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Hedberg Oldfors, C., Garcia Dios, D., Linder, A., Visuttijai, K., Samuelson, E., Karlsson, S., . . . Behboudi, A. (2015). Analysis of an independent tumor suppressor locus telomeric to Tp53 suggested Inpp5k and Myo1c as novel tumor suppressor gene candidates in this region. BMC Genetics, 16(1), Article ID 80.
Open this publication in new window or tab >>Analysis of an independent tumor suppressor locus telomeric to Tp53 suggested Inpp5k and Myo1c as novel tumor suppressor gene candidates in this region
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2015 (English)In: BMC Genetics, ISSN 1471-2156, E-ISSN 1471-2156, Vol. 16, no 1, article id 80Article in journal (Refereed) Published
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.

Keywords
cancer, Myosin-1c, Inpp5k, tumor suppressor
National Category
Basic Medicine
Research subject
Medical sciences
Identifiers
urn:nbn:se:his:diva-12031 (URN)10.1186/s12863-015-0238-4 (DOI)000357852600001 ()26170120 (PubMedID)2-s2.0-84937029410 (Scopus ID)
Funder
Knowledge Foundation, 20120311Åke Wiberg Foundation, 946217602
Available from: 2016-03-14 Created: 2016-03-14 Last updated: 2018-01-10Bibliographically approved
Larsson, D., Jonas, A., Bergsten, N., Ståhl, F. & Karlsson, S. (2012). Membrane Initiated Effects of1α,25-Dihydroxyvitamin D3 inProstate Cancer Cells: Effects on AP1 and CREB Mediated Transcription. In: Stevo Najman (Ed.), Current Frontiers and Perspectives in Cell Biology: (pp. 153-162). InTech
Open this publication in new window or tab >>Membrane Initiated Effects of1α,25-Dihydroxyvitamin D3 inProstate Cancer Cells: Effects on AP1 and CREB Mediated Transcription
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2012 (English)In: Current Frontiers and Perspectives in Cell Biology / [ed] Stevo Najman, InTech, 2012, p. 153-162Chapter in book (Refereed)
Place, publisher, year, edition, pages
InTech, 2012
National Category
Biological Sciences
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-6484 (URN)10.5772/32908 (DOI)978-953-51-0544-2 (ISBN)
Available from: 2012-10-09 Created: 2012-10-09 Last updated: 2017-11-27Bibliographically approved
Falck, E., Karlsson, S., Carlsson, J., Helenius, G., Karlsson, M. & Klinga-Levan, K. (2010). Loss of Glutathione peroxidase 3 expression is correlated with epigenetic mechanisms in endometrial adenocarcinoma. Cancer Cell International, 10, 46
Open this publication in new window or tab >>Loss of Glutathione peroxidase 3 expression is correlated with epigenetic mechanisms in endometrial adenocarcinoma
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2010 (English)In: Cancer Cell International, ISSN 1475-2867, E-ISSN 1475-2867, Vol. 10, p. 46-Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
BioMed Central, 2010
Keywords
Gpx3, endometrial cancer, methylation, real time PCR, FIGO grades
National Category
Natural Sciences
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-4708 (URN)10.1186/1475-2867-10-46 (DOI)000285883400001 ()2-s2.0-78549258157 (Scopus ID)
Available from: 2011-02-02 Created: 2011-02-02 Last updated: 2017-12-11Bibliographically approved
Karlsson, S., Olausson, J., Lundh, D., Sögård, P., Mandal, A., Holmström, K.-O., . . . Larsson, D. (2010). Vitamin D and prostate cancer: The role of membrane initiated signaling pathways in prostate cancer progression. Journal of Steroid Biochemistry and Molecular Biology, 121(1-2), 413-416
Open this publication in new window or tab >>Vitamin D and prostate cancer: The role of membrane initiated signaling pathways in prostate cancer progression
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2010 (English)In: Journal of Steroid Biochemistry and Molecular Biology, ISSN 0960-0760, E-ISSN 1879-1220, Vol. 121, no 1-2, p. 413-416Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
Elsevier, 2010
Keywords
1, 25(OH)2D3, Prostate cancer, Membrane receptors, PDIA3, nVDR, Receptor modeling
National Category
Natural Sciences
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-4528 (URN)10.1016/j.jsbmb.2010.03.083 (DOI)000280600200091 ()20398754 (PubMedID)2-s2.0-77954760891 (Scopus ID)
Available from: 2011-01-03 Created: 2011-01-03 Last updated: 2017-12-20Bibliographically approved
Karlsson, S., Olsson, B. & Klinga-Levan, K. (2009). Gene expression profiling predicts a three-gene expression signature of endometrial adenocarcinoma in a rat model. Cancer Cell International, 9, Article Number: 12
Open this publication in new window or tab >>Gene expression profiling predicts a three-gene expression signature of endometrial adenocarcinoma in a rat model
2009 (English)In: Cancer Cell International, ISSN 1475-2867, E-ISSN 1475-2867, Vol. 9, p. Article Number: 12-Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
BioMed Central, 2009
National Category
Natural Sciences
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-3296 (URN)10.1186/1475-2867-9-12 (DOI)000273352000001 ()19426485 (PubMedID)2-s2.0-66749132843 (Scopus ID)
Available from: 2009-07-09 Created: 2009-07-09 Last updated: 2017-12-13Bibliographically approved
Karlsson, S. & Klinga-Levan, K. (2008). Expression Analysis of Human Endometrial Adenocarcinoma in an Inbred Rat Model. In: Hormonal Carcinogenesis: Proceedings of the Fifth International Symposium. Paper presented at International symposium on Hormonal Carcinogenesis (pp. 503-509). Springer
Open this publication in new window or tab >>Expression Analysis of Human Endometrial Adenocarcinoma in an Inbred Rat Model
2008 (English)In: Hormonal Carcinogenesis: Proceedings of the Fifth International Symposium, Springer , 2008, p. 503-509Conference paper, Published paper (Refereed)
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.

Place, publisher, year, edition, pages
Springer, 2008
Series
Advances in Experimental Medicine and Biology, ISSN 0065-2598 ; 617
National Category
Biochemistry and Molecular Biology
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-2732 (URN)10.1007/978-0-387-69080-3 (DOI)000253701800050 ()2-s2.0-46749125797 (Scopus ID)978-0-387-69078-0 (ISBN)
Conference
International symposium on Hormonal Carcinogenesis
Available from: 2009-02-11 Created: 2009-02-11 Last updated: 2017-11-27Bibliographically approved
Karlsson, S. (2008). Gene Expression Patterns in a Rat Model of Human Endometrial Adenocarcinoma. (Doctoral dissertation). Göteborgs universitet
Open this publication in new window or tab >>Gene Expression Patterns in a Rat Model of Human Endometrial Adenocarcinoma
2008 (English)Doctoral thesis, comprehensive summary (Other academic)
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.

 

Place, publisher, year, edition, pages
Göteborgs universitet, 2008. p. 46
National Category
Cell and Molecular Biology
Research subject
Medical sciences
Identifiers
urn:nbn:se:his:diva-2711 (URN)978-91-628-7648-7 (ISBN)
Public defence
(English)
Note

List of Papers: I. Analysis of chromosome 10 aberrations in rat endometrial cancer-evidence for a tumor suppressor distal to Tp53. Nordlander, C., Karlsson, S., Karlsson, A., Sjöling, A., Winnes, M., Klinga-Levan, K., and Behboudi, A. Int J Cancer. (2007), 120(7), 1472-1481 II. Altered TGF-Beta pathway expression pattern in rat endometrical cancer. Karlsson, S., Holmberg, E., Askerlund, A., and Klinga-Levan, K. Cancer Genet Cytogenet. (2007), 177(1), 43-50 III. Gene expression profiling predicts a three-gene expression signature of endometrical adenocarcinoma in a rat model. Karlsson, S., Olsson, B., and Klinga-Levan, K. Submitted IV. Loss of expression of Glutathione peroxidase 3 in endometrical cancer is correlated with epigenetic mechanisms. Karlsson, S., Falck, E., Carlsson, J., Helenius, G., Karlsson, M., and Klinga-Levan, K. Manuscript

Available from: 2010-04-09 Created: 2009-02-09 Last updated: 2018-01-13Bibliographically approved
Hagberg, M., Holmén, J., Olausson, J., Karlsson, S., Johansson, V. & Larsson, D. (2008). Rapid activation of JNK/SAPK in LNCaP prostate cancer cells by 1α,25-dihydroxyvitamin D3 is independent of PDIA3 (1,25-MARRS). Current Topics in Steroid Research, 5, 17-24
Open this publication in new window or tab >>Rapid activation of JNK/SAPK in LNCaP prostate cancer cells by 1α,25-dihydroxyvitamin D3 is independent of PDIA3 (1,25-MARRS)
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2008 (English)In: Current Topics in Steroid Research, ISSN 0972-4788, Vol. 5, p. 17-24Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
Research Trends, 2008
Keywords
vitamin D, MAP kinase, JNK/SAPK, VDR, PDIA3, LNCaP, prostate cancer, 1α, 25(OH)2D3, siRNA, membrane initiated steroid signaling, MISS, alkaline phosphatase
National Category
Biochemistry and Molecular Biology Cancer and Oncology
Identifiers
urn:nbn:se:his:diva-2429 (URN)
Available from: 2008-12-05 Created: 2008-12-05 Last updated: 2019-07-03Bibliographically approved
Karlsson, S., Holmberg, E., Askerlund, A. & Klinga-Levan, K. (2007). Altered transforming growth factor-β pathway expression pattern in rat endometrial cancer. Cancer Genetics and Cytogenetics, 177(1), 43-50
Open this publication in new window or tab >>Altered transforming growth factor-β pathway expression pattern in rat endometrial cancer
2007 (English)In: Cancer Genetics and Cytogenetics, ISSN 2210-7762, E-ISSN 2210-7770, Vol. 177, no 1, p. 43-50Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
Elsevier, 2007
Identifiers
urn:nbn:se:his:diva-2186 (URN)10.1016/j.cancergencyto.2007.05.010 (DOI)000249038900007 ()17693190 (PubMedID)2-s2.0-34547693516 (Scopus ID)
Available from: 2008-06-12 Created: 2008-06-12 Last updated: 2017-12-12Bibliographically approved
Nordlander, C., Karlsson, S., Karlsson, Å., Sjöling, Å., Winnes, M., Klinga-Levan, K. & Behboudi, A. (2007). Analysis of chromosome 10 aberrations in rat endometrial cancer: evidence for a tumor suppressor locus distal to Tp53. International Journal of Cancer, 120(7), 1472-1481
Open this publication in new window or tab >>Analysis of chromosome 10 aberrations in rat endometrial cancer: evidence for a tumor suppressor locus distal to Tp53
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2007 (English)In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 120, no 7, p. 1472-1481Article in journal (Refereed) Published
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

Place, publisher, year, edition, pages
John Wiley & Sons, 2007
Keywords
BDII, endometrial adenocarcinoma, RNO10, 17p13.3, allelic imbalance, Tp53 mutation, tumor suppressor gene
Identifiers
urn:nbn:se:his:diva-2027 (URN)10.1002/ijc.22533 (DOI)000244610700013 ()17245700 (PubMedID)2-s2.0-33847687821 (Scopus ID)
Available from: 2008-05-07 Created: 2008-05-07 Last updated: 2017-12-12Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-6364-3850

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