bluuebunny/crossref_metadata_2025_split huggingface dataset:
Particle transport method for convection problems with reaction and diffusion
Authors: Shipilova O. , Haario H. , Smolianski A. 
Published: February 2007

AbstractThe paper is devoted to the further development of the particle transport method for the convection problems with diffusion and reaction. Here, the particle transport method for a convection–reaction problem is combined with an Eulerian finite‐element method for diffusion in the framework of the operator‐splitting approach. The technique possesses a special spatial adaptivity to resolve solution singularities possible due to convection and reaction terms. A monotone projection technique is used to transfer the solution of the convection–reaction subproblem from a moving set of particles onto a fixed grid to initialize the diffusion subproblem. The proposed approach exhibits good mass conservation and works with structured and unstructured meshes.The performance of the presented algorithm is tested on one‐ and two‐dimensional benchmark problems. The numerical results confirm that the method demonstrates good accuracy for the convection‐dominated as well as for convection–diffusion problems. Copyright © 2007 John Wiley & Sons, Ltd.
High p21RAS expression levels correlate with chromosome 8 rearrangements in benign human mixed salivary gland tumors
Authors: Stenman Göran , Sandros Jens , Mark Joachim , Nordkvist Anders 
Published: February 2007

AbstractThe expression of RAS oncogenes in benign and malignant salivary gland tumors was studied by immunohistochemistry and by immunoblotting using monoclonal antibodies recognizing the HRAS and KRAS gene 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 that RAS gene 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 of RAS gene expression.
Frequency and extent of allelic loss in the short arm of chromosome 3 in nonsmall‐cell lung cancer
Authors: Rabbitts Pamela , Douglas Jenny , Daly Maria , Sundaresan Vasi , Fox Bernard , Haselton Philip , Wells Frank , Albertson Donna , Waters Jonathan , Bergh Jonas 
Published: February 2007

AbstractDNA was prepared from tumour and normal tissue from 48 patients representing all common histological types of nonsmall‐cell lung cancer. Using eight DNA probes, which detect nine restriction enzyme fragment length polymorphisms (RFLP) on chromosome 3, we established that among the 44 informative patients 32 had lost alleles on the short arm of one of their copies of chromosome 3. Of these 32, at least 13 had also lost alleles on the long arm of chromosome 3, suggesting that the whole chromosome might be lost. For one patient, cytogenetic analysis indicated that the mechanism of allelic loss was reciprocal translocation followed by chromosomal loss of one of the reciprocal products. Two patients with allelic loss distal to the D3S3 locus (which maps to 3p13–14) retained heterozygosity at that locus. These results indicate that loss of alleles on the short arm of chromosome 3 is a common event in lung tumours of the nonsmall‐cell type, that this loss occurs by a variety of chromosomal mechanisms, and that the minimally deleted region is 3p13–14→3pter.
Homozygosity for 8pter→q22 in acute myeloblastic leukemia with t(8;21)(q22;q22)
Authors: Berger Roland 
Published: February 2007

AbstractA case of acute nonlymphocytic leukemia with homozygosity for the chromosome segment 8pter→8q22 is reported. A t(8;21)(q22;q22) translocation was associated with duplication of the derivative chromosome 8q – and absence of the normal chromosome 8. These rearrangements also yielded hemizygosity for 8q22→qter. This case shows that acquired hemizygosity and homozygosity do exist in leukemia as in solid malignant tumors.
Premature chromosome condensation in childhood acute lymphoblastic leukaemia: Correlation of proliferative potential index in blood and marrow
Authors: Macleod Roderick A. F. , Hill Frank G. H. , Creasy Michael R. , Hulten Maj A. 
Published: February 2007

AbstractThe proliferative potential index (PPI), which is the proportion of all G1 cells which are in late G1, has been shown to reflect disease state in patients with acute leukaemia. We have determined PPI in paired blood and marrow samples from children with acute lymphoblastic leukaemia (ALL) at different stages of the disease, and found a close correlation between blood and marrow PPI irrespective of disease stage. Therefore blood PPI can replace marrow PPI for monitoring disease control in ALL.
Gene dosage effect in acquired monosomy 7: Distinct behaviour of β‐glucuronidase and phosphoserine phosphatase
Authors: Minelli Antonella , Piantanida Mauro , Maserati Emanuela , Campagnoli Elena , Pasquali Francesco , Danesino Cesare 
Published: February 2007

AbstractEvidence for gene dosage effect for β‐glucuronidase (GUSB) and phosphoserine phosphatase (PSP), whose genes are mapped on chromosome 7, was searched in a group of 13 patients with myeloproliferative disorders and acquired monosomy 7. The monosomy 7 was the sole anomaly in nine patients and was associated with other chromosome changes in four. A group of 19 patients with similar diseases but with normal karyotype or with anomalies not involving chromosome 7 served as control. β‐galactosidase and arylsulphatase A, whose genes are not on chromosome 7, were tested as control enzymes. We obtained evidence for a gene dosage effect for GUSB, but not for PSP. When all cases with monosomy 7 were compared with controls, no dosage effect was observed for PSP, but when this group was split into two, according to the presence of anomalies additional to the monosomy 7, the values of activity in the group with additional anomalies were significantly lower than in the controls. Thus, in the case of PSP, the loss of one allele is not followed immediately by reduction in activity, and this could be due to the specific importance of PSP in nucleic acid metabolism. We postulate that some regulatory mechanisms are able to keep normal levels of PSP even in the presence of only one allele, and that they are overwhelmed only when additional chromosome changes are present. These changes tend to involve chromosomes carrying genes for enzymes involved in a metabolic pathway closely related to PSP functions, and only then is a gene dosage effect for PSP detectable.
Multiple methylation‐free islands flank a small breakpoint cluster region on 11p13 in the t(11;14)(p13;q11) translocation
Authors: Foroni Letizia , Boehm Thomas , Lampert Fritz , Kaneko Yasuhiko , Raimondi Susanna , Rabbitts Terence H. 
Published: February 2007

AbstractThe t(11;14)(p13;q11) translocation is one of the most frequent chromosomal abnormalities in T‐cell acute lymphoblastic leukemia (ALL). Ten different leukemias carrying this translocation have been analysed and all 10 breakpoints fall within a region of less than 25 kb on chromosome band 11p13. We have used PFGE and cosmid cloning to assess the presence of potential genes by analysing methylation‐free islands in the vicinity. Four methylation‐free islands, within 270 kb, flank the t(11;14)‐associated breakpoint cluster region (T‐ALLbcr), one occurring about 25 kb on the telomeric side and one about 100 kb on the centromeric side of the T‐ALLbcr. Evidence for eight further methylation‐free islands on both sides of the T‐ALLbcr region is also presented. Thus multiple methylation‐free islands exist on 11p13 flanking the t(11;14)(p13;q11) translocation‐associated breakpoint cluster region, representing multiple potential transcription units whose chromosomal environment is altered by chromosome translocation.
Karyotypic changes identified by HaeIII restriction endonuclease banding in a patient with M2 acute non‐lymphoblastic leukemia
Authors: Stuppia Liborio , Palka Giandomenico , Fioritoni Giuseppe , Calabrese Giuseppe , Franchi Paolo Guanciali , D'Arcangelo Luigi , Torlontano Glauco 
Published: February 2007

AbstractA patient with acute non‐lymphoblastic leukemia, FAB type M2, showed a complex karyotype involving chromosomes 1 and 11. The breakpoints could not be exactly identified by GTG and QFQ banding. A subsequent analysis with AluI and HaeIII restriction enzyme staining allowed the detection of a translocation of the heterochromatic region of chromosome 1 to 11q21.
No evidence for loss of alleles at 11p in HBV negative hepatocellular carcinomas
Authors: Kiechle‐Schwarz Marion , Scherer Gerd , Kovacs Gyula 
Published: February 2007

AbstractThe aim of the present study was to determine whether loss of DNA sequences at the chromosome arm 11p, where presumed tumor suppressor genes are located, might occur in hepatocellular carcinomas (HCCs) of hepatitis B virus (HBV) negative patients. Normal liver and HCC genotypes were compared at 6 loci on 11p with 7 polymorphic probes detecting 10 restriction length polymorphisms (RFLPs). Each of the 8 paired normal‐tumor tissue samples was informative for at least three different loci on 11p13‐pter. None of them showed loss of constitutional heterozygosity for those markers. The retainment of 11p alleles suggests that mechanisms other than loss of tumor suppressor genes on 11p are involved in hepatocarcinogenesis of HBV negative patients.
Trisomy 12 is a consistent chromosomal aberration in benign ovarian tumors
Authors: Pejovic Tanja , Heim Sverre , Mandahl Nils , Elmfors Bengt , Flodérus Ulla‐Maria , Furgyik Stefan , Helm Góran , Willén Helena , Mitelman Felix 
Published: February 2007

AbstractClonal karyotypic abnormalities were detected in 7 of 42 cytogenetically analyzed benign ovarian tumors. An adenofibroma had –X and a mucinous cystadenoma had t(1;11)(q25;q23) as the sole abnormality. Trisomy 12 was found in the remaining five tumors. It was the only change in two fibromas and a serous cystadenoma; the fourth tumor, a mucinous cystadenoma, had one clone with + 12 and one with + 12 and + 10, and the fifth tumor, a fibrothecoma, had +4, +9, +12. The finding of trisomy 12 in five of seven karyotypically aberrant tumors suggests that this aberration characterizes a hitherto unrecognized cytogenetic subgroup of benign ovarian neoplasms.
RAS gene activation in acute myelogenous leukemia: Analysis by in vitro amplification and dna base sequence determination
Authors: Mane Shrikant M. , Meltzer Stephen J. , Gutheil John C. , Kapil Vikram , Lee Edward J. , Needleman Samuel W. 
Published: February 2007

AbstractRAS protooncogene activation has been repeatedly demonstrated in neoplastic cell DNA from patients with AML. Despite the convincing demonstration that activating RAS gene point mutations are critical in model systems, their precise prevalence and importance in human cancers such as AML remain speculative. The technology for identifying RAS mutations has changed considerably in recent years. We examined a prospective cohort of 43 acute myeloid leukemia (AML) patients admitted to the University of Maryland Cancer Center for first and second exon mutations of NRAS and KRAS using PCR and DNA sequence analysis. Six (14%) 1st exon NRAS mutations were identified. No clinical or biologic parameter has yet been observed to segregate with RAS activation, although a larger study may be needed to demonstrate this.
New localizations of VH sequences by in situ hybridization with biotinylated probes
Authors: Cherif Dorra , Berger Roland 
Published: February 2007

AbstractThe chromosomal localization of genes of three VH families (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 VH genes on chromosomes other than 14 suggests that several genes of the VH family had been simultaneously translocated in evolution and that the newly localized VH sequences may be pseudogenes.
Monosomy 12p in a radiation‐induced germ cell tumor
Authors: Cowan Janet M. , Beckett Michael A. , Tarbell Nancy J. , Weichselbaum Ralph R. 
Published: February 2007

AbstractWe report results of cytogenetic analysis of a cell line established from a radiation induced germ cell tumor. Tumors of this type are rare, and there is only one other report of chromosome analyses of solid tumors induced by radiotherapy (Cowan et al., 1990). The cells were grown for over a year, and harvested at passage 13. The karyotype was pseudodiploid, with several balanced translocations. Spontaneously occurring germ cell tumors are associated with i(12p). We did not observe an i(12p), but instead found monosomy of 12p and 7q22→q32.
High resolution mapping of consistent leiomyoma breakpoints in chromosomes 12 and 14 to 12q15 and 14q24.1
Authors: Pandis Nikos , Heim Sverre , Bardi Georgia , Mandahl Nils , Mitelman Felix 
Published: February 2007

AbstractA substantial percentage of uterine leiomyomas are cytogenetically characterized by consistent, clonal chromosome abnormalities, including t(12;14)(q14–15;q23–24) and other rearrangements of 12q14–15 that occur without any visible 14q changes. The partly similar banding characteristics of these two regions have hitherto precluded exact mapping of the 12q and 14q breakpoints to any particular band, let alone their assignment to subbands. In the series of four myomas presented here, in which one tumor had inv(12q), two t(12;14), and one a three‐way t(7;12;14), we were able to achieve high resolution banding (550 band stage) of the rearranged chromosomes in several metaphases. This enabled us to assign a 12q breakpoint to 12q15 in all tumors and, in the three cases informative in this regard, the 14q breakpoint to 14q24.1. The more precise breakpoint mapping considerably narrows down the area that must be examined with molecular genetic methods in order to identify the gene loci that are rearranged in leiomyomas with 12q and 14q aberrations. It will also help determine to what extent leiomyoma rearrangements of 12q involve the same loci that are affected in 12q changes in other tumor types, e.g., in pleomorphic adenomas of the salivary gland, in lipomas, and in myxoid liposarcomas. At present it seems that the breakpoint in 12q may be cytogenetically identical in the three benign tumors, whereas it in myxoid liposarcomas appears to be more proximal.
Is the chromosome band 1p36 another hot‐spot for rearrangements in uterine leiomyoma?
Authors: Vanni Roberta , Cin Paola Dal , van den Berghe Herman 
Published: February 2007

AbstractTwo uterine leiomyomas showing involvement of bands 1p36 and 2p24 are reported. These rearrangements may indicate a new hot‐spot for chromosome changes in this neoplasia, 1p36, and confirm the existence of a specific subgroup in leiomyomas, t(1;2)(q36;p24).
Mapping of translocation breakpoints on the short arm of chromosome 19 in acute leukemias by in situ hybridization
Authors: Saltman David L. , Mellentin Julia D. , Smith Stephen D. , Cleary Michael L. 
Published: February 2007

AbstractNon‐random translocations involving the short arm of chromosome 19 are frequently observed in acute leukemias. Recent studies have shown that the 19p13 genes E2A and LYL1, both of which encode helix‐loop‐helix proteins, lie at two different translocation breakpoints in acute lymphoblastic leukemias (ALL). The E2A gene is involved by the t(1;19)(q23;p13) in acute pre‐B‐cell leukemias and the LYL1 gene is structurally altered by a t(7;19)(q34;p13) in T‐cell ALL. To assess the role of these genes in other leukemia‐associated translocations we mapped their locations with respect to the t(11;19)(q23;p13) and t(4;19)(q21;p13) translocation breakpoints carried by T‐ALL cell lines SUP‐T13 and SUP‐T8a, respectively. In situ hybridization studies indicated that the E2A and LYL1 genes are physically distinct from the t(4;19) and t(11;19) breakpoints. Using these and other 19p13 translocation breakpoints as landmarks, we established a partial physical map of 19p: 19pter‐E2A‐INSR‐LYL1‐[t(4;19), t(11;19)]‐19cen. These data should help guide molecular studies to further characterize 19p13 breakpoints and mapping of genes in this chromosomal region.
1P13 is the most frequently involved band in structural chromosomal rearrangements in human breast cancer
Authors: Mitchell Erika L. D. , Santibanez‐Koref Mauro F. 
Published: February 2007

AbstractCytogenetic data on 14 breast carcinomas were examined to determine which chromosome arms and bands are preferentially involved in structural chromosome changes. Chromosome arms 17p, 16q, and 1p and band 1p13 were found to be significantly involved. A review of the world literature confirmed 1p as being the most frequently involved arm in structural chromosome changes in breast cancer and 1p13 as being the band most frequently involved in such changes. The two sets of results were pooled, and the analysis of 113 tumours revealed 229 of 304 bands to be involved, with 1p13 affected in 20% of the tumours.
Comparative cytogenetic analysis between cyclophosphamide‐sensitive and ‐resistant lines of acute myeloid leukemia in the lewis brown norway hybrid rat
Authors: Kearns William , Koelling Todd , Yeager Andrew 
Published: February 2007

AbstractAn animal model of acute myeloid leukemia (AML) has been developed in the Brown Norway (BN) rat and has successfully been introduced into the Lewis x BN F1 hybrid (LBN) and designated LBN AML. The original LBN AML is sensitive to the chemotherapeutic agent cyclophosphamide (CY). Recently, a CY‐resistant cell line of LBN AML has been established. To characterize this animal model of human leukemia better, we analyzed and compared the chromosomal makeup of both the CY‐sensitive and CY‐resistant LBN AML lines. The CY‐sensitive LBN AML cultures contained two cell lines—line 1 (88%):41, XX, –1, –2, –9,del(12)(q16),+der(1)t(1;?8)(p13;q31),+der(2)t(2;9)(p11;q11); and line 11 (12%): 41,XX,–1,–2,–9,del(12),del(20)(q13)+der(1)t(1;?8)(p13;q31),+der(2)t(2;9)(p11;q11). The recently developed CY‐resistant AML cells contained two cell lines—line 1 (88%): 41,XX,–1,–2,–9,del(3)(q36q42.1),del(4)(q42.2),?t(5;?)(q35;?),?t(8;?)(q24;?),del(12)(q16),+der (1)t(1;?8)(p13;q31),+der(2)t(2;9)(p11;q11); and line II (12%): 42,XX (probably represents host contamination). The new chromosomal aberrations in the CY‐resistant line 1 [del(3)(q36q42.1),del(4)(q42.2),?t(5;?)(q35;?), and ?t(8;?)(q24;?)] suggest a possible interrelationship between these secondary karyotypic abnormalities and acquisition of resistance to the chemotherapeutic agent.
Karyotypic evolution in B‐cell chronic lymphocytic leukaemia
Authors: Oscier David , Fitchett Margaret , Herbert Tony , Lambert Richard 
Published: February 2007

AbstractSequential cytogenetic studies were performed on a minimum of two and a maximum of nine occasions (mean 3.6) on the peripheral blood leucocytes of 112 patients with B‐CLL. On initial cytogenetic analysis, 58 had a normal karyotype and 64 had a clonal abnormality. Karyotypic evolution occurred in 18 patients (16%). There was no significant difference in the incidence of disease progression between patients with a stable karyotype and those who underwent karyotypic evolution. In only one patient was there a clear association between disease progression, a change in cell morphology and karyotypic evolution.
Rearrangement of 9p13 as the primary chromosomal aberration in adenoid cystic carcinoma of the respiratory tract
Authors: Higashi Koichiro , Jin Yuesheng , Johansson Maria , Heim Sverre , Mandahl Nils , Biörklund Anders , Wennerberg Johan , Hambraeus Göran , Johansson Leif , Mitelman Felix 
Published: February 2007

AbstractTwo adenoid cystic carcinomas, one of the nasal cavity, the other a bronchial tumor, were cytogenetically analyzed. The former had a t(6;9)(q21‐22;p13‐21) as the sole karyotypic abnormality. The latter had two related abnormal clones, resulting in the mosaic karyotype 46, XY, t(9;17)(p13;p13)/46, Y, t(X;6)(p22;q23), t(9;17)(p13;p13). The karyotypic profiles of the two cases, the only respiratory tract adenoid cystic carcinomas that have been cytogenetically characterized, differ little from those of previously reported adenoid cystic carcinomas of the major salivary glands, underscoring the fundamental biologic similarity among these tumors even when they develop from different structures and in different anatomical sites and organs. Because in the second case the t(9;17) obviously must have preceded the t(X;6), we conclude that both tumors had rearrangement of 9p13 as the primary cytogenetic change. The data thus add to the evidence that 6q changes are frequent, albeit at least sometimes secondary, aberrations in malignant salivary gland tumors. A subset of adenoid cystic carcinomas instead have rearrangement of 9p as the primary, and presumably pathogenetically essential, abnormality.
A chromosome 12 coding region is juxtaposed to the MYC protooncogene locus in a t(8; 12)(q24;q22) translocation in a case of B‐cell chronic lymphocytic leukemia
Authors: Rimokh Ruth , Rouault Jean‐Pierre , Wahbi Kamal , Gadoux Mylène , Lafage Marina , Archimbaud Eric , Charrin Christiane , Gentilhomme Odile , Germain Daniel , Samarut Jacques , Magaud Jean‐Pierre 
Published: February 2007

AbstractWe performed molecular cloning and sequencing of the breakpoints of a new chromosomal translocation involving the MYC protooncogene locus. This secondary t(8; 12)(q24;q22) was associated with a primary t( I I; 14)(q I 3;q32) translocation in a case of B‐cell chronic lymphocytic leukemia (CLL) in blastic transformation. In this leukemia, Northern blot and nuclease analyses SI showed that MYC was strongly expressed with initiation of the transcription at both the 5′ and 3′ promoters as observed in Burkitt's lymphomas; no coding change was observed in MYC putative regulatory sequences. The breakpoint on chromosome 8 mapped to the 3′ end of the MYC locus, in a region containing a potential Z‐DNA tract, and where we identified two DNase I hypersensitive sites. A rearranged MYC gene fragment was cloned and shown to contain chromosome 12 information by Southern blot analysis and by in situ hybridization. A genomic probe subcloned from the isolated region of the chromosome 12 recognized a 1.8 kb transcript in virtually all the tissues tested but a preferential expression of this new gene, which we termed BTGI (for B‐cell translocation gene I) was observed in the CLL cells and in tissues of lymphoid origin. This chromosome 12 coding sequence is conserved in evolution and a transcript of similar size is present in murine tissues.
Translocations t(X;7) and t(7; 14) in a synovial sarcoma
Authors: Verhest Alain , Limon Janusz , Mrózek Krzysztof , Nedoszytko Boguslaw 
Published: February 2007

AbstractCytogenetic analysis of a metastatic biphasic synovial sarcoma showed two structural abnormalities: t(X;7)(q 11 or 12;q32) and t(7;14)(q22;q11.2). This is the first report of a synovial sarcoma without the involvement of either Xp11 or 18q11.