Genes, Chromosomes and CancerThis is an RSS file. You can use it to subscribe to this data in your favourite RSS reader, such as GoogleReader, or to display this data on your own website or blog. Subscribe to this data using MyMedWorm.Subscribe to this data using GoogleReader.Subscribe to this data using Bloglines.Subscribe to this data using MyYahoo.

This page shows you the latest items in this publication.

Pages: 1 2 3 4 5 6 7 8

378 records returned

Definitive molecular cytogenetic characterization of 15 colorectal cancer cell linesEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In defining the genetic profiles in cancer, cytogenetically aberrant cell lines derived from primary tumors are important tools for the study of carcinogenesis. Here, we present the results of a comprehensive investigation of 15 established colorectal cancer cell lines using spectral karyotyping (SKY), fluorescence in situ hybridization, and comparative genomic hybridization (CGH). Detailed karyotypic analysis by SKY on five of the lines (P53HCT116, T84, NCI-H508, NCI-H716, and SK-CO-1) is described here for the first time. The five lines with karyotypes in the diploid range and that are characterized by defects in DNA mis...
Source: Genes, Chromosomes and Cancer - November 20, 2009 Category: Cancer & Oncology Authors: Turid Knutsen, Hesed M. Padilla-Nash, Danny Wangsa, Linda Barenboim-Stapleton, Jordi Camps, Nicole McNeil, Michael J. Difilippantonio, Thomas Ried Source Type: journals

Large intragenic deletions of the NF2 gene: Breakpoints and associated phenotypesEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In this study, the breakpoints of six large intragenic deletions in the NF2 gene are determined, which had initially been detected by multiplex ligation-dependent probe amplification. While one breakpoint occurred within an exon, the remaining 11 lied in the corresponding flanking introns. Two of the deletions were most likely caused by nonallelic homologous recombination between Alu sequences, while the other four appeared to be the result of nonhomologous endjoining, possibly facilitated by rearrangement-promoting elements at the junctions in some cases. The clinical features of patients with large intragenic deletions a...
Source: Genes, Chromosomes and Cancer - November 19, 2009 Category: Cancer & Oncology Authors: Benjamin Abo-Dalo, Kerstin Kutsche, Victor Mautner, Lan Kluwe Source Type: journals

Modeling interactions between leukemia-specific chromosomal changes, somatic mutations, and gene expression patterns during progression of core-binding factor leukemiasEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In cancer genomes, changes observed during tumor progression can be difficult to separate from nonspecific accumulation of cytogenetic changes due to cancer-associated genetic instability. We studied genetic changes occurring over time in cancers presenting with a relatively simple karyotype, namely two related core-binding factor (CBF) acute myeloid leukemias (AMLs), to assess how specific chromosomal changes are selected based on tumor subtype and acquired somatic mutations. Expression profiles for DNA replication/repair genes and the mutation status of KRAS, NRAS, FLT3, and KIT were compared with the karyotypic changes ...
Source: Genes, Chromosomes and Cancer - November 12, 2009 Category: Cancer & Oncology Authors: Dan Jones, Hui Yao, Angela Romans, Caroline Dando, Sherry Pierce, Gautam Borthakur, Amy Hamilton, Carlos Bueso-Ramos, Farhad Ravandi, Guillermo Garcia-Manero, Hagop Kantarjian Source Type: journals

Clinical and molecular features in patients with atypical teratoid rhabdoid tumor or malignant rhabdoid tumorEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
The SMARCB1 gene status in 50 patients with atypical teratoid rhabdoid tumor and/or malignant rhabdoid tumor recruited to a German registry was prospectively analyzed with FISH and PCR. Altogether we found 40 SMARCB1 mutations in 28 patients. Two patients were positive for SMARCB1 staining at immunochemistry. Germline mutations were identified in 10 of 41 patients with CNS disease, including three large heterozygous deletions, six truncating mutations and one donor splice site mutation. No missense mutation was identified. Analysis of first degree relatives did not detect any carriers. Mutations were distributed over the S...
Source: Genes, Chromosomes and Cancer - November 10, 2009 Category: Cancer & Oncology Authors: Uwe Kordes, Stefan Gesk, Michael Christoph Frühwald, Norbert Graf, Ivo Leuschner, Martin Hasselblatt, Astrid Jeibmann, Florian Oyen, Ove Peters, Torsten Pietsch, Reiner Siebert, Reinhard Schneppenheim Source Type: journals

RBSP3 is frequently altered in premalignant cervical lesions: Clinical and prognostic significanceEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
To understand the importance of frequent deletion of 3p22.3 in cervical carcinogenesis, alterations (deletion/methylation/expression) of the candidate genes STAC, MLH1, ITGA9, and RBSP3, located in the region, were analyzed in 24 cervical intraepithelial neoplasia (CIN) and 137 uterine cervical carcinoma (CACX) samples. In CIN, RBSP3 deletion (48%) and methylation (26%) were high compared with the other genes (4-9%). In CACX, alterations of these genes were as follows: deletion: STAC (54%) > MLH1 (46%) > RBSP3 (45%) > ITGA9 (41%), methylation: RBSP3 (25%) > ITGA9 (24%) > STAC (19%) > MLH1 (13%). Overall, alterations of RBS...
Source: Genes, Chromosomes and Cancer - November 3, 2009 Category: Cancer & Oncology Authors: Sraboni Mitra, Dipanjana Mazumder Indra, Nilanjana Bhattacharya, Ratnesh K. Singh, Partha S. Basu, Ranajit K. Mondal, Anup Roy, Eugene R. Zabarovsky, Susanta Roychoudhury, Chinmay K. Panda Source Type: journals

Distinct MHC gene expression patterns during progression of melanomaEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Abnormal expression of major histocompatibility complex (MHC) molecules in melanoma has been reported previously. However, the MHC molecule expression patterns in different growth phases of melanoma and the underlying mechanisms are not well understood. Here, we demonstrate that in vertical growth phase (VGP) melanomas, MHC genes are subject to increased rates of DNA copy number gains, accompanied by increased expression, in comparison to normal melanocytes. In contrast, MHC expression in metastatic melanomas drastically decreased compared to VGP melanomas, despite still prevalent DNA copy number gains. Subsequent investig...
Source: Genes, Chromosomes and Cancer - October 28, 2009 Category: Cancer & Oncology Authors: Yan Degenhardt, Jia Huang, Joel Greshock, Galene Horiates, Katherine Nathanson, Xiaolu Yang, Meenhard Herlyn, Barbara Weber Source Type: journals

Hematopoietic immortalizing function of the NKL-subclass homeobox gene TLX1Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Translocations resulting in ectopic expression of the TLX1 homeobox gene (previously known as HOX11) are recurrent events in human T-cell acute lymphoblastic leukemia (T-ALL). Transduction of primary murine hematopoietic stem/progenitor cells with retroviral vectors expressing TLX1 readily yields immortalized hematopoietic progenitor cell lines. Understanding the processes involved in TLX1-mediated cellular immortalization should yield insights into the growth and differentiation pathways altered by TLX1 during the development of T-ALL. In recent clinical gene therapy trials, hematopoietic clonal dominance or T-ALL-like di...
Source: Genes, Chromosomes and Cancer - October 27, 2009 Category: Cancer & Oncology Authors: Lynnsey A. Zweier-Renn, Teresa S. Hawley, Sandra Burkett, Ali Ramezani, Irene Riz, Rima L. Adler, Dennis D. Hickstein, Robert G. Hawley Source Type: journals

Frequent deletion of CDKN2A and recurrent coamplification of KIT, PDGFRA, and KDR in fibrosarcoma of bone - An array comparative genomic hybridization studyEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In conclusion, our analysis provided novel findings that can be exploited when searching for markers for diagnosis and prognosis, and targets of therapy in this tumor type. © 2009 Wiley-Liss, Inc. (Source: Genes, Chromosomes and Cancer)
Source: Genes, Chromosomes and Cancer - October 27, 2009 Category: Cancer & Oncology Authors: Tarja Niini, José Antonio López-Guerrero, Shinsuke Ninomiya, Mohamed Guled, Claudia Maria Hattinger, Francesca Michelacci, Tom Böhling, Antonio Llombart-Bosch, Piero Picci, Massimo Serra, Sakari Knuutila Source Type: journals

SUZ12 is a candidate target of the non-canonical WNT pathway in the progression of chronic myeloid leukemiaEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Polycomb proteins form multiprotein complexes that repress target genes by chromatin remodeling. In this work, we report that the SUZ12 polycomb gene is over-expressed in bone marrow samples of patients at the blastic phase of chronic myeloid leukemia. We also found a direct interaction between polycomb group genes and the WNT signaling pathway in chronic myeloid leukemia transformation. Electrophoretic mobility shift assay (EMSA), Chromatin immunoprecipitation assay (ChIP), and mass spectrometry assays identified noncanonical WNT pathway members, such as WNT5A and WNT11, bound to the SUZ12 promoter. Immunohistochemistry a...
Source: Genes, Chromosomes and Cancer - October 21, 2009 Category: Cancer & Oncology Authors: Luciana Pizzatti, Renata Binato, Jaime Cofre, Bernadete E. Gomes, Jane Dobbin, Maria Emilia Haussmann, Denise D'Azambuja, Luis Fernando Bouzas, Eliana Abdelhay Source Type: journals

Hereditary gastrointestinal stromal tumors sharing the KIT Exon 17 germline mutation p.Asp820Tyr develop through different cytogenetic progression pathwaysEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
We report the third family with hereditary predisposition to GIST due to the KIT Exon 17 germline mutation p.Asp820Tyr and characterize the cytogenetic progression pathways followed by different GIST sharing the same primary genetic event, using a combination of chromosome banding, comparative genomic hybridization (CGH), and fluorescence in situ hybridization (FISH) analyses. The missense mutation p.Asp820Tyr was detected in the proband's rectal and gastric GIST, as well as in his aunt's GIST epiplon metastasis. The mutation p.Asp820Tyr was subsequently also found in the proband's peripheral blood DNA, as well as in that ...
Source: Genes, Chromosomes and Cancer - October 20, 2009 Category: Cancer & Oncology Authors: Isabel Veiga, Mara Silva, Joana Vieira, Carla Pinto, Manuela Pinheiro, Lurdes Torres, Marta Soares, Lúcio Santos, Hugo Duarte, Artur L. Bastos, Camila Coutinho, José Dinis, Carlos Lopes, Manuel R. Teixeira Source Type: journals

Genome-wide scan identifies a copy number variable region at 3q26 that regulates PPM1L in APC mutation-negative familial colorectal cancer patientsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Familial adenomatous polyposis (FAP) is an autosomal dominantly inherited form of colorectal cancer (CRC) caused by mutation in the adenomatous polyposis coli (APC) gene. However, APC mutations are not detected in 10-50% of FAP patients. We searched for a new cancer gene by performing genome-wide genotyping on members of an APC mutation-negative FAP variant family and ethnicity-matched healthy controls. No common copy number change was found in all affected members using the unaffected members and healthy controls as baseline. A 111 kb copy number variable (CNV) region at 3q26.1 was shown to have copy number loss in all ei...
Source: Genes, Chromosomes and Cancer - October 20, 2009 Category: Cancer & Oncology Authors: L. F. Thean, C. Loi, K. S. Ho, P. K. Koh, K. W. Eu, P. Y. Cheah Source Type: journals

Genomic alterations in histopathologically normal breast tissue from BRCA1 mutation carriers may be caused by BRCA1 haploinsufficiencyEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Multiple biopsies of normal breast tissue from 10 BRCA1 mutation carriers have been analyzed using array-based comparative genomic hybridization. Normal breast tissue from five age-matched control subjects without a family history of breast cancer was included for reference purposes. We repeatedly found multiple low copy number aberrations at a significantly higher frequency in histopathologically normal tissue from BRCA1 mutation carriers than in normal control tissue. Some of these aberrations were similar across samples from different patients and linked to biological functions such as transcriptional regulation and DNA...
Source: Genes, Chromosomes and Cancer - October 16, 2009 Category: Cancer & Oncology Authors: Karin Rennstam, Anita Ringberg, Heather E. Cunliffe, Håkan Olsson, Göran Landberg, Ingrid Hedenfalk Source Type: journals

FAU regulates carboplatin resistance in ovarian cancerEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
The development of chemotherapy resistance by cancer cells is complex, using different mechanisms and pathways. The gene FAU (Finkel-Biskis-Reilly murine sarcoma virus (FBR-MuSV)-associated ubiquitously expressed gene) was identified through functional expression cloning and previous data have shown that overexpression enhances apoptosis in several cell types. We demonstrate that the expression of FAU was reduced in the A2780cis (cisplatin resistant subclone of A2780) cell line compared with the A2780 ovarian cancer cell line, and was directly related to the cell line's sensitivity to carboplatin. Downregulation of FAU in ...
Source: Genes, Chromosomes and Cancer - October 14, 2009 Category: Cancer & Oncology Authors: Esther L. Moss, Mirna Mourtada-Maarabouni, Mark R. Pickard, Charles W. Redman, Gwyn T. Williams Source Type: journals

Unfavorable prognosis of CRTC1-MAML2 positive mucoepidermoid tumors with CDKN2A deletionsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
The CRTC1-MAML2 fusion oncogene underlies the etiology of mucoepidermoid salivary gland carcinoma (MEC) where it confers a favorable survival outcome as compared with fusion-negative MEC. While these analyses suggested that detection of CRTC1-MAML2 serves as a useful prognostic biomarker, we recently identified outlier cases of fusion-positive MEC associated with advanced-staged lethal disease. To identify additional genetic alterations that might cooperate with CRTC1-MAML2 to promote disease progression, we performed a pilot high-resolution oligonucleotide array CGH (aCGH) and PCR-based genotyping study on 23 MEC samples ...
Source: Genes, Chromosomes and Cancer - October 13, 2009 Category: Cancer & Oncology Authors: Sarah L. Anzick, Wei-Dong Chen, Yoonsoo Park, Paul Meltzer, Diana Bell, Adel K. El-Naggar, Frederic J. Kaye Source Type: journals

Population-based survey of cancer risks in chromosome 3 translocation carriersEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
We report a retrospective population-based study using Danish national cytogenetic and cancer registries to clarify tumor risks associated with constitutional translocations involving chromosome 3. We identified 222 (105 females, 117 males) individuals with a constitutional chromosome 3 translocation and compared their cancer risks to those of the Danish population. None of the chromosome 3 translocation carriers had developed RCC at the time of study (female 95% CIs 0.000-0.042, male 95% CIs 0.000-0.038) (P = 1.0 and P = 0.498 for females and males compared to Danish population). Fourteen translocation carriers had develo...
Source: Genes, Chromosomes and Cancer - October 12, 2009 Category: Cancer & Oncology Authors: Emma R. Woodward, Anne-Bine Skytte, Dorthe G. Cruger, Eamonn R. Maher Source Type: journals

PPFIA1 and CCND1 are frequently coamplified in breast cancerEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Recently, amplification of PPFIA1, encoding a member of the liprin family located about 600 kb telomeric to CCND1 on chromosome band 11q13, was described in squamous cell carcinoma of head and neck. Because 11q13 amplification is frequent in breast cancer, and PPFIA1 has been suggested to contribute to mammary gland development, we hypothesized that PPFIA1 might also be involved in the 11q13 amplicon in breast cancer and contribute to breast cancer development. A tissue microarray containing more than 2000 human breast cancers was analyzed for gene copy numbers of PPFIA1 and CCND1 by means of fluorescence in situ hybridiza...
Source: Genes, Chromosomes and Cancer - September 28, 2009 Category: Cancer & Oncology Authors: Ana-Maria Dancau, Laura Wuth, Marcel Waschow, Frederik Holst, Antje Krohn, Matthias Choschzick, Luigi Terracciano, Sotirios Politis, Stefan Kurtz, Annette Lebeau, Kay Friedrichs, Katharina Wencke, Outi Monni, Ronald Simon Source Type: journals

Recurrent copy number gain of transcription factor SOX2 and corresponding high protein expression in oral squamous cell carcinomaEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Gene copy number aberrations are involved in oral squamous cell carcinoma (OSCC) development. To delineate candidate genes inside critical chromosomal regions, array-CGH was applied to 40 OSCC specimens using a microarray covering the whole human genome with an average resolution of 1 Mb. Gene copy number gains were predominantly found at 1q23 (9 cases), 3q26 (11), 5p15 (13), 7p11 (7), 8q24 (17), 11q13 (15), 14q32 (8), 19p13 (8), 19q12 (7), 19q13 (8), and 20q13 (9), whereas gene copy number losses were detected at 3p21-3p12 (15), 8p32 (11), 10p12 (8), and 18q21-q23 (10). Subsequent mRNA expression analyses by quantitative ...
Source: Genes, Chromosomes and Cancer - September 28, 2009 Category: Cancer & Oncology Authors: Kolja Freier, Karl Knoepfle, Christa Flechtenmacher, Susanne Pungs, Frauke Devens, Grischa Toedt, Christof Hofele, Stefan Joos, Peter Lichter, Bernhard Radlwimmer Source Type: journals

Correlation between losses of IGH or its segments and deletions of 13q14 in t(11;14) (q13;q32) multiple myelomaEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In this study we applied a combined cell morphology and FISH method for the analysis of coexistence of t(11;14)(q13;q32) with deletions of the long arm of chromosome 13 ([Delta]13) in PCs from 51 MM patients using several probes for the 13q14, 11q13, and IGH regions. We found 15 different variants of the t(11;14) that are the consequence of different 11q13 breakpoints and various deletions of Variable (del IGH Var) or Constant (del IGH Const) IGH segments and also duplications and losses of the IGH gene on the normal nontranslocated chromosome 14 as well as IGH/Cyclin D1 (CCND1) fusion on der(14) and CCND1/IGH fusions on d...
Source: Genes, Chromosomes and Cancer - September 28, 2009 Category: Cancer & Oncology Authors: Luba Trakhtenbrot, Izhar Hardan, Maya Koren-Michowitz, Shirley Oren, Galina Yshoev, Gideon Rechavi, Arnon Nagler, Ninette Amariglio Source Type: journals

Molecular characterization of commonly used cell lines for bone tumor research: A trans-European EuroBoNet effortEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Usage of cancer cell lines has repeatedly generated conflicting results provoked by differences among subclones or contamination with mycoplasm or other immortal mammalian cells. To overcome these limitations, we decided within the EuroBoNeT consortium to characterize a common set of cell lines including osteosarcomas (OS), Ewing sarcomas (ES), and chondrosarcomas (CS). DNA fingerprinting was used to guarantee the identity of all of the cell lines and to distinguish subclones of osteosarcoma cell line HOS. Screening for homozygous loss of 38 tumor suppressor genes by MLPA revealed deletion of CDKN2A as the most common even...
Source: Genes, Chromosomes and Cancer - September 28, 2009 Category: Cancer & Oncology Authors: Laura Ottaviano, Karl-Ludwig Schaefer, Melanie Gajewski, Wolfgang Huckenbeck, Stefan Baldus, Uwe Rogel, Carlos Mackintosh, Enrique de Alava, Ola Myklebost, Stine H. Kresse, Leonardo A. Meza-Zepeda, Massimo Serra, Anne-Marie Cleton-Jansen, Pancras C. W. Ho Source Type: journals

Gene expression analysis identifies over-expression of CXCL1, SPARC, SPP1, and SULF1 in gastric cancerEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
To elucidate gene expression signatures associated with gastric carcinogenesis, we performed a genome-wide expression analysis of 46 Finnish and 20 Japanese gastric tissues. Comparative analysis between Finnish and Japanese datasets identified 58 common genes that were differentially expressed between cancerous and non-neoplastic gastric tissues. Twenty-six of these genes were up-regulated in cancer and 32 down-regulated. Of these genes, 64% were also differentially expressed in another unrelated publicly available dataset. The expression levels of four of the up-regulated genes, CXCL1, SPARC, SPP1 and SULF, were further a...
Source: Genes, Chromosomes and Cancer - September 24, 2009 Category: Cancer & Oncology Authors: Siina Junnila, Arto Kokkola, Toru Mizuguchi, Koichi Hirata, Marja-Liisa Karjalainen-Lindsberg, Pauli Puolakkainen, Outi Monni Source Type: journals

WTX inactivation is a frequent, but late event in Wilms tumors without apparent clinical impactEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Wilms tumor (WT) is one of the most common solid tumors in childhood. Mutations in WT1 and CTNNB1 are well established as causal alterations in about 10-15% of cases. Recently, WTX (WT gene on the X-chromosome), a gene implicated in WNT signaling, has been identified as a third WT gene. We determined the mutation status of WTX, CTNNB1, and WT1 in a large set of 429 tumors. Genomic WTX alterations were identified in 17% of WTs, equally distributed between males and females. Analysis of 104 WT samples for WTX point mutations revealed a rate of only 2%. An additional 11.5% of tumor samples lacked expression of WTX mRNA. These...
Source: Genes, Chromosomes and Cancer - September 16, 2009 Category: Cancer & Oncology Authors: Jenny Wegert, Stefanie Wittmann, Ivo Leuschner, Eva Geissinger, Norbert Graf, Manfred Gessler Source Type: journals

Characterization of B- and T-lineage acute lymphoblastic leukemia by integrated analysis of MicroRNA and mRNA expression profilesEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In this study, we investigated miRNAs expression profiles in a series of adult ALL cases by microarray analysis. Unsupervised hierarchical clustering largely recapitulated ALL subgroups. Furthermore, we identified miR-148, miR-151, and miR-424 as discriminative of T-lineage versus B-lineage ALL; ANOVA highlighted a set of six miRNAs - namely miR-425-5p, miR-191, miR-146b, miR-128, miR-629, and miR-126 - that can discriminate B-lineage ALL subgroups harboring specific molecular lesions. These results were confirmed and extended by quantitative-PCR on a further cohort of cases. Finally, we used Pearson correlation analysis t...
Source: Genes, Chromosomes and Cancer - September 15, 2009 Category: Cancer & Oncology Authors: Valerio Fulci, Teresa Colombo, Sabina Chiaretti, Monica Messina, Franca Citarella, Simona Tavolaro, Anna Guarini, Robin Foà, Giuseppe Macino Source Type: journals

Two candidate tumor suppressor genes, MEOX2 and SOSTDC1, identified in a 7p21 homozygous deletion region in a Wilms tumorEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
A SNP-based array analysis of 100 Wilms tumors (WT) from 97 patients identified 7p alterations (hemizygous and homozygous deletions and uniparental disomy) in nine tumors. The homozygous deletion (HD) region of 7p21 found in one tumor partially overlapped with another HD region reported previously, and was narrowed down to a 2.1-Mb region. Based on an expression analysis of 10 genes located in the HD region in 3 WT lines and previous studies on tumorigenic roles of MEOX2 and SOSTDC1, we further analyzed these two genes. Sequencing showed no mutation in MEOX2, but two missense mutations (L50F and Q129L) in SOSTDC1 in four t...
Source: Genes, Chromosomes and Cancer - September 15, 2009 Category: Cancer & Oncology Authors: Junjiro Ohshima, Masayuki Haruta, Yasuhito Arai, Fumio Kasai, Yuiko Fujiwara, Tadashi Ariga, Hajime Okita, Masahiro Fukuzawa, Jun-Ichi Hata, Hiroshi Horie, Yasuhiko Kaneko Source Type: journals

t(19;22)(q13;q12) Translocation leading to the novel fusion gene EWSR1-ZNF444 in soft tissue myoepithelial carcinomaEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
We report a myoepithelial carcinoma with an aberrant near-diploid karyotype, 43[sim]47,XX,add(1)(p34)x2,add(3)(q27)x2,del(12)(q22),+add(18)(p11)x2,del(22)(q11),+r, found in cells cultured from a lung metastasis. The deletion in 22q led us to search by molecular cytogenetic means for possible EWSR1 rearrangements, and eventually a novel chimeric gene consisting of the 5[prime]-end of EWSR1 (22q12) and the 3[prime]-end of ZNF444 (19q13) was found. How the new fusion gene contributes to tumorigenesis is unknown, but the finding of an EWSR1 rearrangement suggests that this, possibly even the EWSR1-ZNF444, is a defining pathoge...
Source: Genes, Chromosomes and Cancer - September 15, 2009 Category: Cancer & Oncology Authors: Petter Brandal, Ioannis Panagopoulos, Bodil Bjerkehagen, Sverre Heim Source Type: journals

OCT4B expression in PBMNCs suggests the existence of an alternative OCT4 promoterEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
No abstract. (Source: Genes, Chromosomes and Cancer)
Source: Genes, Chromosomes and Cancer - September 15, 2009 Category: Cancer & Oncology Authors: Spyros I. Papamichos, Alexandros F. Lambropoulos, Vassiliki Kotoula Source Type: journals

Aberrant DNA methylation profile and frequent methylation of KLK10 and OXGR1 genes in hepatocellular carcinomaEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In this study, we combined differential methylation hybridization and a CpG microarray platform to characterize methylation profiles and identify novel candidate genes associated with hepatocellular carcinoma (HCC). The genomic DNA of 21 paired adjacent normal and HCC samples was used, and results were analyzed by hierarchical clustering. Twenty-seven hypermethylated candidates and 38 hypomethylated candidates were obtained. Six candidate genes from the hypermethylated group were validated by combined bisulfite restriction analysis; two genes, human kallikrein 10 gene (KLK10) and oxoglutarate ([alpha]-ketoglutarate) recept...
Source: Genes, Chromosomes and Cancer - September 15, 2009 Category: Cancer & Oncology Authors: Chang-Yi Lu, Sen-Yung Hsieh, Yen-Jung Lu, Chi-Sheng Wu, Lih-Chyang Chen, Shao-Jung Lo, Cheng-Tao Wu, Min-Yuan Chou, Tim Hui-Ming Huang, Yu-Sun Chang Source Type: journals

Claspin inhibition leads to fragile site expressionEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Fragile sites are hot spots for sister chromatid exchanges, translocations, deletions, complex rearrangements, and gene amplification. It has been hypothesized that rearrangements at fragile sites derive from unreplicated regions resulting from stalled forks that escape the ATR replication checkpoint. In the present study, we investigated the role of the Claspin (CLSPN) gene, which codes for an adaptor protein in the ATR pathway, during DNA replication stress in human cells. We show that the inhibition of the CLSPN gene leads to both genome instability and fragile site expression. Following aphidicolin treatment, we found ...
Source: Genes, Chromosomes and Cancer - September 15, 2009 Category: Cancer & Oncology Authors: Maria Luisa Focarelli, Samuela Soza, Linda Mannini, Marianna Paulis, Alessandra Montecucco, Antonio Musio Source Type: journals

Genomic alterations in primary breast cancers compared with their sentinel and more distal lymph node metastases: An aCGH studyEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Metastatic potential of breast cancer may be associated with specific genomic alterations and the earliest metastases are likely to be found in the sentinel lymph nodes (SLN). Using array comparative genomic hybridization (aCGH), we compared the genomes of primary breast invasive duct carcinomas (IDCs), their sentinel and more distal lymph node metastases, and IDCs without nodal metastasis. Thirty-three samples from 22 patients with IDC were subjected to aCGH: 8 IDC samples from patients without lymph node metastasis, 11 IDCs associated with SLN metastases out of which 7 had paired samples of metastases, and 14 samples of ...
Source: Genes, Chromosomes and Cancer - September 15, 2009 Category: Cancer & Oncology Authors: Chunjie Wang, Vladimir V. Iakovlev, Vietty Wong, Stephanie Leung, Keisha Warren, Gaiane Iakovleva, Nona C. R. Arneson, Melania Pintilie, Naomi Miller, Bruce Youngson, David R. McCready, Susan J. Done Source Type: journals

LPXN, a member of the paxillin superfamily, is fused to RUNX1 in an acute myeloid leukemia patient with a t(11;21)(q12;q22) translocationEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
RUNX1 (previously AML1) is involved in multiple recurrent chromosomal rearrangements in hematological malignances. Recently, we identified a novel fusion between RUNX1 and LPXN from an acute myeloid leukemia (AML) patient with t(11;21)(q12;q22). This translocation generated four RUNX1/LPXN and one LPXN/RUNX1 chimeric transcripts. Two representative RUNX1/LPXN fusion proteins, RL and RLs, were both found to localize in the nucleus and could bring the CBFB protein into the nucleus like the wild-type RUNX1. Both fusion proteins inhibit the ability of RUNX1 to transactivate the CSF1R promoter, probably through competition for ...
Source: Genes, Chromosomes and Cancer - September 15, 2009 Category: Cancer & Oncology Authors: Hai-Ping Dai, Yong-Quan Xue, Jian-Wei Zhou, Ai-Ping Li, Ya-Fang Wu, Jin-Lan Pan, Yong Wang, Jun Zhang Source Type: journals

Genomic profiling of pediatric ALK-positive anaplastic large cell lymphoma: A Children's Cancer and Leukaemia Group StudyEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) is a T-cell malignancy in which ALK expression is a consequence of the t(2;5) or a variant translocation involving Chromosome 2. For the most part, this disease presents in the pediatric population and most, but not all, patients are successfully treated. Although the t(2;5) product nucleophosmin-ALK has been extensively studied for its transforming properties, very little is known regarding cooperative genetic mutations that may contribute to lymphomagenesis and may predict survival outcome, specifically in a purely pediatric population. We se...
Source: Genes, Chromosomes and Cancer - August 18, 2009 Category: Cancer & Oncology Authors: Catrin Youssif, Jan Goldenbogen, Rifat Hamoudi, Joaquim Carreras, Maria Viskaduraki, Yu-xin Cui, Chris M. Bacon, G. A. Amos Burke, Suzanne D. Turner Source Type: journals

Integrative genomics reveals mechanisms of copy number alterations responsible for transcriptional deregulation in colorectal cancerEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
To evaluate the mechanisms and consequences of chromosomal aberrations in colorectal cancer (CRC), we used a combination of spectral karyotyping, array comparative genomic hybridization (aCGH), and array-based global gene expression profiling on 31 primary carcinomas and 15 established cell lines. Importantly, aCGH showed that the genomic profiles of primary tumors are recapitulated in the cell lines. We revealed a preponderance of chromosome breakpoints at sites of copy number variants (CNVs) in the CRC cell lines, a novel mechanism of DNA breakage in cancer. The integration of gene expression and aCGH led to the identifi...
Source: Genes, Chromosomes and Cancer - August 17, 2009 Category: Cancer & Oncology Authors: Jordi Camps, Quang Tri Nguyen, Hesed M. Padilla-Nash, Turid Knutsen, Nicole E. McNeil, Danny Wangsa, Amanda B. Hummon, Marian Grade, Thomas Ried, Michael J. Difilippantonio Source Type: journals

Characterization of a hotspot region on chromosome 12 for amplification in ring chromosomes in atypical lipomatous tumorsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Ring chromosomes are cytogenetic hallmarks of genomic amplification in several bone and soft tissue tumors, in particular atypical lipomatous tumors (ALT). In ALT, the ring chromosomes invariably contain amplified material from the central part of the long arm of chromosome 12, mainly 12q12[rarr]15, but often also segments from other chromosomes are involved. Previous studies have shown that one of the recurrent amplicons in ALT, located in 12q13.3-14.1 and harboring the candidate target genes TSPAN31 and CDK4, often has a sharp centromeric border. To characterize this breakpoint region in more detail, 12 cases of ALT with...
Source: Genes, Chromosomes and Cancer - August 17, 2009 Category: Cancer & Oncology Authors: Domenico Trombetta, Fredrik Mertens, Angelo Lonoce, Pietro D'Addabbo, Karin Rennstam, Nils Mandahl, Clelia Tiziana Storlazzi Source Type: journals

Protocadherin PCDH10, involved in tumor progression, is a frequent and early target of promoter hypermethylation in cervical cancerEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Cervical cancer (CC) is the second most common cancer in women. Currently, no tractable molecular-based therapeutic targets exist for patients with invasive CC and no predictive markers of risk assessment for progression of precancerous lesions are identified. New molecular insights into CC pathogenesis are urgently needed. Towards this goal, we first determined the copy number alterations of chromosome 4 and then examined the role of PCDH10 mapped to 4q28 as a candidate tumor suppressor gene. We identified monosomy 4 in 47% of 81 invasive CC studied by SNP array and found that 91% of 130 invasive CC harboring methylation ...
Source: Genes, Chromosomes and Cancer - August 13, 2009 Category: Cancer & Oncology Authors: Gopeshwar Narayan, Luigi Scotto, Vijayalakshmi Neelakantan, Sherine H. Kottoor, Ada Ho Yan Wong, Shee-Loong Loke, Mahesh Mansukhani, Bhavana Pothuri, Jason D. Wright, Andreas M. Kaufmann, Achim Schneider, Hugo Arias-Pulido, Qian Tao, Vundavalli V. Murty Source Type: journals

RAS signaling dysregulation in human embryonal RhabdomyosarcomaEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Rhabdomyosarcoma (RMS) is a common childhood solid tumor, resulting from dysregulation of the skeletal myogenesis program. Two major histological subtypes occur in childhood RMS, embryonal and alveolar. While chromosomal rearrangements account for the majority of alveolar tumors, the genetic defects underlying the pathogenesis of embryonal RMS remain largely undetermined. A few studies performed on small series of embryonal tumors suggest that dysregulation of RAS function may be relevant to disease pathogenesis. To explore further the biological and clinical relevance of mutations with perturbing consequences on RAS signa...
Source: Genes, Chromosomes and Cancer - August 12, 2009 Category: Cancer & Oncology Authors: Simone Martinelli, Heather P. McDowell, Silvia Delle Vigne, George Kokai, Stefania Uccini, Marco Tartaglia, Carlo Dominici Source Type: journals

Rearrangement of upstream sequences of the hTERT gene during cellular immortalizationEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Telomerase expression, resulting from transcriptional activation of the hTERT gene, allows cells to acquire indefinite proliferative potential during cellular immortalization and tumorigenesis. However, mechanisms of hTERT gene activation in many immortal cell lines and cancer cells are poorly understood. Here, we report our studies on hTERT activation using genetically related pairs of telomerase-negative (Tel-) and -positive (Tel+) fibroblast lines. First, whereas transiently transfected plasmid reporters did not recapitulate the endogenous hTERT promoter, the promoter in chromosomally integrated bacterial artificial chr...
Source: Genes, Chromosomes and Cancer - August 11, 2009 Category: Cancer & Oncology Authors: Yuanjun Zhao, Shuwen Wang, Evgenya Y. Popova, Sergei A. Grigoryev, Jiyue Zhu Source Type: journals

Integrative approach for prioritizing cancer genes in sporadic colon cancerEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
The current multistep carcinogenesis models of colon cancer do not fully capture the genetic heterogeneity of the disease, which is additionally complicated by the presence of passenger and driver genetic alterations. The aim of this study was to select in the context of this significant heterogeneity additional genes functionally related to colon cancer development. High-throughput copy number and gene expression data of 36 microsatellite stable sporadic colon cancers resected from patients of a single institution characterized for mutations in APC, KRAS, TP53 and loss of 18q were analyzed. Genes whose expression correlat...
Source: Genes, Chromosomes and Cancer - August 10, 2009 Category: Cancer & Oncology Authors: James F. Reid, Manuela Gariboldi, Viktorija Sokolova, Patrizia Capobianco, Andrea Lampis, Federica Perrone, Stefano Signoroni, Aurora Costa, Ermanno Leo, Silvana Pilotti, Marco A. Pierotti Source Type: journals

Selective elimination of amplified CDK4 sequences correlates with spontaneous adipocytic differentiation in liposarcomaEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Well-differentiated and undifferentiated liposarcomas are characterized by high-level amplifications of chromosome 12 regions including the CDK4 and MDM2 genes. These amplicons are either localized, in well-differentiated liposarcoma (WDLPS), on extrachromosomal structures (ring or rod chromosomes), or integrated into chromosome arms in undifferentiated tumors. Our results reveal that extrachromosomal amplicons are unstable, and frequently lost by micronucleation. This loss correlates with hypermethylation of eliminated sequences and changes of their replication time. Treatment of cells with demethylating agents during ear...
Source: Genes, Chromosomes and Cancer - July 22, 2009 Category: Cancer & Oncology Authors: Zofia Hélias-Rodzewicz, Florence Pédeutour, Jean-Michel Coindre, Philippe Terrier, Alain Aurias Source Type: journals

Genome-wide high-resolution analysis of DNA copy number alterations in NF1-associated malignant peripheral nerve sheath tumors using 32K BAC arrayEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Neurofibromatosis Type I (NF1) is an autosomal dominant disorder characterized by the development of both benign and malignant tumors. The lifetime risk for developing a malignant peripheral nerve sheath tumor (MPNST) in NF1 patients is [sim]10% with poor survival rates. To date, the molecular basis of MPNST development remains unclear. Here, we report the first genome-wide and high-resolution analysis of DNA copy number alterations in MPNST using the 32K bacterial artificial chromosome microarray on a series of 24 MPNSTs and three neurofibroma samples. In the benign neurofibromas, apart from loss of one copy of the NF1 ge...
Source: Genes, Chromosomes and Cancer - July 14, 2009 Category: Cancer & Oncology Authors: Kiran K. Mantripragada, Teresita Díaz de Ståhl, Chris Patridge, Uwe Menzel, Robin Andersson, Nadia Chuzhanova, Lan Kluwe, Abhijit Guha, Victor Mautner, Jan P. Dumanski, Meena Upadhyaya Source Type: journals

Genomic aberrations in 80 cases of primary glioblastoma multiforme: Pathogenetic heterogeneity and putative cytogenetic pathwaysEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Screening the whole glioblastoma multiforme (GBM) genome for aberrations is a good starting point when looking for molecular markers that could potentially stratify patients according to prognosis and optimal treatment. We investigated 80 primary untreated GBM using both G-banding analysis and high-resolution comparative genomic hybridization (HR-CGH). Abnormal karyotypes were found in 83% of the tumors. The most common numerical chromosome aberrations were +7, -10, -13, -14, -15, +20, and -22. Structural abnormalities most commonly involved chromosomes 1 and 3, and the short arm of chromosome 9. HR-CGH verified these find...
Source: Genes, Chromosomes and Cancer - July 13, 2009 Category: Cancer & Oncology Authors: Hanne-Sofie S. Dahlback, Petter Brandal, Torstein R. Meling, Ludmila Gorunova, David Scheie, Sverre Heim Source Type: journals

Identifying the molecular signature of the interstitial deletion 7q subgroup of uterine leiomyomata using a paired analysisEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
This study provides a molecular signature of the del(7q) UL subgroup and will serve as a platform for future studies of tumor pathogenesis. © 2009 Wiley-Liss, Inc. (Source: Genes, Chromosomes and Cancer)
Source: Genes, Chromosomes and Cancer - July 13, 2009 Category: Cancer & Oncology Authors: Jennelle C. Hodge, Peter J. Park, Jonathan M. Dreyfuss, Iman Assil-Kishawi, Priya Somasundaram, Luwam G. Semere, Bradley J. Quade, Allison M. Lynch, Elizabeth A. Stewart, Cynthia C. Morton Source Type: journals

Colocalization of somatic and meiotic double strand breaks near the Myc oncogene on mouse chromosome 15Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Both somatic and meiotic recombinations involve the repair of DNA double strand breaks (DSBs) that occur at preferred locations in the genome. Improper repair of DSBs during either mitosis or meiosis can lead to mutations, chromosomal aberration such as translocations, cancer, and/or cell death. Currently, no model exists that explains the locations of either spontaneous somatic DSBs or programmed meiotic DSBs or relates them to each other. One common class of tumorigenic translocations arising from DSBs is chromosomal rearrangements near the Myc oncogene. Myc translocations have been associated with Burkitt lymphoma in hu...
Source: Genes, Chromosomes and Cancer - July 13, 2009 Category: Cancer & Oncology Authors: Siemon H. Ng, Sarah A. Maas, Petko M. Petkov, Kevin D. Mills, Kenneth Paigen Source Type: journals

Are there any more ovarian tumor suppressor genes? A new perspective using ultra high-resolution copy number and loss of heterozygosity analysisEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
This study shows that recurrent regions of LOH and HD frequently align with known TSGs suggesting that LOH analysis remains a valid approach to discovering new candidates. © 2009 Wiley-Liss, Inc. (Source: Genes, Chromosomes and Cancer)
Source: Genes, Chromosomes and Cancer - July 13, 2009 Category: Cancer & Oncology Authors: Kylie L. Gorringe, Manasa Ramakrishna, Louise H. Williams, Anita Sridhar, Samantha E. Boyle, Jennifer L. Bearfoot, Jason Li, Michael S. Anglesio, Ian G. Campbell Source Type: journals

High density DNA array analysis reveals distinct genomic profiles in a subset of gastrointestinal stromal tumorsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Gastrointestinal stromal tumors (GISTs) generally harbor activating mutations in KIT or platelet-derived growth facter receptor (PDGFRA). Mutations in these receptor tyrosine kinases lead to dysregulation of downstream signaling pathways that contribute to GIST pathogenesis. GISTs with KIT or PDGFRA mutations also undergo secondary cytogenetic alterations that may indicate the involvement of additional genes important in tumor progression. Approximately 10-15% of adult and 85% of pediatric GISTs do not have mutations in KIT or in PDGFRA. Most mutant adult GISTs display large-scale genomic alterations, but little is known a...
Source: Genes, Chromosomes and Cancer - July 7, 2009 Category: Cancer & Oncology Authors: Martin G. Belinsky, Yuliya V. Skorobogatko, Lori Rink, Jianming Pei, Kathy Q. Cai, Lisa A. Vanderveer, David Riddell, Erin Merkel, Chi Tarn, Burton L. Eisenberg, Margaret von Mehren, Joseph R. Testa, Andrew K. Godwin Source Type: journals

Improved detection of chromosomal abnormalities in chronic lymphocytic leukemia by conventional cytogenetics using CpG oligonucleotide and interleukin-2 stimulation: A Belgian multicentric studyEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In conclusion, our results confirm that CpG/IL-2 stimulation increases the detection rate of chromosomal abnormalities in CLL compared with TPA and that further improvement can be obtained by FISH. However, neither conventional cytogenetics nor FISH detected all aberrations, demonstrating the complementary nature of these techniques. © 2009 Wiley-Liss, Inc. (Source: Genes, Chromosomes and Cancer)
Source: Genes, Chromosomes and Cancer - July 6, 2009 Category: Cancer & Oncology Authors: Natalie Put, Peter Konings, Katrina Rack, Mauricette Jamar, Nadine Van Roy, Jeanne-Marie Libouton, Pascal Vannuffel, Daniel Sartenaer, Geneviève Ameye, Frank Speleman, Christian Herens, Hélène A. Poirel, Yves Moreau, Anne Hagemeijer, Peter Vandenberghe Source Type: journals

Characterization and gene expression profiling in glioma cell lines with deletion of chromosome 19 before and after microcell-mediated restoration of normal human chromosome 19Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Nearly 10% of human gliomas are oligodendrogliomas. Deletion of chromosome arm 19q, often in conjunction with deletion of 1p, has been observed in 65-80% of these tumors. This has suggested the presence of a tumor suppressor gene located on the 19q arm. Chromosome 19 deletion is also of interest due to the better prognosis of patients with deletion, including longer survival and better response to chemotherapy, compared with patients without deletion. Two glioma cell lines with deletion of 19q were used for chromosome 19 microcell-mediated transfer, to assess the effect of replacing the deleted segment. Complementation wit...
Source: Genes, Chromosomes and Cancer - June 24, 2009 Category: Cancer & Oncology Authors: Kristen L. Drucker, Gaspar J. Kitange, Thomas M. Kollmeyer, Mark E. Law, Sandra Passe, Amanda L. Rynearson, Hilary Blair, Cheryl L. Soderberg, Bruce W. Morlan, Karla V. Ballman, Caterina Giannini, Robert B. Jenkins Source Type: journals

Rearrangements of the MLL gene are influenced by DNA secondary structure, potentially mediated by topoisomerase II bindingEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
The location of MLL translocation breakpoints within therapy-related acute myeloid leukemia linked to drugs targeting Topoisomerase II and infant acute leukemia (IAL) are biased toward the intron 11-exon 12 region of MLL, although lacking a comprehensive explanation. To address this, blood samples were taken from breast cancer and lymphoma patients receiving Topoisomerase II inhibitor therapy. Inverse PCR analysis was used to interrogate the exon 12 region of MLL for rearrangements. Eleven of 19 observed translocations showed breakpoint junctions restricted to a single 5 bp location within exon 12. A similarly restricted d...
Source: Genes, Chromosomes and Cancer - June 16, 2009 Category: Cancer & Oncology Authors: Hongan Le, Sheetal Singh, Shyh-Jen Shih, Nga Du, Sabine Schnyder, Grace A. Loredo, Christine Bien, Laura Michaelis, Amir Toor, Manuel O. Diaz, Andrew T. Vaughan Source Type: journals

Recurrent chromosomal rearrangements implicate oncogenes contributing to T-cell lymphomagenesis in Lck-MyrAkt2 transgenic miceEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
The oncogene v-akt was isolated from a retrovirus that induced naturally occurring thymic lymphomas in AKR mice. We hypothesized that constitutive activation of Akt2 could serve as a first hit for the clonal expansion of malignant T-cells by promoting cell survival and genomic instability, leading to chromosome alterations. Furthermore, genes that cooperate with Akt2 to promote malignant transformation may reside at translocation/inversion junctions found in spontaneous thymic lymphomas from transgenic mice expressing constitutively active Akt2 specifically in T cells. Cytogenetic analysis revealed that thymic tumors from ...
Source: Genes, Chromosomes and Cancer - June 15, 2009 Category: Cancer & Oncology Authors: Roman A. Timakhov, Yinfei Tan, Mamta Rao, Zemin Liu, Deborah A. Altomare, Jianming Pei, David L. Wiest, Olga O. Favorova, Janice E. Knepper, Joseph R. Testa Source Type: journals

WNT/[beta]-catenin pathway activation in Wilms tumors: A unifying mechanism with multiple entries?Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
We present molecular data supporting that the WNT pathway is involved in both tumor classes, with and without WT1/[beta]-catenin alterations. In the tumor class with WT1/[beta]-catenin alterations, we identified overexpression of 14 previously unreported WNT target genes, including TWIST1. We show that the TWIST1 protein was specifically expressed in these tumors, where staining was restricted to the stromal, nuclear [beta]-catenin positive, component. By comparing the state of the WNT pathway in tumors without WT1/[beta]-catenin alterations and fetal kidneys we provide evidence that suggests that these tumors have a heigh...
Source: Genes, Chromosomes and Cancer - June 15, 2009 Category: Cancer & Oncology Authors: Marie Corbin, Aurélien de Reyniès, David S. Rickman, Dominique Berrebi, Liliane Boccon-Gibod, Sarah Cohen-Gogo, Monique Fabre, Francis Jaubert, Marine Faussillon, Funda Yilmaz, Sabine Sarnacki, Judith Landman-Parker, Catherine Patte, Gudrun Schleiermach Source Type: journals

DNA hypermethylation accompanied by transcriptional repression in follicular lymphomaEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
High-throughput microarray technologies were used to study DNA methylation accompanied by transcriptional changes in follicular lymphoma (FL). Using Methylated CpG Island Amplification with Microarrays to study CpG Island DNA methylation in FL, we discovered widespread hypermethylation of homeobox genes and previously identified targets of polycomb repressive complex 2 (PRC2) in cell lines and primary tumors, but not in benign follicular hyperplasia (BFH). DNA methylation for HOXA11, HOXD10, HOXB7, HOXC12, PAX6, LHX9, SFMBT2, EN2, and PAX7 was independently validated in the RL cell line and HOXA11, HOXD10, PAX6, and EN2 in...
Source: Genes, Chromosomes and Cancer - June 15, 2009 Category: Cancer & Oncology Authors: Lynda B. Bennett, Jennifer L. Schnabel, Jean M. Kelchen, Kristen H. Taylor, Juyuan Guo, Gerald L. Arthur, Christos N. Papageorgio, Huidong Shi, Charles W. Caldwell Source Type: journals

Clinical and cytogenetic features of a population-based consecutive series of 285 pediatric T-cell acute lymphoblastic leukemias: Rare T-cell receptor gene rearrangements are associated with poor outcomeEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In conclusion, in this large series of childhood T-ALLs from the Nordic countries, the cytogenetic findings were not associated with risk of therapy failure with the exception of the TCR;other group. However, further prospective and collaborative investigations of this genetically heterogeneous entity are needed to confirm these results. © 2009 Wiley-Liss, Inc. (Source: Genes, Chromosomes and Cancer)
Source: Genes, Chromosomes and Cancer - June 15, 2009 Category: Cancer & Oncology Authors: Kristina Karrman, Erik Forestier, Mats Heyman, Mette K Andersen, Kirsi Autio, Elisabeth Blennow, Georg Borgström, Hans Ehrencrona, Irina Golovleva, Sverre Heim, Kristiina Heinonen, Randi Hovland, Johann H Johannsson, Gitte Kerndrup, Ann Nordgren, Lars Pa Source Type: journals