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GET /v1/research/project/?format=api&offset=180&ordering=end_planned
{ "count": 2242, "next": "https://api-test.medunigraz.at/v1/research/project/?format=api&limit=20&offset=200&ordering=end_planned", "previous": "https://api-test.medunigraz.at/v1/research/project/?format=api&limit=20&offset=160&ordering=end_planned", "results": [ { "id": 1617, "title": { "de": "Phase 4 development EORTC Quality of Life module specific to Endometrail Cancer (EORTC QLQ-EN34)", "en": "Phase 4 development EORTC Quality of Life module specific to Endometrail Cancer (EORTC QLQ-EN34)" }, "short": "EORTC QLQ-EN34", "url": null, "abstract": { "de": "Endometrial cancer rates have risen over the last two decades, in some countries very significantly due to a combination of factors that includes an ageing population, increased obesity, and exposure to oestrogens.\r\nWith this burgeoning research agenda there is an urgent need to develop a specific quality of life measure for women with endometrial cancer that is sensitive to the impact of treatments so that their affect on quality of life can be assessed. In addition patients are increasingly encouraged to seek information about the impact of treatment on their quality of life so that they can make informed choices about their treatment and care.", "en": "Endometrial cancer rates have risen over the last two decades, in some countries very significantly due to a combination of factors that includes an ageing population, increased obesity, and exposure to oestrogens.\r\nWith this burgeoning research agenda there is an urgent need to develop a specific quality of life measure for women with endometrial cancer that is sensitive to the impact of treatments so that their affect on quality of life can be assessed. In addition patients are increasingly encouraged to seek information about the impact of treatment on their quality of life so that they can make informed choices about their treatment and care." }, "begin_planned": "2008-07-01T02:00:00+02:00", "begin_effective": "2008-07-01T02:00:00+02:00", "end_planned": "2010-09-30T02:00:00+02:00", "end_effective": "2010-09-30T02:00:00+02:00", "assignment": "2008-09-16T16:47:26+02:00", "program": null, "subprogram": null, "organization": 14038, "category": 10, "type": 10, "partner_function": 1, "manager": null, "contact": null, "status": 2, "research": 2, "grant": 10, "event": null, "study": null, "language": null, "funders": [ 442 ], "funder_projectcode": null, "ethics_committee": null, "edudract_number": null, "persons": [ "1617-57392-12" ] }, { "id": 1956, "title": { "de": "Schlaganfallrisikofaktoren in der Grazer Bevölkerung: Was bewirkt eine wiederholte Vorsorgeuntersuchung? Ergebnisse der Austrian Stroke Prevention Study", "en": "Schlaganfallrisikofaktoren in der Grazer Bevölkerung: Was bewirkt eine wiederholte Vorsorgeuntersuchung? Ergebnisse der Austrian Stroke Prevention Study" }, "short": "SCHLAGANFALLRISIKO_GRAZER_BEVOELK", "url": null, "abstract": { "de": null, "en": null }, "begin_planned": "2009-06-01T02:00:00+02:00", "begin_effective": "2009-06-01T02:00:00+02:00", "end_planned": "2010-09-30T02:00:00+02:00", "end_effective": "2010-09-30T02:00:00+02:00", "assignment": "2009-10-22T19:32:12+02:00", "program": null, "subprogram": null, "organization": 14051, "category": 10, "type": 10, "partner_function": 4, "manager": null, "contact": null, "status": 2, "research": 5, "grant": 10, "event": null, "study": null, "language": null, "funders": [ 457 ], "funder_projectcode": null, "ethics_committee": null, "edudract_number": null, "persons": [] }, { "id": 2126, "title": { "de": "Auswirkungen von Stressoren bei Kindern und Jugendlichen", "en": "Effects of stress in adolescents" }, "short": "STRESSOREN_KINDER_JUGENDLICHE", "url": null, "abstract": { "de": null, "en": null }, "begin_planned": "2010-03-01T01:00:00+01:00", "begin_effective": "2010-03-01T01:00:00+01:00", "end_planned": "2010-09-30T02:00:00+02:00", "end_effective": "2010-09-30T02:00:00+02:00", "assignment": "2010-02-22T11:26:29+01:00", "program": null, "subprogram": null, "organization": 29447, "category": 10, "type": 10, "partner_function": 1, "manager": null, "contact": null, "status": 2, "research": 2, "grant": 10, "event": null, "study": null, "language": null, "funders": [ 135 ], "funder_projectcode": null, "ethics_committee": null, "edudract_number": null, "persons": [ "2126-52274-11" ] }, { "id": 1581, "title": { "de": "Identification and functional characterisation of Nuclear Orphan Receptors as Tumor Suppressor Genes in aggressive non-Hodgkin`s Lymphomas and acute lymphoblastic leukemia", "en": "Identification and functional characterisation of Nuclear Orphan Receptors as Tumor Suppressor Genes in aggressive non-Hodgkin`s Lymphomas and acute lymphoblastic leukemia" }, "short": "non-Hodgkin`s Lymphoma", "url": null, "abstract": { "de": "NR4A1 (also called Nur77, TR3, or NGFI-B), NR4A2 (Nurr1 or RNR-1) and NR4A3 (Nor-1 or Minor) are three members of an orphan nuclear hormone receptor family referred to as Nur77 family. They are all transcription factors belonging to the superfamily of steroid nuclear hormone receptors. These nuclear hormone receptors (NR) are classified as early response genes, are induced by a diverse range of signals, including fatty acids, stress, growth factors, cytokines, peptide hormones, neurotransmitters, and physical stimuli for example magnetic fields or shear stress. In line with the pleiotropic physiological stimuli that induce the NR4A subgroup, these orphan NRs have been implicated in cell cycle regulation, apoptosis, inflammation, atherogenesis and more recently in carcinogenesis. \r\nThe ultimate growth of a tumour depends on not only the rate of tumour cell proliferation, but also the rate of tumour cell death (=apoptosis). NR4A1 controls both survival and death of cancer cells. \r\nIn contrast to NR4A1, only pro-survival effects, but not pro-apoptotic effects, have been reported for NR4A2. \r\nNR4A3 has been shown to be functionally redundant with NR4A1 in T-cell apoptosis. Results also suggest that NR4A1 and NR4A3 have non-redundant functions as well.\r\nThe most convincing evidence that nuclear orphan receptors function as critical tumor suppressors is the observation that the abrogation of nuclear receptors Nr4a3 and Nr4a1 leads to rapid development of acute myeloid leukemia. Evidence of nuclear orphan receptors acting as tumor suppressor genes in B-cell malignancies comes from the observation that Epstein-Barr virus EBNA 2 blocks NR4A1 mediated apoptosis in B-cells and from gene expression profiling in diffuse large B-cell lymphoma (DLBCL) in which over expression of NR4A3 is found in cured or refractory DLBCL, as opposed to a fatal course of disease. Hence, it is speculated that NR4A3 increases the apoptotic response to chemotherapy in curable DLBCL.\r\n\r\nThe aim of our study was to comprehensively study NR expression and function in B-cell malignancies and to define the nuclear orphan receptors NR4A1 and NR4A1 as cooperative putative tumor suppressor genes (TSG) in B-cell malignancies.\r\n\r\n", "en": "NR4A1 (also called Nur77, TR3, or NGFI-B), NR4A2 (Nurr1 or RNR-1) and NR4A3 (Nor-1 or Minor) are three members of an orphan nuclear hormone receptor family referred to as Nur77 family. They are all transcription factors belonging to the superfamily of steroid nuclear hormone receptors. These nuclear hormone receptors (NR) are classified as early response genes, are induced by a diverse range of signals, including fatty acids, stress, growth factors, cytokines, peptide hormones, neurotransmitters, and physical stimuli for example magnetic fields or shear stress. In line with the pleiotropic physiological stimuli that induce the NR4A subgroup, these orphan NRs have been implicated in cell cycle regulation, apoptosis, inflammation, atherogenesis and more recently in carcinogenesis. \r\nThe ultimate growth of a tumour depends on not only the rate of tumour cell proliferation, but also the rate of tumour cell death (=apoptosis). NR4A1 controls both survival and death of cancer cells. \r\nIn contrast to NR4A1, only pro-survival effects, but not pro-apoptotic effects, have been reported for NR4A2. \r\nNR4A3 has been shown to be functionally redundant with NR4A1 in T-cell apoptosis. Results also suggest that NR4A1 and NR4A3 have non-redundant functions as well.\r\nThe most convincing evidence that nuclear orphan receptors function as critical tumor suppressors is the observation that the abrogation of nuclear receptors Nr4a3 and Nr4a1 leads to rapid development of acute myeloid leukemia. Evidence of nuclear orphan receptors acting as tumor suppressor genes in B-cell malignancies comes from the observation that Epstein-Barr virus EBNA 2 blocks NR4A1 mediated apoptosis in B-cells and from gene expression profiling in diffuse large B-cell lymphoma (DLBCL) in which over expression of NR4A3 is found in cured or refractory DLBCL, as opposed to a fatal course of disease. Hence, it is speculated that NR4A3 increases the apoptotic response to chemotherapy in curable DLBCL.\r\n\r\nThe aim of our study was to comprehensively study NR expression and function in B-cell malignancies and to define the nuclear orphan receptors NR4A1 and NR4A1 as cooperative putative tumor suppressor genes (TSG) in B-cell malignancies." }, "begin_planned": "2008-10-01T02:00:00+02:00", "begin_effective": "2008-10-01T02:00:00+02:00", "end_planned": "2010-09-30T02:00:00+02:00", "end_effective": "2010-09-30T02:00:00+02:00", "assignment": "2008-07-17T12:24:53+02:00", "program": null, "subprogram": null, "organization": 14082, "category": 10, "type": 10, "partner_function": 4, "manager": 51930, "contact": 51930, "status": 2, "research": 1, "grant": 10, "event": null, "study": null, "language": null, "funders": [ 836 ], "funder_projectcode": null, "ethics_committee": null, "edudract_number": null, "persons": [ "1581-51930-10" ] }, { "id": 2391, "title": { "de": "Einfluss der Knochenentnahmetechnik auf die Osteoblastenaktivität", "en": "Effect of Bone Harvesting Methods to the Osteoblast activity" }, "short": "KNOCHENENTNAHME_OSTEOBLAST", "url": null, "abstract": { "de": null, "en": null }, "begin_planned": "2009-04-01T02:00:00+02:00", "begin_effective": "2011-01-26T01:00:00+01:00", "end_planned": "2010-10-01T02:00:00+02:00", "end_effective": "2017-12-31T01:00:00+01:00", "assignment": "2011-02-04T09:47:14+01:00", "program": null, "subprogram": null, "organization": 14057, "category": 10, "type": 10, "partner_function": 4, "manager": null, "contact": null, "status": 2, "research": 4, "grant": 10, "event": null, "study": null, "language": null, "funders": [ 135 ], "funder_projectcode": null, "ethics_committee": null, "edudract_number": null, "persons": [] }, { "id": 2305, "title": { "de": "Anbahnungsfinanzierung (DEVAG) - Projektnummer: 829019", "en": "Anbahnungsfinanzierung (DEVAG)" }, "short": "DEVAG", "url": null, "abstract": { "de": null, "en": null }, "begin_planned": "2010-06-03T02:00:00+02:00", "begin_effective": "2010-07-01T02:00:00+02:00", "end_planned": "2010-10-13T02:00:00+02:00", "end_effective": "2010-10-16T02:00:00+02:00", "assignment": "2010-09-17T11:46:55+02:00", "program": 54, "subprogram": null, "organization": 14038, "category": 10, "type": 10, "partner_function": 4, "manager": null, "contact": null, "status": 2, "research": 5, "grant": 10, "event": null, "study": null, "language": null, "funders": [ 416 ], "funder_projectcode": "829019", "ethics_committee": null, "edudract_number": null, "persons": [] }, { "id": 2569, "title": { "de": "Anbahnungsfinanzierung: Genetik von Patienten mit Meningokokkeninfektionen Projektnummer: 830184", "en": "host genetics of meningococcal infections" }, "short": "HOST GENETICS MENINGOCOCC INFECT", "url": null, "abstract": { "de": null, "en": null }, "begin_planned": "2010-06-22T02:00:00+02:00", "begin_effective": "2010-06-22T02:00:00+02:00", "end_planned": "2010-10-13T02:00:00+02:00", "end_effective": "2010-10-13T02:00:00+02:00", "assignment": "2011-09-07T13:23:21+02:00", "program": 54, "subprogram": null, "organization": 14091, "category": 10, "type": 10, "partner_function": 4, "manager": 51647, "contact": 51647, "status": 2, "research": 5, "grant": 10, "event": null, "study": null, "language": null, "funders": [ 416 ], "funder_projectcode": null, "ethics_committee": null, "edudract_number": null, "persons": [ "2569-51647-10" ] }, { "id": 1944, "title": { "de": "The role of HOXB4 in renal development, maldevelopment of the kidney and tumorigeneses of renal neoplasms", "en": "The role of HOXB4 in renal development, maldevelopment of the kidney and tumorigeneses of renal neoplasms" }, "short": "ROLE OF HOXB4", "url": null, "abstract": { "de": null, "en": null }, "begin_planned": "2009-11-01T01:00:00+01:00", "begin_effective": "2009-11-01T01:00:00+01:00", "end_planned": "2010-10-31T02:00:00+02:00", "end_effective": "2010-10-31T02:00:00+02:00", "assignment": "2009-10-07T13:44:40+02:00", "program": null, "subprogram": null, "organization": 14020, "category": 10, "type": 10, "partner_function": 4, "manager": 52569, "contact": null, "status": 2, "research": 1, "grant": 10, "event": null, "study": null, "language": null, "funders": [ 530 ], "funder_projectcode": null, "ethics_committee": null, "edudract_number": null, "persons": [ "1944-52569-10" ] }, { "id": 1505, "title": { "de": "Genetische Determinaten zerebraler Kleingefäßerkrankung", "en": "Genetic determinants of cerebral small vessel disease" }, "short": "CEREBRALVESSEL_FWF07", "url": null, "abstract": { "de": "Die Kleingefäßerkrankung ist die zweithäufigste endemische Schädigung des alternden Gehirns nach Alzheimer Pathologie. Leukoaraiose und Lakunen sind die Hauptläsionen dieser Entität und können mittels Magnet Resonanz (MR) Tomografie des Gehirns dargestellt werden. Bis zu 90% aller Personen über dem 65.Lebensjahr zeigen Laukaraiose unterschiedlichen Schweregrades.\r\nDas Ziel unserer Studie ist die Komplexität der zerebralen Kleingefäßerkrankung auf genetischer Basis aufzutrennen, um ein besseres Verständnis des Pathomechanismus dieser Läsion zu erhalten. Im ersten Schritt werden wir eine genomweite Assoziationsstudie und ein Feinmapping der Kopplungsregionen auf Chromosom 4 und 17 in der Austrian Stroke Prevention Study Kohorte durchführen. Im zweiten Schritt werden wir Familien aus der Basiskohorte der Austrian Stroke Prevention Study rekrutieren. Die Familienmitglieder werden dem selben Studienprookoll unterzogen, wie die Probanden der Basiskohorte. In dieser Familienstudie werden wir Schätzungen zur Vererblichkeit der verschiedenen Läsionscharakteristika und die genetische Korrelation zwischen diesen Läsionsmerkmalen und ihren Hauptrisikofaktoren berechnen. Das Spektrum möglicher Endophenotypen der zerebraler Kleingefäßerkrankung soll aufgezeigt werden. In der Familienstudie werden wir Gene verifizieren, die mit dieser Hirnschädigung in früheren Studien identifiziert wurden.\r\nDie gleichzeitige Verfügbarkeit einer Familien- und einer populationsbasierenden Kohorte mit identem Protokoll bietet die einmalige Gelegenheit zur Identifizierung relevanter Gene, da Kopplungs- und Assoziationsstudien in Kombination duchgeführt werden können. Die Identifizierung solcher Gene wird unser äußerst unvollständiges pathophysiologisches Verständnis über die zerebrale Kleingefäßerkrankung verbessern und die Entdeckung neuer therapeutischer Ziele ermöglichen.", "en": "Cerebral small vessel disease is the second most common endemic entity of the ageing brain following Alzheimer pathology. Its hallmark lesions are leuko-araiosis and lacunar infarctions, which can be non-invasively depicted with brain magnetic resonance imaging. Up to 90% of persons above the age of 65 years present with leuko-araiosis. Lacunes occur less common with a frequency of 6% to 20%. Decreased mobility of the elderly due to disequilibrium and gait abnormalities, and progressive cognitive impairment up to dementia are frequent clinical sequelae of cerebral microangiopathy. Established risk factors are arterial hypertension and advancing age. There does not exist any established treatment yet which allows to modify the evolution of small vessel disease-related brain damage. \r\nThe heritability of leukoaraiosis volume ranges between 55% and 73%. There are no heritability estimates of other characteristics of white matter lesions such as type and progression are available. Similarly, the heritability of other components of small vessel disease such as lacunes, brain atrophy and microbleeds have not yet been investigated yet. Association studies indicated that the APOE, ACE, eNOS, MTHFR genes might be related to these pathologies. We found positive associations with APOE, PON1 as well as the AGT, with considerable evidence for a causal relationship for the latter. Very recently, the results of the first genome wide scan on white matter lesion volume have been reported by the Framingham Heart Study describing a significant LOD score on chromosome 4 and a suggestive LOD score for linkage on chromosome 17.\r\n \tThe aim of our study is to genetically dissect the complexity of cerebral small vessel disease in order to better understand the pathomechanisms leading to these lesions. First we will apply genome wide association as well as fine map the linkage regions on Chr 4 and 17 in the the Austrian Stroke Prevention Study cohort, which is one of the largest community-dwelling studies on cerebral small vessel disease and the study with the longest MRI follow up so far. Second, we will recruit families ascertained through participants of the Austrian Stroke Prevention Study. Family members will undergo the same study protocol including brain MRI as the probands in the population based cohort. In the family based cohort we will estimate heritability of and genetic correlation between different lesion characteristics of cerebral small vessel disease and its major risk factors. We aim to develop a spectrum of possible endophenotypes for cerebral small vessel disease. In the family based cohort we also aim to verify genes associated with cerebral small vessel disease in previous studies. \r\nThe co-existence of a family and a population based cohort characterized with identical study protocol will offer a unique and outstanding resource to identify genes by allowing for the combined use of linkage and association. Knowledge of genes involved in cerebral small vessel disease will improve our understanding of the pathogenesis of these lesions and will possibly facilitate the development of novel therapeutic targets.\r\n" }, "begin_planned": "2007-11-01T01:00:00+01:00", "begin_effective": "2008-05-01T02:00:00+02:00", "end_planned": "2010-10-31T02:00:00+02:00", "end_effective": "2012-12-31T01:00:00+01:00", "assignment": "2008-03-31T18:04:38+02:00", "program": 72, "subprogram": null, "organization": 14013, "category": 10, "type": 10, "partner_function": 4, "manager": 51912, "contact": 51912, "status": 2, "research": 1, "grant": 10, "event": null, "study": null, "language": null, "funders": [ 9 ], "funder_projectcode": "P20545", "ethics_committee": null, "edudract_number": null, "persons": [ "1505-51912-10" ] }, { "id": 2323, "title": { "de": "Computermodelle strukturell degenerativer Herzerkrankungen", "en": "Computermodelle strukturell degenerativer Herzerkrankungen" }, "short": "Computermodelle Herzerkrankung", "url": null, "abstract": { "de": null, "en": null }, "begin_planned": "2010-11-01T01:00:00+01:00", "begin_effective": "2010-11-01T01:00:00+01:00", "end_planned": "2010-10-31T02:00:00+02:00", "end_effective": "2010-07-31T02:00:00+02:00", "assignment": "2010-10-05T11:55:03+02:00", "program": null, "subprogram": null, "organization": 14011, "category": 10, "type": 10, "partner_function": 1, "manager": 51502, "contact": 51502, "status": 2, "research": 2, "grant": 10, "event": null, "study": null, "language": null, "funders": [ 135 ], "funder_projectcode": null, "ethics_committee": null, "edudract_number": null, "persons": [ "2323-51502-10" ] }, { "id": 2318, "title": { "de": "Der Einfluss von molekulargenetischen Veränderungen in TGFß1 auf den Schweregrad von strahlentherapiebedingten Toxizitäten bei Prostatakarzinompatienten.", "en": "The association between genetic variants in TGFß1 and radiation induced side effects in prostate cancer patients." }, "short": "MOLECULAR GENETIC VARIANTS", "url": null, "abstract": { "de": null, "en": null }, "begin_planned": "2010-03-01T01:00:00+01:00", "begin_effective": "2010-11-01T01:00:00+01:00", "end_planned": "2010-11-30T01:00:00+01:00", "end_effective": "2011-06-30T02:00:00+02:00", "assignment": "2010-09-29T12:46:53+02:00", "program": null, "subprogram": null, "organization": 14060, "category": 10, "type": 10, "partner_function": 4, "manager": 50495, "contact": 50495, "status": 2, "research": 1, "grant": 10, "event": null, "study": null, "language": null, "funders": [ 135 ], "funder_projectcode": null, "ethics_committee": null, "edudract_number": null, "persons": [ "2318-50495-10" ] }, { "id": 1613, "title": { "de": "Glukose Monitoring bei der Hemodialyse", "en": "Glucose monitoring in hemodialysis" }, "short": "GLUCOSEMONITORING_BRIDGE08", "url": null, "abstract": { "de": "Ziel des Projekts ist die Entwicklung eines Systems zur automatischen und kontinuierlichen Messung der Glukose bei der Hämodialyse und bei verwandten extrakorporalen Blutbehandlungsverfahren, sowie zur indirekten Bestimmung der Glukosekonzentration im Blut und davon abgeleiteter Größen.", "en": "To develop a system for automatic and continuous glucose measurements during hemodialysis and other related extracorporeal blood treatments for indirect estimation of arterial blood glucose and related entities." }, "begin_planned": "2008-10-01T02:00:00+02:00", "begin_effective": "2008-10-01T02:00:00+02:00", "end_planned": "2010-11-30T01:00:00+01:00", "end_effective": "2011-03-31T02:00:00+02:00", "assignment": "2008-09-02T18:21:16+02:00", "program": 60, "subprogram": null, "organization": 14010, "category": 10, "type": 10, "partner_function": 4, "manager": 51834, "contact": 51834, "status": 2, "research": 3, "grant": 10, "event": null, "study": null, "language": null, "funders": [ 416 ], "funder_projectcode": "818127", "ethics_committee": null, "edudract_number": null, "persons": [ "1613-50404-12", "1613-51834-10" ] }, { "id": 2258, "title": { "de": "3D-Densvermessung und Optimierung der OP-Technik mittels Virtual Surgery", "en": "3D-morphometry of dens and improvement of surgical technique via virtual surgery" }, "short": "3D-Densstudie", "url": null, "abstract": { "de": null, "en": null }, "begin_planned": "2010-05-01T02:00:00+02:00", "begin_effective": "2010-08-01T02:00:00+02:00", "end_planned": "2010-12-01T01:00:00+01:00", "end_effective": "2011-07-31T02:00:00+02:00", "assignment": "2010-07-29T15:54:41+02:00", "program": null, "subprogram": null, "organization": 14052, "category": 10, "type": 10, "partner_function": 4, "manager": 62925, "contact": 62925, "status": 2, "research": 1, "grant": 10, "event": null, "study": null, "language": null, "funders": [ 135 ], "funder_projectcode": null, "ethics_committee": null, "edudract_number": null, "persons": [ "2258-62925-10" ] }, { "id": 1436, "title": { "de": "Chromosomale Instabilität bei Alterung und Krebs", "en": "Chromosomal instability in aging and cancer" }, "short": "CHROMOS_INSTAB_AGING_CANCER_2007", "url": null, "abstract": { "de": "This project aims at elucidating factors involved in CIN and age-dependent aneuploidy. We want to address the hypothesis whether CIN or aneuploidy is caused by specific genetic alterations in a single gene or whether it is the consequence of mutations in several or a large number of genes. The project consists of three different steps: In a first, mainly descriptive step, we will employ latest 3D-multicolor FISH imaging techniques directly on tissue sections or on single cell suspensions to identify CIN/aneuploid regions in real biological material. In a second step, we will apply to these CIN/aneuploid regions our unbiased whole genome amplification strategies for subsequent array-CGH. This strategy will yield a high-resolution analysis of the genome of the respective areas or of individual cells. Regions within the tumor genome, which are commonly gained or lost will pinpoint locations of genes, which may be involved in the occurrence of CIN and aneuploidy. Candidate genes identified by this approach will be sequenced. The third, functional step, involves RNAi for gene knockdown of selected genes to verify that their reduced function has indeed an impact on chromosomal stability. Thus, this project combines both descriptive in vivo and functional in vitro technologies to derive significant biological conclusions.\r\n", "en": "This project aims at elucidating factors involved in CIN and age-dependent aneuploidy. We want to address the hypothesis whether CIN or aneuploidy is caused by specific genetic alterations in a single gene or whether it is the consequence of mutations in several or a large number of genes. The project consists of three different steps: In a first, mainly descriptive step, we will employ latest 3D-multicolor FISH imaging techniques directly on tissue sections or on single cell suspensions to identify CIN/aneuploid regions in real biological material. In a second step, we will apply to these CIN/aneuploid regions our unbiased whole genome amplification strategies for subsequent array-CGH. This strategy will yield a high-resolution analysis of the genome of the respective areas or of individual cells. Regions within the tumor genome, which are commonly gained or lost will pinpoint locations of genes, which may be involved in the occurrence of CIN and aneuploidy. Candidate genes identified by this approach will be sequenced. The third, functional step, involves RNAi for gene knockdown of selected genes to verify that their reduced function has indeed an impact on chromosomal stability. Thus, this project combines both descriptive in vivo and functional in vitro technologies to derive significant biological conclusions.\r\n" }, "begin_planned": "2008-01-01T01:00:00+01:00", "begin_effective": "2008-01-01T01:00:00+01:00", "end_planned": "2010-12-31T01:00:00+01:00", "end_effective": "2011-06-30T02:00:00+02:00", "assignment": "2008-01-08T11:42:21+01:00", "program": 72, "subprogram": null, "organization": 14021, "category": 10, "type": 10, "partner_function": 4, "manager": null, "contact": null, "status": 2, "research": 1, "grant": 10, "event": null, "study": null, "language": null, "funders": [ 9 ], "funder_projectcode": "P1234567", "ethics_committee": null, "edudract_number": null, "persons": [] }, { "id": 1702, "title": { "de": "Identification of genes associated with autism spectrum disorder", "en": "Identification of genes associated with autism spectrum disorder" }, "short": "AUTISM SPECTRUM DISORDER", "url": null, "abstract": { "de": "Das \"Autismus-Spektrum\" umfasst insbesondere den frühkindlichen Autismus, den atypischen Autismus und das Asperger-Syndrom. Aufgrund der hohen Konkordanzraten eineiiger Zwillinge geht die Forschung in der Zwischenzeit davon aus, dass Autismus wesentlich auf genetische Ursachen zurückzuführen ist. Durch die in den letzten jahren erfolgte Entwicklung der \"vergleichenden genomischen Hybridisierung (CGH)\" und der sogenannten \"Microarray Analyse\" wird statt nach einzelnen veränderten Bausteinen im Erbgut der Probanden zu suchen, nach ganzen Abschnitten gefahndet, die entweder vollständig fehlen oder aber in doppelter Ausführung vorliegen. Dieser als CNV-Methode (Variationen in der Kopienzahl) bezeichnete Ansatz führte in den letzten beiden Jahren zu ungeahnten Variationen im menschlichen Genom. Unser Konzept im vorliegenden Forschungsantrag sieht vor, 70 bereits gut diagnostizierte Autismus PatientInnen mittels \"state-of-the-art\" Methoden auf Phänotyp-spezifische CNVs zu untersuchen.", "en": "Das \"Autismus-Spektrum\" umfasst insbesondere den frühkindlichen Autismus, den atypischen Autismus und das Asperger-Syndrom. Aufgrund der hohen Konkordanzraten eineiiger Zwillinge geht die Forschung in der Zwischenzeit davon aus, dass Autismus wesentlich auf genetische Ursachen zurückzuführen ist. Durch die in den letzten jahren erfolgte Entwicklung der \"vergleichenden genomischen Hybridisierung (CGH)\" und der sogenannten \"Microarray Analyse\" wird statt nach einzelnen veränderten Bausteinen im Erbgut der Probanden zu suchen, nach ganzen Abschnitten gefahndet, die entweder vollständig fehlen oder aber in doppelter Ausführung vorliegen. Dieser als CNV-Methode (Variationen in der Kopienzahl) bezeichnete Ansatz führte in den letzten beiden Jahren zu ungeahnten Variationen im menschlichen Genom. Unser Konzept im vorliegenden Forschungsantrag sieht vor, 70 bereits gut diagnostizierte Autismus PatientInnen mittels \"state-of-the-art\" Methoden auf Phänotyp-spezifische CNVs zu untersuchen." }, "begin_planned": "2009-01-01T01:00:00+01:00", "begin_effective": "2009-01-01T01:00:00+01:00", "end_planned": "2010-12-31T01:00:00+01:00", "end_effective": "2011-06-30T02:00:00+02:00", "assignment": "2008-12-15T15:19:50+01:00", "program": 79, "subprogram": null, "organization": 14021, "category": 10, "type": 10, "partner_function": 4, "manager": 51996, "contact": null, "status": 2, "research": 1, "grant": 10, "event": null, "study": null, "language": null, "funders": [ 12 ], "funder_projectcode": null, "ethics_committee": null, "edudract_number": null, "persons": [ "1702-51996-10" ] }, { "id": 979, "title": { "de": "SFB LIPOTOXICITY - Part 04: Lipasen und lipotoxische Lipide in Makrophagen: Rolle in der Atherogenese", "en": "SFB LIPOTOXICITY - P04: Lipases and lipotoxic lipids in macrophages: Role in atherogenesis" }, "short": "LIPOTOXICITY P04", "url": null, "abstract": { "de": "Das Ziel des SFB-LIPOTOX ist die Zusammenführung relevanter Forschungsgruppen um gemeinsam ein zentrales Thema zu bearbeiten, Lipotoxizität. Unter Lipotoxizität versteht man die fehlgesteuerte Aufnahme bzw. Produktion von Fettsäuren und Lipiden, die zur Bildung (lipo)toxischer Substanzen führen, die Dysfunktion von Zellen und Geweben bewirken und im Zelltod enden können. Wir wollen jene metabolischen Vorgänge und molekularen Mechanismen untersuchen, die durch lipotoxische Effektoren ausgelöst werden und die pathologische Basis prävalenter Erkrankungen, wie z.B. dem Metabolischen Syndrom, Typ-2 Diabetes und Atherosklerose darstellen. Dieses hochgesteckte Ziel ist nur durch eine gemeinsame Anstrengung innerhalb eines dynamischen und interaktiven Konsortiums, die weit über die Möglichkeiten innerhalb von Einzelprojektförderungen hinausgeht, zu erreichen. Durch Einsatz aktueller genomischer, proteomischer und lipidomischer Methoden sollen neue lipotoxische Stoffwechselwege entdeckt werden. Durch Einsatz mutanter Maus- und Hefemodelle werden jene molekulare Mechanismen untersucht, durch die zelluläre Dysfunktion und Zelltod bewirkt werden. Die gewonnenen Erkenntnisse können somit einen wichtigen Beitrag zur Auffindung neuartiger Diagnose- und Behandlungsmethoden leisten.", "en": "Das Ziel des SFB-LIPOTOX ist die Zusammenführung relevanter Forschungsgruppen um gemeinsam ein zentrales Thema zu bearbeiten, Lipotoxizität. Unter Lipotoxizität versteht man die fehlgesteuerte Aufnahme bzw. Produktion von Fettsäuren und Lipiden, die zur Bildung (lipo)toxischer Substanzen führen, die Dysfunktion von Zellen und Geweben bewirken und im Zelltod enden können. Wir wollen jene metabolischen Vorgänge und molekularen Mechanismen untersuchen, die durch lipotoxische Effektoren ausgelöst werden und die pathologische Basis prävalenter Erkrankungen, wie z.B. dem Metabolischen Syndrom, Typ-2 Diabetes und Atherosklerose darstellen. Dieses hochgesteckte Ziel ist nur durch eine gemeinsame Anstrengung innerhalb eines dynamischen und interaktiven Konsortiums, die weit über die Möglichkeiten innerhalb von Einzelprojektförderungen hinausgeht, zu erreichen. Durch Einsatz aktueller genomischer, proteomischer und lipidomischer Methoden sollen neue lipotoxische Stoffwechselwege entdeckt werden. Durch Einsatz mutanter Maus- und Hefemodelle werden jene molekulare Mechanismen untersucht, durch die zelluläre Dysfunktion und Zelltod bewirkt werden. Die gewonnenen Erkenntnisse können somit einen wichtigen Beitrag zur Auffindung neuartiger Diagnose- und Behandlungsmethoden leisten." }, "begin_planned": "2007-01-01T01:00:00+01:00", "begin_effective": "2007-01-01T01:00:00+01:00", "end_planned": "2010-12-31T01:00:00+01:00", "end_effective": "2011-03-31T02:00:00+02:00", "assignment": "2006-12-27T14:28:13+01:00", "program": 67, "subprogram": null, "organization": 14013, "category": 10, "type": 10, "partner_function": 2, "manager": 51904, "contact": 51904, "status": 2, "research": 1, "grant": 10, "event": null, "study": null, "language": null, "funders": [ 9 ], "funder_projectcode": "F30", "ethics_committee": null, "edudract_number": null, "persons": [ "979-51904-10" ] }, { "id": 1551, "title": { "de": "GENINCA - Genomic instability and genomic alterations in pre-cancerous lesions and/or cancer", "en": "GENINCA - Genomic instability and genomic alterations in pre-cancerous lesions and/or cancer" }, "short": "GENINCA", "url": null, "abstract": { "de": "GENINCA will address two tumor entities, for which we have good access to pre-malignant lesions and in which genomic instability is a common feature: colorectal and liver cancer. \r\nGENINCA represents a collaborative study of 8 academic and 3 industrial partners from 5 European countries. GENINCA will focus on exploring pre-cancerous and cancer lesions of the two aforementioned tumor entities and their respective microenvironment. As the recent identification of human colon-cancer initiating cells by one of our academic consortium members paves the way for completely new strategies for studying mechanisms of tumorgenesis, a particular focus of this grant proposal will be the detailed characterization of these cancer initiating stem cells. At present, it is still a matter of debate which genomic changes are already present in precursor lesions and whether these lesions already show genetic instability. We will therefore address the occurrence of genomic instability and explore their underlying mechanisms especially in pre-cancerous and early cancer lesions. This will be greatly facilitated by in vivo endomicroscopy approaches, sophisticated animal models and large-scale genomic and proteomic analyses. Furthermore, we ill include an in-depth analysis of the corresponding microenvironment. As this represents a translational research effort, we expect to identify markers for novel therapeutic and/or preventative strategies, as well as facilitating tumor diagnosis, prognosis, and monitoring.", "en": "GENINCA will address two tumor entities, for which we have good access to pre-malignant lesions and in which genomic instability is a common feature: colorectal and liver cancer. \r\nGENINCA represents a collaborative study of 8 academic and 3 industrial partners from 5 European countries. GENINCA will focus on exploring pre-cancerous and cancer lesions of the two aforementioned tumor entities and their respective microenvironment. As the recent identification of human colon-cancer initiating cells by one of our academic consortium members paves the way for completely new strategies for studying mechanisms of tumorgenesis, a particular focus of this grant proposal will be the detailed characterization of these cancer initiating stem cells. At present, it is still a matter of debate which genomic changes are already present in precursor lesions and whether these lesions already show genetic instability. We will therefore address the occurrence of genomic instability and explore their underlying mechanisms especially in pre-cancerous and early cancer lesions. This will be greatly facilitated by in vivo endomicroscopy approaches, sophisticated animal models and large-scale genomic and proteomic analyses. Furthermore, we ill include an in-depth analysis of the corresponding microenvironment. As this represents a translational research effort, we expect to identify markers for novel therapeutic and/or preventative strategies, as well as facilitating tumor diagnosis, prognosis, and monitoring." }, "begin_planned": "2008-01-01T01:00:00+01:00", "begin_effective": "2008-01-01T01:00:00+01:00", "end_planned": "2010-12-31T01:00:00+01:00", "end_effective": "2011-06-30T02:00:00+02:00", "assignment": "2008-06-09T13:23:20+02:00", "program": 24, "subprogram": "HEALTH-2007-2.4.1-3", "organization": 14021, "category": 10, "type": 10, "partner_function": 3, "manager": null, "contact": null, "status": 2, "research": 2, "grant": 10, "event": null, "study": null, "language": null, "funders": [ 10 ], "funder_projectcode": null, "ethics_committee": null, "edudract_number": null, "persons": [] }, { "id": 2051, "title": { "de": "Bedeutung des Endothelinsystems bei der Pathogenese der Präeklamsie", "en": "Bedeutung des Endothelinsystems bei der Pathogenese der Präeklamsie" }, "short": "Endothelinsystems und Präeklamsie", "url": null, "abstract": { "de": null, "en": null }, "begin_planned": "2010-01-01T01:00:00+01:00", "begin_effective": "2010-01-01T01:00:00+01:00", "end_planned": "2010-12-31T01:00:00+01:00", "end_effective": "2011-07-30T02:00:00+02:00", "assignment": "2010-01-21T12:47:04+01:00", "program": null, "subprogram": "Land Steiermark-Projekt über 5.000,- Euro Antragssumme", "organization": 14038, "category": 10, "type": 10, "partner_function": 4, "manager": null, "contact": null, "status": 2, "research": 1, "grant": 10, "event": null, "study": null, "language": null, "funders": [ 135 ], "funder_projectcode": null, "ethics_committee": null, "edudract_number": null, "persons": [] }, { "id": 2220, "title": { "de": "Stratifizierung genetischer Veränderungen von malignen Kindertumoren - Grundlage für eine personalisierte Therapie", "en": "Stratifizierung genetischer Veränderungen von malignen Kindertumoren - Grundlage für eine personalisierte Therapie" }, "short": "MALIGNE KINDERTUMORE", "url": null, "abstract": { "de": null, "en": null }, "begin_planned": "2010-01-01T01:00:00+01:00", "begin_effective": "2010-07-01T02:00:00+02:00", "end_planned": "2010-12-31T01:00:00+01:00", "end_effective": "2012-12-31T01:00:00+01:00", "assignment": "2010-06-09T10:58:03+02:00", "program": null, "subprogram": "MAE: IANr. eingetragen (01.06.2010)", "organization": 14020, "category": 10, "type": 10, "partner_function": 4, "manager": 52569, "contact": 52569, "status": 2, "research": 2, "grant": 10, "event": null, "study": null, "language": null, "funders": [ 135 ], "funder_projectcode": null, "ethics_committee": null, "edudract_number": null, "persons": [ "2220-52569-10" ] }, { "id": 2630, "title": { "de": "Angiogeneseleistung von mesenchymalen Zellen der Plazenta in 3-D Zellkulturmodellen", "en": "Angiogenesis of mesenchymal cells of the placenta in 3-D cell culture models " }, "short": null, "url": null, "abstract": { "de": null, "en": null }, "begin_planned": "2010-03-01T01:00:00+01:00", "begin_effective": "2010-03-01T01:00:00+01:00", "end_planned": "2010-12-31T01:00:00+01:00", "end_effective": "2010-12-31T01:00:00+01:00", "assignment": "2011-11-09T12:43:52+01:00", "program": null, "subprogram": null, "organization": 14017, "category": 10, "type": 10, "partner_function": 4, "manager": 51718, "contact": 51718, "status": 2, "research": 1, "grant": 10, "event": null, "study": null, "language": null, "funders": [ 530 ], "funder_projectcode": null, "ethics_committee": null, "edudract_number": null, "persons": [ "2630-51718-10" ] } ] }