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C Turc-Carel

Publications and source records attributed to C Turc-Carel.

At least 19 recordsLinked to original sources
PubMed1992

In vitro karyotypic and immunophenotypic characterisation of primitive neuroectodermal tumours: similarities to malignant gliomas.

Monoclonal antibody (Mab) mediated immunotherapy of brain tumours requires the identification of tumour-restricted cell surface antigens. We have characterised four primitive neuroectodermal tumours, which included pineoblastoma, medulloblastoma and ependymoblastoma cultures, that demonstrated in vitro evidence of malignant behaviour (anchorage-independent growth and nu/nu xenograft tumour formation). The cytogenetic findings ranged from normal G-banded and Q-banded karyotypes through mixed near-diploid/hyperdiploid. These cultures resembled the cell surface immunophenotypic spectrum of malignant gliomas. They were distinguished from normal glia in vitro by the expression of restricted fetal mesenchymal, neuronal, myoblastic, melanocytic, epidermal, chondrocytic, lymphoid and epithelial antigens. Certain antigens appeared sufficiently represented among central nervous system (CNS) neoplasms to afford potential targets for Mab-mediated immunotherapy.

Adolescent↗
PubMed1992

Abnormal expression of neurofilament proteins in Ewing's sarcoma cell cultures.

A neural origin of Ewing's sarcoma (ES) has often been suggested and we have demonstrated neurofilament protein expression in ES cells. However, only the 200-kD subunit has been revealed in all of the ES cells analyzed. The 160- and 68-kD subunits were always absent. For these reasons, we have attempted to induce neural differentiation in 3 ES cell lines with different types of inducers: tetradecanoylphorbol-13-acetate (TPA) retinoic acid and nerve growth factor. When the cell lines were cultured for 7 days with TPA (10(-9) M) or retinoic acid (10(-7) M), only the 68-kD neurofilament subunit was slightly induced. No inducation was obtained when nerve growth factor was used, even at a 21-day culture. These results are in agreement with the putative neural origin of ES and may indicate an abnormal expression of neurofilament proteins in this tumor.

Cell Division↗
PubMed1991

Transfection of lipoma cells with papilloma bovine virus subgenomic fragment.

Lipoma cells with consistent chromosomal aberration have been transfected with plasmids carrying papilloma bovine virus subgenomic fragment (PBV 69). The successful transformation of the cells was ascerted on the changed growth pattern of the cells in liquid medium, colony formation in soft agar and modified cell appearance in electron microscopy; transfection with PBV 69 has not been, however, sufficient to immortalize lipoma cells.

Adipose Tissue↗
PubMed1990

Myxoid liposarcoma with t(12;16) (q13;p11) contains site-specific differences in methylation patterns surrounding a zinc-finger gene mapped to the breakpoint region on chromosome 12.

The q13 to q15 region of human chromosome 12 is frequently and consistently rearranged in malignant and benign adipose tissue tumors as well as benign tumors of smooth muscle and salivary glands. A reciprocal translocation, (12;16) (q13;p11), is characteristic of the myxoid subtype of liposarcoma, whereas translocations within 12q13-14 are frequently observed in benign lipomas. We are using pulsed-field gel electrophoresis to study the 12q13-q14 region in order to detect and clone the respective translocation breakpoints in these tumors. The locus GLI, which encodes a zinc-finger protein, has been mapped to the same region as the myxoid liposarcoma breakpoint. Pulsed-field analysis of myxoid liposarcoma and lipoma DNA has allowed us to construct a 600-kilobase physical map surrounding the GLI locus, which shows that breakpoints in both types of tumor are outside this region. However, myxoid liposarcoma DNA samples contained altered restriction fragments detectable with GLI probes that were highly specific and reproducible from case to case. These altered fragments are due to highly specific and reproducible methylation differences that are unique to myxoid liposarcoma DNA. These methylation changes may prove to be useful clinically as a diagnostic tool to differentiate subtypes of liposarcoma.

Cell Line↗
PubMed1989

Three possible cytogenetic subgroups of leiomyosarcoma.

Cytogenetic analysis was performed on short-term cultured tumor cells from ten patients diagnosed as having leiomyosarcoma. Of these, five tumors from five unrelated patients had clonal chromosome abnormalities. The combined data from this report and previous studies on leiomyosarcomas indicate that at least three subtypes may be identified chromosomally within leiomyosarcomas. One subtype is characterized by a hypodiploid chromosome number ranging from 41 to 43 and a common chromosome pattern of monosomies of chromosomes specific to this subgroup, including partial monosomy of the short arm of chromosome 1 (1p13----pter), monosomy 18, and consistent monosomy 22. In contrast to the previous subtype, for the pathogenesis of which the "tumor suppressor gene" hypothesis may be suggested, another subtype was characterized by a pseudodiploid chromosome number associated with simple reciprocal translocations; so far, these translocations are unique to individual tumors, the pathogenesis of which may involve a translocation-mediated gene deregulation pathway. A third subtype contained tumors with heterogeneous karyotypic findings.

Adult↗
PubMed1989

Immunologic characterization of Ewing's sarcoma using mesenchymal and neural markers.

The two most recent hypotheses about the histogenesis of Ewing's Sarcoma (ES) are that it has a mesenchymal or neuroectodermal origin. Immunologic markers specific to these two tissue origins were tested on cryostat sections from three primary tumors carrying the chromosomal translocation t(11;22)(q24;q12). Cell lines established in vitro from two of these three primary tumors were also analyzed. Using antibodies directed against neural components (neurone-specific-enolase [NSE], HNK-1, and neurofilament triplet proteins [NFTP]), positive reactions were observed in cells from two primary tumors and their corresponding cell lines. Results of electron microscopic examination of the primary tumors were compatible with the diagnosis of ES. When using antibodies directed against mesenchymal cell surface antigens (common leucocytes, Leu M1, Leu M2, and Leu M3), the weak positive reactions observed in the three primary tumors were attributed to lymphoid infiltrates within tumor cells. Six additional ES cell lines carrying the translocation t(11;22) were also analyzed by immunocytochemical and flow cytometry methods using antibodies directed against mesenchymal and neural components. Positive reactions were observed in all seven cell lines tested using antibodies directed against NSE, HNK-1, and 200 KD subunit of the NFTP, whereas negative reactions were obtained with Leu M2 antibody. These results are consistent with a neuroectodermal origin of ES cells.

Antibodies, Monoclonal↗
PubMed1988

Normal blood lymphocytes from patients with adipose tissue tumors with rearrangements at 12q13-q14 do not express the fragile site fra(12)(q13.1).

An association between chromosomal fragile sites and cancer-specific breakpoints has been found to be statistically significant. Cancer patients have been shown to be carriers of fragile sites in chromosome regions involved in rearrangements in malignant cells. Based on these observations it has been hypothesized that fragile sites may be involved in the pathogenesis of human tumors. We have recently described a new recurrent cancer breakpoint at chromosomal region 12q13-q14 in adipose tissue tumors. The possible involvement in these tumors of the rare folate-sensitive fragile site 12q13.1 has been investigated in PHA-stimulated peripheral blood cells from three patients carrying the t(12;16)(q13;p11) in their liposarcoma cells and one patient with the t(3;12)(q28;q14) in his lipoma cells. No expression of the fragile site 12q13.1 could be detected in the blood lymphocytes of any of the patients. The involvement of the fragile site 12q13.1 in the pathogenesis of adipose tissue tumors with a 12q13-q14 breakpoint remains to be established.

Chromosome Banding↗
PubMed1988

Breakpoints in benign lipoma may be at 12q13 or 12q14.

Chromosomal investigations in two unrelated lipoma samples are reported. The breakpoint involving 12q in chromosomal rearrangements could be assigned to band 12q13 in one case and 12q14 in the other case. Evidence is provided that cytogenetically distinct breakpoints on 12q may be found in lipoma cells, resolving previous disagreements based on interpretational difficulties.

Chromosome Aberrations↗
PubMed1988

Translocation (7;21) in a lipoma.

Cytogenetic analysis was performed on a solitary lipoma from the flank of a 38-year-old male. A translocation t(7;21)(p22;q11.2) was found as the sole clonal chromosomal abnormality. The results are discussed in relation to other cytogenetic abnormalities found in benign adipose tumors.

Adult↗
PubMed1988

Recurrent breakpoints at 9q31 and 22q12.2 in extraskeletal myxoid chondrosarcoma.

A cytogenetic study of extraskeletal myxoid chondrosarcoma cells revealed a complex t(9;22;15)(q31;q12.2;q25) as a primary chromosome change. A reciprocal translocation involving identical breakpoints on chromosomes #9 and #22 in this tumor has been reported in the literature. We suggest that the breakpoints 9q31 and 22.q12.2 are associated with extraskeletal myxoid chondrosarcoma, a comparatively rare tumor of adulthood.

Aged↗
PubMed1988

Consistent involvement of band 12q14 in two different translocations in three lipomas from the same patient.

We studied cytogenetically three distinct lipomas from a patient with multiple subcutaneous lipomas in the left shoulder area. A breakpoint at 12q14 was involved in structural rearrangements in the three lipomas resulting in two different reciprocal translocations, i.e., t(3;12)(q28;q14) in two and a t(1;12)(q34.2;q14) in the third. These results confirm the consistency of involvement of the breakpoint at 12q14 in lipomas and give support to the hypothesis that multiple lipomas evolve from different stem cells.

Chromosome Banding↗
PubMed1988

Association of breakpoint 14q23 with uterine leiomyoma.

A chromosomal study of short-term cultured tumor cells from a benign uterine leiomyoma showed a clonal insertion, dir ins(14;6)(q23;p23p25) as a unique change. This finding supports the hypothesis of a specific association of the breakpoint 14q23 with uterine leiomyoma.

Chromosome Banding↗
PubMed1988

Chromosomes in Ewing's sarcoma. I. An evaluation of 85 cases of remarkable consistency of t(11;22)(q24;q12).

Since our initial reports on chromosomal studies in eight Ewing's sarcomas (ES), we have carried out similar investigations on 23 additional ES specimens following short-term culture of tumor cells (16 cases), and established in vitro cell lines (three cases) and on xenografted tumors in nude mice (four cases). We demonstrated the presence of the reciprocal t(11;22)(q24;q12) in every case except one that exhibited a complex t(11;22;14)(q24;q12;q11). On the basis of results from these additional 23 cases, we confirm the consistency of the t(11;22)(q24;q12) in ES. Moreover, we reviewed 54 ES cases reported by other investigators; when added to our 31 cases, this brings the total number to 85 unrelated cases of ES available for an evaluation of the frequency of involvement of bands 11q24 and 22q12 in translocations in ES. The standard t(11;22)(q24;q12) proved to be a remarkably consistent event, present in 83% of the cases. Five percent of the cases exhibited complex translocations involving a third chromosome in addition to chromosomes #11 and #22. In 4% of the cases variant translocations involved 22q12 but with a chromosome(s) other than #11. The breakpoint on chromosome 22q12 appears to be the most consistently observed event in 92% of the cases, whereas, the breakpoint at chromosome 11q24 was observed in 88% of the cases.

Adolescent↗
PubMed1988

Chromosomes in Ewing's sarcoma. II. Nonrandom additional changes, trisomy 8 and der(16)t(1;16).

Chromosomal data from 82 informative, unrelated Ewing's sarcoma (ES) specimens (including 20 personal specimens) were reviewed for secondary changes additional to the t(11;22)(q24;q12). Additional numerical and/or structural changes were found in 75 specimens. Trisomy 8 was observed consistently in half of the 43 cases selected for analysis of numerical changes. A nonrandom der(16) was observed as a result of an unbalanced t(1;16) in 18% of the 82 analyzed for structural changes. Consistent involvement of chromosome #16 in rearrangements with chromosome #1 may be an additional chromosome change specifically associated with ES.

Bone Neoplasms↗