Találati lista | Tudóstér

001-es BibID:	BIBFORM074852
Első szerző:	Myllykangas, Samuel
Cím:	Helicobacter pylori infection activates FOS and stress-response genes and alters expression of genes in gastric cancer-specific loci / Samuel Myllykangas, Outi Monni, Bálint Nagy, Hilpi Rautelin, Sakari Knuutila
Dátum:	2004
ISSN:	1045-2257
Megjegyzések:	We studied human gene expression changes caused by Helicobacter pylori infection by using an in vitro model and 13k cDNA microarrays. A gastric cancer cell line was infected with H. pylori strain NCTC 11637. H. pylori infection was found to induce differential expression of genes in chromosomal locations known to contain frequent chromosomal aberrations and gene mutations specific to gastric cancer. Based on the results of time series experiments, the primary transcription target of the infection seemed to be FOS, the expression of which significantly increased after H. pylori infection. H. pylori infection also activated transcription of several stress-response genes. H. pylori infection may predispose the host cell to DNA damage in the chromosomal locations specific to gastric cancer by activating transcription and promoting histone removal from these sites, thus exposing its target DNA to mutations.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Helicobacter pylori FOS gene expression
Megjelenés:	Genes Chromosomes & Cancer. - 40 : 4 (2004), p. 334-341. -
További szerzők:	Monni, Outi Nagy Bálint (1956-) (molekuláris genetikus) Rautelin, Hilpi Knuutila, Sakari
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:

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:
Saját polcon:

001-es BibID:	BIBFORM065301
Első szerző:	Rautava, J.
Cím:	ERBB receptors in developing, dysplastic and malignant oral epithelia / J. Rautava, K. J. Jee, P. J. Miettinen, B. Nagy, S. Myllykangas, E. W. Odell, T. Soukka, P. R. Morgan, K. Heikinheimo
Dátum:	2008
ISSN:	1368-8375
Megjegyzések:	Some oral squamous cell carcinomas (OSCCs) overexpress epidermal growth factor receptor (EGFR) but little is known about the receptor system overall during oral carcinogenesis. We studied all four ERBB receptors (EGFR, ERBB2-4) in developing (n = 2), normal (n = 7), dysplastic (n = 23) and malignant (n = 26) oral epithelia by means of immunohistochemistry. The investigations were supplemented by conducting reverse transcription-polymerase chain reactions in relation to 13 OSCC samples. All four ERBB receptors were detected in developing oral epithelium and, to a lesser degree, in mature oral epithelium. An increase in EGFR immunoreactivity was seen in 61% and 54% of dysplasias and OSCCs, respectively. The corresponding percentages for ERBB2 were 48 and 12, for ERBB3 48 and 43. ERBB4 nuclear staining was increased in 30% of dysplasias and 26% of OSCCs. Changes in ERBB receptor mRNA levels were not statistically significant. The results show that ERBB receptor profiles are specific to each tumour. Increased nuclear translocation of ERBB4 in some OSCCs may alter transcription of target genes and be associated with cancer progression. This information may be useful for clinicians as EGFR inhibitors are becoming treatment options in modern oncology.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban ERBB Receptor oral Epithelial cancer
Megjelenés:	Oral Oncology. - 44 : 3 (2008), p. 227-235. -
További szerzők:	Jee, Kowan Ja Miettinen, Päivi J. Nagy Bálint (1956-) (molekuláris genetikus) Myllykangas, Samuel Odell, Edward William Soukka, Tero Morgan, Peter R. Heikinheimo, Kristiina
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon: