|
1. |
The 11q23 breakpoint in acute leukemia with t(11;19)(q23;p13) is distal to those of t(4;11), t(6;11) and t(9;11) |
|
Genes, Chromosomes and Cancer,
Volume 4,
Issue 2,
1992,
Page 107-112
Dorra Cherif,
Hera Der‐Sarkissian,
Josette Derré,
Roland Berger,
Takashi Tokino,
Yusuke Nakamura,
Preview
|
PDF (543KB)
|
|
摘要:
AbstractThirteen cosmid probes were mapped on the long arm of chromosome 11 between 11q22 and 11q24 by nonradioactive in situ hybridization. Starting with these localizations and those of other probes mapped to 11q23, four acute leukemias with translocations involving 11q23 were studied with the same method. The translocation breakpoints of the t(4;11)(q21;q23), t(6;11)(q27;q23), t(9;11)(p21–p22;q23), and t(11;19)(q23;p13) were confirmed to be distal to CD3D. The probe cC11 1–304 was proximal to the t(11;19) breakpoint while distal to the breakpoints of the other rearrangements. In view of the diversity of chromosomal abnormalities involving band 11q23, our finding extends the molecular heterogeneity of the breakpoint localization in leukemias with rearrangements involving 11
ISSN:1045-2257
DOI:10.1002/gcc.2870040202
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1992
数据来源: WILEY
|
2. |
Genetic alterations of the tumour suppressor gene regions 3p, 11p, 13q, 17p, and 17q in human breast carcinomas |
|
Genes, Chromosomes and Cancer,
Volume 4,
Issue 2,
1992,
Page 113-121
Tone I. Andersen,
Astrid Gaustad,
Anne‐Lise Børresen,
George W. Farrants,
Jahn M. Nesland,
Lars Ottestad,
Kjell M. Tveit,
Preview
|
PDF (843KB)
|
|
摘要:
AbstractFifty‐nine primary breast carcinomas and 11 metastases were examined to identify genetic alterations in the tumour suppressor gene regions 3p, 11p, 13q, 17p, and 17q. Loss of heterozygosity (LOH) was frequently observed on chromosome arms 17p (p144D6 lost in 75%, pYNZ22.1 in 55%, andTP53in 48% of the primary tumours), 13q (RBIlost in 40% of the primary tumours), and 17q (pRMU3 lost in 35%, pTHH59 in 29%, andNM23HIin 26% of the primary tumours). Loss of all the markers except p144D6 was observed even more frequently in the metastases. Pairwise comparisons for concordance of allele losses on 17p indicated that there might be two genes on 17p implicated in breast cancer development; theTP53gene and a gene located close to the p144D6 and pYNZ22.1 markers. LOH of theRBIgene was associated with LOH of pYNZ22.1 and p144D6, but not with LOH ofTP53.LOH ofRBIandTP53was associated with occurrence of ductal carcinomas,RBIand p144D6 losses with tumour size, and p144D6 losses with positive node status as well. LOH ofTP53and the three 17q markersNM23HI, pTHH59, and pRMU3 was most frequently observed in tumours from postmenopausal women. p144D6 losses occurred most frequently in progesterone receptor‐negative tumours, whereas pTHH59 losses occurred most frequently in oestrogen receptor‐negative tumours. LOH of the investigated loci was not associated withERBB2protooncogene amplification, with positive family history of breast cancer, or with sur
ISSN:1045-2257
DOI:10.1002/gcc.2870040203
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1992
数据来源: WILEY
|
3. |
Reciprocal translocation t(12;22)(q13;q13) in clearcell sarcoma of tendons and aponeuroses |
|
Genes, Chromosomes and Cancer,
Volume 4,
Issue 2,
1992,
Page 122-127
Göran Stenman,
Larsgunnar Kindblom,
Lennart Angervall,
Preview
|
PDF (687KB)
|
|
摘要:
AbstractClearcell sarcoma is a rare soft tissue sarcoma that displays certain similarities to malignant melanoma. In this paper we describe the karyotypic findings and in vitro growth characteristics of a shorttermcultured clearcell sarcoma. The cultured tumor cells had preserved immunohistochemical characteristics and certain ultrastructural features of the primary tumor, including positivity for vimentin, S‐100 protein, and a melanomaassociated antigen, supporting the authenticity of the cultured cells. Cytogenetic analysis revealed an abnormal stemline karyotype of 49,XY, –1, + 8, + 8, + 12, + der(l)t(1;?)(p36.1 –.3;?), t(12,22)(q13;q13). A similar or identical t(12;22) was recently reported in two of four clear‐cell sarcomas. It is suggested that the t(12;22)(q13;q13) is a primary cytogenetic abnormality in clear‐cell sarcoma and distinguishes this tumor type from malignant
ISSN:1045-2257
DOI:10.1002/gcc.2870040204
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1992
数据来源: WILEY
|
4. |
Nonradioactive in situ hybridisation of the translocation t(1;7) in myeloid malignancies |
|
Genes, Chromosomes and Cancer,
Volume 4,
Issue 2,
1992,
Page 128-134
Robert E. Kibbelaar,
Jan‐Willem R. Mulder,
Enno J. Dreef,
Philip M. Kluin,
Harmen Van Kamp,
Hans L. Haak,
Anton K. Raap,
Hans W. Wessels,
Geoffrey C. Beverstock,
Preview
|
PDF (649KB)
|
|
摘要:
AbstractBone marrow cells of four patients with t(1;7) and myelodysplasia or acute myeloid leukemia were analyzed using nonradioactive in situ hybridisation. As probes, centromeric alphoid DNA sequences of chromosomes 1 and 7, a satellite DNA probe for 1q12, and chromosomespecific libraries of chromosomes 1 and 7 were used. The breakpoints of the t(1;7)(p11;p11) as determined by banding analysis could be studied more accurately, and the recently proposed designation t(1;7)(cen;cen) was confirmed in all four cases. Colocalization of alphoid DNA sequences of chromosomes 1 and 7 by double target in situ hybridisation was demonstrated in metaphase cells and also in interphase nuclei. The in situ hybridisation method described is applicable for the screening of peripheral blood cells or archival material.
ISSN:1045-2257
DOI:10.1002/gcc.2870040205
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1992
数据来源: WILEY
|
5. |
Chromosomal in situ suppression hybridization of immunologically classified mitotic cells in hematologic malignancies |
|
Genes, Chromosomes and Cancer,
Volume 4,
Issue 2,
1992,
Page 135-140
Marianne Tiainen,
Sakari Knuutila,
Susanne Popp,
Patricia Emmerich,
Thomas Cremer,
Valerie Parlier,
Martine Jotterand Bellomo,
Tapani Ruutu,
Preview
|
PDF (646KB)
|
|
摘要:
AbstractChromosomal in situ suppression (CISS) hybridization was performed with library DNA from sorted human chromosomes 8, 9, 15, 17, 21, and 22 on immunologically stained bone marrow cells of four patients with a hematologic neoplasm, including two patients with myelodysplastic syndrome and trisomy 8, one patient with promyelocytic leukemia bearing the translocation t(15;17)(q22;q11–12), and one patient with chronic myeloid leukemia and the translocation t(9;22)(q34;q11). In all patients, the results of conventional karyotype analysis could be confirmed by one‐ or two‐color CISS hybridization using the appropriate chromosome‐specific libraries. Our results show that CISS hybridization can detect both numerical and structural chromosome changes in immunologically classified cells with high specificity and reliability. The fact that chromosome spreads of very poor quality can now be included in such analyses is a decisive advantage of this approach. In addition, the suitability of this approach for interphase cytogenetics is di
ISSN:1045-2257
DOI:10.1002/gcc.2870040206
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1992
数据来源: WILEY
|
6. |
Chromosomal abnormalities in skin following total body or total lymphoid irradiation |
|
Genes, Chromosomes and Cancer,
Volume 4,
Issue 2,
1992,
Page 141-145
Charles M. Rubin,
Mark E. Nesbit,
John H. Kersey,
Diane C. Arthur,
Tae H. Kim,
Preview
|
PDF (500KB)
|
|
摘要:
AbstractPatients undergoing bone marrow transplantation often receive total body or total lymphoid irradiation as part of the conditioning regimen prior to marrow infusion. The cytogenetic effects of this therapy on skin fibroblasts were studied. Fibroblast cultures from eight skin biopsies were harvested in early passages for G‐banded chromosome analysis. Four biopsies were from three patients who had high‐dose cyclophosphamide and total body radiotherapy; one was from within and one was from outside the radiation field of a patient who had high‐dose cyclophosphamide and lymphoid radiotherapy, one was from a patient who had combination chemotherapy alone, and one was from a normal control. No abnormal mitoses were found in the control or the patient who had chemotherapy alone, and only two of 30 mitoses from skin outside the lymphoid radiotherapy field were abnormal. However, most cells (49–88%) from five biopsies within radiotherapy fields were abnormal. Typically, abnormal karyotypes were pseudodiploid and contained multiple balanced rearrangements, of which reciprocal translocations were most common. The data indicate that the radiotherapy used for bone marrow transplantation induces extensive, sustained chromosome abnormalities in vivo in skin fibr
ISSN:1045-2257
DOI:10.1002/gcc.2870040207
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1992
数据来源: WILEY
|
7. |
Cytogenetic abnormalities in an ossifying fibroma from a patient with bilateral retinoblastoma |
|
Genes, Chromosomes and Cancer,
Volume 4,
Issue 2,
1992,
Page 146-152
Susanne M. Gollin,
Patrick D. Storto,
Patrick S. Malone,
Janice A. Washington,
Abirami Chidambaram,
Leon Barnes,
Ivo P. Janecka,
Preview
|
PDF (698KB)
|
|
摘要:
AbstractCytogenetic analysis of a cemento‐ossifying fibroma from a patient with nonfamilial bilateral multicentric retinoblastoma revealed three reciprocal translocations with the karyotype 46,XY,t(1;18)(q21;q21.3),t(3;10)(p13;q22),t(6;11)(p22;p15). Routine and high‐resolution cytogenetic analysis of peripheral blood leukocytes showed an apparently normal, 46,XY chromosome pattern with no deletion of chromosome 13. Molecular analysis demonstrated no gross differences in the retinoblastoma gene or theTP53gene between constitutional and tumor DNA. This is the first cytogenetic analysis of a cemento‐ossifying fibroma and the first report of this tumor in a retinoblastoma patient. The data may be added to the small, but growing literature on cytogenetic aberrations in benign tumors and may lend insight into genes involved in cell proliferation and neoplastic transform
ISSN:1045-2257
DOI:10.1002/gcc.2870040208
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1992
数据来源: WILEY
|
8. |
t(11;18)(q21;q21) is a recurrent chromosome abnormality in small lymphocytic lymphoma |
|
Genes, Chromosomes and Cancer,
Volume 4,
Issue 2,
1992,
Page 153-157
Constance A. Griffin,
Barbara A. Zehnbauer,
Richard Ambinder,
William E. Beschorner,
Risa Mann,
Preview
|
PDF (527KB)
|
|
摘要:
AbstractWe have identified two cases of previously untreated, small lymphocytic lymphoma with extranodal involvement, which had a reciprocal translocation, t(11;18)(q21;q21), as the sole cytogenetic abnormality. These two cases are remarkably similar to two previously reported cases carrying this translocation with regard to clinical features, cytogenetic abnormality, histologic subtype, and immunophenotype. Molecular genetic analysis of these two cases revealed clonal gene rearrangement of theIGHlocus but only germline configuration of theBCL2oncogene at 18q21 when probes and conditions that usually identifyBCL2rearrangement in lymphomas were used. Lymphomas bearing an (11;18) rearrangement appear to make up a phenotypically identifiable subgroup. Identification of the genes at the translocation breakpoints will be important.
ISSN:1045-2257
DOI:10.1002/gcc.2870040209
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1992
数据来源: WILEY
|
9. |
Losses of 3p, 11p, and 13q in ej/ras‐ transformable simian virus 40‐immortalized human uroepithelial cells |
|
Genes, Chromosomes and Cancer,
Volume 4,
Issue 2,
1992,
Page 158-168
Chinghai Kao,
Shi‐Qi Wu,
Manju Bhatthacharya,
Lorraine F. Meisner,
Catherine A. Reznikoff,
Preview
|
PDF (1047KB)
|
|
摘要:
AbstractFive independent clones of Simian virus 40 (SV40)‐immortalized human uroepithelial cells (CK/SV‐HUC) were established after transfection of HUC cultures from the same tissue donor with plasmids encoding SV40 large T and small t antigen genes. Each CK/SV‐HUC clone contained a unique SV40 integration site, and all expressed similar levels of SV40 mRNA. All five clones were nontumorigenic, but clones 2, 4, and 5 tumorigenically transformed after transfection at P19 with mutant EJ/rasand also spontaneously after 40 serial passages in vitro. In contrast, CK/SV‐HUC clones 1 and 3 did not transform when either approach was used. These differences in transformability among CK/SV‐HUC clones could not be predicted based on differences in SV40 gene expression nor on any in vitro growth property tested. In cytogenetic analyses, a transformable clone showed losses of three chromosome arms containing putative cancer suppressor gene regions, including 3p14→pter, 13q, and 11p, whereas the nontransformable clones showed none of these losses. Thus these data indicate that genetic losses on 3p, 11p, and 13q may contribute to tumorigenic transformation of SV40‐immortalized human uroepi
ISSN:1045-2257
DOI:10.1002/gcc.2870040210
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1992
数据来源: WILEY
|
10. |
Amplification of the topoisomerase ii α gene in a non‐small cell lung cancer cell line and characterisation of polymorphisms at the human topoisomerase ii α and β loci in normal tissue |
|
Genes, Chromosomes and Cancer,
Volume 4,
Issue 2,
1992,
Page 169-175
W. Nicol Keith,
Robert Brown,
K. B. Tan,
Preview
|
PDF (738KB)
|
|
摘要:
AbstractDNA was prepared from normal tissue and 19 lung cancer cell lines. Using probes which detect restriction fragment length polymorphisms at both the topoisomerase II α and β loci, heterozygosity was detected at a frequency of 0.17 and 0.37 for the α and β loci, respectively. Southern blot analysis of DNA extracted from lung cancer cell lines detected amplification of both the topoisomerase II α andERBB2genes in the adenocarcinoma line Calu3. These results indicate that topoisomerase II α andERBB2may be closely linked on chromosome 17 and coamplified during adenocarcinoma progression. Since topoisomerase II is a target for several anticancer drugs, it will be of interest to study alterations to topoisomerase II genes during tumour development, as these may in part determine the response of the tumour to chemoth
ISSN:1045-2257
DOI:10.1002/gcc.2870040211
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1992
数据来源: WILEY
|
|