Transfection of the mouse MyoD1 gene into the human rhabdomyosarcoma cell line RD increased the ability of the tumor cells to differentiate into multinucleated myotubes and enhanced myosin heavy-chain gene expression but did not decrease tumorigenicity in nude mice.
Using a probe that detects a polymorphic locus within the RB1 gene we found loss of only one allele (heterozygous deletion) in 33% of soft tissue sarcomas examined, including two leiomyosarcomas, a malignant peripheral nerve sheath tumour, a rhabdomyosarcoma and a chondrosarcoma.
To determine whether selection for primary resistance to L-PAM conferred cross-resistance to VCR we selected an L-PAM-resistant subline of rhabdomyosarcoma xenograft HxRh28 (HxRh28/L-PAM-13).
By use of an enzyme-linked immunosorbent assay, we have found that phorbol 12-myristate 13-acetate (PMA) causes an approximately 10-fold increase in the level of type-1 plasminogen activator inhibitor (PAI-1) accumulated in conditioned medium of the human rhabdomyosarcoma cell line.
Fragments of human genomic DNA corresponding to the promoter region of the gene for the transferrin receptor have been cloned upstream of the bacterial gene for chloramphenicol acetyltransferase and these constructs used to assess promoter activity following transfection into a human rhabdomyosarcoma cell line.
Taken together with the results of recent reports indicating that the cardiac alpha-actin type is a marker of embryonic and fetal skeletal muscle, our findings indicate that rhabdomyosarcomas express the embryonic sarcomeric actin isoform.
We now report on a family of fibronectin mRNAs identified by Northern blotting analysis in two normal human fibroblast strains (HEL 299 and Flow 7000) and five transformed cell lines (8387 and HT-1080, fibrosarcomas; G-361, melanoma; JEG-3, choriocarcinoma; and RD, rhabdomyosarcoma).
Translocation of the 5' region of the FKHR gene to the derivative chromosome 2, and retention of the 3' region of FKHR on the derivative chromosome 13 [(der(13)], were demonstrated in metaphase cells from a rhabdomyosarcoma cell line with a previously identified t(2;13) translocation.
We conclude that IN157 cells express high levels of bioactive 10 kDa IGF-II and 7.5 kDa IGF-II that may stimulate the proliferation of rhabdomyosarcomas by interaction with IGF-I receptors on the cells.
We conclude that IN157 cells express high levels of bioactive 10 kDa IGF-II and 7.5 kDa IGF-II that may stimulate the proliferation of rhabdomyosarcomas by interaction with IGF-I receptors on the cells.
RANTES-promoter-luciferase gene fusion assays demonstrate high levels of reporter gene activity in a "mature" T cell line Hut78, the erythroleukemic cell line HEL, and the rhabdomyosarcoma cell line RD, with little or no activity in the "early" T cell line Jurkat, the gamma delta T cell line PEER, the thymic tumor Molt4, or the pre-erythroid cell line K562.
These results in children with RMS corroborates previous findings in other clinical settings suggesting that the mutant p53 carrier state may predispose individuals to malignancy at an early age.
We conclude that IGF-II overexpression in muscle myoblasts induces morphological and biological changes typical of the malignant phenotype and represents a fundamental event in the pathogenesis of RMS and possibly of other embryonal tumors.
Sequential immunoprecipitations with anti-PAX3 and anti-FKHR sera demonstrated expression of a 97-kDa PAX3-FKHR fusion protein in the t(2;13)-positive rhabdomyosarcoma Rh30 cell line and verified that a single polypeptide contains epitopes derived from each protein.
Sequential immunoprecipitations with anti-PAX3 and anti-FKHR sera demonstrated expression of a 97-kDa PAX3-FKHR fusion protein in the t(2;13)-positive rhabdomyosarcoma Rh30 cell line and verified that a single polypeptide contains epitopes derived from each protein.