ISSN:1045-2257    

DOI:10.1002/gcc.2870010102

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

ISSN:1045-2257    

DOI:10.1002/gcc.2870010103

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

摘要:

AbstractCytogenetic analysis of short‐term cultures from 25 malignant fibrous histiocytomas (MFH) revealed clonal chromosome abnormalities in 17 tumors: ten storiform‐pleomorphic and seven myxoid MFH. Telomeric associations, rings, and dicentric chromosomes were present in 11 tumors and cytogenetic signs of gene amplification (homogeneously staining regions and double minute chromosomes) in four. The breakpoint distribution of the numerous structural rearrangements was nonrandom. The chromosome bands most frequently affected were 19p13 (in eight tumors; eight rearrangements gave rise to 19p+ markers, some of which looked similar, and an r(19) was found in one case), 11p11 (in seven tumors; three translocations and four deletions), 1q11 (in seven tumors; one translocation and six deletions), and 3p12 (in six tumors; all deletions). Other bands involved at least four times were 1p36, 5p15, and 20q13. Of particular clinical interest was the observation that tumors with 19p+ seemed to have a pronounced tendency to recur locally (local recurrence in five of eight tumors with 19p+ compared to one of nine in tumors without this aberration; observation period 4–16 mo

ISSN:1045-2257    

DOI:10.1002/gcc.2870010104

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

摘要:

AbstractWe describe a t(8;14)(q24;q11) involving the T‐cell receptor α‐chain gene (TCRA) and the 3′ region of theMYCprotooncogene in a B‐cell lymphoma. The B‐cell origin of this tumor was determined by its histological architecture, by immunophenotypic analysis, and by Southern analysis of immunoglobulin gene rearrangements. An identical fragment encompassing the translocation breakpoint junction was detected through Southern analysis using both aTCRAJ and aMYCprobe. The other alleles at theTCRAJ andMYCloci were in the germline configuration. Restriction enzyme and nucleotide sequencing analyses revealed that the breakpoint junction on chromosome 8 lies approximately 700 base pairs (bp) downstream of the 3′ end of the thirdMYCexon; on chromosome 14, the break is located 12.6 kilobases (kb) downstream of the 3′ end of the Cδ fourth exon. A heptamer‐like consensus sequence on chromosome 14 adjacent to the translocation breakpoint implies the involvement of recombinase activity. However, no consensus sequences were found on chromosome 8 within 140 bp in either direction from the breakpoint. It is possible that this translocation involvingMYCoccurred during an attempt at an inappropriate rearrangement of theTCRAlocus in a cell

ISSN:1045-2257    

DOI:10.1002/gcc.2870010105

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

摘要:

AbstractTumors of the soft tissues are classified histogenetically according to their phenotypic resemblance to normal adult tissue. Here we describe molecular approaches that make it possible to distinguish between one class of these tumors, rhabdomyosarcoma, and other small‐, round‐cell tumors. We show that the ascertainment of specific genotypic changes can be used to distinguish further between the embryonal and alveolar subtypes of rhabdomyosarcoma. We tested our model in two ways: first, in a retrospective analysis of diagnostically problematic cases of undifferentiated, small‐cell tumors and, second, in a blind study of pediatric tumors. Rhabdomyosarcoma was correctly identified in all cases using this strategy alone. The underlying simplicity of the strategy used to define rhabdomyosarcoma subtypes with molecular markers suggests a model by which tumors can be unequivocally identified, which may apply equally well to other human solid t

ISSN:1045-2257    

DOI:10.1002/gcc.2870010106

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

摘要:

AbstractThe most common inherited syndrome in man predisposing to neoplasia is neurofibromatosis‐1 (von Recklinghausen disease) (NF1). We investigated the hypothesis that affected individuals carry a single inactive allele at theNF1locus in the germline and that a tumor arises from a cell in a susceptible tissue in which the remaining normal allele has been lost or inactivated. DNA from tumor and nontumor tissue from 27NF1patients was analyzed with three markers closely linked to theNF1locus and two additional markers from chromosome 17. No loss of heterozygosity was observed in neurofibromas, plexiform or not. For other tumor types analyzed, seven of 14 showed a loss. A loss of heterozygosity was observed in six of 11 of the malignant peripheral nerve tumors analyzed. Of the seven malignancies demonstrating a loss, five involved a neurofibrosarcoma. These findings suggest that the pathogenesis of neurofibrosarcoma inNF1involves a deficiency of the NF1 gene product. In any given patient, loss of heterozygosity was detected at some marker loci but not others. Thus the mutations demonstrated in these tumors comprise a set of overlapping mutations, which may facilitate more precise localization of theNF1gen

ISSN:1045-2257    

DOI:10.1002/gcc.2870010107

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

ISSN:1045-2257    

DOI:10.1002/gcc.2870010108

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

摘要:

AbstractA continuous line of human mammary tumor cells, called 21MT, has been established in culture from a pleural effusion of a 36‐year‐old woman with metastatic breast cancer. The cells are epithelial as shown by morphology and expression of keratins and are mammary tumor cells as shown by expression of the HMFG‐2 antigenic determinant. The cells grow well both in DFCI‐1, a partially defined medium containing pituitary extract and 1% fetal bovine serum, and in α‐minimum essential medium (α‐MEM) supplemented with 10% serum, epidermal growth factor (EGF), insulin, and hydrocortisone. Karyotypic analysis of cells at early passage has shown the presence of rearranged (marker) chromosomes as well as aneuploidy with a net DNA content in the tetraploid range, confirmed by DNA cytofluorography, as well as double minute chromosomes in about 5% of the cells. Southern blots have revealed a 40‐fold amplification of theERBB2gene and a 50‐fold overexpression of its mRNA. The amplification ofERBB2DNA was localized by in situ hybridization to one of the marker chromosomes but not to the double minutes. It is inferred, therefore, that at least two genes have been amplifi

ISSN:1045-2257    

DOI:10.1002/gcc.2870010109

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

摘要:

AbstractThe expression ofRASoncogenes in benign and malignant salivary gland tumors was studied by immunohistochemistry and by immunoblotting using monoclonal antibodies recognizing theHRASandKRASgene products. Twenty‐eight out of 29 benign pleomorphic adenomas overexpressed p21RAS, whereas only 12 out of 18 malignant salivary gland tumors expressed the p21 protein. The expression levels were also substantially higher in the adenomas than in the malignant tumors, indicating thatRASgene activation appears to be more frequent and of greater importance for benign than for malignant salivary gland tumors. Comparisons of the p21 expression levels with the karyotypes of the pleomorphic adenomas revealed a novel correlation between high p21 expression and chromosome 8 rearrangements. As a hypothesis, it is suggested that a novel gene located on the proximal long arm of chromosome 8, most likely at band q12, is involved in the regulation ofRASgene expressio

ISSN:1045-2257    

DOI:10.1002/gcc.2870010110

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY

摘要:

AbstractHuman neuroblastomas show a high incidence of deletions in the distal region of the short arm of chromosome 1. In pursuit of a molecular analysis of these deletions, we have generated a microclone bank from microdissected 1p35‐pter chromosomal fragments. To allow a rapid localization of the microclones, we have also generated a panel of (human X mouse) hybrid cell lines through microcell‐mediated chromosome transfer. The hybrid cells contained different portions of the human chromosome 1 on a murine background. A total of 20 randomly chosen single or low‐copy microclones were localized by Southern analysis on DNA of the hybrid panel: All probes were derived from chromosome 1. Sixteen mapped in region 1p36.I‐pter, two in 1p22‐p36.1, and another two in 1 cen‐qter. The mapping of ten of these microclones was further refined by in situ hybridization. Cells of the neuroblastoma line GI‐ME‐N carry two types of chromosome 1, one cytogenetically normal and another with a translocation reported to be in 1p36.2, i.e., a t(1;?)(p36.2;?) marker. Using cell hybridization, we separated the two chromosome 1 types of GI‐ME‐N into different hybrid cell clones. Southern hybridization of three microclones from distal 1p to DNA of the hybrid cell clones revealed that the breakpoint in the translocated chromosome 1 wa

ISSN:1045-2257    

DOI:10.1002/gcc.2870010111

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1989

数据来源: WILEY