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Cytogenetic analysis of paediatric solid tumors
Abstracts 35
165 CYTOGENETIC STUDIES OF CHILDHOOD SOLID TUMORS. N. P. Bown, E. V. Davison, A. D. J. Pearson, and M. M. Reid. Department of Human Genetics, University of Newcaslle upon Tyne, England.
Three case reports of paediatric solid tumours are presented, and the observed karyotypic abnormalities are described; (i) a stage IV neuroblastoma demonstrating a rearrangement of lp in the primary tumour after chemotherapy, (ii) an ependymoma showing six karyotypically distinct cell lines in long-term cultures, and (iii) a primitive neuroectodermal tumour showing multiple chromosome abnormalities in one cell line, and t(3;10)(inv(7)) in a second cell line in long-term cultures. The methods used in solid tumour cytogenetics are described, and the chromosome results related to the patient's clinical status and to previous reports in the literature.
36
CYTOGENETIC ANALYSIS OF PAEDIATRIC SOLID TUMORS. P. A. Gorman, M. Malone*, J. Pritchard*, D. Sheer. Imperial Cancer Research Fund, London WC2A 3PX, U.K. * The Hospital for Sick Children at Great Ormond Street, London WCIN 3HJ, U.K.
We are carrying out a detailed cytogenetic investigation of selected solid tumours in children. Many of the tumours we have examined so far have simple rearrangements involving only a few chromosomes, suggesting that it may he possible to identify sites of consistent chromosome aberrations within particular turnout types. For example, a fibrosarcoma had as its only visible aberrations, +7, +15 and +17p-. Only one of four primitive neuroectodermal turnouts analysed in detail had a t(11;22)(q24;q12} which appears identical to that described previously for this tumour type and Ewing's sarcomas, together with an i(lq) and several trisomies. A second neuroectodermal tumour showed rearranged chromosomes 11 and 22 which did not appear to be derived from the usual t(11;22), as well as a three-way translocation t{2;15;21). A third neuroectodermal tumour had a deleted 11p, monosomy 22, and several other rearrangements. A fourth neuroectodermal tumour had apparently normal chromosomes 11 or 22 and the only chromosome rearrangement present was a t(10;12}(q22;q24}. A Ewing's sarcoma had the typical t(11;22) together with trisomy 12.
37
CYTOGENETICINVESTIGATION OF PEDIATRIC SOLID TUMORS WITH THE USE OF COLLAGENAgE DISAGGREGATION. F. Speleman, G, Laureys*, Y. Benoit*, J. G. Leroy*. Centre of Medical Genetics, * Department of Pediatric Hematology and Oncology, University Hospital Gent, Belgium.
We report on the results of a short term collagenase disa~regation technique used for cytogenetic analysis of solid tumors. Tissue slices are incubated for I to 2 hr at 37°C in 5% CO2/95% air atmosphere in MEM with 10% fetal calf serum and collagenase II (200 u/ml). After washing, the cells are resuspended in I to 4 culture flasks, depending on the amount of cells obtained. A first culture is harvested as soon as possible, usually after I to 4 days. From January till July 1988 we have karyotyped successfully 11 different pediatric tumors (7 malignant, 4 benign) with this new method. Clonal abnormalities were detected in 5 tumors. The karyotypes are: 48, XY,+8,+11/49,XY,+8,+ 11,+20 (infantile fibrosarcoma); 46,XX,der(2)t(2;?)(q14;?)(fibrous dysplasia); 48,XY,+12,+13 (Wilms' tumor); 45,XY,t(1;2)(q23;q11),del(2)(p21---~qter),-2,-6,del(7)(q32-~qter),-10,der •1•)t(1•;?)(q25;?)•-14•der•15)(15;16)(q15;q23)•-16•-17•-2••-2••-22•+7mar(•ip•sarc•ma); 61 chromosomes with structural abnormalities (malignant fibrous histiocytoma, secondary tumor in a patient treated for bilateral relinoblastoma). Except for the histiocytoma sufficient metaphases with good quality chromosomes were found in all tumors. We conclude that with enzymatic treatment of tumor tissue with high concentrations of collagenase a higher success rate can he obtained.
165 CYTOGENETIC STUDIES OF CHILDHOOD SOLID TUMORS. N. P. Bown, E. V. Davison, A. D. J. Pearson, and M. M. Reid. Department of Human Genetics, University of Newcaslle upon Tyne, England.
Three case reports of paediatric solid tumours are presented, and the observed karyotypic abnormalities are described; (i) a stage IV neuroblastoma demonstrating a rearrangement of lp in the primary tumour after chemotherapy, (ii) an ependymoma showing six karyotypically distinct cell lines in long-term cultures, and (iii) a primitive neuroectodermal tumour showing multiple chromosome abnormalities in one cell line, and t(3;10)(inv(7)) in a second cell line in long-term cultures. The methods used in solid tumour cytogenetics are described, and the chromosome results related to the patient's clinical status and to previous reports in the literature.
36
CYTOGENETIC ANALYSIS OF PAEDIATRIC SOLID TUMORS. P. A. Gorman, M. Malone*, J. Pritchard*, D. Sheer. Imperial Cancer Research Fund, London WC2A 3PX, U.K. * The Hospital for Sick Children at Great Ormond Street, London WCIN 3HJ, U.K.
We are carrying out a detailed cytogenetic investigation of selected solid tumours in children. Many of the tumours we have examined so far have simple rearrangements involving only a few chromosomes, suggesting that it may he possible to identify sites of consistent chromosome aberrations within particular turnout types. For example, a fibrosarcoma had as its only visible aberrations, +7, +15 and +17p-. Only one of four primitive neuroectodermal turnouts analysed in detail had a t(11;22)(q24;q12} which appears identical to that described previously for this tumour type and Ewing's sarcomas, together with an i(lq) and several trisomies. A second neuroectodermal tumour showed rearranged chromosomes 11 and 22 which did not appear to be derived from the usual t(11;22), as well as a three-way translocation t{2;15;21). A third neuroectodermal tumour had a deleted 11p, monosomy 22, and several other rearrangements. A fourth neuroectodermal tumour had apparently normal chromosomes 11 or 22 and the only chromosome rearrangement present was a t(10;12}(q22;q24}. A Ewing's sarcoma had the typical t(11;22) together with trisomy 12.
37
CYTOGENETICINVESTIGATION OF PEDIATRIC SOLID TUMORS WITH THE USE OF COLLAGENAgE DISAGGREGATION. F. Speleman, G, Laureys*, Y. Benoit*, J. G. Leroy*. Centre of Medical Genetics, * Department of Pediatric Hematology and Oncology, University Hospital Gent, Belgium.
We report on the results of a short term collagenase disa~regation technique used for cytogenetic analysis of solid tumors. Tissue slices are incubated for I to 2 hr at 37°C in 5% CO2/95% air atmosphere in MEM with 10% fetal calf serum and collagenase II (200 u/ml). After washing, the cells are resuspended in I to 4 culture flasks, depending on the amount of cells obtained. A first culture is harvested as soon as possible, usually after I to 4 days. From January till July 1988 we have karyotyped successfully 11 different pediatric tumors (7 malignant, 4 benign) with this new method. Clonal abnormalities were detected in 5 tumors. The karyotypes are: 48, XY,+8,+11/49,XY,+8,+ 11,+20 (infantile fibrosarcoma); 46,XX,der(2)t(2;?)(q14;?)(fibrous dysplasia); 48,XY,+12,+13 (Wilms' tumor); 45,XY,t(1;2)(q23;q11),del(2)(p21---~qter),-2,-6,del(7)(q32-~qter),-10,der •1•)t(1•;?)(q25;?)•-14•der•15)(15;16)(q15;q23)•-16•-17•-2••-2••-22•+7mar(•ip•sarc•ma); 61 chromosomes with structural abnormalities (malignant fibrous histiocytoma, secondary tumor in a patient treated for bilateral relinoblastoma). Except for the histiocytoma sufficient metaphases with good quality chromosomes were found in all tumors. We conclude that with enzymatic treatment of tumor tissue with high concentrations of collagenase a higher success rate can he obtained.