Global ETD Search

321	Untersuchungen zur Kombinationswirkung von Valproat und Bestrahlung in Bezug auf klonogenes Überleben, Apoptose, Polyploidie und chromosomale Instabilität in Prostatakarzinom- und Prostatahyperplasie-Zelllinien / The combined effect of valproate and radiation on clonogenic survival, apoptosis, polyplodity and chromosomal instability in prostate cancer cells and prostate hyperplasia cells Friedrich, Christiane 23 November 2010 (has links) No description available. 610 Medizin, Gesundheit Medicine Valproat Bestrahlung Prostata-Karzinom DU-145 PC-3 BPH-1 PTN-2 klonogenes Überleben Apoptose Polyploidie chromsomale Instabilität Valproate valproic acid radiation prostate cancer prostate carcinoma DU-145 PC-3 BPH-1 PTN-2 clonogenic survival assays apoptosis polyploidity chromosomal instability 44.00 44.52 44.64 44.88 MED 371: Radiologie
322	Zytogenetische Grundlage der malignen Progression anaplastischer Astrozytome: Chromosomale Aberrationen von Primärtumoren, Rezidiven und ihr Einfluss auf das Überleben / Cytogenetic basics of malignant progression of anaplastic astrocytoma: Chromosomal aberrations of primary and recurrent tumors and their influence on survival Haupt, Jörn 02 November 2011 (has links) No description available. 610 Medizin, Gesundheit Medicine Anaplastische Astrozytome CGH maligne Progression sekundäres Glioblastom chromosomale Aberrationen cgh secondary glioblastoma chromosomal aberrations malignant progression 44.47 44.65 44.81 MED 391: Pathologie {Medizin} MED 424: Onkologie MED 533: Neurochirurgie
323	Implication de MEK1 et MEK2 dans l'initiation et la progression du cancer colorectal Duhamel, Stéphanie 08 1900 (has links) Une dérégulation de la voie de signalisation Ras/Raf/MEK/ERK1/2 est observée dans plus de 30% des cancers et des mutations activatrices de RAS sont observées dans 30% à 50% des adénomes colorectaux. À la suite d’une analyse extensive de biopsies de tumeurs colorectales humaines par micromatrices tissulaires (TMA), nous avons observé que 44% des tissus cancéreux exprimaient MEK1/2 phosphorylés, contre 10% des tissus normaux. L'analyse des TMA a également révélé que 79% des tumeurs arboraient un marquage nucléaire de MEK1/2 phosphorylés, contre 4 % pour les tissus normaux. Bien que la voie MEK/ERK1/2 soit fréquemment activée dans les cancers, le rôle précis des isoformes de MEK1 et de MEK2 n'a jamais été clairement établie. De même, l'impact de cette localisation nucléaire aberrante de phospho-MEK1/2, dans l'initiation et la progression des cancers colorectaux, est inconnu. Lors d'un premier projet, nous avons démontré, que l’expression de MEK1 ou MEK2 activé est suffisante pour transformer in vitro des cellules intestinales épithéliales de rat (IEC-6). L'expression des mutants actifs de MEK1 ou MEK2 est suffisante pour induire une dérégulation de la prolifération cellulaire et engendrer la formation d'adénocarcinomes invasifs dans un modèle de greffe orthotopique du côlon chez la souris. Nous avons également démontré que l'inhibition de MEK2 par shRNA supprime complètement la prolifération des lignées humaines de cancer du côlon, alors que la suppression de MEK1 a peu d'effet sur la capacité de prolifération. Le deuxième projet, nous a permis d'observer que l'expression d'un mutant nucléaire de MEK1 dans les cellules IEC-6 transforme drastiquement les cellules. Une augmentation de prolifération, une résistance à l'anoikose, un dérèglement du cycle cellulaire, de l'instabilité chromosomique (CIN), de la tétra/aneuploïdie sont observés. La caractérisation des mécanismes responsables de cette localisation aberrante de MEK1/2 phosphorylés, a permis d'identifier la protéine Sef, un régulateur de la localisation cytoplasmique de MEK/ERK1/2. Nous avons démontré que l'expression d'une forme oncogénique de Ras (H-RasV12) inhibe l'expression de Sef, engendrant alors une accumulation nucléaire de MEK1/2 activés. Plus encore, la réexpression de Sef restaure la localisation cytoplasmique de MEK1/2 et renverse les propriétés tumorigéniques ainsi que l'aneuploïdie induite par Ras activé. Un troisième projet, visant la caractérisation des mécanismes associés à la CIN et à l'aneuploïde engendrés par l'activation aberrante de la voie de Ras-ERK1/2, a permis d'observer que l'hyperactivation de ERK1/2 induit des anomalies mitotiques menant à la binucléation. Une localisation erronée et une surexpression de la kinase Aurora A, de même que des protéines de passage du complexe chromosomique (CPC), Aurora B, Survivine et INCENP, sont observées. L'inhibition partielle de l'activation de ERK1/2 par de faible dose de PD184352, un inhibiteur de MEK1/2, est suffisante pour renverser la surexpression de ces régulateurs mitotiques, de même que corriger les anomalies de la mitose et réduire la tétra/aneuploïdie engendrée par Ras oncogénique. Ainsi, nous avons démontré, pour la première fois, que la voie des MAP kinases ERK1/2 est impliquée dans la CIN, la tétraploïdie et l'aneuploïdie. Nos résultats suggèrent que la perte de Sef est un événement oncogénique précoce, qui contribue à la localisation nucléaire aberrante de MEK1/2 qui est observée dans les tumeurs colorectales. Cette localisation anormale de MEK1/2 est associée à l'initiation de la transformation, la progression tumorale et la CIN, via l'activité soutenue de ERK1/2. Ces informations sont capitales et démontrent l’importance de la voie de signalisation Ras/Raf/MEK/ERK1/2 dans le processus de tumorigénèse colorectale. / The Ras-dependent Raf/MEK/ERK1/2 signaling pathway is frequently hyperactivated in human cancer as a result of receptor tyrosine kinase overexpression or gain-of-function mutations in RAS or RAF genes. More specificaly, activating mutation in RAS genes are found in ~ 30-50% of colorectal adenomas and phosphorylation of ERK1/2 is frequently observed in human colorectal cancer cells and tumor specimens. In a large TMA analysis, we found that MEK1/MEK2 are aberrantly activated in 44% of human colorectal cancers. In addition, our analysis revealed that 79% of colorectal cancers exhibit aberrant phospho-MEK1/2 staining in the nucleus, as compared to 4% of normal tissue. How dysregulation and mislocalization of MEK1/2 contribute to tumor initiation and progression is not well understood. In order to determine the exact contribution of MEK1 and MEK2 to the pathogenesis of colorectal cancer, wild type and constitutively active forms of MEK1 and MEK2 were ectopically expressed by retroviral gene transfer in the normal intestinal epithelial cell line IEC-6. We found that the expression of activated MEK1 or MEK2 is sufficient to morphologically transform intestinal epithelial cells, dysregulate cell proliferation and induce the formation of high-grade adenocarcinomas after orthotopic transplantation in mice. A large proportion of these intestinal tumors metastasize to the liver and lung. Importantly, we show that silencing of MEK2 expression completely suppresses the proliferation of human colon carcinoma cell lines, whereas inactivation of MEK1 has a much weaker effect. In a second project, we have investigated the impact of the nuclear mislocalization of phosphorylated MEK1/2 observed in colorectal tumors. We show that oncogenic activation of Ras is sufficient to induce the nuclear accumulation of phosphorylated MEK1/2 and ERK1/2 in intestinal epithelial cells. To evaluate the biological impact of the mislocalization of MEK1/2, we have forced the localization of MEK1 in the nucleus of epithelial cells. We found that sustained nuclear MEK1 signaling leads to hyperactivation of ERK1/2 and to enhanced cell proliferation. Nuclear localization of MEK1 also leads to tetraploidization, chromosomal instability (CIN) and tumorigenesis. Importantly, we show that oncogenic Ras downregulates the spatial regulator Sef, concomitant to nuclear accumulation of activated MEK1/2. Moreover, re-expression of Sef is sufficient to restore the normal localization of MEK1/2 and to revert the cell cycle defects and tumorigenesis induced by oncogenic Ras. Another project was initiated to characterize the tetraploidy and CIN observed upon hyperactivation of the Ras-ERK1/2 pathway. Aneuploidy and CIN are observed in the majority of colorectal cancers and are associated with a poorer prognosis. We show that hyperactivation of ERK1/2 by oncogenic Ras or sustained nuclear MEK-ERK1/2 signaling induces mitotic defects that lead to tetraploidy, aneuploidy and CIN. We also found that dysregulation of Ras-ERK1/2 signaling alters the expression and localization of Aurora A and the Chromosomal passenger complex proteins. In conclusion, we show for the first time that the MEK/ERK1/2 signaling pathway is implicated in aneuploidy and CIN. Our results suggest that sustained nuclear ERK1/2 signaling may contribute to the initiation and progression of colorectal cancer by rapidly inducing aneuploidy and CIN. We suggest that loss of Sef is an early oncogenic event that contributes to genetic instability and tumor progression by sustaining nuclear ERK1/2 signaling. These observations are significant and highlight the importance of the Ras-ERK1/2 signaling pathway in colorectal tumorigenesis. Voie de signalisation Signaling pathway RAS oncogénique Oncogenic RAS MEK1/2 MEK1/2 ERK1/2 ERK1/2 Cancer colorectal Colorectal cancer Tumorigénèse Tumorigenesis Transformation Transformation Aneuploïdie Aneuploidy Instabilité chromosomique Chromosomal instability Inhibiteur de MEK1/2 MEK1/2 inhhibitor
324	Évaluation de la cytogénotoxicité humaine induite par l’exposition à de faibles doses de benzo-a-pyrène, à l’aide de biomarqueurs précoces Fortin, Fléchère 04 1900 (has links) Le benzo-a-pyrène (BaP) est un hydrocarbure aromatique polycyclique (HAP) cancérogène pour l’homme, qui contamine toutes les sphères de notre environnement. Son métabolite, le BaP-7,8-diol-9,10-époxyde (BPDE) est considéré comme son cancérogène ultime. Le BPDE se lie à l’ADN, formant des adduits qui doivent être réparés et qui seraient responsables des dommages à l’ADN et de la cancérogenèse induite par le BaP. Les adduits BPDE-ADN et les dommages à l’ADN (bris simple-brin [BSB] à l’ADN, aberrations chromosomiques [AC], échanges entre chromatides-sœurs [ÉCS] et micronoyaux [MN]) ont été mesurés dans les lymphocytes humains exposés à de faibles concentrations de BaP, provenant de jeunes volontaires non-fumeurs et en santé. Suite à l’exposition au BaP, le niveau d’adduits BPDE-ADN et la fréquence des AC et des MN augmentent significativement, puis diminuent aux concentrations les plus élevées de BaP testées, suggérant une induction du métabolisme de phase II du BaP. Lors de la mesure des ÉCS, nous obtenons une courbe dose-réponse linéaire, indiquant la production d’un autre type de lésions devant être réparées par le système de réparation par recombinaison homologue. Ces lésions pourraient être des bris à l’ADN ou des bases oxydées (8-OH-dG), ce qui est suggéré par l’analyse des corrélations existant entre nos biomarqueurs. Par ailleurs, la comparaison de la courbe dose-réponse des hommes et des femmes montre que des différences existent entre les sexes. Ainsi, les ÉCS, les AC et les MN sont significativement augmentés chez les hommes à la plus faible concentration de BaP, alors que chez les femmes cette augmentation, quoique présente, est non significative. Des différences interindividuelles sont également observées et sont plus importantes pour les adduits BPDE-ADN, les MN et les AC, alors que pour les ÉCS elles sont minimes. Les analyses statistiques effectuées ont permis d’établir que quatre facteurs (niveau d’exposition au BaP, adduits BPDE-ADN, fréquence des AC et nombre de MN par cellule micronucléée) expliquent jusqu’à 59 % de la variabilité observée dans le test des ÉCS, alors qu’aucun facteur significatif n’a pu être identifié dans le test des AC et des MN. L’analyse du mécanisme de formation de nos biomarqueurs précoces permet de suggérer que les bris à l’ADN et les bases oxydées devraient être classées comme biomarqueurs de dose biologique efficace, au sein des biomarqueurs d’exposition, dans le continuum exposition-maladie du BaP, étant donné qu’ils causent la formation des biomarqueurs de génotoxicité (ÉCS, AC et MN). Par ailleurs, le test des AC et des MN ont permis de confirmer l’action clastogénique du BaP en plus de mettre en évidence des effets aneugènes affectant surtout la ségrégation des chromosomes lors de la division cellulaire. Ces effets aneugènes, reliés à l’étape de progression dans la cancérogenèse, pourraient être particulièrement importants puisque l’exposition au BaP et aux HAP est chronique et dure plusieurs années, voire des décennies. La compréhension des mécanismes régissant la formation des biomarqueurs étudiés dans cette étude, ainsi que des relations existant entre eux, peut être appliquée à de nombreux contaminants connus et émergents de notre environnement et contribuer à en évaluer le mode d’action. / Benzo-a-pyrene (BaP) is a polycyclic aromatic hydrocarbon (PAH) classified as carcinogenic to human, and is present throughout our environment. Metabolic activation of BaP leads to production of BaP-7,8-diol-9,10-epoxide (BPDE), considered as its ultimate carcinogenic metabolite. BPDE can bind to DNA, forming BPDE-DNA adducts at the origin of BaP-induced DNA damage and carcinogenesis. BPDE-DNA adducts and DNA damages (DNA single-strand breaks [SSBs], chromosomal aberrations [CAs], sister chromatid exchanges [SCEs] and micronuclei [MNs]) are measured in human lymphocytes exposed to low BaP concentrations, taken from non-smoking healthy young subjects. Following BaP exposure, BPDE-DNA adduct levels, as well as CA and MN frequencies raise significantly, and then decrease to the higher BaP concentrations tested, suggesting metabolic enzyme saturation or induction of BaP phase II metabolism. As for SCEs test, a linear dose response curve is obtained, suggesting that production of additional DNA lesions requiring homologous recombination repair may occur. These lesions could be DNA breaks or oxidized DNA bases (8-OH-dG), as indicated by correlation analysis performed between our biomarkers. Additionally, when comparing the dose-response curves for men and women separately, some differences show up. Indeed, SCEs, CAs, and MNs are significantly increased in men at the lowest BaP concentration tested, while in women, this increase is present but not significant. Interindividual differences are also present and are more considerable for BPDE-DNA adducts, MNs and CAs, whereas they are very low for SCEs. Statistical analysis showed that four factors (BaP exposure level, BPDE-DNA adducts, CA frequency and number of MN per micronucleated cell) significantly explained up to 59 % of observed variability in SCE test, while no such factors could explain the observed variability in CA and MN test. Following analysis of mechanisms underlying the formation of early biomarkers, we suggest a modification of the Exposure-Disease Continuum of BaP. We propose that DNA breaks and oxidized DNA bases should be classified as biomarkers of biologically effective dose (part of the exposure biomarkers), as their presence are at origin of early biomarkers of genotoxicity (SCEs, CAs and MNs). On the other hand, CA and MN tests confirmed clastogenic properties of BaP, and highlighted aneugenic effects influencing mostly chromosome segregation during cell division. These aneugenic effects, linked to the progression step of carcinogenesis, could be of particular importance given that exposure to BaP and other PAHs (smoking, occupational exposure) are chronic and may last for decades. Understanding the mechanisms playing a role in early biomarkers formation, as well as the relations existing between them, can be largely applied in our environment to many known and emerging contaminants, thus contributing to characterize their mode of action. Bris simple-brin à l'ADN Échanges entre chromatides-sœurs Aberrations chromosomiques Micronoyaux Lymphocytes Adduits BPDE-ADN Benzo-a-pyrène-diol-époxyde Stress oxydatif Différences entre les sexes Différences interindividuelles DNA single-strand breaks Sister chromatid exchanges Chromosomal aberrations Micronuclei BPDE-DNA adducts Benzo-a-pyrene-diol-epoxide Oxydative stress Sex differences Interindividual differences
325	Genetic, genomic and epigenetic alterations in congenital malformations : implications in genetic counseling Serra Juhé, Clara, 1984- 20 October 2012 (has links) Mechanisms underlying congenital malformations are largely unknown despite its high incidence, affecting 2-3% of liveborn infants. A broader knowledge about the causes of birth defects would provide valuable information regarding the outcome and prognosis of the anomaly, the development and establishment of diagnostic protocols, the design of therapeutic strategies and genetic counseling to the family. Different approaches have been used in the present thesis regarding technologies and model diseases to elucidate the contribution of genetic and epigenetic alterations in the etiopathogenesis of congenital malformations. Copy number variations, methylation patterns, as well as point mutations have been explored. Moreover, a study to analyze genetic counseling in relation to one of the new molecular techniques used has been performed. Obtained data reveal a relevant role of genetic and epigenetic alterations in congenital malformations, in some cases as a unique cause to explain the disease and in others as part of an oligogenic or multifactorial model. / Els mecanismes causants de les malformacions congènites són poc coneguts malgrat l’elevada incidència d’aquestes patologies, que afecten el 2-3% de recent nascuts. Un coneixement més ampli de les causes de les anomalies congènites proporcionaria informació rellevant pel que fa al pronòstic de l’anomalia, el desenvolupament i establiment de protocols diagnòstics, el disseny d’estratègies terapèutiques, així com l’assessorament genètic a la família. En la tesi que es presenta s’han utilitzat diferents estratègies, pel que fa a tecnologies i models de malalties, amb l’objectiu d’esbrinar la contribució d’alteracions genètiques i epigenètiques en l’etiopatogènia de les malformacions congènites. S’han analitzat variacions en número de còpia, patrons de metilació, així com mutacions puntuals. D’altra banda, també s’ha realitzat un estudi per aprofundir en l’assessorament genètic en relació a una de les noves tècniques moleculars utilitzades. Els resultats obtinguts indiquen que les altercacions genètiques i epigenètiques tenen una contribució molt rellevant en l’etiologia de les malformacions congènites, en alguns casos com a causa única de la malaltia i en altres com a component d’un model oligogènic o multifactorial. Malformacions congènites Malformacions cardíaques congènites Epigenètica Variacions en número de còpia (CNV) Mutacions puntuals Assessorament genètic Análisis cromosòmica en micromatrius Seqüenciació d’exoma Metilació del DNA Congenital malformations Congenital heart defects Epigenetics Copy number variation (CNV) Point mutations Genetic counseling Chromosomal microarray analysis Exome sequencing DNA methylation 575
326	Duplicacions segmentàries a la regió cromosòmica humana 8P23.1: evolució i expansió d'una nova família gènica Bosch Pages, Nina 19 December 2008 (has links) Les duplicacions segmentàries (DSs), o també anomenades duplicons o Low copy Repeats (LCRs), són regions de coma mínim 1 kb amb un alt nivell d'identitat (>90%), que estan presents almenys dues vegades en el genoma. La regió 8p23.1 consta de 6.5 Mb a la part distal del braç curt del cromosoma 8 i està flanquejada per duplicacions segmentàries. Degut a la seva arquitectura genòmica aquesta regió és susceptible a patir reordenaments mediats per recombinació homòloga no al·lèlica entre les DSs, com per exemple la inversió polimòrfica de 8p23.1 [inv(8)(p23)], present en un de cada quatre individus de la població general europea i japonesa, així com d'altres reorganitzacions menys corrents.El treball realitzat en aquesta tesi doctoral pretén aprofundir en la caracterització de la complexa arquitectura genòmica d'aquesta regió. En la nostra primera aproximació a l'estudi de les DSs que flanquegen la regió cromosòmica 8p23.1, es va identificar una nova família gènica específica de primats, la família gènica FAM90A.Així, bona part d'aquesta tesi doctoral està centrada en l'anàlisi de l'origen, formació, evolució i expansió de FAM90A en els homínids. Per altra banda també s'ha analitzant en detall la variabilitat de FAM90A com a variant en número de còpia (CNV) en diferents poblacions humanes.Finalment, s'ha establert la freqüència de la inversió que afecta a 8p23.1 en població espanyola. També s'ha procedit a genotipar diversos individus homozigots per la inversió i s'ha predit l' estatus de la inversió en 150 individus del projecte HapMap i s'ha analitzat l'efecte que té aquesta reorganització sobre els nivells d'expressió dels gens de la regió. / Segmental duplications (SDs), also known as duplicons or Low Copy Repeats (LCRs), are regions of a minimum of 1 kb with a high sequence identity level (>90%), which are present at least two times in the genome. The 8p23.1 region extends 6.5 Mb at the distal part of the short arm of chromosome 8 and it is flanked by segmental duplications. Due to its genomic architecture the region is prone to suffer rearrangements mediated by non-allelic homologous recombination between these SDs, such as the polymorphic inversion of 8p23.1 [inv(8)(p23)], which is present in one out of every four of European and Japanese general population individuals, as well as other less frequent rearrangements.The aim of the work presented in this doctoral thesis is to get insights in the characterization of the genomic architecture of this complex region. Our first approach to study the SDs flanking 8p23.1 region resulted in the identification of a novel gene family which is primate specific, the FAM90A gene family. Thus, this doctoral thesis is mainly focused on the analysis of the origins, formation, evolution and expansion of FAM90A in hominoids. It has also been analyzed in detail the variability of FAM90A as a copy number variant (CNV) in different human populations.Finally, it has been established the frequency of the inversion affecting 8p23.1 region in the Spanish population. Several homozygous inverted individuals have been genotyped and the status for the inversion has been predicted for 150 HapMap individuals, as well as the effect of this rearrangement on the gene expression levels of the genes contained in the region. NAHR Chromosomal rearrangements 8p23.1 Defensins Correlation Gene fusion Gene expansion Mosaicism Inversions Primates Structural variant Copy number variant or CNV Gene family FAM90A Segmental duplicactions Illumina SNPassoc WGS Real time- PCR FISH Ka/Ks Polimorfisme Trastorn genòmic NAHR Reordenaments cromosòmics 8p23.1 Defensines Correlació Fusió gènica Expansió gènica Mosaicisme Inversions Primats Variant estructural Variant en número de còpia o CNV Família gènica FAM90A Duplicacions segmentàries Genomic disorder Polymorphism Ka/Ks FISH Real time PCR WGS SNPassoc Illumina 57
327	Cascades of genetic instability resulting from compromised break-induced replication Vasan, Soumini January 2013 (has links) Indiana University-Purdue University Indianapolis (IUPUI) / Break-induced replication (BIR) is a mechanism to repair double-strand breaks (DSBs) that possess only a single end that can find homology in the genome. This situation can result from the collapse of replication forks or telomere erosion. BIR frequently produces various genetic instabilities including mutations, loss of heterozygosity, deletions, duplications, and template switching that can result in copy-number variations (CNVs). An important type of genomic rearrangement specifically linked to BIR is half crossovers (HCs), which result from fusions between parts of recombining chromosomes. Because HC formation produces a fused molecule as well as a broken chromosome fragment, these events could be highly destabilizing. Here I demonstrate that HC formation results from the interruption of BIR caused by a defective replisome or premature onset of mitosis. Additionally, I document the existence of half crossover instability cascades (HCC) that resemble cycles of non-reciprocal translocations (NRTs) previously described in human tumors. I postulate that HCs represent a potent source of genetic destabilization with significant consequences that mimic those observed in human diseases, including cancer. Comparative Genomic Hybridization Break-induced Replication Copy Number Variations Chromosomal Rearrangements Double-strand Break Repair Half Crossover Homologous Recombination Non-reciprocal Translocation Half crossover instability cascades DNA double-strand break DNA repair Genetic instabilities Array-CGH DNA repair -- Research -- Analysis DNA damage -- Research -- Analysis DNA microarrays -- Research -- Analysis DNA replication -- Regulation DNA -- Analysis Genetic recombination -- Research Mutagenesis -- Research Molecular biology -- Research Mitosis -- Regulation -- Research DNA polymerases DNA -- Synthesis Tumors -- Genetic aspects Cancer -- Genetic aspects
328	Jesus Christ’s humanity in the contexts of the pre-fall and post-fall natures of humanity: a comparative and critical evaluative study of the views of Jack Sequeira, Millard J. Erickson and Norman R. Gulley Mwale, Emanuel 12 1900 (has links) Bibliography: leaves 653-669 / Before God created human beings, He devised a plan to save them in case they sinned. In this plan, the second Person of the Godhead would become human. Thus, the incarnation of the second Person of the Godhead was solely for the purpose of saving fallen, sinful human beings. There would have been no incarnation if human beings had not sinned. Thus, the nature of the mission that necessitated the incarnation determined what kind of human nature Jesus was to assume. It was sin that necessitated the incarnation – sin as a tendency and sin as an act of disobedience. In His incarnational life and later through His death on Calvary’s cross, Jesus needed to deal with this dual problem of sin. In order for Him to achieve this, He needed to identify Himself with the fallen humanity in such a way that He would qualify to be the substitute for the fallen humanity. In His role as fallen humanity’s substitute, He would die vicariously and at the same time have sin as a tendency rendered impotent. Jesus needed to assume a human nature that would qualify Him to be an understanding and sympathetic High Priest. He needed to assume a nature that would qualify Him to be an example in overcoming temptation and suffering. Thus, in this study, after comparing and critically evaluating the Christological views of Jack Sequeira, Millard J. Erickson and Norman R. Gulley, I propose that Jesus assumed a unique post-fall (postlapsarian) human nature. He assumed the very nature that all human beings since humankind’s fall have, with its tendency or leaning towards sin. However, unlike other human beings, who are sinners by nature and need a saviour, Jesus was not a sinner. I contend that Jesus was unique because, first and foremost, He was conceived in Mary’s womb by the power of the Holy Spirit and was filled with the Holy Spirit throughout His earthly life. Second; He was the God-Man; and third, He lived a sinless life. This study contributes to literature on Christology, and uniquely to Christological dialogue between Evangelical and Seventh-day Adventist theologians. / Philosophy, Practical and Systematic Theology / D. Phil. (Systematic Theology) Adoptionism Alleles Anhypostatic Christology Anthropotokos Alternative Christology Apollinarianism Apthartodocetism Arianism Augustinian model Autosomal chromosomes Autosomal inheritance Born-again Christology Chalcedonian creed Christology from above Christotokos Chromosomes Chromosomal abnormalities Cloning Co-dominance Communicatio idiomatum Complementary base pairing Cri-du-chat syndrome Deoxyribonucleic acid (DNA) Diploid cell Docetism Dominant gene Down syndrome Dynamic incarnation Dynamic monarchianism Eastern Orthodox Christology Ebionitism Embryogenesis Eutychianism Evangelical Christology Existential Christology Functional Christology Genes Gene mutation Gene expression Genome Genotype Gnosticism Hamartiology Haploid cell Heterozygous History of Jesus’ Christology Homoiousios Theology Homozygous Human cloning Immaculate conception Incarnation Incarnational life Inheritance Karyotype Kenoticism Klinefelter syndrome Logos-flesh Christology Meiosis Mitosis Modalistic monarchianism Monarchianism Monophysitism Mutation Nestorianism Nicene Creed One-nature Christology Ontological Christology Organogenesis Patripassianism Phenotype Polygenic inheritance Post lapsarian view/model Prelapsarian view/model Recessive gene Roman Catholic Christology Sabellianism Seventh-day Adventist Christology Sex chromosomes Sex-linked inheritance Speculative Christology Theotokos Turner syndrome Two-natures Christology Unique post-fall Christology Socinianism Soteriology Theotokos Turner syndrome Two-natures Christology Unique post-fall Christology Virginal conception 231.4 Seventh-Day Adventists -- Doctrines Salvation -- Seventh-Day Adventists Fall of man -- History of doctrines Jesus Christ -- History of doctrines Sequerra, Jack Erickson, Millard J. Gulley, Norman R.

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