摘要:

AbstractA reciprocal chromosomal translocation, t(15;17)(q22;q11.2‐12), is characteristic of acute promyelocytic leukemia (APL) of French‐American‐British (FAB) subtype M3, and is not associated with any other human malignancy. The non‐random pattern of the APL translocations suggests that specific genes on chromosomes 15 and 17 are somehow altered or deregulated as a consequence of the rearrangement. Translocation breakpoints in APL patients provide physical landmarks that suggest an approach to isolating the APL gene(s). Genetic and physical maps constructed for the APL breakpoint region on chromosome 17 have indicated that two fully‐linked DNA markers, defining loci forTHRA1and D17S80, map to opposite sides of an APL breakpoint yet reside on a common 350‐kbCla1 fragment. Cosmid‐walking experiments to clone this APL breakpoint have revealed a 38‐kilobase deletion on chromosome 17. Studies in additional APL patients have shown that the breakpoint region on chromosome 17 spans at lea

ISSN:1045-2257    

DOI:10.1002/gcc.2870020202

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

年代:1990

数据来源: WILEY

摘要:

AbstractClonal abnormalities of chromosome(s) 7 were investigated in two patients with acute lymphoblastic leukemia. The abnormal karyotypes were 46,XY,–7,del(6)(q13q21),+i(7q)/47,XY,del(6),+i(7q) in case 1, and 46,XX,–7,t(4;11)(q21;q23),+i(7q) in case 2. DNA from leukemic tissue was investigated with Southern blotting using hypervariable DNA probes λMS31 and pλg3 located on 7p and 7q, respectively. Restriction fragment length polymorphisms (RFLPs) were detected on the short arm in case 1 and on both arms in case 2, and a marked difference in intensity between the two alleles was observed. In case 1 the acquired hemizygosity of 7p, suggested by the cytogenetic findings, was confirmed by Southern blotting. Thus, one chromosome 7 formed the i(7q) and the other No. 7 was duplicated. In case 2 the results of the Southern blotting indicated that the size of the clone with i(7q) was considerably greater than suggested by cytogenetic analysis of the few available metaphase

ISSN:1045-2257    

DOI:10.1002/gcc.2870020203

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

年代:1990

数据来源: WILEY

摘要:

AbstractThe clonal loss of genetic information as revealed by the comparison of normal and tumor DNA restriction fragment length alleles has permitted the determination of the genomic positions of cancer‐recessive mutations. Here we have applied this approach to the analysis of 19 central nervous system tumors that constitute four histologic groups and occur most frequently in children and young adults. The detectable loss of genetic information from cases of medulloblastoma (11 examined) indicates that among such tumors, loss occurs most frequently from the short arm of chromosome 17. For the ependymomas examined (four cases), chromosome 22 was the preferred site for detectable loss. Analysis of pilocytic astrocytomas of the cerebellum (three cases) failed to reveal genetic alterations of any type among such tumors, a finding unique to this histologic group. The single choroid plexus papilloma examined demonstrated loss of genetic information from chromosome 3. Among the 19 tumors, multiple cases of loss were observed from chromosomes 10, 11, 13, and 22, and from the short arm of chromosome 17. Therefore, with regard to the chromosomal locations of implied tumor suppressor genes, these results are consistent with those described for intracranial tumors occurring more commonly in adults of middle to advanced ag

ISSN:1045-2257    

DOI:10.1002/gcc.2870020204

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

年代:1990

数据来源: WILEY

摘要:

AbstractThe chromosomal localization of genes of three VHfamilies (VH1–3) was performed using in situ hybridization with biotinylated probes. Significantly strong signals were observed on chromosome 14, band 14q32, and on bands 16p11 and 15q11, although less frequently. Signal intensity and frequency were more important on chromosome 14 with all three probes, and on chromosome 16 with the VH2 and VH3 probes, while chromosome 15 was more marked than 16 with the VH1 probe. The localization of VHgenes on chromosomes other than 14 suggests that several genes of the VHfamily had been simultaneously translocated in evolution and that the newly localized VHsequences may be pseudogene

ISSN:1045-2257    

DOI:10.1002/gcc.2870020205

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

年代:1990

数据来源: WILEY

摘要:

AbstractStable integration of polyoma viral DNA into the host‐cell genome is a prerequisite for continuous expression of the transformed phenotype. In this study we have mapped the chromosomal location of integrated viral DNA sequences in a polyoma‐induced mouse salivary gland adenocarcinoma. By in situ hybridization, a major integration site was assigned to chromosome 14, band B. The combined results from in situ hybridizations to metaphase chromosomes, primary tumors, and cultured tumor cells indicate the presence of both integrated and free polyoma viral DNA in the tumors. Cytogenetically, the tumors were characterized by a pronounced karyotypic instability. No abnormal cells with the same karyotype were observed in any of the tumors. Nevertheless, it was possible to recognize a preferential pattern of chromosome variation with certain common recurrent and sporadic deviations. Clonal gains and/or losses of single chromosomes were seen in all tumors. It is concluded from these results that karyotypic instability may play an important role in the genesis and progression of polyoma virus‐induced salivary gland t

ISSN:1045-2257    

DOI:10.1002/gcc.2870020206

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

年代:1990

数据来源: WILEY

摘要:

AbstractCytogenetic analysis of ten primary non‐small cell lung carcinomas (NSCLC), including five adenocarcinomas (ADC), three squamous cell (SQC), and two large cell (LCC) carcinomas has been carried out in an attempt to determine karyotype changes involved in the early stage of disease. The tumors were all aneuploid and exhibited complex karyotypes with multiple structural and numerical abnormalities. Clonal structural rearrangements were identified and in particular loss of material from the short arm of chromosome 9 had a 90% incidence. This loss was due to non‐reciprocal translocation, deletion, or chromosome loss. Breakpoints were in the region 9q13 to p22. Other chromosome regions that were non‐randomly involved are as follows: 1 cen to p13, 3p, 5q11 to q13, 6p, 6q15 to q27, 7p, 8p, 11q12 to q23, 13p, 14p, 15p, 17p, and 19p. While a primary cytogenetic change in NSCLC has not been identified conclusively, our findings implicate loss of material from 9p as a potentially important

ISSN:1045-2257    

DOI:10.1002/gcc.2870020207

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

年代:1990

数据来源: WILEY

摘要:

AbstractThe cytosolic protein p18 which is expressed in increased amounts in acute leukemia cells is variably phosphorylated as a function of growth and differentiation. Proteins with identical amino acid sequence were independently found to be highly expressed in normal brain tissue and neuroendocrine tumor cells. Here we describe the mapping of the recently cloned p18 gene to chromosome 1, band p35–36.1 by Southern blot analysis of human–rodent somatic cell hybrid DNA and by chromosome in situ hybridization using a p18 genomic probe. This region of the distal short arm of chromosome 1 is a frequent site of deletions or loss of heterozygosity in tumors derived from neural crest cells, particularly neuroblastomas and melanomas. The high levels of expression of p18 in brain and neuroendocrine tumor cells, its possible role in growth regulation, and its chromosomal location in a region frequently deleted in neuroectodermal tumors suggest that this gene may be involved in common genetic events occurring in these tum

ISSN:1045-2257    

DOI:10.1002/gcc.2870020208

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

年代:1990

数据来源: WILEY

摘要:

AbstractDNA adduct induction by N‐acetoxy‐N‐2‐acetylaminofluorene (N‐Ac‐AAF) has been investigated in Chinese hamster ovary (CHO) cells using immunoelectron microscopy. The major RNA and DNA adducts, N‐(guanosin‐8‐yl)‐2‐aminofluorene (G‐C8‐AF) and N‐(deoxyguanosin‐8‐yl)‐2‐aminofluorene (dG‐C8‐AF), were localized with a rabbit anti‐G‐C8‐AF antiserum and colloidal gold cytochemistry. Appropriate controls, including incubation of untreated cells with normal rabbit serum and immunogen‐absorbed serum, demonstrated that colloidal gold deposits were indicative of the presence of adducts. The localization of gold particles in close association with nuclear chromatin revealed high concentrations of adducts in DNA and RNA of nuclei. Morphometric evaluation of adduct formation in organelles of cells from different carcinogen exposures showed that 85–88% of total adducts were concentrated in nuclei. DNA adducts remaining in nuclei after RNAse treatment appeared to concentrate in heterochromatic areas, and these areas contained 59% of bound gold particles by morphometry. A total of 137–178 particles were found in nuclei of treated cells vs. 15–26 in the surrounding cytoplasm. Treated cells incubated with normal rabbit serum or specific adduct‐absorbed ser

ISSN:1045-2257    

DOI:10.1002/gcc.2870020209

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

年代:1990

数据来源: WILEY

摘要:

AbstractCytogenetic analyses have documented the consistent deletion of part of the short arm of chromosome 1 in neuroblastoma cells suggesting the presence of a suppressor gene in this chromosomal region. To determine the smallest region of deletion overlap at the molecular level on independently derived tumors and to define the location of the breakpoints more precisely, Southern analyses were performed on a somatic cell hybrid panel containing the normal and altered chromosomes 1 from seven neuroblastoma lines. By this method we were able to analyze a panel of 20 cloned sequences and two isozymes to determine the location of the breakpoints. Our findings indicate that the proximal breakpoints of chromosome 1 deletions range over a distance of more than 50 cM with the most distal deletion breakpoint occurring betweenMYCL1and DIS57. In addition, using restriction fragment length polymorphisms, it was determined that in at least three of the five cell lines in whichMYCL1was deleted from a chromosome I, the gene was translocated to another chromosome thus retaining the diploid complement. We propose that the neuroblastoma susceptibility gene is located distal toMYCL1and that there is another gene which is linked toMYCL1that may be involved in this neoplasm.

ISSN:1045-2257    

DOI:10.1002/gcc.2870020210

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

年代:1990

数据来源: WILEY

摘要:

AbstractSix patients with an aggressive leukemia/lymphoma disorder had a t(14;18) as well as either a t(8;14) (three patients) or a t(8;22) (three patients). Leukemia cells from all three patients with the t(8;22) had a mature B cell phenotype (Smlg+and TdT−), whereas two of three patients with the t(8;14) had a pre‐B phenotype and were Smlg−. None of the patients with the t(8;22) had a prior history of follicular lymphoma, whereas two of the three patients with the t(8;14) had had a follicular lymphoma. The clinical, cytogenetic, and morphologic characteristics of these six patients along with eight previously reported cases with both the t(14;18), and the t(8;14), the t(8;22) or the t(2;8) are disc

ISSN:1045-2257    

DOI:10.1002/gcc.2870020211

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

年代:1990

数据来源: WILEY