CCL

Összesen 5 találat.
#/oldal:
Részletezés:
Rendezés:

1.

001-es BibID:BIBFORM065330
Első szerző:Kettunen, Eeva
Cím:L1CAM, INP10, P-cadherin, tPA and ITGB4 over-expression in malignant pleural mesotheliomas revealed by combined use of cDNA and tissue microarray / E. Kettunen, A. G. Nicholson, B. Nagy, H. Wikman, J. K. Seppänen, T. Stjernvall, T. Ollikainen, V. Kinnula, S. Nordling, J. Hollmén, S. Anttila, S. Knuutila
Dátum:2004
ISSN:1460-2180
Megjegyzések:Malignant pleural mesothelioma (MM) is a rare tumour with high mortality, which can exhibit various morphologies classified as epithelioid, biphasic and sarcomatoid subtypes. To investigate the molecular changes in these tumours, we studied gene expression patterns by combined use of cDNA arrays and tumour tissue microarrays (TMA). Deregulation of the expression of 588 cancer-related genes was screened in 16 MM comprising all three subtypes and compared with references, i.e. normal mesothelial cell lines and pleural mesothelium. Array data were analysed using three statistical methods; principal component analysis (PCA), permutation test and receiver operating characteristic (ROC) curves. Eleven genes were verified by real-time RT-PCR. Genes encoding two adhesion molecules [COL1A2 and integrin beta4 (ITGB4)] and a chemokine (INP10) were up-regulated in MM compared with both the cell lines and pleural mesothelium. There was a type-specific up-regulation of semaphorin E, ITGB4 and P-cadherin in epithelioid MM, matrix metalloproteinase 9 (MMP9) and tissue-type plasminogen activator (tPA) in sarcomatoid MM and neural cell adhesion molecule L1 (L1CAM) and INP10 in biphasic MM. Immunohistochemistry on TMA containing 47 MM (26 epithelioid, 15 sarcomatoid and six biphasic) was performed for five proteins, ITGB4, P-cadherin, tPA, INP10 and L1CAM. INP10 expression was increased in MM in general compared with normal mesothelium, while increased expression of P-cadherin, L1CAM and ITGB4 was more specific in MMs exhibiting an epithelioid growth pattern. The over-expression of tPA was more frequent in epithelioid MM despite higher mRNA levels in sarcomatoid and biphasic MM. We conclude that several proteins, associated with cell adhesion either directly (ITGB4, L1CAM, P-cadherin) or as a regulatory factor (INP10), are differentially expressed in MM. In particular, INP10, ITGB4 and COL1A2 were up-regulated in MM compared with both reference sample types, suggesting a relationship with development of these tumours.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
L1CAM
INP10
P-cadherin
tPA
ITGB4
overexpression
mesothelioma
Megjelenés:Carcinogenesis. - 26 : 1 (2004), p. 17-25. -
További szerzők:Nicholson, Andrew Gordon Nagy Bálint (1956-) (molekuláris genetikus) Wikman, Harriet Seppänen, Jouni K. Stjernvall, Tuula Ollikainen, Tiina Kinnula, Vuokko Nordling, Stig Hollmén, Jaakko Anttila, Sisko Knuutila, Sakari
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

2.

001-es BibID:BIBFORM065323
Első szerző:Myllykangas, Samuel
Cím:DNA copy number amplification profiling of human neoplasms / S. Myllykangas, J. Himberg, T. Böhling, B. Nagy, J. Hollmén, S. Knuutila
Dátum:2006
ISSN:0950-9232
Megjegyzések:DNA copy number amplifications activate oncogenes and are hallmarks of nearly all advanced tumors. Amplified genes represent attractive targets for therapy, diagnostics and prognostics. To investigate DNA amplifications in different neoplasms, we performed a bibliomics survey using 838 published chromosomal comparative genomic hybridization studies and collected amplification data at chromosome band resolution from more than 4500 cases. Amplification profiles were determined for 73 distinct neoplasms. Neoplasms were clustered according to the amplification profiles, and frequently amplified chromosomal loci (amplification hot spots) were identified using computational modeling. To investigate the site specificity and mechanisms of gene amplifications, colocalization of amplification hot spots, cancer genes, fragile sites, virus integration sites and gene size cohorts were tested in a statistical framework. Amplification-based clustering demonstrated that cancers with similar etiology, cell-of-origin or topographical location have a tendency to obtain convergent amplification profiles. The identified amplification hot spots were colocalized with the known fragile sites, cancer genes and virus integration sites, but global statistical significance could not be ascertained. Large genes were significantly overrepresented on the fragile sites and the reported amplification hot spots. These findings indicate that amplifications are selected in the cancer tissue environment according to the qualitative traits and localization of cancer genes.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
DNA
copy
number
profiling
human
neoplasms
Megjelenés:Oncogene. - 25 : 55 (2006), p. 7324-7332. -
További szerzők:Himberg, J. Böhling, T. Nagy Bálint (1956-) (molekuláris genetikus) Hollmén, Jaakko Knuutila, Sakari
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

3.

001-es BibID:BIBFORM065344
Első szerző:Niini, Tarja
Cím:Expression of myeloid-specific genes in childhood acute lymphoblastic leukemia : a cDNA array study / T. Niini, K. Vettenranta, J. Hollmén, M. L. Larramendy, Y. Aalto, H. Wikman, B. Nagy, J. K. Seppänen, A. Ferrer Salvador, H. Mannila, U. M. Saarinen-Pihkala, S. Knuutila
Dátum:2002
ISSN:0887-6924
Megjegyzések:Several specific cytogenetic changes are known to be associated with childhood acute lymphoblastic leukemia (ALL), and many of them are important prognostic factors for the disease. Little is known, however, about the changes in gene expression in ALL. Recently, the development of cDNA array technology has enabled the study of expression of hundreds to thousands of genes in a single experiment. We used the cDNA array method to study the gene expression profiles of 17 children with precursor-B ALL. Normal B cells from adenoids were used as reference material. We discuss the 25 genes that were most over-expressed compared to the reference. These included four genes that are normally expressed only in the myeloid lineages of the hematopoietic cells: RNASE2, GCSFR, PRTN3 and CLC. We also detected over-expression of S100A12, expressed in nerve cells but also in myeloid cells. In addition to the myeloid-specific genes, other over-expressed genes included AML1, LCP2 and FGF6. In conclusion, our study revealed novel information about gene expression in childhood ALL. The data obtained may contribute to further studies of the pathogenesis and prognosis of childhood ALL.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
expression
gene
myeloid
ALL
CDNA
array
Megjelenés:Leukemia. - 16 : 11 (2002), p. 2213-2221. -
További szerzők:Vettenranta, Kim Hollmén, Jaakko Larramendy, Marcelo L. Aalto, Yan Wikman, Harriet Nagy Bálint (1956-) (molekuláris genetikus) Seppänen, Jouni K. Salvador, Aurora Ferrer Mannila, Heikki Saarinen-Pihkala, Ulla Maija Knuutila, Sakari
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

4.

001-es BibID:BIBFORM065334
Első szerző:Wikman, Harriet
Cím:Caveolins as tumour markers in lung cancer detected by combined use of cDNA and tissue microarrays / Harriet Wikman, Jouni K. Seppänen, Virinder K. Sarhadi, Eeva Kettunen, Kaisa Salmenkivi, Eeva Kuosma, Katri Vainio-Siukola, Balint Nagy, Antti Karjalainen, Thanos Sioris, Jarmo Salo, Jaakko Hollmén, Sakari Knuutila, Sisko Anttila
Dátum:2004
ISSN:0022-3417
Megjegyzések:To identify new potential diagnostic markers for lung cancer, the expression profiles of 37 lung tumours were analysed using cDNA arrays. Seven samples were from small-cell lung cancer (SCLC), two from large-cell neuroendocrine tumours (LCNEC), and 28 from other non-small-cell lung cancers (mainly squamous cell cancer and adenocarcinoma). Principal component analysis and the permutation test were used to detect differences in the gene expression profiles and a set of genes was found that distinguished high-grade neuroendocrine carcinomas (SCLC and LCNEC) from other lung cancers. In addition, several genes, such as caveolin-1 (CAV1) and caveolin-2 (CAV2), were constantly deregulated in all types of tumour sample, compared with normal tissue. The expression of these two genes was investigated further at the protein level on a tissue microarray containing tumours from 161 patients and normal tissues. Immunostaining for CAV1 was negative in 48% of tumours, whereas 28% of the tumours did not express CAV2. Lack of CAV1 protein expression was not caused by methylation or mutation. In stage I adenocarcinomas, CAV2 protein expression correlated with shorter survival. In conclusion, the present study was able to identify genes that have not previously been implicated in lung cancer by the combined use of two different array techniques. Some of these genes may provide novel diagnostic markers for lung cancer.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
caveolins
tumor
marker
lung cancer
cDNA
tissue
microarray
Megjelenés:Journal Of Pathology. - 203 : 1 (2004), p. 584-593. -
További szerzők:Seppänen, Jouni K. Sarhadi, Virinder K. Kettunen, Eeva Salmenkivi, Kaisa Kuosma, Eeva Vainio-Siukola, Katri Nagy Bálint (1956-) (molekuláris genetikus) Karjalainen, Antti Sioris, Thanos Salo, Jarmo Hollmén, Jaakko Knuutila, Sakari Anttila, Sisko
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

5.

001-es BibID:BIBFORM065342
Első szerző:Zhu, Ying
Cím:Investigatory and analytical approaches to differential gene expression profiling in mantle cell lymphoma / Ying Zhu, Jaakko Hollmén, Riikka Räty, Yan Aalto, Balint Nagy, Erkki Elonen, Juha Kere, Heikki Mannila, Kaarle Franssila, Sakari Knuutila
Dátum:2002
ISSN:0007-1048
Megjegyzések:Mantle cell lymphoma (MCL) is a non-Hodgkin's lymphoma of B-cell lineage. The blastoid variant of MCL, characterized by high mitotic rate, is clinically more aggressive than common MCL. We used the cDNA array technology to examine the gene expression profiles of both blastoid variant and common MCL. The data was analysed by regression analysis, principal component analysis and the naive Bayes' classifier. Eight genes were identified as differentially deregulated between the two groups. Oncogenes CMYC, BCL2 and PIM1 were upregulated more frequently in the blastoid variant than in common MCL. This implied that the gp130-mediated signal transducer and activator of transcription 3 (STAT3) signalling pathway was involved in the blastoid variant transformation of MCL. Other differentially deregulated genes were TOP1, CD23, CD45, CD70 and NFATC. By using the eight differentially deregulated genes, we created a classifier to distinguish the blastoid variant from common MCL with high accuracy. We also identified 18 genes that were deregulated in both groups. Among them, BCL1, CALLA/CD10 and GRN were suggested to be oncogenes. The products of RGS1, RGS2, ANX2 and CD44H were suggested to promote tumour metastasis. CD66D was suggested to be a tumour suppressor gene.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
gene
expression
mantle cell
lymphoma
Megjelenés:British Journal Of Haematology. - 119 (2002), p. 905-915. -
További szerzők:Hollmén, Jaakko Räty, Riikka Aalto, Yan Nagy Bálint (1956-) (molekuláris genetikus) Elonen, Erkki Kere, Juha Mannila, Heikki Franssila, Kaarle Knuutila, Sakari
Internet cím:DOI
Szerző által megadott URL
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Rekordok letöltése1 
Corvina könyvtári katalógus v8.2.27 © 2023 Monguz kft. Minden jog fenntartva.