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Behboudi, Afrouz, ProfessorORCID iD iconorcid.org/0000-0003-2525-3752
Publications (10 of 35) Show all publications
Peker, Y., Celik, Y., Yucel-Lindberg, T. & Behboudi, A. (2023). Association of TNF-α (-308 G/A) Gene Polymorphism With the Changes in Circulating TNF-α Levels Over 12 Months in Response to CPAP Treatment in the RICCADSA Cohort. Paper presented at American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Journal of Respiratory and Critical Care Medicine, 207, Article ID A2714.
Open this publication in new window or tab >>Association of TNF-α (-308 G/A) Gene Polymorphism With the Changes in Circulating TNF-α Levels Over 12 Months in Response to CPAP Treatment in the RICCADSA Cohort
2023 (English)In: American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, E-ISSN 1535-4970, Vol. 207, article id A2714Article in journal, Meeting abstract (Other academic) Published
Place, publisher, year, edition, pages
American Thoracic Society, 2023
National Category
Respiratory Medicine and Allergy
Research subject
Translational Medicine TRIM
Identifiers
urn:nbn:se:his:diva-22572 (URN)10.1164/ajrccm-conference.2023.207.1_MeetingAbstracts.A2714 (DOI)
Conference
American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC
Funder
Swedish Research CouncilSwedish Heart Lung Foundation
Note

A109. MICE TO HUMANS: MECHANISTIC DISCOVERIES IN SLEEP APNEA

This abstract is funded by: Swedish Research Council, Swedish Heart and Lung Foundation, Resmed Foundation, and resMed Inc

Available from: 2023-05-24 Created: 2023-05-24 Last updated: 2023-06-12Bibliographically approved
Celik, Y., Peker, Y., Yucel-Lindberg, T., Thelander, T. & Behboudi, A. (2023). Association of TNF-α (-308G/A) Gene Polymorphism with Changes in Circulating TNF-α Levels in Response to CPAP Treatment in Adults with Coronary Artery Disease and Obstructive Sleep Apnea. Journal of Clinical Medicine, 12(16), Article ID 5325.
Open this publication in new window or tab >>Association of TNF-α (-308G/A) Gene Polymorphism with Changes in Circulating TNF-α Levels in Response to CPAP Treatment in Adults with Coronary Artery Disease and Obstructive Sleep Apnea
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2023 (English)In: Journal of Clinical Medicine, E-ISSN 2077-0383, Vol. 12, no 16, article id 5325Article in journal (Refereed) Published
Abstract [en]

Rationale: We recently demonstrated that patients with coronary artery disease (CAD) and obstructive sleep apnea (OSA) carrying the tumor necrosis factor-alpha (TNF-α) A allele had increased circulating TNF-α levels compared with the ones carrying the TNF-α G allele. In the current study, we addressed the effect of TNF-α (-308G/A) gene polymorphism on circulating TNF-α levels following continuous positive airway pressure (CPAP) therapy. Methods: This study was a secondary analysis of the RICCADSA trial (NCT00519597) conducted in Sweden. CAD patients with OSA (apnea–hypopnea index) of ≥15 events/h and an Epworth Sleepiness Scale (ESS) score of <10 were randomized to CPAP or no-CPAP groups, and OSA patients with an ESS score of ≥10 were offered CPAP treatment. Blood samples were obtained at baseline and 12-month follow-up visits. TNF-α was measured by immunoassay (Luminex, R&D Systems). Genotyping of TNF-α-308G/A (single nucleotide polymorphism Rs1800629) was performed by polymerase chain reaction–restriction fragment length polymorphism. Results: In all, 239 participants (206 men and 33 women; mean age 64.9 (SD 7.7) years) with polymorphism data and circulating levels of TNF-α at baseline and 1-year follow-up visits were included. The median circulating TNF-α values fell in both groups between baseline and 12 months with no significant within- or between-group differences. In a multivariate linear regression model, a significant change in circulating TNF-α levels from baseline across the genotypes from GA to GA and GA to AA (standardized β-coefficient −0.129, 95% confidence interval (CI) −1.82; −0.12; p = 0.025) was observed in the entire cohort. The association was more pronounced among the individuals who were using the device for at least 4 h/night (n = 86; standardized β-coefficient −2.979 (95% CI −6.11; −1.21); p = 0.004)), whereas no significant association was found among the patients who were non-adherent or randomized to no-CPAP. The participants carrying the TNF-α A allele were less responsive to CPAP treatment regarding the decline in circulating TNF-α despite CPAP adherence (standardized β-coefficient −0.212, (95% CI −5.66; −1.01); p = 0.005). Conclusions: Our results suggest that TNF-α (-308G/A) gene polymorphism is associated with changes in circulating TNF-α levels in response to CPAP treatment in adults with CAD and OSA. 

Place, publisher, year, edition, pages
MDPI, 2023
Keywords
coronary artery disease, obstructive sleep apnea, tumor necrosis factor
National Category
Cardiac and Cardiovascular Systems Neurology Rheumatology and Autoimmunity
Research subject
Translational Medicine TRIM
Identifiers
urn:nbn:se:his:diva-23190 (URN)10.3390/jcm12165325 (DOI)001057693200001 ()37629366 (PubMedID)2-s2.0-85169096048 (Scopus ID)
Funder
Swedish Research Council, 521-2011-537, 521-2013-3439Swedish Heart Lung Foundation, 20080592, 20090708, 20100664Region Västra Götaland, ALFGBG-11538, ALFGBG-150801Lund University
Note

CC BY 4.0

© 2023 by the authors.

Correspondence: yuksel.peker@lungall.gu.se

This study was supported by grants from the Swedish Research Council (521-2011-537 and 521-2013-3439); the Swedish Heart–Lung Foundation (20080592, 20090708, and 20100664); the “Agreement concerning research and education of doctors” of Västra Götalandsregionen (ALFGBG-11538 and ALFGBG-150801); the research fund at Skaraborg Hospital (VGSKAS-4731, VGSKAS-5908,VGSKAS-9134, VGSKAS-14781, VGSKAS-40271, and VGSKAS-116431); Skaraborg Research and Development Council (VGFOUSKB-46371); Lund University; the Heart Foundation of Kärnsjukhuset; the ResMed Foundation; and ResMed Ltd. None of the funders had any direct influence on the design of the study, the analysis of the data, data collection, the drafting of the manuscript, or the decision to publish.

Available from: 2023-09-07 Created: 2023-09-07 Last updated: 2024-01-26Bibliographically approved
Celik, Y., Behboudi, A., Peker, Y., Redline, S. S., Jelic, S. & Gottlieb, D. J. (2023). Impact of Continuous Positive Airway Pressure on Serum Angiopoietin-2 Following Coronary Revascularization in Patients With Obstructive Sleep Apnea: The RICCADSA Study. Paper presented at American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Journal of Respiratory and Critical Care Medicine, 207, Article ID A6268.
Open this publication in new window or tab >>Impact of Continuous Positive Airway Pressure on Serum Angiopoietin-2 Following Coronary Revascularization in Patients With Obstructive Sleep Apnea: The RICCADSA Study
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2023 (English)In: American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, E-ISSN 1535-4970, Vol. 207, article id A6268Article in journal, Meeting abstract (Other academic) Published
Place, publisher, year, edition, pages
American Thoracic Society, 2023
National Category
Respiratory Medicine and Allergy
Research subject
Translational Medicine TRIM
Identifiers
urn:nbn:se:his:diva-22573 (URN)10.1164/ajrccm-conference.2023.207.1_MeetingAbstracts.A6268 (DOI)
Conference
American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC
Funder
Swedish Research CouncilSwedish Heart Lung FoundationNIH (National Institutes of Health), R01HL137234, R01 HL106041
Note

D20. MECHANISTIC INSIGHTS IN SLEEP DISORDERED BREATHING

The main RICCADSA trial was supported by the Swedish Research Council, the Swedish Heart and Lung Foundation, ResMed Foundation and ResMed Inc. The present study was supported by NIH grants R01HL137234 and R01 HL106041.

Available from: 2023-05-24 Created: 2023-05-24 Last updated: 2023-11-28Bibliographically approved
Behboudi, A., Thelander, T., Yazici, D., Celik, Y., Yucel-Lindberg, T., Thunström, E. & Peker, Y. (2021). Association of TNF-alpha (-308G/A) Gene Polymorphism with Circulating TNF-alpha Levels and Excessive Daytime Sleepiness in Adults with Coronary Artery Disease and Concomitant Obstructive Sleep Apnea. Journal of Clinical Medicine, 10(15), Article ID 3413.
Open this publication in new window or tab >>Association of TNF-alpha (-308G/A) Gene Polymorphism with Circulating TNF-alpha Levels and Excessive Daytime Sleepiness in Adults with Coronary Artery Disease and Concomitant Obstructive Sleep Apnea
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2021 (English)In: Journal of Clinical Medicine, E-ISSN 2077-0383, Vol. 10, no 15, article id 3413Article in journal (Refereed) Published
Abstract [en]

Obstructive sleep apnea (OSA) is common in patients with coronary artery disease (CAD), in which inflammatory activity has a crucial role. The manifestation of OSA varies significantly between individuals in clinical cohorts; not all adults with OSA demonstrate the same set of symptoms; i.e., excessive daytime sleepiness (EDS) and/or increased levels of inflammatory biomarkers. The further exploration of the molecular basis of these differences is therefore essential for a better understanding of the OSA phenotypes in cardiac patients. In this current secondary analysis of the Randomized Intervention with Continuous Positive Airway Pressure in CAD and OSA (RICCADSA) trial (Trial Registry: ClinicalTrials.gov; No: NCT 00519597), we aimed to address the association of tumor necrosis factor alpha (TNF-α)-308G/A gene polymorphism with circulating TNF-α levels and EDS among 326 participants. CAD patients with OSA (apnea–hypopnea-index (AHI) ≥ 15 events/h; n = 256) were categorized as having EDS (n = 100) or no-EDS (n = 156) based on the Epworth Sleepiness Scale score with a cut-off of 10. CAD patients with no-OSA (AHI < 5 events/h; n = 70) were included as a control group. The results demonstrated no significant differences regarding the distribution of the TNF-α alleles and genotypes between CAD patients with vs. without OSA. In a multivariate analysis, the oxygen desaturation index and TNF-α genotypes from GG to GA and GA to AA as well as the TNF-α-308A allele carriage were significantly associated with the circulating TNF-α levels. Moreover, the TNF-α-308A allele was associated with a decreased risk for EDS (odds ratio 0.64, 95% confidence interval 0.41–0.99; p = 0.043) independent of age, sex, obesity, OSA severity and the circulating TNF-α levels. We conclude that the TNF-α-308A allele appears to modulate circulatory TNF-α levels and mitigate EDS in adults with CAD and concomitant OSA.

Place, publisher, year, edition, pages
MDPI, 2021
Keywords
coronary artery disease, obstructive sleep apnea, tumor necrosis factor
National Category
Cardiac and Cardiovascular Systems Respiratory Medicine and Allergy Medical Genetics
Research subject
Translational Medicine TRIM
Identifiers
urn:nbn:se:his:diva-20494 (URN)10.3390/jcm10153413 (DOI)000682078800001 ()34362196 (PubMedID)2-s2.0-85114081185 (Scopus ID)
Note

CC BY 4.0

Available from: 2021-08-20 Created: 2021-08-20 Last updated: 2022-09-02Bibliographically approved
Peker, Y., Thelander, T., Yazici, D., Celik, Y., Yucel-Lindberg, T., Thunström, E. & Behboudi, A. (2021). Association of TNF-α (-308G/A) Gene Polymorphism with Circulating TNF-α Levels and Excessive Daytime Sleepiness in Adults with Coronary Artery Disease and Concomitant Obstructive Sleep Apnea. Paper presented at American Thoracic Society 2021 International Conference, May 14-19, 2021. American Journal of Respiratory and Critical Care Medicine, 203(9 suppl S), Article ID A4713.
Open this publication in new window or tab >>Association of TNF-α (-308G/A) Gene Polymorphism with Circulating TNF-α Levels and Excessive Daytime Sleepiness in Adults with Coronary Artery Disease and Concomitant Obstructive Sleep Apnea
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2021 (English)In: American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, E-ISSN 1535-4970, Vol. 203, no 9 suppl S, article id A4713Article in journal, Meeting abstract (Other academic) Published
Place, publisher, year, edition, pages
American Thoracic Society, 2021
National Category
Cardiac and Cardiovascular Systems
Research subject
Translational Medicine TRIM
Identifiers
urn:nbn:se:his:diva-22571 (URN)10.1164/ajrccm-conference.2021.203.1_MeetingAbstracts.A4713 (DOI)000685468904693 ()
Conference
American Thoracic Society 2021 International Conference, May 14-19, 2021
Funder
Swedish Research CouncilSwedish Heart Lung Foundation
Note

TP132. TP132 EPIDEMIOLOGY AND GENETICS OF SLEEP DISORDERS: EXAMINE THE LATEST ADVANCES!

This abstract is funded by: The Swedish Research Council, The Swedish Heart and Lung Foundation, The Resmed Foundation

Available from: 2023-05-24 Created: 2023-05-24 Last updated: 2023-08-22Bibliographically approved
Visuttijai, K., Pettersson, J., Mehrbani Azar, Y., van den Bout, I., Örndal, C., Marcickiewicz, J., . . . Behboudi, A. (2016). Lowered Expression of Tumor Suppressor Candidate MYO1C Stimulates Cell Proliferation, Suppresses Cell Adhesion and Activates AKT. PLOS ONE, 11(10), Article ID e0164063.
Open this publication in new window or tab >>Lowered Expression of Tumor Suppressor Candidate MYO1C Stimulates Cell Proliferation, Suppresses Cell Adhesion and Activates AKT
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2016 (English)In: PLOS ONE, E-ISSN 1932-6203, Vol. 11, no 10, article id e0164063Article in journal (Refereed) Published
Abstract [en]

Myosin-1C (MYO1C) is a tumor suppressor candidate located in a region of recurrent losses distal to TP53. Myo1c can tightly and specifically bind to PIP2, the substrate of Phosphoinositide 3-kinase (PI3K), and to Rictor, suggesting a role for MYO1C in the PI3K pathway. This study was designed to examine MYO1C expression status in a panel of well-stratified endometrial carcinomas as well as to assess the biological significance of MYO1C as a tumor suppressor in vitro. We found a significant correlation between the tumor stage and lowered expression of MYO1C in endometrial carcinoma samples. In cell transfection experiments, we found a negative correlation between MYO1C expression and cell proliferation, and MYO1C silencing resulted in diminished cell migration and adhesion. Cells expressing excess of MYO1C had low basal level of phosphorylated protein kinase B (PKB, a.k.a. AKT) and cells with knocked down MYO1C expression showed a quicker phosphorylated AKT (pAKT) response in reaction to serum stimulation. Taken together the present study gives further evidence for tumor suppressor activity of MYO1C and suggests MYO1C mediates its tumor suppressor function through inhibition of PI3K pathway and its involvement in loss of contact inhibition.

Place, publisher, year, edition, pages
Public Library of Science, 2016
Keywords
MYO1C, myosin-1c, tumor suppressor, AKT signaling
National Category
Other Medical Sciences
Research subject
Medical sciences; Bioinformatics
Identifiers
urn:nbn:se:his:diva-13020 (URN)10.1371/journal.pone.0164063 (DOI)000385698100017 ()27716847 (PubMedID)2-s2.0-84991449467 (Scopus ID)
Projects
Cellular, Molecular and Functional Characterization of the Tumor Suppressor Candidate MYO1C
Note

CC BY 4.0

Available from: 2016-10-11 Created: 2016-10-11 Last updated: 2023-09-21
Visuttijai, K., Ejeskär, K. & Behboudi, A. (2015). Analyses of protein expression of PI 3-kinase/AKT signaling in response to altered expression of motor protein MYO1C. Paper presented at 106th Annual Meeting of the American Association for Cancer Research (AACR), Philadelphia, PA, April 18-22, 2015. Cancer Research, 75(15 Supplement), Article ID 2166.
Open this publication in new window or tab >>Analyses of protein expression of PI 3-kinase/AKT signaling in response to altered expression of motor protein MYO1C
2015 (English)In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 75, no 15 Supplement, article id 2166Article in journal, Meeting abstract (Refereed) Published
Place, publisher, year, edition, pages
American Association for Cancer Research, 2015
National Category
Genetics Cancer and Oncology
Identifiers
urn:nbn:se:his:diva-22682 (URN)10.1158/1538-7445.am2015-2166 (DOI)000371578504271 ()
Conference
106th Annual Meeting of the American Association for Cancer Research (AACR), Philadelphia, PA, April 18-22, 2015
Available from: 2023-06-12 Created: 2023-06-12 Last updated: 2023-06-13Bibliographically approved
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, 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.

Place, publisher, year, edition, pages
Biomed Central, 2015
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: 2024-01-17Bibliographically approved
Samuelson, E., Karlsson, S., Partheen, K., Nilsson, S., Szpirer, C. & Behboudi, A. (2012). BAC CGH-array identified specific small-scale genomic imbalances in diploid DMBA-induced rat mammary tumors. BMC Cancer, 12, Article ID 352.
Open this publication in new window or tab >>BAC CGH-array identified specific small-scale genomic imbalances in diploid DMBA-induced rat mammary tumors
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2012 (English)In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 12, article id 352Article in journal (Refereed) Published
Abstract [en]

Background: Development of breast cancer is a multistage process influenced by hormonal and environmental factors as well as by genetic background. The search for genes underlying this malignancy has recently been highly productive, but the etiology behind this complex disease is still not understood. In studies using animal cancer models, heterogeneity of the   genetic background and environmental factors is reduced and thus analysis and identification of genetic aberrations in tumors may become easier. To identify chromosomal regions   potentially involved in the initiation and progression of mammary cancer, in the present   work we subjected a subset of experimental mammary tumors to cytogenetic and molecular   genetic analysis.

Methods: Mammary tumors were induced with DMBA (7,12-dimethylbenz[a]anthrazene) in female rats from the susceptible SPRD-Cu3 strain and from crosses and backcrosses between this strain and the resistant WKY strain. We first produced a general overview of chromosomal aberrations in the tumors using conventional kartyotyping (G-banding) and Comparative Genome Hybridization (CGH) analyses. Particular chromosomal changes were then analyzed in more details using an in-house developed BAC (bacterial artificial chromosome) CGH-array platform.

Results: Tumors appeared to be diploid by conventional karyotyping, however several sub-microscopic chromosome gains or losses in the tumor material were identified by BAC CGH-array analysis. An oncogenetic tree analysis based on the BAC CGH-array data suggested gain of rat chromosome (RNO) band 12q11, loss of RNO5q32 or RNO6q21 as the earliest events in the development of these mammary tumors.

Conclusions: Some of the identified changes appear to be more specific for DMBA-induced mammary tumors and some are similar to those previously reported in ACI rat model for estradiol-induced mammary tumors. The later group of changes is more interesting, since they may represent anomalies that involve genes with a critical role in mammary tumor development. Genetic changes identified in this work are at very small scales and thus may provide a more feasible basis for the identification of the target gene(s). Identification of the genes underlying these chromosome changes can provide new insights to the mechanisms   of mammary carcinogenesis.

Place, publisher, year, edition, pages
BioMed Central (BMC), 2012
National Category
Biological Sciences
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-6545 (URN)10.1186/1471-2407-12-352 (DOI)000310632100001 ()22894538 (PubMedID)2-s2.0-84864931479 (Scopus ID)
Funder
The Royal Swedish Academy of Sciences, FOA07B-089Royal Physiographic Society in LundAdlerbertska Research Foundation
Note

CC BY 2.0

This work was supported by The Royal Swedish Academy of Sciences (FOA07B-089), The Royal Physiographic Society in Lund (Nilsson-Ehle Foundation), Assar Gabrielsson Research Foundation for Clinical Cancer Research (FB07-87), Gunvor and Ivan Svensson Foundation, The Royal Society of Arts and Sciences in Gothenburg, Adlerbertska Research Foundation and the Fund for Scientific Medical Research (FRSM, 3.4517.05)

Available from: 2012-10-17 Created: 2012-10-17 Last updated: 2023-06-12
Falck, E., Behboudi, A. & Klinga-Levan, K. (2012). The impact of the genetic background on the genome make-up of tumor cells. Genes, Chromosomes and Cancer, 51(5), 438-446
Open this publication in new window or tab >>The impact of the genetic background on the genome make-up of tumor cells
2012 (English)In: Genes, Chromosomes and Cancer, ISSN 1045-2257, E-ISSN 1098-2264, Vol. 51, no 5, p. 438-446Article in journal (Refereed) Published
Abstract [en]

Endometrial adenocarcinoma (EAC) is the most common form of malignancy in the female genital tract, ranking as the fourth leading form of invasive tumors that affect women. The BDII inbred rat strain has been used as a powerful tumor model in studies of the genetic background of EAC. Females from the BDII strain are prone to develop tumors with an incidence of more than 90%. Development of EAC in BDII female rats has similarities in pathogenesis, histopathological, and molecular properties to that of human, and thus represents a unique model for analysis of EAC tumorigenesis and for comparative studies in human EACs. In a previous study, a set of rat EAC cell lines derived from tumors developed in female crossprogenies between BDII and nonsusceptible rat strains were analyzed by spectral karyotyping (SKY). Here we present an analysis with specific focus on the impact of different genetic backgrounds on the rate and occurrence of genetic aberrations in experimental tumors using data presented in the previous report. We could reveal that the ploidy state, and the abundance and type of structural as well as numerical change differed between the two genetic setups. We have also identified chromosomes harboring aberrations independent of genetic input from the nonsusceptible strains, which provide valuable information for the identification of the genes involved in the development of EAC in the BDII model as well as in human endometrial tumors.

Place, publisher, year, edition, pages
Wiley-Blackwell, 2012
National Category
Cancer and Oncology
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-5665 (URN)10.1002/gcc.21929 (DOI)000301118100003 ()22250046 (PubMedID)2-s2.0-84857997916 (Scopus ID)
Available from: 2012-04-02 Created: 2012-04-02 Last updated: 2023-05-25Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0003-2525-3752

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