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N Pandis

Publications and source records attributed to N Pandis.

At least 19 recordsLinked to original sources
PubMed2006

Maxillary incisor torque with conventional and self-ligating brackets: a prospective clinical trial.

OBJECTIVES: To test the hypothesis that the engagement mode of wire to bracket affects the buccolingual inclination of maxillary incisors in extraction and non-extraction treatment with self-ligating and conventional brackets. DESIGN: A randomized clinical trial employing a random distribution of variables among the studied populations. SETTING AND SAMPLE POPULATION: Private practice of one author. A total of 105 patients followed prospectively, were divided into two groups based on the inclusion of extraction in the treatment planning. These groups were further divided in two subgroups each, one receiving a self-ligating bracket and the other treated with a conventional Edgewise appliance of the same slot size and prescription. EXPERIMENTAL VARIABLE: Difference in the buccolingual inclination of maxillary incisors before and after treatment with the two appliances across the two treatment groups (extraction and non-extraction). OUTCOME MEASURE: Angular measurements of the Sella-Nasion and Nasion-A point to maxillary incisor axis. RESULTS: No difference was found in the mean difference of the two angles measured for the two bracket groups studied. CONCLUSION: Self-ligating brackets seem to be equally efficient in delivering torque to maxillary incisors relative to conventional brackets in extraction and non-extraction cases.

Adolescent↗
PubMed2004

Assessment of clonal relationships in ipsilateral and bilateral multiple breast carcinomas by comparative genomic hybridisation and hierarchical clustering analysis.

The issue of whether multiple, ipsilateral or bilateral, breast carcinomas represent multiple primary tumours or dissemination of a single carcinomatous process has been difficult to resolve, especially for individual patients. We have addressed the problem by comparative genomic hybridisation analysis of 26 tumours from 12 breast cancer patients with multiple ipsilateral and/or bilateral carcinoma lesions. Genomic imbalances were detected in 25 of the 26 (96%) tumours. Using the genomic imbalances detected in these 26 lesions as well as those previously found by us in an independent series of 35 unifocal breast carcinomas, we compared a probabilistic model for likelihood of independence with unsupervised hierarchical clustering methodologies to determine the clonal relatedness of multiple tumours in breast cancer patients. We conclude that CGH analysis of multiple breast carcinomas followed by unsupervised hierarchical clustering of the genomic imbalances is more reliable than previous criteria to determine the tumours' clonal relationship in individual patients, that most ipsilateral breast carcinomas arise through intramammary spreading of a single breast cancer, and that most patients with bilateral breast carcinomas have two different diseases.

Adult↗
PubMed2002

Germ line BRCA1 & BRCA2 mutations in Greek breast/ovarian cancer families: 5382insC is the most frequent mutation observed.

BRCA1 and BRCA2 genes were screened for loss-of-function mutations in a series of 85 patients having at least one first- or second-degree relative affected by breast and/or ovarian cancer. All BRCA1 exons and BRCA2 exons 10 and 11 were screened with a combination of methods including SSCP, PTT and direct sequencing. We have found disease-associated mutations in 14 families (16.5%), eleven in BRCA1 and three in BRCA2. The known founder mutation 5382insC of BRCA1 was identified in seven unrelated families. The other mutations identified include the non-sense R1751X, the splice junction variant 5586G>A of BRCA1 and three frameshifts, 2024del5, 3034del4, and 6631del5, of BRCA2. Nine out of these 14 families had a family history of three or more breast/ovarian cancer cases. A large number of polymorphic or unclassified variants is also reported. Combined with our previously published data 5382insC was found in nine out of 20 families (45%), suggesting that this mutation may represent a common founder mutation in the Greek population.

Adult↗
PubMed2001

Are some breast carcinomas polyclonal in origin?

This editorial comments on the important study by Going et al. published in the present issue of the Journal [1]. Using a molecular genetic assay based on the X-chromosome inactivation principle, they found that 4 out of 12 breast carcinomas examined exhibited what the authors call "clonal mosaicism" that is, two or more monoclonal samples were mosaic (polyclonal) in respect of X chromosome inactivation between separate, morphologically homogeneous tumour areas. The authors very carefully discuss potential methodological errors that could have led to this surprising finding, which seems to run counter to the almost unanimously held conviction that carcinomas are monoclonal in origin, but none of these potential errors would explain the results. As often in such situations, the authors prudently state that further studies using independent analytical techniques are necessary to find out whether a significant proportion of mammary carcinomas are indeed polyclonal. However, there already exists a substantial body of evidence from cytogenetic studies of breast cancers indicating that many of them are polyclonal. Although there is still room for interpretation and some doubt remains as to exactly which role should be ascribed to the observed clonal heterogeneity in our models of carcinogenesis, it seems obvious that more attention than before ought to be paid to this now well documented fact.

Breast Neoplasms↗
PubMed2001

C-MYC and IGF-II mRNA-binding protein (CRD-BP/IMP-1) in benign and malignant mesenchymal tumors.

Mouse coding region determinant-binding (mCRD-BP) and human IGF-II mRNA-binding 1 (hIMP-1) proteins are orthologous mRNA-binding proteins that recognize c-myc and IGF-II mRNA, respectively, and regulate their expression posttranscriptionally. Here, we confirm that human CRD-BP/IMP-1 binds to c-myc mRNA and that it is predominantly expressed in fetal tissues. Moreover, hCRD-BP/IMP-1 expression was detected in cell lines of neoplastic origin and in selected primary tumors. In a series of 33 malignant and 10 benign mesenchymal tumors, 73% and 40%, respectively, were found to express hCRD-BP/IMP-1. In particular, expression was significant in 14 Ewing's sarcomas, all of which were positive. The data suggest that hCRD-BP/IMP-1 plays a role in abnormal cell proliferation in mesenchymal tumors.

Amino Acid Motifs↗
PubMed2000

Cytogenetic heterogeneity and clonal evolution in synchronous bilateral breast carcinomas and their lymph node metastases from a male patient without any detectable BRCA2 germline mutation.

Two synchronous bilateral breast carcinomas and their matched lymph node metastases from a 70-year-old man were cytogenetically analyzed. All four tumors were near-diploid, and except for the primary tumor from the right breast, had a 45,X,-Y clone in common. The loss of the Y chromosome was, however, common to all four tumors, whereas metaphase cells from peripheral blood lymphocytes showed a normal 46, XY chromosome complement. The primary tumor from the right breast was monoclonal, with loss of the Y chromosome and gain of 1q, whereas its metastasis had two related clones: the 45,X,-Y clone, and the other a more complex version of the clone in the primary tumor, with inv(3), -14, and del(16)(q13) as additional changes. The primary tumor from the left breast was polyclonal with three unrelated clones: 45,X,-Y/45,XY,-18/47,XY,+20, two of which were present in its metastasis. DNA flow cytometric studies showed diploidy for both primary tumors. No mutation in the BRCA2 gene was found on analysis of DNA from peripheral blood lymphocytes. The present findings show that del(16)(q13) is a recurrent finding among male breast carcinomas and that some of the primary cytogenetic abnormalities, as well as the pattern of chromosomal changes during the progression of sporadic breast carcinoma in the male, are similar to those in the female. In addition, the loss of the Y chromosome in the tumors but not in peripheral blood lymphocytes, suggests a possible role for this abnormality in the pathogenesis of male breast carcinoma.

Aged↗
PubMed2000

Spectral karyotyping and chromosome banding studies of primary breast carcinomas and their lymph node metastases.

Three primary breast tumors and their lymph node metastases were characterized by G-banding, spectral karyotyping (SKY), and fluorescence in situ hybridization (FISH). In each case, the karyotypic abnormalities detected were similar in the primary tumor and its matched metastasis. Two of the pairs had near-diploid karyotypes with three to four chromosomal aberrations, whereas the third pair had a near-pentaploid chromosome content and many marker chromosomes in the primary tumor and a near-tetraploid chromosome number with almost the same marker chromosomes in the metastasis. SKY and FISH confirmed the karyotypic similarities between the primary tumors and their metastases and, in addition, improved the identification and characterization of marker chromosomes. One of the tumor pairs with near-diploid karyotypes had gain of 8q, 16q, and 17q, whereas the other had gain of 1q and chromosome 8 material in the form of ring chromosomes. The third pair had more complex chromosomal translocations and numerical changes resulting in net gain of material from chromosomes X, 1, 2, 6, 7, 14, 16, 19, and 20, and chromosome arms 8q and 11q, as well as net loss of material from chromosomes 3, 13, 18, 21, and 22. The present study underscores the need to combine conventional chromosome banding and molecular cytogenetic techniques in the cytogenetic analysis of solid tumors.

Breast Neoplasms↗
PubMed2000

High frequency of clonal chromosome abnormalities in prostatic neoplasms sampled by prostatectomy or ultrasound-guided needle biopsy.

Cancer of the prostate remains poorly characterized cytogenetically. This is due in part to methodological problems and in part to the paucity of radical prostatectomies, until now the main source of material for cytogenetic analyses. We have improved existing techniques for the culturing of prostatic neoplasms removed by radical prostatectomy or sampled by ultrasound-guided needle biopsy. Successful short-term cultures were obtained from all 10 prostatectomy samples and from all 10 ultrasound-guided needle biopsies, always with a pure epithelial morphology. Of the 19 cases yielding a sufficient number of high-quality metaphases for chromosome banding analysis, the single atypical epithelial hyperplasia had a normal karyotype, whereas both prostatic intraepithelial neoplasias and 12 of 16 (75%) invasive carcinomas were shown to have clonal abnormalities. Ten of the 12 (83%) karyotypically abnormal invasive carcinomas presented structural chromosomal rearrangements. A recurrent deletion, del(10)(p13), was seen in three tumors; in one of them the terminal nature of the deletion was confirmed by two-color FISH. A del(17)(p11) was seen in one PIN lesion, but since the analysis of exons 4-8 of the TP53 tumor suppressor gene revealed no mutations, there probably was no inactivation of the second TP53 allele. Our study thus leads to the following main conclusions. First, better culturing methods allow the detection of abnormal karyotypes in a much higher percentage of prostatic neoplasms than has hitherto been possible. Second, ultrasound-guided needle biopsies of prostatic neoplasms are a sufficient source of material for cytogenetic analysis. Third, a terminal deletion of the short arm of chromosome 10, del(10)(p13), seems to identify a subgroup of prostatic cancer.

Biopsy, Needle↗
PubMed1999

Different patterns of chromosomal imbalances in metastasising and non-metastasising primary breast carcinomas.

In an attempt to identify chromosomal abnormalities that may be associated with a metastatic phenotype, we investigated the pattern of chromosomal gains and losses in 66 node-positive and 63 node-negative primary breast carcinomas. For both subgroups of tumours, losses were more common than gains and the losses were most often the result of structural aberrations. The exceptions were the long arm of chromosome 1, and chromosomes 7, 8, 12, 18 and 20, which were more often gained than lost. Node-negative tumours were preferentially characterised by loss of 6q10-21 and loss of 16q, whereas loss of chromosome 18 was significant for node-positive tumours. Other aberrations that tended to be associated with one of the phenotypes, though not statistically significant, were gain of chromosome 18 and loss of chromosome 10 in node-negative tumours, and gain of chromosome 14 and loss of 12p in node-positive tumours. Our data show that there are differences among the genetic lesions present in node-negative and node-positive breast tumours. Int. J. Cancer (Pred. Oncol.) 84:370-375, 1999.

Breast Neoplasms↗
PubMed1999

Recurrent t(16;17)(q22;p13) in aneurysmal bone cysts.

Aneurysmal bone cyst (ABC) is a benign bone lesion for which no previous cytogenetic data exist. We describe the finding of clonal chromosome aberrations in three tumors; two had a t(16;17)(q22;p13) as the sole anomaly, and the third had a del(16)(q22) as the only change. These findings show that somatic mutations contribute to the development of ABC and furthermore indicate that bands 16q22 and 17p13 may harbor genes of importance in this process.

Adolescent↗
PubMed1999

Multiple polysomies in breast carcinomas: preferential gain of chromosomes 1, 5, 6, 7, 12, 16, 17, 18, and 19.

Chromosome G-banding analysis of metaphase cells from 16 primary breast carcinomas revealed the presence of multiple polysomies in near-diploid as well as in polyploid cells. Chromosome 17 was preferentially gained in 7 tumors, followed in frequency by chromosomes 1, 12, and 19 (5 tumors each), and chromosomes 5, 6, 7, 16, and 18 (4 tumors each). Eleven of the 16 carcinomas had, apart from the clones exhibiting the numerical gains, other unrelated clones. Nine of these 11 cases had clones with structural chromosome aberrations, 5 of which had structural aberrations involving the short arm of chromosome 3. The biologic significance, if any, of this seemingly nonrandom coexistence of multiple polysomies with structural aberrations of 3p is at present not known. The pattern of numerical chromosome aberrations observed in the present study is comparable to previous results from fluorescence in situ hybridization (FISH) studies, with the use of centromeric probes on interphase cells. However, unlike FISH studies, which have been focused on chromosomes 1, 3, 7, 8, 11, 16, and 17, the cytogenetic results reveal that other chromosomes also may be nonrandomly gained as part of multiple polysomies in breast carcinomas. In addition, the tumors with multiple polysomies were generally of high histologic grade and with metastasis to axillary lymph nodes, suggesting that multiple wholechromosome gains may be a pathway of genetic evolution or progression or both in some breast carcinomas.

Adult↗
PubMed1999

Karyotypic evolution in breast carcinomas with i(1)(q10) and der(1;16)(q10;p10) as the primary chromosome abnormality.

The pattern of clonal karyotypic evolution in breast carcinomas carrying an i(1q) or a der(1;16)(q10;p10) as the primary chromosome abnormality was assessed in a series of 42 tumors, including 8 described here for the first time, with either or both (3 tumors) of them defining cytogenetic features. Evidence of clonal evolution was seen in somewhat more than half of all cases in both subgroups. The secondarily acquired aberrations appeared to be nonrandom in distribution. This was especially so for structural rearrangements of 11q leading to loss of material from this arm, which were clearly more common in both subgroups than in karyotypically abnormal breast carcinomas in general. Other deviations from random were less certain but seemed to include the frequent occurrence of +20 in tumors with i(1q) and +7 in tumors with der(1;16)(q10;p10). That differences were observed between i(1q) carcinomas and der(1;16)(q10;p10) carcinomas with regard to their patterns of clonal evolution hints that the pathogenetic effect of the primary change in these two situations may be more than the mere gain of an extra copy of 1q.

Breast Neoplasms↗
PubMed1999

Chromosomal aberrations in breast cancer: a comparison between cytogenetics and comparative genomic hybridization.

The analysis of chromosomal imbalances in solid tumors using comparative genetic hybridization (CGH) has gained much attention. A survey of the literature suggests that CGH is more sensitive in detecting copy number aberrations than is karyotyping, although careful comparisons between CGH and cytogenetics have not been performed. Here, we compared cytogenetics and CGH in 29 invasive breast cancers after converting the karyotypes into net copy number gains and losses. We found 15 tumors (56%) with a significant agreement between the two methods and 12 tumors (44%) where the methods were in disagreement (two cases failed CGH analysis). Interestingly, in 13 of the 15 tumors where the two methods were concordant, there was also a strong correlation between chromosome index and DNA index by flow cytometry. In the opposite situation, i.e., when chromosome and DNA indices were not matching, there was disagreement between cytogenetics and CGH in 10 of the 12 tumors. Of the discordant cases, all except one had a "simple" abnormal karyotype. Unresolved chromosomal aberrations (marker chromosomes, homogeneously staining regions, double minutes) could not completely explain the differences between CGH and karyotyping. A likely explanation for the discrepancies is that the methods analyzed different cell populations. Gains and losses found by CGH represented the predominant (often aneuploid) clone, whereas the abnormal, near-diploid karyotypes represented minor cell clone(s), which, for unknown reasons, had a growth advantage in vitro.

Aneuploidy↗
PubMed1998

Cytogenetic analysis of colorectal adenomas: karyotypic comparisons of synchronous tumors.

The phenotypic progression of colorectal tumors is driven by their step-by-step acquisition of genomic alterations. These pathogenetically important mutations are at the same time markers of tumor clonality. The aim of this study was to describe the clonal relation among synchronous colorectal adenomas. Twenty-four colorectal adenomas from 11 patients were subjected to chromosome banding analysis. Clonal chromosome abnormalities were found in 20 tumors. Recurrent structural rearrangements involved chromosomes 1, 13, 17, and 18. The most common numerical changes were gain of chromosomes 7, 13, 20, and 3 and loss of chromosome 18. Eight adenomas had subclones as evidence of clonal evolution. Similar clones in separate polyps were seen in tumors from 6 patients; these adenomas were always located in the same part of the large bowel. In 2 patients, both with one rectal adenoma and one adenoma in the colon, no karyotypic similarity between the lesions was found. Our findings indicate that whereas close, but macroscopically distinct, synchronous colorectal adenomas usually have a common pathway of progression, perhaps even the same clonal origin, large bowel adenomas at a considerable distance from one another exhibit karyotypic differences, indicating that they arise independently.

Adenoma↗
PubMed1998

Cytogenetic findings in invasive breast carcinomas with prognostically favourable histology: a less complex karyotypic pattern?

Seventeen invasive primary breast carcinomas of histological types usually considered to be prognostically favourable (2 medullary, 3 papillary, 3 tubular, and 9 mucinous carcinomas) were analysed as part of an ongoing study of the cytogenetics of breast cancer. Thirteen of the tumours (7 mucinous, 2 medullary, 2 papillary, and 2 tubular carcinomas) showed clonal chromosome aberrations. Trisomy 7 and i(1q) were present as sole and recurrent aberrations in the mucinous tumours. The 2 tubular carcinomas and I papillary carcinoma had simple numerical changes only, whereas the second papillary tumour had a balanced translocation as the sole anomaly. Both medullary carcinomas had chromosome numbers in the triploid range, with clones displaying structural and numerical changes. Our data, especially when collated with information on previously published cases of mucinous, papillary, tubular, and medullary breast carcinomas, show that the former 3 histological types, in keeping with their recognised prognostic advantage, appear to exhibit relatively simple karyotypic changes, i.e., numerical aberrations, balanced translocations, and near-diploid chromosome numbers. Medullary carcinomas on the other hand, appear to have more complex karyotypes, similar to those described for the more common ductal and lobular subtypes of breast carcinoma.

Adenocarcinoma, Mucinous↗