|
1. |
Preferential clustering of chromosomal breakpoints in Burkitt's lymphomas and L3 type acute lymphoblastic leukemias with a t(8;14) translocation |
|
Genes, Chromosomes and Cancer,
Volume 8,
Issue 1,
1993,
Page 1-7
Giuseppe Saglio,
Maria Grazia Borrello,
Angelo Guerrasio,
Gabriella Sozzi,
Anna Serra,
Paola Francia Di Celle,
Robin Foa,
Manlio Ferrarini,
Silvio Roncella,
Caterina Borgna Pignatti,
Pierluigi Marradi,
Pietro Izzo,
Jesus Soler,
Marco Pierotti,
Preview
|
PDF (538KB)
|
|
摘要:
AbstractWe have analyzed the type ofMYC/IGheavy‐chain locus (IGH) rearrangement present in 15 patients affected by t(8; 14)‐positive primary Burkitt's lymphoma or acute lymphoblastic leukemia of the L3 type in an attempt to map in detail the locations of the chromosome 8 and chromosome 14 breakpoints. The almost constant position of the chromosome 8 breakpoint (within or immediately 5′ of theMYCgene) together with two distinct clusters of breakpoints on chromosome 14 resulted in two main types ofMYC/IGH(present in 12 of 15 cases). In the first type (six cases), theMYCgene or at least its coding portion was joined with theJHregion on chromosome 14, whereas in the second, present in another six cases, theMYCgene and theCαlregion were juxtaposed. Physical linkage between the translocatedMYCand a known enhancer element of theIGHlocus is the common feature in the two types of rearrangement, suggesting that a high‐level constitutive expression plays a prominent role inMYCactivation. Interestingly, the chromosome 14 break site within the switch α1region, which has been only occasionally described in other cases, is present in 40% of our patients, suggesting the existence of preferential breakpoint cluster regions in cases of similar geographic origin. © 1993 Wiley
ISSN:1045-2257
DOI:10.1002/gcc.2870080102
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1993
数据来源: WILEY
|
2. |
Chromosomal radiosensitivity at intrachromosomal telomeric sites |
|
Genes, Chromosomes and Cancer,
Volume 8,
Issue 1,
1993,
Page 8-14
Luis Alvarez,
James W. Evans,
Rebecah Wilks,
Joe N. Lucas,
J. Martin Brown,
Amato J. Giaccia,
Preview
|
PDF (637KB)
|
|
摘要:
AbstractTelomeric DNA is composed of highly conserved sequences which are present at the termini of chromosomes as well as at intrachromosomal locations. Here, we studied a Chinese hamster ovary (CHO) cell line, BL‐10, with highly stable amplified telomeric DNA at the termini as well as at intrachromosomal locations. We show that intrachromosomal or interstitial telomeric sites in this cell line and in another CHO cell line, HA‐1, are radiosensitive in that they are more prone to breakage than would be expected based on the percentage of the genome composed of telomeric sequences. The frequency of breakage at interstitial telomeric sites is 4.3 to 8.3 times higher than that in the CHO genome overall. These conclusions are reached by both conventional cytogenetic analysis of two CHO cell lines which have the same survival rates after exposure to ionizing radiation, and by use of double fluorescence in situ hybridization (FISH) with a pan‐telomere‐specific probe and a CHO chromosome‐specific library in the same metaphase cells after irradiation. © 1993 Wiley
ISSN:1045-2257
DOI:10.1002/gcc.2870080103
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1993
数据来源: WILEY
|
3. |
Structural organization ofMYCNamplicons of neuroblastoma tumors, xenografts, and cell lines characterized by the sequences encompassing theMYCNamplicons in a human neuroblastoma cell line |
|
Genes, Chromosomes and Cancer,
Volume 8,
Issue 1,
1993,
Page 15-21
Kiyotaka Akiyama,
Naotoshi Kanda,
Masao Yamada,
Mieko Kato,
Keiko Tadokoro,
Tadashi Matsunaga,
Yoshisuke Nishi,
Preview
|
PDF (554KB)
|
|
摘要:
AbstractWe characterized differences in the structural organization of theMYCNamplicons of a number of neuroblastomas by analyzing 8 contigs spanning 330 kb cloned from theMYCNamplicon of a neuroblastoma cell line. Some regions were amplified in almost all specimens, the conserved regions (CRs), and others were differentially amplified in some subsets, the non‐conserved regions (NCRs). CRs constituted only 20% of the 330 kb region, with the remainder being NCRs. The regions that inevitably co‐segregate with theMYCNgene make up the core, whereas flanking regions are retained at random. If a histogram of the frequency with which the amplified NCR sequences from one specimen match those of the cell line MC‐NB‐1 shows a random distribution, the NCRs would co‐segregate withMYCNas a result of random events. However, both the tumors and cell lines/xenografts showed a distribution with two distinct peaks; one from a group containing a small number of sequences with a fairly high degree of homology to the NCRs of MC‐NB‐1, and the other from a group containing a large number of sequences with little homology. These results indicate that the flanking segments are preferentially co‐segregated withMYCNby a non‐random mechanism. © 19
ISSN:1045-2257
DOI:10.1002/gcc.2870080104
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1993
数据来源: WILEY
|
4. |
Tissue culture loss of aneuploid cells from carcinomas of the prostate |
|
Genes, Chromosomes and Cancer,
Volume 8,
Issue 1,
1993,
Page 22-27
Josée J. König,
Wilma Teubel,
Jan Willem Van Dongen,
Anne Hagemeijer,
Johannes C. Romijn,
Fritz H. Schröder,
Preview
|
PDF (484KB)
|
|
摘要:
AbstractThe frequency of aneuploid cells in cultured prostate carcinoma specimens was investigated. Ploidy distribution of the original tissue was established by flow cytometry (FCM). Fluorescence in situ hybridization (FISH) of chromosome I was applied to directly isolated and cultured cells to investigate whether any modifications in the ploidy distribution of chromosome I took place during tissue culture. In six tumor specimens that were diploid by FCM and FISH, no differences were found in the ploidy distribution of chromosome I before and after tissue culture. In eight tumors that were aneuploid by FISH, the percentage of aneuploid nuclei was significantly reduced from 28.0 ± 15.0 (range 13ndash;59%) in uncultured cells to 9.1 ± 4.4 (range 4ndash;18%) after tissue culture. The reduction of aneuploid nuclei ranged from 44 to 85%, which means that the majority of the aneuploid cell populations that were observed in the original specimens were undetectable in cultured samples. This suggests a preferential growth of normal epithelial cells. The data presented can explain the high percentage of diploid karyotypes usually found in short‐term cultured prostate carcinoma specimens. © 1993 Wiley‐Lis
ISSN:1045-2257
DOI:10.1002/gcc.2870080105
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1993
数据来源: WILEY
|
5. |
Detection of sex‐region Y (SRY) transcripts in human prostate adenocarcinoma and benign prostatic hypertrophy |
|
Genes, Chromosomes and Cancer,
Volume 8,
Issue 1,
1993,
Page 28-33
James V. Tricoli,
Joyce L. Yao,
Sharon A. D'Souza,
R. Bruce Bracken,
Preview
|
PDF (531KB)
|
|
摘要:
AbstractThe human sex‐region Y (SRY) gene maps to Yp 11.3 and encodes a protein that shares significant sequence homology with a conserved DNA binding motif found in the nonhistone high‐mobility group (HMG) proteins. In the mouse,Sryis required for normal testicular development and is expressed in the developing male gonadal ridge as well as in the adult testis. In man,SRYexpression has been observed in the adult testis, but not in other adult male tissues. We have analyzed samples from human prostate adenocarcinoma and benign prostatic hypertrophy (BPH) for the expression of theSRYgene. We found expression ofSRYin 60% of malignant prostate tumors and in three of six samples of BPH. We did not find expression in male or female colon mucosa, or in tissue from a cystic ovary. Malignant and atrophic testicular tissue both containedSRYtranscript and served as positive controls in these experiments. We also foundSRYtranscript in the DU‐145 prostate adenocarcinoma cell line. Interestingly,SRYexpression is absent in the Tera‐2 teratocarcinoma cell line. The potential for theSRYgene product to bind HMG core response elements in vitro suggests thatSRYcould participate in the cascade of gene regulatory events that result in aberrant cell growth or malignancy. © 1993 Wiley
ISSN:1045-2257
DOI:10.1002/gcc.2870080106
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1993
数据来源: WILEY
|
6. |
Mapping of the gene for interferon‐inducible dsRNA‐dependent protein kinase to chromosome region 2p21‐22: A site of rearrangements in myeloproliferative disorders |
|
Genes, Chromosomes and Cancer,
Volume 8,
Issue 1,
1993,
Page 34-37
Samir M. Hanash,
Laura Beretta,
Christine L. Barcroft,
Susan Sheldon,
Thomas W. Glover,
David Ungar,
Nahum Sonenberg,
Preview
|
PDF (303KB)
|
|
摘要:
AbstractRecent evidence suggests that the human interferon‐inducible double‐stranded RNA‐dependent protein kinase may function as a tumor suppressor. Here we describe the mapping of the gene for this kinase to chromosome region 2p21‐22 by fluorescence in situ hybridization. A combined analysis of cytogenetic data from a series of 341 patients with hematologic disorders that exhibited cytogenetic abnormalities and from published reports indicates that abnormalities involving 2p21‐22 occur nonrandomly and are observed among patients with acute myelogenous leukemia, raising the possibility of a role for this protein kinase in leukemogenesis. © 1993 Wiley
ISSN:1045-2257
DOI:10.1002/gcc.2870080107
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1993
数据来源: WILEY
|
7. |
Non‐random integration of epstein‐barr virus in lymphoblastoid cell lines |
|
Genes, Chromosomes and Cancer,
Volume 8,
Issue 1,
1993,
Page 38-48
Valia S. Lestou,
Marc De Braekeleer,
Sabine Strehl,
German Ott,
Helmut Gadner,
Peter F. Ambros,
Preview
|
PDF (823KB)
|
|
摘要:
AbstractIn order to examine the role of Epstein‐Barr virus (EBV) in the immortalization of human 6 lymphocytes and in the pathogenesis of lymphoid malignancies, we investigated whether the EBV integration into the human genome is randomly distributed or whether the virus integrates preferentially at certain sites. Twelve in vitro immortalized human lymphoblastoid cell lines (LCLs), two in vivo infected LCLs, and one Burkitt's lymphoma cell line (EB2) were examined by non‐radioactive in situ hybridization (ISH) with a biotinylated EBV probe. Recurrent hybridization sites were detected in all 15 cell lines. The chromosomes frequently carrying the EBV genome were chromosomes 1, 2, 4, and 5. In more than 70 chromosomal bands, a greater number of integration sites than expected was found (p<0.05). Approximately half of these bands were involved in the majority of the cell lines (for example, 1p31, 1q43, 2p22, 3q28, 4q13, 5p14, 5q12, and 11p15) whereby band 5p14 was involved in all LCLs analyzed. Virtually no viral integrations were found on the sex chromosomes (X, Y). The majority of the EBV integrations was found in G‐band‐positive material (p<0.0001). Thus, our findings clearly show that EBV integrates into the human genome in a non‐random manner. © 1993 Wiley
ISSN:1045-2257
DOI:10.1002/gcc.2870080108
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1993
数据来源: WILEY
|
8. |
Oligoclonal B‐cell leukemia characterized by spontaneous cell division and telomere association |
|
Genes, Chromosomes and Cancer,
Volume 8,
Issue 1,
1993,
Page 49-59
Peter E. Crossen,
Sandra M. Tully,
Suzanne M. Benjes,
Peter E. Hollings,
Michael E. J. Beard,
Joy C. Nimmo,
Mary J. Morrison,
Preview
|
PDF (898KB)
|
|
摘要:
AbstractCytogenetic analysis of unstimulated cultures from a female patient with chronic B‐cell leukemia (CLL) revealed three cytogenetically distinct clones, suggesting that the patient's leukemia was oligoclonal. Immunoglobulin heavy chain gene rearrangement studies revealed 1 germline and 4 rearranged bands, indicative of an oligoclonal leukemc population. Further evidence of oligoclonality was provided by X‐linked RFLP studies. This is the first report of oligoclonality in CLL demonstrated by cytogenetic, immunoglobulin gene rearrangement, and X‐chromosome inactivation studies. In addition to oligoclonality, the patient's leukemk cells exhibited telomere association, a Robertsonian translocation, and clonal evolution, suggesting an underlying genomic instability. © 1993 Wiley‐L
ISSN:1045-2257
DOI:10.1002/gcc.2870080109
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1993
数据来源: WILEY
|
9. |
Cloning and sequencing of a t(14;19) breakpoint that involves the Cμ switch region |
|
Genes, Chromosomes and Cancer,
Volume 8,
Issue 1,
1993,
Page 60-62
Peter E. Crossen,
Martin A. Kennedy,
David C. Heaton,
Mary J. Morrison,
Preview
|
PDF (264KB)
|
|
摘要:
AbstractThe t(14;19) is a recurring translocation found in a small number of cases of chronic B‐cell leukemia (CLL). We have cloned and sequenced the breakpoint in a patient with a t(14;19) and shown that the breakpoint on chromosome 14 occurred in the Cμ switch region, and that the breakpoint on chromosome 19 occurred in the 5′ untranslated region of theBCL3 gene. This is in contrast to all the other reported cases with a t(14;19) in which the breakpoints on chromosome 14 occurred in the Cαl or Cα2 switch region, and the breakpoints on chromosome 19 occurred upstream of theBCL3 gene. Our results further emphasize the importance of the switch region in the t(14;19) translocation. © 1993 Wiley‐
ISSN:1045-2257
DOI:10.1002/gcc.2870080110
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1993
数据来源: WILEY
|
10. |
Numerical aberrations, including trisomy 22 as the sole anomaly, are recurrent in follicular thyroid adenomas |
|
Genes, Chromosomes and Cancer,
Volume 8,
Issue 1,
1993,
Page 63-66
Patrick Antonini,
Nicolas Lévy,
Bernard Caillou,
Anne‐Marie Vénuat,
Martin Schlumberger,
Claude Parmentier,
Alain Bernheim,
Preview
|
PDF (348KB)
|
|
摘要:
AbstractShort‐term cultures from 38 follicular thyroid adenomas revealed clonal numerical and/or structural chromosomal changes in 8 tumors, nonclonal changes in I tumor, and only normal karyotypes in 29 tumors. Three cases had trisomy 22 as the sole anomaly. Two cases had a combination of trisomies for chromosomes 5, 7, 9, 12, and 16. © 1993 Wiley‐Liss,
ISSN:1045-2257
DOI:10.1002/gcc.2870080111
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1993
数据来源: WILEY
|
|