his.sePublikationer
Ändra sökning
Avgränsa sökresultatet
1 - 12 av 12
RefereraExporteraLänk till träfflistan
Permanent länk
Referera
Referensformat
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annat format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annat språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf
Träffar per sida
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sortering
  • Standard (Relevans)
  • Författare A-Ö
  • Författare Ö-A
  • Titel A-Ö
  • Titel Ö-A
  • Publikationstyp A-Ö
  • Publikationstyp Ö-A
  • Äldst först
  • Nyast först
  • Skapad (Äldst först)
  • Skapad (Nyast först)
  • Senast uppdaterad (Äldst först)
  • Senast uppdaterad (Nyast först)
  • Disputationsdatum (tidigaste först)
  • Disputationsdatum (senaste först)
  • Standard (Relevans)
  • Författare A-Ö
  • Författare Ö-A
  • Titel A-Ö
  • Titel Ö-A
  • Publikationstyp A-Ö
  • Publikationstyp Ö-A
  • Äldst först
  • Nyast först
  • Skapad (Äldst först)
  • Skapad (Nyast först)
  • Senast uppdaterad (Äldst först)
  • Senast uppdaterad (Nyast först)
  • Disputationsdatum (tidigaste först)
  • Disputationsdatum (senaste först)
Markera
Maxantalet träffar du kan exportera från sökgränssnittet är 250. Vid större uttag använd dig av utsökningar.
  • 1.
    Fagerlind, Magnus
    et al.
    Högskolan i Skövde, Institutionen för vård och natur.
    Nilsson, Patric
    Högskolan i Skövde, Institutionen för vård och natur.
    Harlén, Mikael
    Högskolan i Skövde, Institutionen för vård och natur.
    Karlsson, Sandra
    Högskolan i Skövde, Institutionen för vård och natur.
    Rice, Scott A.
    Sch. of Biotech. and Biomol. Sci., University of New South Wales, Sydney, NSW 2052, Australia / Ctr. Mar. Biofouling and Bio-Innov., University of New South Wales, Sydney, NSW 2052, Australia.
    Kjelleberg, Staffan
    Sch. of Biotech. and Biomol. Sci., University of New South Wales, Sydney, NSW 2052, Australia / Ctr. Mar. Biofouling and Bio-Innov., University of New South Wales, Sydney, NSW 2052, Australia.
    Modeling the effect of acylated homoserine lactone antagonists in Pseudomonas aeruginosa2005Ingår i: Biosystems (Amsterdam. Print), ISSN 0303-2647, E-ISSN 1872-8324, Vol. 80, nr 2, s. 201-213Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Pseudomonas aeruginosa is a gram-negative bacterium that causes serious illnesses, particularly in immunocompromised individuals, often with a fatal outcome. The finding that the acylated homoserine lactone quorum sensing (QS) system controls the production of virulence factors in P. aeruginosa makes this system a possible target for antimicrobial therapy. It has been suggested that an N-(3-oxododecanoyl)-homoserine lactone (3O-C12-HSL) antagonist, a QS blocker (QSB), would interfere efficiently with the quorum sensing system in P. aeruginosa and thus reduce the virulence of this pathogen. In this work, a mathematical model of the QS system in P. aeruginosa has been developed. The model was used to virtually add 3O-C12-HSL antagonists that differed in their affinity for the receptor protein and for their ability to mediate degradation of the receptor. The model suggests that very small differences in these parameters for different 3O-C12-HSL antagonists can greatly affect the success of QSB based inhibition of the QS system in P. aeruginosa. Most importantly, it is proposed that the ability of the 3O-C12-HSL antagonist to mediate degradation of LasR is the core parameter for successful QSB based inhibition of the QS system in P. aeruginosa. Finally, this study demonstrates that QSBs can shift the system to a low steady state, corresponding to an uninduced state and thus, suggests that the use of 3O-C12-HSL antagonists may constitute a promising therapeutic approach against P. aeruginosa involved infections.

  • 2.
    Falck, Eva
    et al.
    Högskolan i Skövde, Forskningscentrum för Systembiologi. Högskolan i Skövde, Institutionen för vård och natur.
    Karlsson, Sandra
    Högskolan i Skövde, Forskningscentrum för Systembiologi. Högskolan i Skövde, Institutionen för vård och natur.
    Carlsson, Jessica
    Högskolan i Skövde, Forskningscentrum för Systembiologi. Högskolan i Skövde, Institutionen för vård och natur.
    Helenius, Gisela
    Örebro University Hospital.
    Karlsson, Mats
    Örebro University Hospital.
    Klinga-Levan, Karin
    Högskolan i Skövde, Forskningscentrum för Systembiologi. Högskolan i Skövde, Institutionen för vård och natur.
    Loss of Glutathione peroxidase 3 expression is correlated with epigenetic mechanisms in endometrial adenocarcinoma2010Ingår i: Cancer Cell International, ISSN 1475-2867, E-ISSN 1475-2867, Vol. 10, s. 46-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Glutathione peroxidase 3 (GPX3) is one of the key enzymes in the cellular defense against oxidative stress and the hepatocyte growth factor receptor, (MET) has been suggested to be influenced by the GPX3 gene expression. In a previous microarray study performed by our group, Gpx3 was identified as a potential biomarker for rat endometrial adenocarcinoma (EAC), since the expression was highly downregulated in rat EAC tumors. Herein, we have investigated the mRNA expression and Gpx3 and Met in rat EAC by real time quantitative PCR (qPCR), and the methylation status of Gpx3. In addition we have examined the expression of GPX3 and MET in 30 human EACs of different FIGO grades and 20 benign endometrial tissues. We found that the expression of GPX3 was uniformly down regulated in both rat and human EAC, regardless of tumor grade or histopathological subtype, implying that the down-regulation is an early event in EAC. The rate of Gpx3 promoter methylation reaches 91%, where biallelic methylation was present in 90% of the methylated tumors. The expression of the Met oncogene was slightly upregulated in EACs that showed loss of expression of Gpx3, but no tumor suppressor activity of Gpx3/GPX3 was detected. Preliminary results also suggest that the production of H2O2 is higher in rat endometrial tumors with down-regulated Gpx3 expression. A likely consequence of loss of GPX3 protein function would be a higher amount of ROS in the cancer cell environment. Thus, the results suggest important clinical implications of the GPX3 expression in EAC, both as a molecular biomarker for EAC and as a potential target for therapeutic interventions.

  • 3.
    Hagberg, Malin
    et al.
    Högskolan i Skövde, Institutionen för vård och natur.
    Holmén, Jonathan
    Högskolan i Skövde, Institutionen för vård och natur.
    Olausson, Josefin
    Högskolan i Skövde, Institutionen för vård och natur.
    Karlsson, Sandra
    Högskolan i Skövde, Institutionen för vård och natur.
    Johansson, Viktoria
    Högskolan i Skövde, Institutionen för vård och natur.
    Larsson, Dennis
    Högskolan i Skövde, Institutionen för vård och natur.
    Rapid activation of JNK/SAPK in LNCaP prostate cancer cells by 1α,25-dihydroxyvitamin D3 is independent of PDIA3 (1,25-MARRS)2008Ingår i: Current Topics in Steroid Research, ISSN 0972-4788, Vol. 5, s. 17-24Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    1α,25-dihydroxyvitamin D3 (1,25D3 ) is a highly potential anti-cancerous agent for prevention and treatment of prostate cancer, the most commonly diagnosed cancer type of males in western countries. A recent study by our laboratory, demonstrates that LNCaP cancer cells treated with 1,25D3, evoked dose-dependent activation of the JNK/SAPK MAPK signaling pathway within 10 minutes after hormone treatment, indicative of membrane-initiated steroid signaling (MISS) by 1,25D3. This confirms previous reports on intestinal-, chondrocyte- and osteoblast cells, where 1,25D3 operates through pharmacologically distinct nuclear-initiated mechanisms (NISS) and plasma membrane-initiated mechanisms. NISS is mediated via the vitamin D receptor (nVDR) and MISS is mediated through 1,25D3-MARRS (PDIA3, 1,25D3-membraneassociated rapid response steroid binding protein) or nVDR. The aims of the present study were to investigate the mechanisms of MISS evoked effects on alkaline phosphatase (ALP) and activation of the JNK/SAPK by 1,25D3, and the involvement of PDIA3 in 1,25D3 initiated activation of the JNK/SAPK signaling pathway. Furthermore, 1,25D3-treated LNCaP cells were transfected with siRNA against PDIA3 and phosphorylated JNK/SAPK was estimated by western analysis. Western analysis and ALP-assays demonstrated rapid activation of both JNK/SAPK as well as ALP. Silencing of PDIA3 did not affect 1,25D3 mediated activation of JNK/SAPK, suggesting that PDIA3 is not involved in the 1,25D3-initiated activation of the JNK/SAPK signaling pathway.

  • 4.
    Hedberg Oldfors, Carola
    et al.
    Sahlgrenska Academy, University of Gothenburg.
    Garcia Dios, Diego
    Sahlgrenska Academy, University of Gothenburg.
    Linder, Anna
    Sahlgrenska Academy, University of Gothenburg.
    Visuttijai, Kittichate
    Högskolan i Skövde, Institutionen för biovetenskap. Högskolan i Skövde, Forskningscentrum för Systembiologi. Sahlgrenska Academy, University of Gothenburg.
    Samuelson, Emma
    Sahlgrenska Academy, University of Gothenburg.
    Karlsson, Sandra
    Högskolan i Skövde, Institutionen för biovetenskap. Högskolan i Skövde, Forskningscentrum för Systembiologi.
    Nilsson, Staffan
    Chalmers University of Technology.
    Behboudi, Afrouz
    Högskolan i Skövde, Institutionen för biovetenskap. Högskolan i Skövde, Forskningscentrum för Systembiologi.
    Analysis of an independent tumor suppressor locus telomeric to Tp53 suggested Inpp5k and Myo1c as novel tumor suppressor gene candidates in this region2015Ingår i: BMC Genetics, ISSN 1471-2156, E-ISSN 1471-2156, Vol. 16, nr 1, artikel-id 80Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Several reports indicate a commonly deleted chromosomal region independent from, and distal to the TP53 locus in a variety of human tumors. In a previous study, we reported a similar finding in a rat tumor model for endometrial carcinoma (EC) and through developing a deletion map, narrowed the candidate region to 700 kb, harboring 19 genes. In the present work real-time qPCR analysis, Western blot, semi-quantitative qPCR, sequencing, promoter methylation analysis, and epigenetic gene expression restoration analyses (5-aza-2'-deoxycytidine and/or trichostatin A treatments) were used to analyze the 19 genes located within the candidate region in a panel of experimental tumors compared to control samples.

    RESULTS:

    Real-time qPCR analysis suggested Hic1 (hypermethylated in cancer 1), Inpp5k (inositol polyphosphate-5-phosphatase K; a.k.a. Skip, skeletal muscle and kidney enriched inositol phosphatase) and Myo1c (myosin 1c) as the best targets for the observed deletions. No mutation in coding sequences of these genes was detected, hence the observed low expression levels suggest a haploinsufficient mode of function for these potential tumor suppressor genes. Both Inpp5k and Myo1c were down regulated at mRNA and/or protein levels, which could be rescued in gene expression restoration assays. This could not be shown for Hic1.

    CONCLUSION:

    Innp5k and Myo1c were identified as the best targets for the deletions in the region. INPP5K and MYO1C are located adjacent to each other within the reported independent region of tumor suppressor activity located at chromosome arm 17p distal to TP53 in human tumors. There is no earlier report on the potential tumor suppressor activity of INPP5K and MYO1C, however, overlapping roles in phosphoinositide (PI) 3-kinase/Akt signaling, known to be vital for the cell growth and survival, are reported for both. Moreover, there are reports on tumor suppressor activity of other members of the gene families that INPP5K and MYO1C belong to. Functional significance of these two candidate tumor suppressor genes in cancerogenesis pathways remains to be investigated.

  • 5.
    Karlsson, Sandra
    Högskolan i Skövde, Institutionen för vård och natur.
    Expression analysis of genes involved in the development of endometrial adenocarcinoma in a rat model of human cancer2006Licentiatavhandling, monografi (Övrigt vetenskapligt)
  • 6.
    Karlsson, Sandra
    Högskolan i Skövde, Forskningscentrum för Systembiologi. Högskolan i Skövde, Institutionen för vård och natur.
    Gene Expression Patterns in a Rat Model of Human Endometrial Adenocarcinoma2008Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
    Abstract [en]

    Endometrial cancer develops from the endometrium of the uterus and is the most common pelvic malignancy diagnosed in women in the western society. Similar to all cancer diseases, endometrial cancer is a disorder that results from complex patterns of genetic and epigenetic alterations involved in the malignant transformation. The BDII/Han rat model is unique for spontaneous hormonal carcinogenesis since more than 90% of the female virgins spontaneously develop endometrial cancer. The possibility to perform global gene expression profiling of tumor cells would likely provide important information of the genes and pathways that are aberrant in endometrial adenocarcinoma (EAC). The works in the present thesis have been focused on investigating the expression patterns in endometrial tumors.  The findings in this thesis involve the identification of a novel candidate tumor suppressor region of rat chromosome 10. This genomic segment contains 18 potential tumor suppressor genes. Preliminary microarray data analysis confirmed that this region might contain relevant candidate genes as the EACs on average had 3.8 times lower expression of Crk in comparison to the normal/premalignant endometrial tissue cultures. Furthermore, an expression analysis using qPCR, revealed a significant down-regulation of Myo1c and Hic.   We were also able to identify a group of genes associated with the TGF-Beta pathway that were differentially expressed between endometrial tumors and normal/pre-malignant endometrium. These results suggest that the TGF-Beta signaling pathway is disrupted in EAC. This has previously been demonstrated in human EAC, although this is the first report on aberrant expression of TGF-Beta downstream target genes.  Evaluation of Gpx3 down-regulation in the rat EAC cell lines revealed an almost complete loss of expression in a majority of the endometrial tumors. From methylation studies, we could conclude that the loss of expression of Gpx3 is correlated with biallelic hypermethylation in the Gpx3 promoter region. This result was confirmed with a demethylation study of EAC cell lines, where the Gpx3 mRNA expression was restored after treatment with a demethylation agent and a deacetylation inhibitor. We also showed that mRNA expression of the well-known oncogene, Met, was slightly higher in endometrial tumors with loss of Gpx3 expression. A likely consequence of loss of Gpx3 function is a higher amount of reactive oxygen species (ROS) in the cancer cell environment. Since it has been proposed that overproduction of ROS is required for the hypoxic activation of HIF-1, we suggest that loss of Gpx3 expression activates transcription of Met through induction of the transcription factor HIF-1. The loss of the protective properties of GPX3 most likely makes the endometrial cells more vulnerable to ROS damage and genome instability.  We extended the results obtained from the rat endometrial tumors to human material, and conducted expression analysis of GPX3 in 30 endometrial human tumors using qPCR. The results showed a uniformly down-regulation of GPX3 in 29 of the tumors, independent of tumor grade. We thus concluded that the down-regulation of GPX3 probably occurs at an early stage of EAC and therefore contributes to the EAC carcinogenesis. These results suggest that there are important clinical implications of GPX3 expression in EAC, both as a biomarker for EAC and as a potential target for therapeutics.

     

  • 7.
    Karlsson, Sandra
    et al.
    Högskolan i Skövde, Institutionen för vård och natur.
    Holmberg, Erik
    Högskolan i Skövde, Institutionen för vård och natur.
    Askerlund, Anders
    Högskolan i Skövde, Institutionen för vård och natur.
    Klinga-Levan, Karin
    Högskolan i Skövde, Institutionen för vård och natur.
    Altered transforming growth factor-β pathway expression pattern in rat endometrial cancer2007Ingår i: Cancer Genetics and Cytogenetics, ISSN 2210-7762, E-ISSN 2210-7770, Vol. 177, nr 1, s. 43-50Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Endometrial cancer is the most abundant female gynecologic malignancy, ranking fourth in incidence among invasive tumors in women. Females of the BDII inbred rat strain are extremely prone to endometrial adenocarcinoma (EAC), and approximately 90% of virgin females spontaneously develop EAC during their lifetime. Thus, these rats serve as a useful model for the genetic analysis of this malignancy. In the present work, gene expression profiling, by means of cDNA microarrays, was performed on cDNA from endometrial tumor cell lines and from cell lines derived from nonmalignant lesions/normal tissues of the endometrium. We identified several genes associated with the transforming growth factor-β (TGF-β) pathway to be differentially expressed between endometrial tumor cell lines and nonmalignant lesions by using clustering and statistical inference analyses. The expression levels of the genes involved in the TGF-β pathway were independently verified using semiquantitative reverse-transcription polymerase chain reaction. Repressed TGF-β signaling has been reported previously in EAC carcinogenesis, but this is the first report demonstrating aberrations in the expression of TGF-β downstream target genes. We propose that the irregularities present in TGF-β pathway among the majority of the EAC tumor cell lines may affect EAC carcinogenesis.

  • 8.
    Karlsson, Sandra
    et al.
    Högskolan i Skövde, Institutionen för vård och natur.
    Klinga-Levan, Karin
    Högskolan i Skövde, Institutionen för vård och natur.
    Expression Analysis of Human Endometrial Adenocarcinoma in an Inbred Rat Model2008Ingår i: Hormonal Carcinogenesis: Proceedings of the Fifth International Symposium, Springer , 2008, s. 503-509Konferensbidrag (Refereegranskat)
    Abstract [en]

    Endometrial cancer (EC) is the most abundant female gynaecologic malignancy, ranking fourth in incidence among invasive tumors in women. Hormone-related (estrogen-dependent) EC is the prevalent subtype and accounts for approximately 75% of these cancers. Females of the BDII inbred rat strain are extremely prone to endometrial adenocarcinoma, (EAC) and approximately 90% of virgin females spontaneously develop EAC during their life span. Thus, these rats serve as a useful model for the genetic analysis of this malignancy. In the present work, gene expression profiling, by means of cDNA microarrays, was performed on cDNA from endometrial tumor cell lines and from cell lines derived from nonmalignant lesions/normal tissues of the endometrium without specific findings (WSF). We identified numerous genes differentially expressed between endometrial cell lines and WSFs employing clustering analysis and statistical inference analysis. Many of the genes identified are located within or close to the chromosomal regions earlier identified to be associated with EAC susceptibility and development. Several of the genes identified are involved in pathways commonly altered in carcinogenesis, such as the TGF-pathway.

  • 9.
    Karlsson, Sandra
    et al.
    Högskolan i Skövde, Forskningscentrum för Systembiologi. Högskolan i Skövde, Institutionen för vård och natur.
    Olausson, Josefin
    Högskolan i Skövde, Institutionen för vård och natur.
    Lundh, Dan
    Högskolan i Skövde, Forskningscentrum för Systembiologi. Högskolan i Skövde, Institutionen för vård och natur.
    Sögård, Peter
    Högskolan i Skövde, Institutionen för vård och natur. Högskolan i Skövde, Forskningscentrum för Systembiologi.
    Mandal, Abul
    Högskolan i Skövde, Forskningscentrum för Systembiologi. Högskolan i Skövde, Institutionen för vård och natur.
    Holmström, Kjell-Ove
    Högskolan i Skövde, Forskningscentrum för Systembiologi. Högskolan i Skövde, Institutionen för vård och natur.
    Stahel, Anette
    Högskolan i Skövde, Institutionen för vård och natur.
    Bengtsson, Jenny
    Högskolan i Skövde, Institutionen för vård och natur.
    Larsson, Dennis
    Högskolan i Skövde, Forskningscentrum för Systembiologi. Högskolan i Skövde, Institutionen för vård och natur.
    Vitamin D and prostate cancer: The role of membrane initiated signaling pathways in prostate cancer progression2010Ingår i: Journal of Steroid Biochemistry and Molecular Biology, ISSN 0960-0760, E-ISSN 1879-1220, Vol. 121, nr 1-2, s. 413-416Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) has been demonstrated to mediate both genomic and non-genomic responses in prostate cancer (CaP) cells. Here, we give an overview of membrane initiated 1,25(OH)2D3 signaling in prostate cancer cell progression. The presence of PDIA3 was investigated and homologous modeling of the putative PDIA3 receptor complex was conducted. Furthermore, the cellular distribution of nVDR was analyzed. We could show that both nVDR and PDIA3 are expressed in the prostate cancer cell lines investigated. The homologous modeling of PDIA3 showed that the receptor complex exists in a trimer formation, which suggests for allosteric activity. Our findings support previous reports and suggest that 1,25(OH)2D3 is an important therapeutic agent in inhibiting prostate cancer progression. Furthermore, our data show that 1,25(OH)2D3 regulate prostate cell biology via multiple pathways and targeting specific pathways for 1,25(OH)2D3 might provide more effective therapies compared to the vitamin D therapies currently clinically tested.

  • 10.
    Karlsson, Sandra
    et al.
    Högskolan i Skövde, Forskningscentrum för Systembiologi. Högskolan i Skövde, Institutionen för vård och natur.
    Olsson, Björn
    Högskolan i Skövde, Forskningscentrum för Systembiologi. Högskolan i Skövde, Institutionen för vård och natur.
    Klinga-Levan, Karin
    Högskolan i Skövde, Forskningscentrum för Systembiologi. Högskolan i Skövde, Institutionen för vård och natur.
    Gene expression profiling predicts a three-gene expression signature of endometrial adenocarcinoma in a rat model2009Ingår i: Cancer Cell International, ISSN 1475-2867, E-ISSN 1475-2867, Vol. 9, s. Article Number: 12-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

     

    Background: In the Western world, endometrial cancers are the most common gynaecological neoplastic disorders among women. Initial symptoms are often vague and may be confused with several other conditions or disorders. Thus, there is a need for an easy and reliable diagnostic tool. The objective of this work was to identify a gene expression signature specific for endometrial adenocarcinomas to be used for testing potential endometrial biomarkers.

    Results: Changes in expression between endometrial adenocarcinomas and non-/pre-malignant endometrium from the BDII EAC rat model were compared in cDNA microarray assays. By employing classification analysis (Weka) on the expression data from approximately 5600 cDNA clones and TDT analysis on genotype data, we identified a three-gene signature (Gpx3, Bgn and Tgfb3). An independent analysis of differential expression, revealed a total of 354 cDNA clones with significant changes in expression. Among the 10 best ranked clones, Gpx3, Bgn and Tgfb3 were found.

     

    Conclusion: Taken together, we present a unique data set of genes with different expression patterns between EACs and non-/pre-malignant endometrium, and specifically we found three genes that were confirmed in two independent analyses. These three genes are candidates for an EAC signature and further evaluations of their involvement in EAC tumorigenesis will be undertaken.

  • 11.
    Larsson, Dennis
    et al.
    Högskolan i Skövde, Institutionen för vård och natur. Högskolan i Skövde, Forskningscentrum för Systembiologi.
    Jonas, Adele
    Högskolan i Skövde, Institutionen för vård och natur. Högskolan i Skövde, Forskningscentrum för Systembiologi.
    Bergsten, Niklas
    Högskolan i Skövde, Institutionen för vård och natur. Högskolan i Skövde, Forskningscentrum för Systembiologi.
    Ståhl, Fredrik
    University College of Borås, School of Health Sciences, Sweden.
    Karlsson, Sandra
    Högskolan i Skövde, Institutionen för vård och natur. Högskolan i Skövde, Forskningscentrum för Systembiologi.
    Membrane Initiated Effects of1α,25-Dihydroxyvitamin D3 inProstate Cancer Cells: Effects on AP1 and CREB Mediated Transcription2012Ingår i: Current Frontiers and Perspectives in Cell Biology / [ed] Stevo Najman, InTech, 2012, s. 153-162Kapitel i bok, del av antologi (Refereegranskat)
  • 12.
    Nordlander, Carola
    et al.
    CMB-Genetics, Lundberg Laboratory, Göteborg University, SE 40530 Gothenhurg, Sweden.
    Karlsson, Sandra
    Högskolan i Skövde, Institutionen för vård och natur.
    Karlsson, Åsa
    CMB-Genetics, Lundberg Laboratory, Göteborg University, SE 40530 Gothenhurg, Sweden / Division of Medicine/Oncology, Stanford School of Medicine, Stanford, CA 94305, United States.
    Sjöling, Åsa
    Institute of Biomedicine, Department of Microbiology and Immunology, Göteborg University, SE 40530 Gothenburg, Sweden.
    Winnes, Marta
    CMB-Genetics, Lundberg Laboratory, Göteborg University, SE 40530 Gothenhurg, Sweden / Lundberg Laboratory for Cancer Research, Department of Pathology, Göteborg University, 41345 Gothenburg, Sweden.
    Klinga-Levan, Karin
    Högskolan i Skövde, Institutionen för vård och natur.
    Behboudi, Afousz
    Institute of Biomedicine, Department of Clinical Genetics, Göteborg University, SE 40530 Gothenburg, Sweden / Institute of Biomedicine, Dept. Clinical Genetics, Göteborg University, 40530 Gothenburg, Sweden.
    Analysis of chromosome 10 aberrations in rat endometrial cancer: evidence for a tumor suppressor locus distal to Tp532007Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 120, nr 7, s. 1472-1481Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    We have recently shown in the BDII rat model of human endometrial adenocarcinoma (EAC), rat chromosome 10 (RNO10) is frequently involved in chromosomal aberrations. In the present study, we investigated the association between RNO10 deletions, allelic imbalance (AI) at RNO10q24 and Tp53 mutation in 27 rat EAC tumors. We detected chromosomal breakage accompanied by loss of proximal and/or gain of distal parts of RNO10 in approximately 2/3 of the tumors. This finding is suggestive of a tumor suppressor activity encoded from the proximal RNO10. Given the fact that Tp53 is located at RNO10q24-q25, we then performed Tp53 mutation analysis. However, we could not find a strong correlation between AI/deletions at RNO10q24 and Tp53 mutation. Instead, the observed patterns for AI, chromosomal breaks and deletions suggest that major selection was directed against a region located close to, but distal of Tp53. In different human malignancies a similar situation of AI at chromosome band 17p13.3 (HSA17p13.3) unassociated with TP53 mutation has been observed. Although RNO10 is largely homologous to HSA17, the conservation with respect to gene order among them is not extensive. We utilized publicly available draft DNA sequences to study intrachromosomal rearrangement during the divergence between HSA17 and RNO10. By using reciprocal comparison of rat and human genome data, we could substantially narrow down the candidate tumor suppressor region in rat from 3 Mb to a chromosomal segment of about 0.5 Mb in size. These results provide scientific groundwork for identification of the putative tumor suppressor gene(s) at 17p13.3 in human tumors

1 - 12 av 12
RefereraExporteraLänk till träfflistan
Permanent länk
Referera
Referensformat
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annat format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annat språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf