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N Pandis

Publications and source records attributed to N Pandis.

87 records · Page 5Linked to original sources
PubMed1992

Cytogenetic findings in three primary hepatocellular carcinomas.

Short-term cultures of three primary hepatocellular carcinomas were cytogenetically analyzed. Case 1 displayed a normal karyotype. Case 2 had, in addition to cells with a normal male chromosome complement, a clone with -Y. In case 3, two abnormal clones were found, one with -Y and one with a highly aberrant karyotype: [formula: see text] Our results, collated with the findings in one previously published primary hepatocellular carcinoma and in three cell lines, suggest that structural changes of chromosomes 1 and 6, leading to loss of 1p and 6q material, and loss of chromosome 16 are frequent events in hepatocellular carcinogenesis.

Aged↗
PubMed1992

Chromosome aberrations and expression of ras and myc oncogenes in leiomyomas and a leiomyosarcoma of the uterus.

Twenty eight leiomyomas and one leiomyosarcoma were cytogenetically analysed and also examined for ras and myc oncoprotein expression. Chromosome alterations were found in seven leiomyoma cases. In four of them 12q14-15 was involved. P21 product of H-ras and P62 product of c-myc genes were detected in paraffin embedded parallel tissue sections. A high expression of H-ras was apparent in most tumors. C-myc expression was weak or negative in most leiomyomas with normal karyotype while on the contrary in three out of seven cases with abnormal cytogenetic findings the gene product stained moderately positive. Considerable chromosome abnormalities and oncogene overexpression were also identified in the leiomyosarcoma.

Adult↗
PubMed1991

Trisomy 7 in short-term cultures of colorectal adenocarcinomas.

Cytogenetic analysis of short-term cultures from six adenocarcinomas of the colon revealed trisomy 7 as a recurrent clonal chromosomal abnormality. In three tumors, +7 was the sole change. In the fourth carcinoma, two aberrant clones with simple numerical aberrations were detected; one with +7 and one with +3. Tumors 5 and 6 both displayed two completely different abnormal clones; one had numerous numerical and structural abnormalities and thus was undoubtedly representative of the cancer parenchyma, and the other had only +7. The karyotypic differences between the coexisting clones in the latter two cases seem to argue against an evolutionary scenario in which the karyotypically more complex clones have evolved from the clones carrying trisomy 7 only. Furthermore, in tumor 6 the metaphases with trisomy 7 were found in colonies of fibroblast-like cells whereas those with a large number of abnormalities grew in colonies of epithelial-like cells. The combined results indicate that mitoses with trisomy 7 as the sole chromosomal change do not represent the neoplastic parenchyma of colorectal adenocarcinomas.

Adenocarcinoma↗
PubMed1991

Chromosomal abnormalities in giant cell tumors of bone.

Cytogenetic analysis of short-term cultures from ten giant cell tumors of bone revealed clonal and nonclonal chromosome abnormalities in three tumors and nonclonal changes only in seven. None of the clonal aberrations, inv(21)(p11q21) in one tumor, +5 in another, and t(15q22q), dic(4;22)(p16;p1?), double minutes, dicentrics, and ring chromosomes present in three separate clones in the third tumor, were identical to previously reported clonal changes in giant cell tumors. Telomeric associations were found in five tumors. The telomeres of chromosome arms 19q and 15p were particularly frequently involved.

Adolescent↗
PubMed1991

Chromosome analysis of 96 uterine leiomyomas.

From September 1989 to May 1990, we attempted cytogenetic analysis on 96 uterine leiomyomas removed from 64 women. Of the 90 tumors in which analysis was successful, 59 had a normal karyotype while 31 had clonal abnormalities. The most common aberration (13 tumors) was 7q-, mostly del(7)(q21.2q31.2); in two tumors with +12 and t(12;14) as the primary abnormalities, the 7q- was obviously a secondary change since it was found only in a subclone. A t(12;14)(q14-15;q23-24) was detected in two tumors, complex aberrations involving both 12q14-15 and 14q23-24 were also present in two, and rearrangements of 12q without concomitant 14q changes were seen in another two myomas. Rearrangements of 6p were present in five tumors, and trisomy 12 was found in two. More than one abnormality could be detected in 17 leiomyomas. Evidence of clonal evolution in the form of subclones was found in eight tumors, all of which were cellular and had histologically detectable mitotic activity. In addition to their clonal complexity, these myomas also frequently exhibited clonal telomeric associations (four tumors) and ring chromosome formation (three tumors; twice affecting chromosome 1). Monosomy 22 occurred as a secondary abnormality in three tumors; it, too, may reflect a preferred pathway in the karyotypic evolution of uterine leiomyomas.

Chromosome Aberrations↗
PubMed1991

A radiographic study of condyle position at various depths of cut in dry skulls with axially corrected lateral tomograms.

Fifty dry skulls were evaluated by means of submental vertex radiographs and axially corrected tomograms. The condyles were classified into four groups according to anterior surface and shape as viewed on the submentovertex radiograph. Thirty condyles were classified as having a flat anterior surface, 27 as convex, 19 as concave, and 24 as triangular. The analysis of variance for the depth of cut demonstrated (1) no statistically significant difference between the condyle/fossa relationship at the various depths of cut for the convex, flat, and triangular condyles and (2) a statistically significant difference between the condyle/fossa relationship of the concave condyles. The difference was significant at the p = 0.107 level for the anterior joint space (A), and at the p = 0.0671 level for the posterior joint space (B). The analysis of variance, in regard to the subject variable, demonstrated a statistically significant difference at the p = 0.0001 level for all condyles.

Analysis of Variance↗
PubMed1990

Complex chromosome rearrangements involving 12q14 in two uterine leiomyomas.

Cytogenetic analysis of short-term cultures from 10 uterine leiomyomas revealed normal karyotypes in 8 and clonal complex chromosome rearrangements in 2 tumors. In both leiomyomas with clonal abnormalities, 12q14, but not 14q22-24, was involved in translocations with 1q43 in one tumor and with 12q24 in the other. Additional chromosome abnormalities were found in both cases: 1-5 rings and monosomy of chromosome 9 in case 1, and complex numerical and structural abnormalities of chromosomes 1, 6-8, 11, 13, 16, 17, and 22 in case 2. The consistent cytogenetic rearrangement of 12q14 in uterine leiomyomas, sometimes without concomitant 14q changes, indicates that a gene of critical importance for leiomyoma development may be found in this band.

Adult↗
PubMed1990

High resolution mapping of consistent leiomyoma breakpoints in chromosomes 12 and 14 to 12q15 and 14q24.1.

A 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.

Chromosome Aberrations↗
PubMed1990

Parallel karyotypic evolution and tumor progression in uterine leiomyoma.

Cytogenetic evidence of clonal evolution was detected in five uterine leiomyomas. In two tumors, two clones were found, the third tumor had four, the fourth had nine, and the fifth had 12 clones. The first tumor had trisomy 12 as the primary anomaly and a sideline that also contained a del(7)(q21q31). Both clones of the second tumor had three structural changes in common but differed by the presence in the more advanced clone of an inv(7)(q31q34). Two cytogenetically unrelated pairs of clones were seen in the third tumor. One clone had a stemline of 46 and an r(1); a sideline had developed through duplication of this clone. The other pair had a del(7)(q21q31) in common. The last two tumors both had t(12;14)(q14-15;q23-24) as the primary abnormality. They also had a high frequency of telomeric associations that involved certain chromosome arms only. One of the secondary changes in the fourth tumor was a del(7)(q21q31); the principal secondary change in the fifth case was a ring chromosome 1 of variable size in the different clones. The analysis of these five uterine leiomyomas and the collation of the results with previously obtained data lead us to conclude that del(7)(q21q31) is secondary to t(12;14) and + 12 in this tumor type, and that ring formation involving chromosome 1 material, often with duplication of segments, is a common phenomenon during clonal evolution. The fact that the tumors were classified as cellular and had an increased mitotic rate indicates a parallel development between histologically detectable tumor progression and cytogenetically recognizable clonal evolution in uterine leiomyomas.

Chromosome Aberrations↗
PubMed1989

Mixed lineage leukemia with cytogenetically unrelated abnormal clones.

We present a case of acute leukemia with morphologic, cytochemical, and immunophenotypic markers indicating that the population of blasts have characteristics of lymphoid and myelomonocytic origin. The cytogenetic study revealed the following mosaic abnormal karyotype: 46XX,dup(1)(q21----32)/46,XX,dup(11)(q13----25)/47,XX,trip(11) (q13----25),+der(17)t(17;?) (q24;?). The two clones involving #11 are obviously related. It is reasonable to assume that the third clone is an evolutionary result of the second one. Because no cytogenetic similarities were found among the first clone and the other two, we suggest that this mixed leukemia was of biclonal origin. To our knowledge, acute leukemia with mixed lineage characteristics and with the simultaneous presence of cytogenetically unrelated clones has not previously been reported.

Adult↗
PubMed1983

Karyotypic abnormalities of squamous cell carcinoma of the oral cavity.

The karyotypic abnormalities in 18 squamous cell carcinomas of the oral cavity were studied in unbanded chromosomes on direct preparations of the tumor material. The chromosome counts revealed a great variability in the number of chromosomes per cell of each tumor, the range being from 31 to 148 in all cases studied. The modal population of cells was diploid in five cases, triploid in eight cases, tetraploid and pentaploid in one case each. Reduction of the number of chromosomes was more consistently observed in groups A and B, frequently involving chromosome No 1 and increases in groups C, D, E, F and G. Markers were frequently present, the most common being an almost metacentric chromosome of the size of the chromosomes of Group C.

Aged↗
PubMedDate not supplied

Evaluation of breast cancer polyclonality by combined chromosome banding and comparative genomic hybridization analysis.

Cytogenetically unrelated clones have been detected by chromosome banding analysis in many breast carcinomas. Because these karyotypic studies were performed on short-term cultured samples, it may be argued that in vitro selection occurred or that small clones may have arisen during culturing. To address this issue, we analyzed 37 breast carcinomas by G-banding and comparative genomic hybridization (CGH), a fluorescent in situ hybridization--based screening technique that does not require culturing or tumor metaphases. All but two of the 37 karyotypically abnormal cases presented copy number changes by CGH. The picture of genomic alterations revealed by the two techniques overlapped only partly. Sometimes the CGH analysis revealed genomic imbalances that belonged to cell populations not picked up by the cytogenetic analysis and in other cases, especially when the karyotypes had many markers and chromosomes with additional material of unknown origin, CGH gave a more reliable overall picture of the copy number gains and losses. However, besides sometimes revealing cell populations with balanced chromosome aberrations or unbalanced changes that nevertheless remained undetected by CGH, G-banding analysis was essential to understand how the genomic imbalances arose in the many cases in which both techniques detected the same clonal abnormalities. Furthermore, because CGH pictures only imbalances present in a significant proportion of the test sample, the very detection by this technique of imbalances belonging to apparently small, cytogenetically unrelated clones of cells proves that these clones must have been present in vivo. This constitutes compelling evidence that the cytogenetic polyclonality observed after short-term culturing of breast carcinomas is not an artifact.

Breast Neoplasms↗
PubMedDate not supplied

CRD-BP: a c-Myc mRNA stabilizing protein with an oncofetal pattern of expression.

The Coding Region Determinant-Binding Protein (CRD-BP) is an RRM and KH-domain-containing protein that recognizes specifically at least three RNAs. It binds to one of the two c-myc mRNA instability elements, to the 5'Un Translated Region (UTR) of the leader 3 IGF-II mRNA and to the oncofetal H19 RNA. CRD-BP has been assigned a role in stabilizing c-myc mRNA by preventing its endonucleolytic cleavage and in repressing the translation of the leader 3 IGF-II mRNA, the major embryonic species of this message. CRD-BP is normally expressed only in fetal tissues. However, its expression is detected in primary tumors and transformed cell lines of different origins. The vast majority of colon (80%) and breast (60%) tumors and sarcomas (73%) express CRD-BP whereas in other tumor types, for example prostate carcinomas, its expression is rare. CRD-BP expression has also been detected in benign tumors such as breast fibroadenomas, meningiomas and other benign mesenchymal tumors, implying a role for this gene in abnormal cell proliferation. In breast carcinomas, CRD-BP expression and or gene copy number gains in the region encompassing the c-myc locus were detected in approximately 75% of tumors, implying that the deregulated expression of c-myc may be more widespread than previously believed. Infiltrated lymph nodes, corresponding to CRD-BP-positive primary tumors, were also found positive indicating that monitoring for CRD-BP could prove useful for the detection and monitoring of disseminated disease.

Animals↗