bluuebunny/crossref_metadata_2025_split huggingface dataset:
Trisomy 7: A potential cytogenetic marker of human prostate cancer progression
Authors: Bandyk Mark G. , Pisters Louis L. , Von Eshenbach Andrew C. , Chung Leland W. K. , Zhao Lian , Liang Jan C. , Troncoso Patricia , Palmer Judy L. 
Published: February 2007

AbstractWe used the fluorescence in situ hybridization (FISH) method to show that chromosome 7 trisomy is associated with the progression of human prostate cancer. Thirty‐six specimens including 15 primary prostate carcinomas, 16 metastatic lesions, and 5 normal prostate tissues, as well as 2 prostate carcinoma cell lines of different tumorigenic potential, were examined for chromosome 7 aneuplaidy. Our results showed that the androgen‐unresponsive tumorigenic cell line PC‐3 exhibited a significantly higher ratio of chromosome 7 to total chromosome number than the androgen‐responsive nontumorigenic cell line LNCaP (P = 0.001). In prostate specimens, the frequency of trisomy 7 cells was significantly increased (P < 0.05) in the advanced stage tumors (C and D1) but not in the early (6) stage tumors or normal prostatic tissue. Furthermore, metastases showed a higher frequency of trisomy 7 cells than primary tumors (P = 0.005). In 2 patients with paired primary and metastatic tumors, trisomy 7 cells increased from 4‐7% in the primary tumors to 42‐45% in the metastatic tumor cells in the bone marrow. Therefore, our data suggest that trisomy 7 may be a common feature associated with local and metastatic progression and serve as a novel marker for human prostate cancer progression. Genes Chrom Concer 9:/9‐27 (1994). © 1994 Wiley‐Liss, Inc.
Molecular and cytogenetic analysis of chromosome 9 deletions in 75 malignant gliomas
Authors: Josefa Bello M. , Pestaña Angel , Rey Juan A. , De Campos Jose M. , Vaquero Jesus , Elena Kusak M. , Sarasa Jose L. 
Published: February 2007

AbstractA deletion mapping analysis of chromosome 9 has been performed on a series of 75 samples derived from malignant gliomas. A total of 27 tumors displayed different deletions for the loci studied (D9S1, NRASL1, D9S18, IFNA, and IFNB1). In most instances, losses involving the markers located on the short arm of chromosome 9 were observed, and only two samples were characterized by losses of the short and long arms. Either partial or complete homozygous deletions of IFN genes were observed in 15 cases, and 12 other samples showed hemizygous deletions for these genes. The results show that the 9p abnormalities are not exclusive to high‐grade astrocytic tumors, as some low‐grade samples (two astrocytomas grade II and six oligodendrogliomas) displayed this anomaly which, in a few instances, was the sole abnormality detected. Genes Chrom Cancer 9:33‐41 (1994). © 1994 Wiley‐Liss, Inc.
Chromosome abnormalities in pancreatic adenocarcinoma
Authors: Griffin Constance A. , Long Patricia P. , Morsberger Laura A. , Douna‐Issa Fadia , Hruban Ralph H. , Yeo Charles J. 
Published: February 2007

AbstractAdenocarcinoma of the pancreas is the fifth most common cause of cancer deaths in the United States, yet few cytogenetic studies of this tumor have been reported. We analyzed 26 primary tumors to identify which chromosome abnormalities occur most frequently in this neoplasm. One carcinoma was well differentiated and mucin producing, 18 were moderately well differentiated, and seven were poorly differentiated. Only normal karyotypes were obtained from nine carcinomas. The remaining 17 carcinomas frequently had normal metaphase cells in addition to simple to highly complex karyotypes. The modal chromosome number in 20 carcinomas was diploid or near‐diploid; four carcinomas had both a major near‐diploid and near‐triploid or near‐tetraploid component, and two were near‐tetraploid. Numerical abnormalities included loss of whole copies of chromosomes 6, 17, and 18, and gains of chromosome 20. Structural abnormalities were frequent, with 1p, 2p, 3p, 4q, 6q, 7q, 1 1q, and 17p recurrently involved. Results of this study were combined with karyotypes of 19 other primary adenocarcinomas of the pancreas reported in the literature. The combined data involving 1 17 breakpoints suggest that careful analysis of chromosome 20, proximal 1 q. 6q, proximal 8p. and proximal 17p could be productive in defining genes involved in adenocarcinoma of the pancreas. Genes Chrom Cancer 9:93‐100 (1994).© 1994 Wiley‐Liss, Inc.
At least two different regions are involved in allelic imbalance on chromosome arm 16q in breast cancer
Authors: Cleton‐Jansen Anne‐Marie , Moerland Elna W. , Kuipers‐Dijkshoorn Net J. , Cornelisse Cees J. , Devilee Peter , Callen David F. , Sutherland Grant R , Hansen Bettine 
Published: February 2007

AbstractLoss of heterozygosity (LOH) or allelic imbalance, the latter term referring to both loss and gain of an allele, on the long arm of chromosome 16 has been repeatedly found in cancers of, e.g., the breast and prostate. This indicates the presence of one or more tumor suppressor genes on 16q. To locate the gene(s) more precisely, a detailed allelic imbalance map of 20 polymorphic markers on this chromosome arm was made for 79 sporadic breast carcinomas. LOH of one or more markers was found in 63% of the tumors. Some had allelic imbalance on a region of 16q which failed to overlap with the LOH in other tumors. We therefore assigned two separate “smallest regions of overlap” to 16q and suggest that this chromosome arm contains at least two different tumor suppressor genes. Genes Chrom Cancer 9:101‐107 (1994).© 1994 Wiley‐Liss, Inc.
Constitutional DNA‐level aberrations in chromosome 22 in a patient with multiple meningiomas
Authors: Deprez Ronald H. Lekanne , Groen Nicole A. , Louz Derrick , Van Der Kwast Theo H. , Zwarthoff Ellen C. , Hagemeijer Anne , Van Drunen Ellen , Bootsma Dirk , Koper Jan W. , Avezaat Cees J. J. 
Published: February 2007

AbstractWe describe a patient who developed multiple meningiomas but had no clear evidence of neurofibromatosis type 2. Four of the tumors, derived from three different sites, were analyzed cytogenetically and/or at the DNA level using chromosome 22 specific probes. All four tumors showed loss of the same copy of chromosome 22. On the chromosome that was retained in the tumors, we found two constitutional aberrations, a 1.5 kb deletion and a point mutation. The patient had inherited both alterations from her father. The father has not developed any meningiomas so far but he has been treated for a well‐differentiated adenocarcinoma of the lung and a brain metastasis from this tumor. The mother and 75 unrelated individuals did not show any of the chromosome 22 alterations. The multiple tumors found in the patient suggest that she has a predisposing gene for the development of meningiomas. The finding that all investigated tumors lost the same, constitutionally normal copy of chromosome 22 could indicate that the predisposing gene resides on chromosome 22 and was affected by the constitutional mutations. Genes Chrom Cancer 9:124‐128 (1994).© 1994 Wiley‐Liss, Inc.
Amplification of the anonymous marker D17S67 in malignant astrocytomas
Authors: Bijlsma Emilia K. , Westerveld Andries , Hulsebos Theo J. M. , Leenstra Sieger , Bosch D. Andries 
Published: February 2007

AbstractLoss of heterozygosity (LOH) for chromosome arms 9p, 10p, 10q, and 17p and amplification of the epidermal growth factor receptor (EGFR) gene have been identified as frequent genetic changes in malignant astrocytomas. We have found amplification of the anonymous marker D17S67 on chromosome arm 17p in 10% (3 of 30 cases) of astrocytomas of the highest malignancy grade. The tumors with D17S67 amplification displayed other genetic changes on chromosome 17, including additional amplifications and deletions. All three patients with D17S67 amplification developed severe brain edema and died within I month after operation. Genes Chrom Cancer 9:148‐152 (1994). © 1994 Wiley‐Liss, Inc.
A 3‐Mb physical map of the chromosome region 8p21.3‐p22, including a 600‐kb region commonly deleted in human hepatocellular carcinoma, colorectal cancer, and non‐small cell lung cancer
Authors: Fujiwara Yoshiyuki , Ohata Hiroyuki , Emi Mitsuru , Okui Keiko , Koyama Kumiko , Tsuchiya Eiju , Nakajima Toshifusa , Monden Morito , Mori Takesada , Kurimasa Akihito , Oshimura Mitsuo , Nakamura Yusuke 
Published: February 2007

AbstractTo isolate a putative tumor suppressor gene(s), we have constructed a physical map and a detailed deletion map of chromosome region 8p21.3‐p22, where loss of heterozygosity (LOH) has been frequently seen in human hepatocellular carcinomas (HCC), colorectal cancers (CRC), and non‐small cell lung cancers (NSCLC). The smallest commonly deleted region at 8p21.3‐p22 in HCC and CRC was between the loci defined by CI8‐245 and CI8‐2644; in NSCLC, a region between CI8‐1051 and CI8‐2644 was commonly deleted. A contiguous physical map of 12 cosmid markers in the 8p21.3‐p22 region was constructed by means of multi‐color fluorescence in situ hybridization (FISH) and pulsed‐field gel electrophoresis (PFGE). On the basis of this physical map, which spans roughly 3.1 Mb, the estimated sizes of the commonly deleted regions were at most 1.2 Mb in HCC and CRC and 0.6 Mb in NSCLC. As four of the 12 physically ordered markers are located within the 0.6 Mb region commonly deleted in all three tumor types, nearly one fourth to one fifth of the target region has already been covered with cosmid inserts. Genes Chrom Cancer 10:7–14 (1994). © 1994 Wiley‐Liss, Inc.
Identification of genetically aberrant cell lineages in Wilms' tumors
Authors: Weremowicz Stanislawa , Kozakewich Harry P. , Haber Daniel , Park Seon , Morton Cynthia C. , Fletcher Jonathan A. 
Published: February 2007

AbstractMost Wilms' tumors contain several predominant cell types, of which a primitive blastemal population is often the most prominent. Other typical components include undifferentiated mesenchymal and epithelial cells, but it has not been demonstrated that these components are neoplastic. We used a combined cytogenetic and fluorescence in situ hybridization approach to determine the clonal relationship of different cell populations within six Wilms' tumors. Clonal numerical chromosome aberrations in three Wilms' tumors were found in blastemal cells, but not in mesenchymal cells. Loss of one WTl allele in two other tumors was detected in both blastemal and mesenchymal cells. Tetrasomy 18 in a sixth case was observed in mesenchymal and epithelial cells; blastemal cells could not be evaluated in this tumor. These findings demonstrate that mesenchymal and epithelial cells in some Wilms' tumors are neoplastic. Different histologic components in some Wilms' tumors derive from a single chromosomally aberrant ancestor which is most likely to be the primitive blastemal cell. Genes Chrom Cancer 10:40–48 (1994). © 1994 Wiley‐Liss, Inc.
Induction of senescence and control of tumorigenicity in BK virus transformed mouse cells by human chromosome 6
Authors: Gualandi Francesca , Morelli Cristina , Pavan Jorge V. , Rimessi Paola , Sensi Alberto , Bonfatti Alessandra , Gruppioni Rita , Possati Laura , Stanbridge Eric J. , Barbanti‐Brodano Giuseppe 
Published: February 2007

AbstractViral transformation models may be useful to detect and map human tumor suppressor genes. BK virus (BKV), a human papovavirus, readily transforms rodent cells but is unable to transform human cells, suggesting that oncosuppressive functions expressed in human cells control BKV oncogenic activity. We have transferred human chromosome 6 to BKV‐transformed mouse pRPcTlssI cells. The great majority of the colonies growing in selective medium degenerated by senescence. Only five hybrid pRPcTIssI/H6 clones maintained the immortalized phenotype of the recipient cell line. All the immortalized clones had two common regions of deletion involving bands 6q21–22 and the SOD2 gene in 6q25. Senescent colonies carried an intact chromosome 6. A specific human sequence in 6q21–22 was amplified by PCR in senescent cells, suggesting that this region harbors a gene inducing senescence. The SOD2 deletion confirms recent data on the role of the Mn‐dependent superoxide dismutase in inhibition of proliferation. The monochromosomic hybrids bearing a deleted chromosome 6 showed a reverted phenotype in vitro and a significantly longer latency period before they were tumorigenic in nude mice, indicating the presence of a tumor suppressor gene in the residual regions of chromosome 6. Molecular mapping suggests that this gene is located in 6q27. The BKV transformation model detects genes inducing senescence and tumor suppressor genes on human chromosome 6 and may represent a useful system to isolate and clone such genes. Genes Chromosom Cancer 10:77–84 (1994). © 1994 Wiley‐Liss, Inc.
Cell lineage involvement of recurrent chromosomal abnormalities in hematologic neoplasms
Authors: Knuutila Sakari , Teerenhovi Lasse , Larramendy Marcelo L. , Elonen Erkki , Franssila Kaarle O. , Nylund Stella J. , Timonen Time , Heinonen Kristiina , Mahlamäki Eija , Winqvist Robert , Ruutu Tapani 
Published: February 2007

AbstractAnalysis of most hematologic neoplasms indicates the involvement of one or more cell lineages in the bone marrow and/or the blood but rules out the involvement of all lineages in any one neoplasm. It is important to detect lineage involvement in order to clarify which stem cells are involved in leukemia, to predict prognosis, and to select appropriate treatment. Our aim was to study the cell lineage involvement of some of the recurrent chromosomal abnormalities seen in hematological neoplasms. The direct morphology‐antibody‐chromosomes (MAC) method was used. The deletion 20q in myeloproliferative diseases (MPD), the deletion of 5q and t(1;7) in myelodysplastic syndromes (MDS), and t(3;3) in acute myeloid leukemia subtype M7 (AML‐M7) were seen in all or at least in two myeloid lineages. These were interpreted as stem cell abnormalities. Deletion 13q in MPD, t(8;21) in AML‐M2 and t(15;17) in AML‐M3 were seen in granulocytic lineages only; t(14;18) in non‐Hodgkin's lymphoma and trisomy 12 as the sole abnormality in chronic lymphocytic leukemia (B‐CLL) were seen only in immunoglobulin light chain clonal B cells; inversion 14 in T‐CLL was seen only in T cells, whereas t(15;14) in acute lymphocytic leukemia with eosinophilia (ALL‐EO) was seen in lymphoid stem cells but not in mature granulocytes or lymphocytes. Additional abnormalities (in addition to the Philadelphia chromosome) in chronic myeloid leukemia (CML) were seen in all myeloid cell lineages and also in mature granulocytes, B cells, and large granular lymphocytes. Abnormalities in Hodgkin's disease were restricted to CD30‐positive Reed‐Sternberg cells. Trisomy 8 and monosomy 7 are abnormalities that may be present in either stem cells or any of the single cell lineages. Genes Chromosom Cancer 10:95–102 (1994). © 1994 Wiley‐Liss, Inc.
Some desmoid tumors are characterized by trisomy 8
Authors: Cin Paola Dal , Sciot Raf , Aly Magdy S. , Delabie Jan , Stas Margareta , De Wever Ivo , Van Damme Boudewijn , Van Den Berghe Herman 
Published: February 2007

AbstractTen desmoid tumors were examined by chromosome banding analysis and by in situ hybridization on short‐term cultures and frozen sections. Trisomy 8 was detected in four out of ten tumors, of which only one had shown trisomy 8 by karyotype analysis. Since trisomy 8 has been reported in superficial fibromatoses, which are clinically distinct but histologically similar to desmoid tumors, the occurrence of trisomy 8 in both may be a further indication of a close relationship. Genes Chromosom Cancer 10:131–135 (1994). © 1994 Wiley‐Liss, Inc.
TP53 alterations and clinical outcome in low grade astrocytomas
Authors: Kraus Jürgen A. , Bolln Carsten , Wolf Helmut K. , Neumann Jürgen , Kindermann Dietmar , Fimmers Rolf , Forster Frank , Baumann Axel , Schlegel Uwe 
Published: February 2007

AbstractThirty‐eight WHO grade II astrocytomas and 10 malignant recurrent gliomas in these patients were examined for the presence of TP53 alterations. Seventeen/38 low grade astrocytomas and 6/10 malignant recurrent tumors harbored mutations of the gene detected by SSCP analysis and direct sequencing of PCR products. TP53 mutations in five out of six high grade mutant tumors were already present in the corresponding low grade astrocytomas. In two cases, TP53 mutations present in the low grade astrocytoma could not be demonstrated in the recurrent glioma. Immunohistochemistry with two different antibodies to the human TP53 protein revealed nuclear immunoreaction of tumor cells in 11/38 low grade and in 8/10 recurrent tumors. There was no correlation between the presence of TP53 alteration and clinical course. We conclude that, although TP53 mutations are detectable in a substantial fraction of WHO grade II astrocytomas, they do not appear to play a role in the malignant progression of these tumors and they are not of prognostic significance. Genes Chromosom Cancer 10:143–149 (1994). © 1994 Wiley‐Liss, Inc.
Characterization of homogeneously staining regions in a small cell lung cancer cell line, using in situ hybridization with an MYCN probe
Authors: Dietzsch Erin , Lukeis Robyn E. , Vrazas Vickie , Hasthorpe Suzanne , Garson O. Margaret 
Published: February 2007

AbstractThe cell line CIPL38 was derived from the pleural effusion of a patient with small cell lung cancer. The karyotype was hyperdiploid and complex with a variable number of marker chromosomes. Two of the markers had large homogeneously staining regions (hsr), which were shown to consist of amplified MYCN by in situ hybridization. One hsr bearing a marker chromosome could not be identified with G‐banding, but the other was situated on a der(14). This was elucidated further with FISH analysis, which enabled the identification of sequences of chromosome I involved in a complex rearrangement with chromosome 14 and the hsr. Genes Chromosom Cancer 10:213–216 (1994). © 1994 Wiley‐Liss, Inc.
Fluorescence in situ hybridisation studies to characterise complete and partial monosomy 7 in myeloid disorders
Authors: Gibbons Barbara , Lillington Debra M. , Monard Simon , Young Bryan D. , Cheung Kan Luk , Lister T. Andrew , Kearney Lyndal 
Published: February 2007

AbstractEight patients with myeloid disorders characterised by a karyotype including apparent monosomy or partial monosomy 7, in the presence of a ring or marker chromosome, were investigated by fluorescence in situ hybridisation (FISH) with a chromosome 7 centromere‐specific probe and an Alu‐PCR derived chromosome 7 paint. In 4 of 5 cases a ring chromosome was shown to be of chromosome 7 origin; in one of these the apparent ring was shown to consist solely of chromosome 7 centromeric material, and in the fifth case the ring was derived from chromosome 18. In three cases monosomy 7 had arisen during the course of karyotype evolution and was clearly not the primary cytogenetic abnormality. One further case demonstrated fragmentation and cryptic translocation of chromosome 7 material. In the last case a chromosome described as der(I)t(I;7)(p II;pII) was redefined as dic(I;7)(pII;qII). The application of FISH has enabled a more accurate characterisation of chromosome abnormalities, and extended studies of this type may eventually lead to more precise prognostic groups defined by karyotype. Genes Chromosom Cancer 10:244–249 (1994). © 1994 Wiley‐Liss, Inc.
Analysis of androgen receptor DNA reveals the independent clonal origins of uterine leiomyomata and the secondary nature of cytogenetic aberrations in the development of leiomyomata
Authors: Mashal Robert D. , Fejzo Marlena L. Schoenberg , Friedman Andrew J. , Mitchner Natasha , Nowak Romana A. , Rein Mitchell S. , Morton Cynthia C. , Sklar Jeffrey 
Published: February 2007

AbstractUterine leiomyomata are thought to be monoclonal neoplasms. Accordingly, investigations of clonality with G6PD isoforms used as a marker for X chromosome inactivation have suggested independent origins for multiple tumors within individual uteri. However, results from a recent study assessing methylation differences between DNA of active and inactive X chromosomes have been interpreted to suggest that multiple tumors may arise from a common precursor. We have examined the clonality of 36 leiomyomata from 16 patients by analyzing X chromosome inactivation as indicated by the methylation status of the X‐linked androgen receptor gene. As shown by this assay, all informative leiomyomata were monoclonal in origin. In patients with multiple leiomyomata, a random distribution of inactivation between the X homologs was noted, consistent with an independent origin of each tumor. Cytogenetic analysis was also performed on short‐term cell cultures of 27 of the 36 tumors. In each of two tumors that had both cells with a clonal karyotypic abnormality and karyotypically normal cells, DNA prepared from short‐term cultures showed a monoclonal pattern of X inactivation identical to that of the leiomyoma from which they were derived. These data suggest that karyotypically normal cells present in short‐term cultures of uterine leiomyomata are part of the tumor clone, and that clonal expansion of tumor cells precedes the development of cytogenetic aberrations.
Loss of heterozygosity on the short arm of chromosome 3 in mesothelioma cell lines and solid tumors
Authors: Zeiger Martha A. , Gnarra James R. , Zbar Berton , Linehan W. Marston , Pass Harvey I. 
Published: February 2007

AbstractCytogenetic analysis of mesothelioma cell lines and solid tumors has documented non‐random chromosomal abnormalities on the short arm of chromosome 3 from 3p 14 to 3p25. We therefore examined nine mesothelioma cell lines, their corresponding tumors, and 15 additional mesothelioma tumors for loss of heterozygosity on 3p from 3p 13 to 3p25.5 by polymerase chain reaction and restriction fragment length polymorphism analysis at 8 loci: D3S3, D3S30, D3S6, D3S2, D3S32, D3FI5S2, THRB, and VHL Loss of heterozygosity was documented by loss of one of two alleles in the tumor DNA whose corresponding normal DNA was heterozygous and was documented in four of nine mesothelioma cell lines and six of 15 mesothelioma tumors or a total of 42% of the mesotheliomas evaluated. This study suggests the involvement of a gene on the short arm of chromosome 3 in the development of mesotheliomas.
The insulin‐like growth factor I receptor gene is the target for the 15q26 amplicon in breast cancer
Authors: Almeida Anna , Muleris Martine , Dutrillaux Bernard , Malfoy Bernard 
Published: February 2007

AbstractWe report the amplification and overexpression of the IGFIR (insulin‐like growth factor I receptor) gene in primary breast cancers with an amplification of band 15q26. The involvement of IGFIR, which may vary in frequency from 2‐3% in unselected tumor series to more than 10% in breast cancers with hsr, may represent an important event in tumor progression.