In this study we analysed by immunohistochemistry the expression of p53 protein in 14 malignant fibrous histocytomas (MFHs), 22 other types of sarcoma (eight leiomyosarcomas, four rhabdomyosarcomas, four liposarcomas, two fibrosarcomas, two chondrosarcomas, one malignant schwannoma, and one dermatofibrosarcoma protuberans), and 25 non-malignant mesenchymal lesions (eight dermatofibromas, four cases of nodular fasciitis, three leiomyomas, three fibromatoses, two epithelioid.leiomyomas, two neurofibromas, one schwannoma, one myositis ossificans, and one giant cell tumour of tendon sheath).
The expression of mRNAs encoding EGF and the EGF receptor in myometrial and leiomyoma cultures suggest that EGF may be involved in the autocrine/paracrine regulation of human uterine leiomyomata and myometrial growth.
The three previously identified cytogenetic subgroups were all represented in this series: del(7) (q21.2q31.2) was found in 11, trisomy 12 in five, and t(12;14)(q14-15;q23-24) in one leiomyoma.
The cytogenetic profiles of leiomyoma and lipoma are strikingly similar; both tumor types have nonrandom rearrangements of 12q13-15, t(12;14) in leiomyoma and t(3;12) in lipoma, as well as variant rearrangements of the same 12q segment.
The finding in these leiomyosarcomas of rearrangements of the same regions of chromosomes 12 and 14 that are involved in the tumor-specific t(12;14)(q14-15;q23-24) of uterine leiomyoma indicates that the same genes in 12q and 14q might be important in the pathogenesis of benign and malignant smooth muscle tumors.
The objective of this study was to examine the possible steroid dependence of IGF, IGFBP and IGF receptor gene expression and IGFBP synthesis in uterine leiomyomata, using tissues from women cycling normally and made hypo-oestrogenic by a gonadtrophin-releasing hormone agonist (GnRHa).
Western ligand blotting showed the presence of IGFBP-2 and -3 proteins, and when compared with a group of women with fibroids not treated with LHRHa (B.J.Vollenhoven et al., 1993, J. Clin.Endocrinol.
Analysis of androgen receptor DNA reveals the independent clonal origins of uterine leiomyomata and the secondary nature of cytogenetic aberrations in the development of leiomyomata.
As an initial step toward finding the gene or genes that are interrupted by the translocation breakpoint, a somatic cell hybrid carrying the derivative 14 as the single t(12;14) translocated chromosome was constructed from a leiomyoma cell line with this translocation.
We evaluated the presence of growth hormone receptor messenger ribonucleic acid in the human uterus and leiomyomas to investigate whether growth hormone might act directly rather than by hepatic generation of insulin-like growth factor-I.
We used a digoxigenin-labeled oligoprobe sharing no homology to the growth hormone-binding protein or to the prolactin receptor, to investigate whether growth hormone receptor messenger ribonucleic acid was present in tissue sections or amplified complementary deoxyribonucleic acid from leiomyoma and the surrounding myometrium.