[Somatic cell hybrids used in cytogenetic analysis of transformation mechanism of uterine endometrial cell].
6-Thioguanine and Neomycin resistant human endometrial carcinoma cells were established from parental HHUA 95 cells in the present study. The karyotype was 46,XX although chromosome abnormalities had been observed occasionally. Cell hybrids between 6-TGr neor 95 and rat immortalized, non-tumorigenic 3Y1 cells were formed to analyze for cosegregation of chromosomes and tumorigenicity. However, the morphology of 3 hybrid clones was a spindle form, similar to the 3Y1 cells. In spite of the consistent presence of human chromosomes, negative anchorage independent growth in these clones suggested that none of the chromosomes involved in fused cells was associated with tumorigenicity of endometrial carcinoma. Loci on a few human chromosomes of a normal cell cause suppression in several hybrid systems. Cell fusion between 6-TGr 95 and normal human fibroblasts (HF) was performed to confirm whether this is also true in endometrial carcinoma. Hybrid cells had four copies of homologous chromosomes (two from each of the parent cells). These had a polygonal appearance, being similar to the HHUA 95 cells. Both anchorage independence and tumorigenesis were negative. Those results suggested that malignant transformation of endometrial cells was the result of multiple genetic changes. In this respect, the loss of genes implicated in the suppression plays an important role in endometrial carcinogenesis.
Yamada
H
H
Department of Obstetrics and Gynecology, Hokkaido University School of Medicine, Sapporo.
Wake
N
N
Fujino
T
T
Aihara
T
T
Tanaka
S
S
Tanaka
T
T
Fujimoto
S
S
Ishiwata
I
I
D000230:Adenocarcinoma / Q000235:genetics* / Q000473:pathology; D000818:Animals; D002459:Cell Fusion; D002471:Cell Transformation, Neoplastic; D004715:Endometriosis / Q000235:genetics* / Q000473:pathology; D005260:Female; D006801:Humans; D006822:Hybrid Cells; D007621:Karyotyping; D051379:Mice; D051381:Rats; D014594:Uterine Neoplasms / Q000235:genetics* / Q000473:pathology