The congenital mesoblastic nephroma: a case report of prenatal diagnosis.

The congenital mesoblastic nephroma is a very rare benign congenital renal tumor. It is the most common renal tumor before the age of 6 months (50%) and it constitutes only 5% of renal tumors before 15 years. The authors report a case of prenatal diagnosis of congenital mesoblastic nephroma revealed by an acute polyhydramnios at 33 weeks of pregnancy. After a preterm labor, the patient delivered at 35 weeks. The newborn underwent a radical nephrectomy. No recurrence was noticed at 10 months. This case of prenatal diagnosis is compared to the 12 cases previously reported. The prognosis of CMN depends on histologic findings, but also on the severity of prematurity induced by the polyhydramnios. The main treatment of this pathology if diagnosed during pregnancy remains the prevention of preterm labor, and after birth the removal of the kidney.

Increase in epidermal growth factor receptor and its mRNA levels by parathyroid hormone (1-34) and parathyroid hormone-related protein (1-34) during differentiation of human trophoblast cells in culture.

Human cytotrophoblasts in culture aggregate and fuse to form syncytiotrophoblasts. This process is associated with an increase in epidermal growth factor receptor (EGFR) expression [Alsat et al.: J Cell Physiol 154:122-128, 1993]. Recent studies have demonstrated the presence of parathyroid hormone-related protein (PTHrP) in the human uterus and placenta. This led us to study the effect of PTH (1-34) and PTHrP (1-34) on the expression of EGFR during this differentiation process. Both peptides induced a concentration-dependent increase in EGF binding, with a maximal effect at the physiological concentration of 1 nM. EGFR protein level assessed by cross-linking and immunoblotting and EGFR biological activity assessed by measuring its EGF-induced autophosphorylation were increased 2- and 2.5-fold, respectively, when cells were treated for 24 h with 0.1 microM PTHrP or PTH compared to control cells. This effect was time-dependent with a maximum at 3 h of treatment. This treatment also increased trophoblast cell EGFR mRNA levels, suggesting transcriptional regulation of the EGFR. To ascertain whether activation of protein kinase C (PKC) or protein kinase A (PKA) is involved in this PTH effect, we determined EGFR protein level and EGFR autophosphorylation after exposure of cells to PKA inhibitor and PKC inhibitor, alone or together with the peptide. The presence of a PKC inhibitor blocked a further increase in EGFR number by PTH, while PKA inhibitor had no effect. These results show that PTH and PTHrP increase the synthesis of EGF receptors which are strongly expressed in syncytiotrophoblasts and suggested that these peptides might be involved in human placental development.

Increase in epidermal growth factor receptor and its messenger ribonucleic acid levels with differentiation of human trophoblast cells in culture.

Epidermal growth factor receptor (EGFR) expression was studied during the differentiation of human trophoblast cells in culture. In vitro, intravillous mononuclear cytotrophoblasts aggregate and fuse within 24 h to form a syncytium. This morphological differentiation was associated with a significant twofold increase in specific 125I-EGF binding capacity (P < 0.01). Scatchard analyses showed an apparent rise in the number of high-affinity binding sites (0.33 +/- 0.04 and 0.63 +/- 0.07 pmol/mg protein at 24 and 48 h, respectively), with no change in their affinity (1.34 and 1.42 x 10(-10) mol/L). Affinity labeling of 125I-EGF in cultured trophoblast cells followed by SDS-PAGE and autoradiography revealed a band of 175 KDa corresponding to EGFR, the intensity of which increased with the time in culture. EGF-dependent phosphorylation of membrane proteins from cultured trophoblast cells revealed major phosphorylated proteins of 170 KDa (EGFR) and 35 KDa, which were both increased at 48 h, indicating a rise in EGFR-kinase activity during syncytium formation. Northern blot analysis of EGFR-mRNA, followed by hybridization with a 32P-cDNA probe for EGFR, revealed an increase in EGFR gene expression in syncytiotrophoblasts, as compared to cytotrophoblasts. Thus, the increase in bioactive EGFR observed during the differentiation of trophoblast cells was due to an increase in their synthesis. Cultured trophoblast cells are therefore a good model of spontaneous up-regulation of EGFR expression with cell differentiation.