摘要:

AbstractCytogenetic analysis was performed on a selected series of short‐term cultures of primary breast carcinomas from 28 patients. All patients had histopathologically confirmed malignancies, with the majority (25/28 cases) demonstrating infiltrating ductal carcinoma. All 28 cases evidenced clonal chromosome abnormalities, with 10/28 displaying only numeric aberrations, whereas 18/28 displayed clonal structural alterations. In near‐diploid tumors the most common numeric changes were — 17 and — 19. However, trisomy 7 was the only numeric change in two near‐diploid tumors. Structural chromosome alterations were primarily isochromosomes, apparent terminal deletions, and unbalanced non‐reciprocal translocations. Chromosomes 1 (10/18–56%) and 6 (8/18–44%) were most frequently altered in this series. Breakpoints of clonal structural abnormalities were shown to cluster to several chromosome segments, including 1p22‐q11, 3p11, 6p11–13, 7p11‐q11, 8p11‐q11, and 19q13. Analysis of the gain or loss of specific chromosome segments revealed that the most consistent tendency was over‐representation of 1q, 3q, and 6

ISSN:1045-2257    

DOI:10.1002/gcc.2870070402

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

年代:1993

数据来源: WILEY

摘要:

AbstractCytogenetic analysis was performed on a selected series of short‐term cultures from 34 patients with documented metastatic breast carcinoma. The majority of tumor cells were hyperdiploid, with clonal structural alterations observed in 94% of patients (32/34). The most common numeric changes were –2, –15, and –18. Chromosome 20 was the most frequently overrepresented (in near‐3n tumors only). Clonal structural chromosome alterations included isochromosomes, terminal deletions, and, most frequently, unbalanced non‐reciprocal translocations. Chromosomes most often involved in structural rearrangements included 1, 7, 11, and 6 (accounting for 24.7%, 10.3%, 9.1%, and 7.0% of breakpoints, respectively). When the breakpoints of clonal structural abnormalities were analyzed, they were shown to cluster to several chromosome segments, including 1p11‐q21, 7pter, 11p12‐q12, and 6q11–21. An analysis of the net gain or loss of specific chromosome segments was also performed, with the most consistent tendency observed being the over‐representation of 1q, 6p, 7, and 11. The most frequent losses included 1p, 6q, 7, and 11q. ©

ISSN:1045-2257    

DOI:10.1002/gcc.2870070403

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

年代:1993

数据来源: WILEY

摘要:

AbstractFluorescence in situ hybridization (FISH) was performed on bone marrow or peripheral blood cells thought to contain a del(11)(q23q25) from four patients who had acute leukemia or myelodysplasia. Cells from all patients were shown to contain translocations that involved chromosome 6 in three of them. Our data suggest that a large proportion of presumptive del(11)(q23) or del(11)(q23q25) chromosomes may represent previously unidentified translocations that can be detected by FISH. © 1993 Wiley‐Liss, I

ISSN:1045-2257    

DOI:10.1002/gcc.2870070404

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

年代:1993

数据来源: WILEY

摘要:

AbstractCytogenetic analysis of a squamous cell lung carcinoma revealed a near‐haploid karyotype with 27 chromosomes, in both primary cultures and an established cell line. The only chromosomes with two homologs present were chromosomes X, 5, 7, and 22. The two X chromosomes were early and late replicating, respectively. No structural rearrangements could be detected. In vitro, the clone evolved by duplication towards hyperdiploidy with 54 chromosomes. © 1993 Wiley‐Liss,

ISSN:1045-2257    

DOI:10.1002/gcc.2870070405

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

年代:1993

数据来源: WILEY

摘要:

AbstractParathyroid hormone‐related protein (PTHRP) is expressed in a large number of tumors and is the mediator of parathyroid hormone‐like effects seen in humoral hypercalcemia of malignancy. The gene coding forPTHRPhas been localised to the short arm of chromosome 12. This is at the same region as the oncogeneKRAS2, and amplification ofKRAS2has previously been found in human lung cancer. The BEN cell line which is known to express PTHRP was established from a patient who had squamous cell carcinoma of the lung with hypercalcemia. Cytogenetic analysis of the BEN cell line revealed a very complex karyotype with many marker chromosomes. Chromosomal in situ hybridization with biotinylated DNA probes visualized by a biotin‐streptavidin‐polyalkaline‐phosphatase complex was used to analyse two dicentric marker chromosomes containing homogeneously staining regions (hsr) in BEN. The hsr were found to contain amplifiedPTHRPandKRAS2at levels of 30‐fold and 14‐fold per cell, respectively. The higher level of amplification of thePTHRPgene would suggest thatPTHRPis the target gene of amplification in the amplicon. This is the first report of gene amplification ofPTHRPand in addition its co‐amplification withKRAS2. © 1993

ISSN:1045-2257    

DOI:10.1002/gcc.2870070406

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

年代:1993

数据来源: WILEY

摘要:

AbstractSeveral chromosomal regions are found to be consistently amplified in human breast cancers. For two of these regions, 8p 12 and 10q26, we previously reported the amplification of genes encoding FGF receptors,FGFR1/FLGandFGFR2/BEK, in about 12% of breast tumors. ThePLATgene, encoding the tissue‐type plasminogen activator, is also located close to or within the 8p 12 region. In the present study, we show that bothFGFR1andPLATcan be amplified in breast as well as ovarian carcinomas.FGFR1amplification was detected in 14.5% of breast and 7.8% of ovarian tumors, whereasPLATwas found to be amplified in 15.6% and 19.4% of the tumors, respectively. Each gene could be amplified independently of the other. These data raised the question of which gene is selected for amplification at 8p 12. In most cases, the levels of expression ofFGFR1andPLATin breast tumors were comparable to their level of expression in normal mammary tissue. However,FGFR1was expressed above the normal level in a certain number of cases. This gene could be a good candidate as “driver” of the 8p 12 amplification, but it cannot account for all complex molecular events taking place in this region. © 1993 Wiley‐L

ISSN:1045-2257    

DOI:10.1002/gcc.2870070407

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

年代:1993

数据来源: WILEY

摘要:

AbstractWe present the case of a 14‐year‐old girl in whom a myelodysplastic syndrome was diagnosed 9 months after surgical resection and chemotherapy for an ovarian germ cell tumor. Cells from her marrow were characterized by trisomy 8 and an isochromosome 12p, a marker that appears to be unique to germ cell tumors. The presence of the same two anomalies in her original tumor was demonstrated by fluorescence in situ hybridization study of interphase cells in paraffin‐embedded tissues and thus provided strong evidence that the two neoplasms had a common clonal origin. © 1993 Wiley‐L

ISSN:1045-2257    

DOI:10.1002/gcc.2870070408

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

年代:1993

数据来源: WILEY

摘要:

AbstractChromosomal in situ suppression (CISS) hybridization with biotin labeled chromosome‐specific libraries was performed on short‐term cultures from five cases of non‐Hodgkin's lymphoma (NHL). The painting analysis proceeded in three stages. First‐stage CISS hybridization was done with libraries specific for chromosomes that seemed to be lost or rearranged as judged by banding analysis. Second‐stage CISS included hybridization with probes specific for chromosomes that, because of banding pattern similarities, were considered to be likely candidates to have contributed unidentified chromatin blocks in the abnormal karyotype. The third and final stage was a confirmation hybridization with a library specific for the chromosome that, at the stage two analysis, was found to have donated the previously unknown chromosomal segment. The aberrant chromosomes were often more complex than the banding analysis had led us to believe. Among the rearrangements whose nature was determined by CISS hybridization were two add(1)(p36) which, in both cases, were shown to be a der(1)t(1;2)(p36;q31). This study illustrates the potential use of chromosome painting in resolving karyotypic uncertainties in NHL, and it shows that new cytogenetic subgroups may emerge when classical banding analysis is supplemented with fluorescence in situ hybridization techniques. © 1993 Wiley

ISSN:1045-2257    

DOI:10.1002/gcc.2870070409

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

年代:1993

数据来源: WILEY

摘要:

AbstractAn embryonal rhabdomyosarcoma was analyzed cytogenetically. In primary cultures fed a serum‐containing medium, 11 clones with karyotypic abnormalities were found. One had trisomy 8 only. The other 10 clones had trisomy 8 as well as additional evolutionary changes that included trisomy for part or all of chromosome 2, isochromosomes for the short and long arms of chromosome 11, isochromosomes for the long arm of chromosome 8, and extra copies of chromosome 8, some of which had an interstitial deletion in 8q. In those primary cultures that had grown in a chemically defined, serum‐free medium and in all passaged cultures, trisomy 8 was the only aberration. Our findings and a survey of published information point to gain of one chromosome 8 as a frequent primary karyotypic abnormality in embryonal rhabdomyosarcomas. Trisomy for part or all of chromosomes 2 and 11 and additional gains of chromosome 8 material seem to be common secondary changes. © 1993 Wiley‐Lis

ISSN:1045-2257    

DOI:10.1002/gcc.2870070410

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

年代:1993

数据来源: WILEY

ISSN:1045-2257    

DOI:10.1002/gcc.2870070411

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

年代:1993

数据来源: WILEY