺癌病理类型及有否巴结转移有关（P〈0.05）。TopoⅡα阳性表达率与是否有淋巴结转移有关（P〈0.05）。结论：检测MT和TopoⅡα对提示预后和临床选择化疗方案有指导意义。     

MT1-MMP和TIMP-2在非小细胞肺癌中的表达及与病理特征的相关性

目的：研究NSCLC中MT1-MMP及TIMP-2的表达及与病理类型分型、淋巴结转移和TNM分期关系。方法：采用免疫组化SP法检测MT1-MMP及TIMP-2在80例NSCLC患者和80例癌旁组织中的表达。结果：在NSCLC中MT1-MMP阳性表达率为73.8%,癌旁组织中为52.5%,（P〈0.05）。在NSCLC中TIMP-2的阳性表达率为42.5%,癌旁组织为72.5%,（P〈0.05）。MT1-MMP和TIMP-2的表达与肺癌的病理分类及肿瘤大小无关,而与TNM分期及淋巴结转移有关。MT1-MMP和TIMP-2的表达呈负相关（r=-0.635,P〈0.05）。结论：MT1-MMP和TIMP-2可能参与了NSCLC的发生发展过程,有望成为判断肺癌转移和预后的指标。     

膜型基质金属蛋白酶-1在乳腺癌中表达的预后价值

目的探讨膜型基质金属蛋白酶-1（MT1-MMP）蛋白在乳腺癌中表达的临床意义。方法采用免疫组织化学方法检测106例乳腺癌患者手术标本中MT1-MMP蛋白的表达;用统计学软件SPSS11．0作为统计分析的工具,MT1-MMP表达与临床病理因子的关系用卡方检验和Pearson等级相关分析检验;预后分析采用Kaplan—Meier检验Cox Regression。结果乳腺癌组织中MT1-MMP蛋白表达阳性率为62．3％,表达强度在不同分期和不同淋巴结转移数目患者间差异有统计学意义且呈正相关（P〈0．050）,在不同大小肿瘤间及在ER、PR和HER-2不同表达的患者间差异无统计学意义。MT1-MMP阴性患者与弱至中度阳性或强阳性患者间的无病生存期比较,MT1-MMP（-）为65．0％,MT1-MMP（＋-＋＋）为27．1％,MT1-MMP（＋＋＋）为27．8％,差异有统计学意义（P〈0．050）。不同MT1-MMP免疫组织化学染色强度患者的7年生存率也明显不同,MT1-MMP（-）为77．5％,MT1-MMP（＋-＋＋）为60．4％,MT1-MMP（＋＋＋）为50．0％,差异有统计学意义（P〈0．050）。根据不同分期和不同淋巴结转移状态分层分析发现,MT1-MMP蛋白不同表达强度的患者预后差异有统计学意义（P〈0．050）;根据不同肿瘤大小的分层分析发现,不同MT1-MMP表达强度的T2期和T4期患者预后差别有统计学意义（P〈0．050）,但T1和T3期患者预后没有差别。多因素分析显示MT1-MMP是有意义的预后因子,MT1-MMP强阳性患者死亡风险增加2倍,弱到中度阳性患者死亡风险增加1．3倍。结论MT1-MMP的表达与乳腺癌侵袭转移有关,MT1-MMP是乳腺癌的预后因子。     

RNA干扰沉默MIF基因对宫颈癌SiHa细胞上皮细胞间质变的影响

[目的]探讨巨噬细胞移动抑制因子（MIF）对人宫颈癌SiHa细胞上皮间质转化（EMT）的影响。[方法]构建并鉴定重组真核表达质粒Genesil-MIF siRNA,转染人宫颈癌细胞SiHa细胞。RT-PCR检测各组细胞中MIF、E-cadherin、Vimentin mRNA表达水平。免疫细胞化学法组检测E-cadherin、Vimentin蛋白表达水平。[结果]重组质粒Genesil-MIF siRNA成功构建并转染至人宫颈癌SiHa细胞。RT-PCR法证实实验组细胞中E-cadherin mRNA相对高表达（P〈0.05）,而Vimentin、MIF mRNA相对低表达（P〈0.05）。免疫细胞化学法证实实验组细胞中E-cadherin蛋白表达水平升高,Vimentin蛋白表达水平明显降低。[结论]MIF沉默通过促进SiHa细胞中E-cadherin表达,抑制Vimentin表达从而抑制EMT发生。     

乳腺癌组织中MT1-MMP、VEGF的表达及其相关性

目的 探讨MT1-MMP和VEGF在乳腺癌组织中的表达及其与乳腺癌临床病理特征间的关系.方法 采用免疫组织化学方法检测67例乳腺癌组织和癌旁正常组织中MT1-MMP和VEGF的表达情况,并与临床病理特征进行相关性分析.结果 MT1-MMP和VEGF在乳腺癌组织中的表达水平显著高于在癌旁正常组织中的表达水平（P＜0.05）.VEGF 和MT1-MMP在乳腺癌组织中的表达呈正相关（P=0.005）.VEGF的表达与乳腺癌的TNM分期和淋巴结转移相关（P＜0.05）;MT1-MMP表达与乳腺癌的TNM分期和腋窝淋巴结转移相关（P＜0.05）.结论 MT1-MMP和VEGF的过表达与乳腺癌的浸润转移有关,二者联合检测对判断乳腺癌的恶性程度和预后具有重要价值.     

HIF-1α基因沉默对人肺腺癌细胞A549裸鼠移植瘤生长及survivin表达的影响

目的观察缺氧诱导因子-1α（HIF-1α）基因沉默对肺癌的抑瘤效应和survivin表达的影响。方法将实验用肺腺癌A549细胞分为空白对照组、无意义序列转染组和实验组,接种裸鼠,建立裸鼠荷瘤模型,观测HIF-1α-MiRNA对裸鼠皮下移植瘤的生长抑制作用和对survivin表达的影响。采用免疫组化SP法,检测HIF-1α和survivin蛋白在裸鼠移植瘤中的表达。采用逆转录聚合酶链反应（RT-PCR）法检测HIF-1α和survivin mRNA的表达。采用原位末端标记（TUNEL）法检测肿瘤组织中细胞凋亡。结果实验组裸鼠肿瘤的生长速度较空白对照组、无意义序列转染组明显减慢（P〈0.05）。接种60 d后处死裸鼠,实验组裸鼠的肿瘤重量为（0.59±0.28）g,明显轻于空白对照组[（1.90±0.18）g]和无意义序列转染组[（1.66±0.24）g,P〈0.01]。实验组肿瘤组织中HIF-1αmRNA和蛋白的相对表达量分别为（0.45±0.04）%和（24.56±5.83）%,survivin mRNA和蛋白的相对表达量分别为（0.32±0.02）%和（29.08±3.99）%,均明显低于空白对照组、无意义序列转染组（P均〈0.05）。但实验组肿瘤组织中凋亡细胞的数量显著高于对照组。结论以HIF-1α为靶点的基因治疗,可能通过下调靶基因survivin的表达促进肺癌细胞凋亡,发挥抑制肿瘤生长的作用。     

表达MT1-MMP的乳腺癌细胞株对蒽环类药物敏感性研究

目的观察表达MT1-MMP的乳腺癌细胞株对蒽环类化疗药物敏感性的影响。方法用脂质体Lipofectamine 2000将pcDNA3.1-MT1-MMP真核表达载体转染乳腺癌细胞株MDA-MB-453,然后用含G418的培养基筛选获得过表达MT1-MMP的乳腺癌细胞株。蛋白印迹（Western blotting）技术检测MDA-MB-453细胞内MT1-MMP的表达情况。四唑蓝（MTT）法检测各组细胞对化疗药物的敏感性。结果 Western blotting实验证实,重组载体pcDNA3.1-MT1-MMP真核表达载体成功转入乳腺癌细胞内,并稳定过表达MT1-MMP。MTT法检测发现,阿霉素（ADH）、表阿霉素（EPI）、吡喃阿霉素（THP）转染组细胞的抑制率分别为41.38±1.34%、37.69±1.93%和57.96±3.19%,均明显低于未转染组（70.22±2.55%、70.35±1.21%、76.97±2.70%）和空白质粒组（68.94±1.89%、69.43±1.27%、73.06±1.65%,P〈0.05）。结论表达MT1-MMP的乳腺癌细胞株MDA-MB-453对蒽环类化疗药物具有耐药性,MT1-MMP有可能成为一个新的蒽环类化疗药物敏感性预测因子。     

血清瘦素水平在急性白血病患者体内表达的研究

目的观察急性白血病（AL）患者血清瘦素（LEP）水平的表达。方法AL患者25例（实验组）,健康人25例（对照组）,分别以放射免疫法测量AL患者治疗前血清LEP水平及健康人血清LEP水平。结果两组血清LEP水平分别为（19．6±3．48）μg／L和（32．89±6．56）μg／L,差异有统计学意义（P〈0．05）。结论AL患者血清瘦素水平较健康人为低。     

电子垃圾拆解区人群甲状腺激素水平改变的 Meta分析

目的：评价暴露于电子垃圾拆解区对人体血清甲状腺激素水平的影响。方法：检索PubMed、Web of Science、Elsevier电子期刊、中国知网、万方数据库等中英文数据库,收集国内外发表的评价人体血清甲状腺激素水平与电子垃圾拆解区暴露相关性的随机对照研究,检索时间从建库至2017年4月。应用RevMan 5.2软件进行Meta分析。结果：共纳入9篇相关研究,样本量包括暴露组489例、对照组489例。结果显示,电子垃圾拆解区人群血清总甲状腺素（T4）、游离甲状腺素（FT4）水平较对照组低（P < 0.05）,但游离三碘甲状腺原氨酸（FT3）、血清总三碘甲状腺原氨酸（T3）和促甲状腺激素（TSH）与对照组的差异无统计学意义（P > 0.05）。结论：暴露于电子垃圾拆解区可能会引起人甲状腺功能的改变。     

Determinants of polycyclic aromatic hydrocarbon-DNA adducts in human placenta.

To determine the relative contributions of tobacco smoking and P-450 metabolism (cytochrome P-450IAI) in the formation of benzo(a)pyrenediol-epoxide and other polycyclic aromatic hydrocarbon-DNA adducts in vivo, 16 human placentas were assayed for aryl hydrocarbon hydroxylase activity and (+/-)r-7,t-8-dihydroxy-c-9,10-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene-DN A adduct levels. Immunoaffinity chromatography columns, conjugated with monoclonal antibodies raised against benzo(a)-pyrene-diol-epoxide-deoxyguanosine, were used to concentrate polycyclic aromatic hydrocarbon-DNA adducted nucleotides, and synchronous fluorescence spectroscopy was used specifically to detect r-7,t-8,t-9,c-10-tetrahydroxy-7,8,9,10-tetrahydrobenzo(a)pyrene (BP-tetrol) extracted from acid hydrolysates of immunoconcentrated materials. Data were analyzed for associations with maternal dietary and smoking habits, umbilical cord blood cotinine levels, and placental aryl hydrocarbon hydroxylase levels. Complex mixtures of fluorescent materials were present in organic solvent extracts of acid hydrolysates of immunoconcentrated nucleotide-adducts from all placentas with patterns of fluorescence that may be associated with tobacco smoking determined by generation of spectral fluorescence excitation-emission matrices. BP-tetrols were detected in extracts from 8 placentas: 5 of 7 from smokers and 3 of 9 from nonsmokers. Placental aryl hydrocarbon hydroxylase activity was significantly higher in placentas from which BP-tetrols were extracted [3.9 +/- 2.4 [corrected] (mean +/- SE) pmol 3-hydroxybenzo(a)pyrene mg protein-1 min-1], than among placentas from which BP-tetrols were not extracted (0.4 +/- 0.2 [corrected] pmol 3-hydroxybenzo(a)pyrene mg protein-1 min-1) (P = 0.03, Student's t test). This association was independent of maternal smoking or umbilical cord blood cotinine levels. These results indicate that while maternal tobacco smoking is associated with the accumulation of putative, but as yet unidentified, polycyclic aromatic hydrocarbon-DNA adducts in placenta, metabolic capacity appears to be the principal determinant for the (+/-)r-7,t-8-dihydroxy-c-9,10 epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene-DNA adduct levels detected.     

Morphologic aspect of the placenta in young and adult pregnant rats bearing Walker 256 carcinoma

In the present study we investigated the influence of Walker 256 tumor growth on the modification of placental morphology and on fetal development in young and adult pregnant rats. After mating, female rats were divided into six groups: young control pregnant (Y), young pregnant with tumor (Yw), young pregnant injected with ascitic fluid (Ya), adult control pregnant (A), adult pregnant with tumor (Aw), and adult pregnant injected with ascitic fluid (Aa). Rats from tumor-bearing groups (Yw and Aw) were injected with 2.5 x 10(6) viable tumor cells into the right flank. Rats from Ya and Aa groups received daily inoculations of ascitic fluid (2.0 ml, i.p.) obtained from tumor-bearing rats without tumor cells. After 21 days, all animals were killed and the placentas were weighed and fixed with paraformaldehyde for histological analysis. Compared with control groups (Y and A), both tumor-bearing groups (Yw and Aw) presented the following changes: i) hemorrhage in the decidua and in the trophoblast giant cell layer; ii) disarrangement of the spongy zone, iii) restricted delimitation of the maternal and fetal blood vessels in the placental labyrinth; iv) hemorrhage and edema in the placental labyrinth. Similar results were observed in the placenta of groups injected with ascitic fluid (Ya and Aa). These results indicate that tumor development during pregnancy can have deleterious effects on placenta and fetus. These observations extend our previous data of extensive fetal reabsorption in both pregnant tumor-bearing and ascitic fluid-injected animals. These changes in placental morphology may be related to the synthesis and release of some factors by the tumor and the host cells, which could act directly or indirectly on placental tissue.     

Placental characteristics and reduced risk of maternal breast cancer

BACKGROUND: Women who have preeclampsia during pregnancy are at reduced risk of subsequent breast cancer. We examined whether other markers of reduced placental size or function, including increased blood pressure during pregnancy, predict a reduction in maternal breast cancer. METHODS: The Child Health and Development Studies is a 40-year follow-up of pregnant women enrolled in the Kaiser Permanente health plan between 1959 and 1967. We identified 3804 white women for whom data were available on placental examinations and other study variables. As of 1997, 146 women had developed invasive breast cancer. Proportional hazards models were used to estimate associations of breast cancer with markers of placental function. All statistical tests were two-sided. RESULTS: A blood pressure increase between the second and third trimesters exhibited a linear relationship with breast cancer rate, with the highest quartile showing a 51% reduction (95% confidence interval [CI] = 20% to 70%) that was not explained by preeclampsia. Smaller placental diameter was independently associated with a reduced breast cancer rate; the association increased with age at first pregnancy (P =.008). Maternal floor infarction of the placenta was associated with a 60% reduction in breast cancer rate (95% CI = 12% to 82%). In combination, placental risk factors were associated with a reduction in the breast cancer rate of as high as 94% (95% CI = 80% to 98%). CONCLUSIONS: Smaller placentas, maternal floor infarction of the placenta, and increasing blood pressure during pregnancy were associated with reduced maternal breast cancer. In the case of smaller placental diameter, the larger reduction observed with older age at first pregnancy suggests a process in which promotion of an existing lesion is blocked. Elucidating the mechanisms for these associations could provide clues to breast cancer prevention and treatment.     

Birth weight of children and cadmium accumulation in placentas of female nickel-cadmium (long-life) battery workers.

In a retrospective epidemiological study on the birth weight of 266 children of 137 female workers in a nickel-cadmium battery factory, 157 children of workers occupationally exposed to cadmium were compared with 109 born to non-occupationally exposed workers. No effect of cadmium exposure on birth weight was detected, but a statistically significant effect on birth weight of smoking during pregnancy was observed. In a prospective study on the same population of female battery workers, 27 placentas were collected and the cadmium distribution and concentration in tissue subsamples determined. Placental cadmium concentrations were positively correlated with maternal blood cadmium. The cadmium concentration in placentas ranged from < 0.002 to 0.095 microgram/g (wet weight), the mean concentration +/- SD was 0.021 +/- 0.022 microgram/g (wet weight). Morphological and ultrastructural studies of placental tissues did not reveal any effect of cadmium. This study did not provide any evidence in support of the hypothesis that the placenta may be the critical organ in exposure to cadmium.     

Histological, histochemical and electron microscopic changes of the placenta induced by maternal exposure to hyperthermia in the rat.

Both clinical and experimental investigations have shown that maternal hyperthermia during critical stages of embryo development can induce malformations in the offspring. Studies of the effect of heat stress on the placental functions are limited to the ewes, but that on microscopic structure is unknown. In the present study, rats were exposed to 41 or 42 degrees C for 1 h on gestation day (GD) 9. The controls were sham treated. Fetuses and placentas were collected on GD 20. Intrauterine growth retardation (IUGR) and several craniofacial malformations were observed in the fetuses of the heat-treated group. The placentas of the 42 degrees C group were significantly lighter in weight than those of the control. Light microscopy (LM) revealed thickening, hyalinization and occasional lymphocytic infiltration of the decidua basalis. Giant cells were prominent and glycogen cells had degenerated, leaving behind large cysts in the basal (spongy) zone. Best's carmine stain with or without diastase indicated the reduction in number and degeneration of glycogen cells and cyst formation. The labyrinthine zone was relatively thin in comparison to that of the controls. Perivascular fibrosis and paucity of vascularization were other features of the placentas of the hyperthermia group. Electron microscopy (EM) revealed lipid droplet accumulation in the trophoblast, the presence of myelin bodies and an increased production of collagen in the basal zone. Perivascular fibrosis appeared to have contributed to placental barrier thickening. EM also revealed accumulation of glycogen and lipid droplets in the trophoblasts and fibrin secretion into the extracellular space of the labyrinthine zone. These data suggest that placental pathology possibly contributes to fetal growth retardation in maternally heat-stressed rat fetuses.     

Population distribution of placental benzo(a)pyrene metabolism in smokers

Human placental microsomes isolated from term placentas derived from nonsmoking women and women smoking 1 to 40 cigarettes a day were analyzed for the metabolism of benzo(a)pyrene measured as various metabolites by HPLC and/or as aryl hydrocarbon hydroxylase (AHH)6 activity. In accordance with other reports, AHH activity was several times higher in smokers than in nonsmokers. Regression analysis on 13 different placental tissues from women smoking from 1 to 40 cigarettes demonstrated a high correlation (r = 0.8 to 0.9) between AHH activity (or the formation of benzo(a)pyrene phenols resolved by HPLC) versus the formation of the procarcinogenic benzo(a)pyrene-7,8-diol. Subsequent studies on placentas derived from 67 women who smoked 10 to 40 cigarettes per day demonstrated a definite dose-response relationship between AHH activity and the number of cigarettes smoked/day. The dose-response curve was sigmoidal in shape; however, when the data were plotted on a semi-log scale the curve assumed a linear shape, reaching saturation of AHH induction beyond 20 to 25 cigarettes/day. While mean AHH activity was dependent upon the number of cigarettes smoked/day, considerable interindividual variability in AHH (ranging more than 1,000-fold in some cases) was observed among individuals with comparable smoking histories, i.e. smoking the same number of cigarettes. Population distribution suggested clustering of the population in the low-AHH-activity region while cord-blood thiocyanate analysis and twin studies suggested that genetic factors contributed to a major portion of the inter-individual variability in AHH activity observed among smokers.     

Human placental aryl hydrocarbon hydroxylase: studies with fluorescence histochemistry.

Tissue sections from human placentas taken at term were studied after time-sequential incubations with benzo[a]pyrene and appropriate cofactors for mixed-function oxidation. Fluorescence microscopy revealed that the enzymic reaction appeared to be most active in the syncytial trophoblast, though the fluorescence of hydroxylated metabolites also could be observed in other placental cell types. A comparison of sections from placentas with very low versus very high aryl hydrocarbon hydroxylase activities provided evidence that induction of the human placental enzyme system with pol7cyclic aromatic hydrocarbons also appeared to occur primarily in the syncytium. When considered in conjunction with previous studies on human placental aryl hydrocarbon hydroxylase, the results tended to indicate that fetal elements of the human placenta contain the necessary electron-transport components for catalysis of mixed-function oxidations of chemical carcinogens and other foreign compounds and that this hydroxtlase system is readily inducible in the same fetal cells by components present in cigarette smoke.     

Metastatic melanoma in pregnancy: risk of transplacental metastases in the infant.

PURPOSE: Although metastases to the fetus via the placenta are rare, melanoma is the most common culprit. When it occurs, maternally derived melanoma metastasis in the infant is almost invariably fatal. PATIENTS AND METHODS: This article reviews current guidelines for placental evaluation in pregnant women with metastatic melanoma and presents surveillance recommendations for their infants. Comprehensive literature reviews were performed on melanoma in pregnancy and melanoma metastasis to the placenta and fetus. The use of interferon alfa in the pediatric population was also reviewed. A comprehensive search of the MEDLINE database (1966 to 2002) was performed. Articles were reviewed and additional references were obtained from the bibliographies. Translation of non-English articles was performed, and authors of previous publications were contacted. RESULTS: Eighty-seven patients with placental or fetal metastasis were identified. Twenty-seven occurrences were attributed to melanoma (31%). The fetus was affected in six of 27 melanoma patients (22%), with five of six infants dying of disease. The use of high-dose interferon alfa adjuvant therapy in pediatric patients has not been reported. CONCLUSION: The placentas of women with known or suspected metastatic melanoma should be carefully examined grossly and histologically by pathologists. With placental involvement, fetal risk of melanoma metastasis is approximately 22%. Neonates delivered with concomitant placental involvement should be considered a high-risk population. The risk-benefit ratio of adjuvant treatment for a potentially affected infant should be carefully weighed.     

Monoclonal antibody to human T-cell leukemia virus p19 defines polypeptide antigen in human choriocarcinoma cells and syncytiotrophoblasts of first-trimester placentas

In previous studies we detected retrovirus RD114 p30-related antigen in human placental syncytiotrophoblasts and antibodies in cord blood sera. We now report that a monoclonal IgG antibody specific for the p19 protein of human T-cell leukemia virus (HTLV) reacts with human syncytiotrophoblastic antigen. When used in the immunoperoxidase tissue-staining procedure, the monoclonal antibody reacted with the syncytiotrophoblastic cells in sections of all early placentas (less than 15 weeks of gestation), blighted ova and benign (hydatidiform mole) or malignant placental tumors (destructive mole, choriocarcinoma). In all cases the reactivity was mainly confined to the cytoplasm of the cells with syncytiotrophoblastic morphology. Normal embryonal or adult tissues tested were negative. In immunoblotting of cultured choriocarcinoma cells, anti-HTLV p19 detected a single polypeptide at mol.wt 28,000 from proteins separated by electrophoresis.