Academic literature on the topic 'Fancg gene'
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Journal articles on the topic "Fancg gene"
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Taniguchi, Toshiyasu, and Alan D. D'Andrea. "The Fanconi anemia protein, FANCE, promotes the nuclear accumulation of FANCC." Blood 100, no. 7 (October 1, 2002): 2457–62. http://dx.doi.org/10.1182/blood-2002-03-0860.
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Fanconi anemia is an autosomal recessive disorder characterized by aplastic anemia, cancer susceptibility, and cellular sensitivity to mitomycin C. The 6 known Fanconi anemia gene products (FANCA, FANCC, FANCD2, FANCE, FANCF, and FANCG proteins) interact in a common pathway. The monoubiquitination and nuclear foci formation of FANCD2 are essential for the function of this pathway. FANCA, FANCC, FANCG, and FANCF proteins form a multisubunit nuclear complex (FA complex) required for FANCD2 monoubiquitination. Because FANCE and FANCC interact in vitro and FANCE is required for FANCD2 monoubiquitination, we reasoned that FANCE is a component of the FA complex in vivo. Here we demonstrate that retroviral transduction of Fanconi anemia subtype E (FA-E) cells with the FANCE cDNA restores the nuclear accumulation of FANCC protein, FANCA–FANCC complex formation, monoubiquitination and nuclear foci formation of FANCD2, and mitomycin C resistance. Hemagglutinin (HA)-tagged FANCE protein localizes diffusely in the nucleus. In normal cells, HA-tagged FANCE protein coimmunoprecipitates with FANCA, FANCC, and FANCG but not with FANCD2. Our data indicate that FANCE is a component of the nuclear FA complex in vivo and is required for the monoubiquitination of FANCD2 and the downstream events in the FA pathway.
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Guardiola, Ph, P. Ladne, J. Soulier, F. Siclon, J. Delrow, E. Gluckman, F. Sigaux, and J. P. Radich. "Involvement of Fanconi Anemia (FA) Genes FANCG and FANCA in Human DNA Replication, Mitosis and Chromosome Segregation: A Gene Expression Profiling Study." Blood 104, no. 11 (November 16, 2004): 2836. http://dx.doi.org/10.1182/blood.v104.11.2836.2836.
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Abstract FA is an autosomal recessive disorder with diverse clinical symptoms, including developmental anomalies, progressive bone marrow failure, and a predisposition to the development of malignancies. FA cells are hypersensitive to DNA cross-linking agents, and display chromosomal instability and defective DNA repair. FANCG-deficient pts accounts for 10% of all FA pts, and are a high risk FA population for acute myeloblastic leukemia. FANCG protein is part of the FA nuclear core complex, interacting with FANCA and FANCF. It can also interact with FANCD1, RAD51, and CYP2E1, suggesting roles in homologous recombination DNA repair and oxidative DNA-damage protection. However, FANCG lack apparent homology to other proteins involved in such processes. To address whether FANCG mRNA expression level was associated with some microarray-based functional signatures using Affymetrix HG-U133A Genechips, we first used a dataset including 111 T-acute lymphoblastic leukemia (T-ALL) samples. This large series was selected because FA pts do not usually develop T-ALL (risk of FANC gene mutation/inactivation low), FANCG is highly expressed in thymus and lymphoblasts, FANCG gene expression was significantly varying across these samples. We first selected samples having the lowest (FANCGlow) and highest (FANCGhigh) FANCG expression levels (n=15 per group, median expression values: 36 vs. 329), and identified genes differentially expressed between these 2 groups using SAM (fold change>3; qvalue<1%). Among the 368 probesets (308 known genes) significantly up-regulated in FANCGhigh group (likely to be co-expressed/regulated with FANCG), 55 were correlated to FANCG expression profile (>.75) when analyzing all 111 T-ALL samples. These genes were mainly involved in cell proliferation, mitotic cell cycle and its regulation (DNA replication, traversing Start control point, G2/M transition, chromosome segregation and cytokinesis), and were also representing cellular components involved in such processes (kinesin complex, spindle, and kinetochore). FANCA, RAD51, RAD51C, and PIR51 were also among the genes having expression patterns close to FANCG one. In addition, 11 of these 55 genes, all involved in DNA replication, were also correlated with FANCA (>.75). A robust regression analysis identified CKS1B, CCNB2, RFC5, MELK, STK18, and CENPF as the genes most significantly associated with FANCG expression profile (p<.0001, power=100%). Finally, we compared normal fibroblasts (CCL153) to primary fibroblasts from 2 FANCG-deficient pts grown under normal conditions or with MMC 100 nM for 36 hours (PD829, PD352). Fifty-eight of the 585 probesets down-regulated in FANCG-deficient fibroblasts (fold change>2; qvalue<1%) were also present in the FANCGhigh list of genes, and were mainly involved in DNA replication, mitotic chromosomal positioning and segregation, as well as in cytokinesis. Among these genes, GMNN (DNA replication inhibition by preventing MCM complex incorporation), MCM10 (DNA replication initiation), POLE2 (DNA replication and repair), and RRM2 (DNA synthesis) were also correlated with FANCA expression pattern. Of note, FANCC, FANCE, FANCF, FANCD1/BRCA2, and FANCL expression patterns were not significantly correlated with the one of FANCG or FANCA. Conclusion: these results suggest that the FA core complex, and especially FANCG and FANCA, is involved in DNA replication and mitosis.
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Ali, Abdullah M., Thiyam R. Singh, and Ruhikanta A. Meetei. "Identification and Partial Characterization of Fanconi Anemia Associated Polypeptides (FAAPs) Using a Versatile Multiprotein-Complex Purification Method." Blood 108, no. 11 (November 16, 2006): 989. http://dx.doi.org/10.1182/blood.v108.11.989.989.
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Abstract Fanconi Anemia (FA) is an autosomal recessive and X-linked disorder characterized by congenital abnormalities, progressive bone marrow failure, and a high incidence of hematological (acute leukemia) and non-hematological malignancies (squamous cell carcinomas of the head and neck or gynecologic system). FA is genetically heterogeneous disease and to date 12 complementation groups are known of which 11 gene products have been identified (FANC- A, B, C, D1, D2, E, F, G, J, L, M). Eight of the FA gene products, FANCA, FANCB, FANC, FANCE, FANCF, FANCG, FANCL and FANCM form a multiprotein FA core complex. This complex is required for the monoubiquitination of FANCD2 upon DNA damage by various genotoxic agents. The other two FA proteins; FANCD1/BRCA2 and FANCJ are believed to act “downstream” of FANCD2. In order to understand the role of FA proteins in DNA repair pathway it is necessary to find all the FA genes and their interacting partners. We have established a two-step purification method using 6XHis and FLAG tags for the biochemical and functional characterization of the FA core complex proteins. In an attempt to isolate interacting partners of FANCM and FANCL proteins; we have established two different HeLa cell lines; HeLa-HF-FANCM and HeLa-HF-FANCL, stably expressing HF-FANCM and HF-FANCL recombinant proteins respectively. Two step affinity purification was carried out to isolate the complexes from the extracts prepared from stable cell lines. Two polypeptides, namely, FAAP16 and FAAP100 were identified by mass-spectrometry as major interacting partners of FANCM and FANCL respectively. The interaction of FAAP16 and FAAP100 with other FA core complex proteins was confirmed by reciprocal affinity purification coupled mass-spectrometry using HeLa cells stably expressing HF-FAAP16 and HF-FAAP100 proteins. Furthermore, suppression of FAAP16 and FAAP100 in HeLa cells using siRNA resulted in a reduced MMC-induced FANCD2 monoubiquitination. Studies are being carried out to understand the precise role of these proteins in the FA core complex. These data suggest additional proteins interact with FA core complex members and demonstrate the utility of the purification method in delineating interacting proteins involved in FA.
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Reuter, Tanja, Sabine Herterich, Oliver Bernhard, Holger Hoehn, and Hans J. Gross. "Strong FANCA/FANCG but weak FANCA/FANCC interaction in the yeast 2-hybrid system." Blood 95, no. 2 (January 15, 2000): 719–20. http://dx.doi.org/10.1182/blood.v95.2.719.
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Three of at least 8 Fanconi anemia (FA) genes have been cloned (FANCA, FANCC, FANCG), but their functions remain unknown. Using the yeast 2-hybrid system and full-length cDNA, the authors found a strong interaction between FANCA and FANCG proteins. They also obtained evidence for a weak interaction between FANCA and FANCC. Neither FANCA nor FANCC was found to interact with itself. These results support the notion of a functional association between the FA gene products.
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Galimi, Francesco, Meenakshi Noll, Yoshiyuki Kanazawa, Timothy Lax, Cindy Chen, Markus Grompe, and Inder M. Verma. "Gene therapy of Fanconi anemia: preclinical efficacy using lentiviral vectors." Blood 100, no. 8 (October 15, 2002): 2732–36. http://dx.doi.org/10.1182/blood-2002-04-1245.
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Fanconi anemia (FA) is an inherited cancer susceptibility syndrome caused by mutations in a DNA repair pathway including at least 6 genes(FANCA, FANCC, FANCD2, FANCE, FANCF, and FANCG). The clinical course of the disease is dominated by progressive, life-threatening bone marrow failure and high incidence of acute myelogenous leukemia and solid tumors. Allogeneic bone marrow transplantation (BMT) is a therapeutic option but requires HLA-matched donors. Gene therapy holds great promise for FA, but previous attempts to use retroviral vectors in humans have proven ineffective given the impaired proliferation potential of human FA hematopoietic progenitors (HPCs). In this work, we show that using lentiviral vectors efficient genetic correction can be achieved in quiescent hematopoietic progenitors from Fanca−/− andFancc−/−mice. Long-term repopulating HPCs were transduced by a single exposure of unfractionated bone marrow mononuclear cells to lentivectors carrying the normal gene. Notably, no cell purification or cytokine prestimulation was necessary. Resistance to DNA- damaging agents was fully restored by lentiviral transduction, allowing for in vivo selection of the corrected cells with nonablative doses of cyclophosphamide. This study strongly supports the use of lentiviral vectors for FA gene therapy in humans.
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Yarde, Danielle N., Lori A. Hazlehurst, Vasco A. Oliveira, Qing Chen, and William S. Dalton. "Bortezomib Enhances Melphalan Response by Altering Fanconi Anemia (FA)/BRCA Pathway Expression and Function." Blood 108, no. 11 (November 16, 2006): 840. http://dx.doi.org/10.1182/blood.v108.11.840.840.
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Abstract The FA/BRCA pathway is involved in DNA damage repair and its importance in oncogenesis has only recently been implicated. Briefly, 8 FA/BRCA pathway family members facilitate the monoubiquitination of FANCD2. Upon monoubiquitination, FANCD2 translocates to the DNA repair foci where it interacts with other proteins to initiate DNA repair. Previously, we reported that the FA/BRCA pathway is upregulated in multiple myeloma cell lines selected for resistance to melphalan (Chen, et al, Blood 2005). Further, reducing FANCF in the melphalan resistant 8226/LR5 myeloma cell line partially reversed resistance, whereas overexpressing FANCF in the drug sensitive 8226/S myeloma line conferred resistance to melphalan. Others have reported, and we have also verified, that bortezomib enhances melphalan response in myeloma cells; however, the mechanism of enhanced melphalan activity in combination with bortezomib has not been reported. Based on our observation that the FA/BRCA pathway confers melphalan resistance, we hypothesized that bortezomib enhances melphalan response by targeting FA/BRCA DNA damage repair pathway genes. To investigate this hypothesis, we first analyzed FA/BRCA gene expression in 8226/S and 8226/LR5 cells treated with bortezomib, using a customized microfluidic card (to detect BRCA1, BRCA2, FANCA, FANCC, FANCD2, FANCE, FANCF, FANCG, FANCL, RAD51 and RAD51C) and q-PCR. Interestingly, we found that low dose (5nM) bortezomib decreased many FA/BRCA pathway genes as early as 2 hours, with maximal decreases seen at 24 hours. Specifically, 1.5- to 2.5-fold decreases in FANCA, FANCC, FANCD2, FANCE and RAD51C were seen 24 hours post bortezomib exposure. Moreover, pre-treatment of myeloma cells with low dose bortezomib followed by melphalan treatment revealed a greater than 2-fold reduction in FANCD2 gene expression levels. We also found that melphalan treatment alone enhanced FANCD2 protein expression and activation (monoubiquitination), whereas the combination treatment of bortezomib followed by melphalan decreased activation and overall expression of FANCD2 protein. Taken together, these results suggest that bortezomib enhances melphalan response in myeloma by targeting the FA/BRCA pathway. Further understanding of the role of the FA/BRCA pathway in determining melphalan response may allow for more customized and effective treatment of myeloma.
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Heinrich, Michael C., Kirsten V. Silvey, Stacie Stone, Amy J. Zigler, Diana J. Griffith, Michelle Montalto, Lin Chai, Yu Zhi, and Maureen E. Hoatlin. "Posttranscriptional cell cycle–dependent regulation of human FANCC expression." Blood 95, no. 12 (June 15, 2000): 3970–77. http://dx.doi.org/10.1182/blood.v95.12.3970.
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Abstract The Fanconi Anemia (FA) Group C complementation group gene (FANCC) encodes a protein, FANCC, with a predicted Mr of 63000 daltons. FANCC is found in both the cytoplasmic and the nuclear compartments and interacts with certain other FA complementation group proteins as well as with non-FA proteins. Despite intensive investigation, the biologic roles of FANCC and of the other cloned FA gene products (FANCA and FANCG) remain unknown. As an approach to understanding FANCC function, we have studied the molecular regulation of FANCC expression. We found that although FANCCmRNA levels are constant throughout the cell cycle, FANCC is expressed in a cell cycle-dependent manner, with the lowest levels seen in cells synchronized at the G1/S boundary and the highest levels in the M-phase. Cell cycle–dependent regulation occurred despite deletion of the 5′ and 3′ FANCC untranslated regions, indicating that information in the FANCC coding sequence is sufficient to mediate cell cycle–dependent regulation. Moreover, inhibitors of proteasome function blocked the observed regulation. We conclude that FANCC expression is controlled by posttranscriptional mechanisms that are proteasome dependent. Recent work has demonstrated that the functional activity of FA proteins requires the physical interaction of at least FANCA, FANCC, and FANCG, and possibly of other FA and non-FA proteins. Our observation of dynamic control of FANCC expression by the proteasome has important implications for understanding the molecular regulation of the multiprotein complex.
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Heinrich, Michael C., Kirsten V. Silvey, Stacie Stone, Amy J. Zigler, Diana J. Griffith, Michelle Montalto, Lin Chai, Yu Zhi, and Maureen E. Hoatlin. "Posttranscriptional cell cycle–dependent regulation of human FANCC expression." Blood 95, no. 12 (June 15, 2000): 3970–77. http://dx.doi.org/10.1182/blood.v95.12.3970.012k33_3970_3977.
Full textAbstract:
The Fanconi Anemia (FA) Group C complementation group gene (FANCC) encodes a protein, FANCC, with a predicted Mr of 63000 daltons. FANCC is found in both the cytoplasmic and the nuclear compartments and interacts with certain other FA complementation group proteins as well as with non-FA proteins. Despite intensive investigation, the biologic roles of FANCC and of the other cloned FA gene products (FANCA and FANCG) remain unknown. As an approach to understanding FANCC function, we have studied the molecular regulation of FANCC expression. We found that although FANCCmRNA levels are constant throughout the cell cycle, FANCC is expressed in a cell cycle-dependent manner, with the lowest levels seen in cells synchronized at the G1/S boundary and the highest levels in the M-phase. Cell cycle–dependent regulation occurred despite deletion of the 5′ and 3′ FANCC untranslated regions, indicating that information in the FANCC coding sequence is sufficient to mediate cell cycle–dependent regulation. Moreover, inhibitors of proteasome function blocked the observed regulation. We conclude that FANCC expression is controlled by posttranscriptional mechanisms that are proteasome dependent. Recent work has demonstrated that the functional activity of FA proteins requires the physical interaction of at least FANCA, FANCC, and FANCG, and possibly of other FA and non-FA proteins. Our observation of dynamic control of FANCC expression by the proteasome has important implications for understanding the molecular regulation of the multiprotein complex.
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Ciccone, Samantha, Anna Pulliam, Xiaohong Li, Yue Si, Attilio Orazi, Grover C. Bagby, and D. Wade Clapp. "A Model of Clonal Evolution and Myelodysplasia (MDS) on Mice with Genetic Disruption of Both Fancc and Fancg." Blood 108, no. 11 (November 16, 2006): 2627. http://dx.doi.org/10.1182/blood.v108.11.2627.2627.
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Abstract Fanconi anemia (FA) is a rare inherited chromosomal instability syndrome characterized by bone marrow failure and a high relative risk of MDS. Eight FA proteins associate in a core nuclear complex and function at least in part to catalyze the monoubiquitination of the downstream target protein, FANCD2 in response to DNA damage. In this nuclear pathway the FA proteins are epistatic in the activation of FANCD2 since inactivation of any one of the eight FA proteins results in failure of FANCD2 monoubiquitination and hypersensitivity to cross-linking agents. Although biochemical studies have attributed additional survival signaling functions to the FA proteins, these functions have not been evaluated using a genetic model. Murine models of FA have been established using homologous recombination for gene disruption. Although all strains of knockout mice are hypersensitive to mitomycin c, none of the single gene knockout mice display bone marrow failure, MDS, or myeloid leukemia. Seeking to develop such a model, we utilized a genetic intercross to generate mice that harbor disruptions in both Fancc and Fancg. Genetic disruption of both Fancc and Fancg predispose Fancc−/−;Fancg −/− mice or recipients adoptively transferred with Fancc −/−; Fancg −/− hematopoietic stem cells to MDS analogous to the disease phenotype in FA patients as defined histologically and by cytogenetic analysis. Genome wide transcriptomal analysis and hierarchical clustering by genotypic group of bone marrow cells from wild type, single knockout, and double knockout mice (n=3 each) confirmed substantial differences between hematopoietic cells of Fancc, Fancg and double knockout (DKO) mice. Serial pairwise analysis and gene pattern analyses (GeneSifter) showed that of the 1190 genes expressed differentially (by a factor of >1.5, FDR adjusted p<0.05) in Fancc−/− marrow cells only 134 were differentially expressed in Fancg−/− cells. Of the 524 genes expressed differentially in Fancg−/− marrow compared to WT, 277 were not expressed differentially in Fancc−/− marrow compared to WT. In pairwise analysis of Fancc−/− vs. Fancg−/− gene expression, ontologies of those genes more highly expressed in Fancc −/− cells included responses to biotic stress, defense and immune response. The most over-represented ontological category of those genes more highly expressed in Fancg−/− cells was response to oxidative stress. Since these genes are not epistatic in regards to the hematopoietic phenotype, and the transcriptomal consequences of their loss-of-function in marrow cells are significantly different, this genetic model confirms that the Fancc and Fancg proteins are multi-functional. Transcriptosomal analyses were conducted on DKO mice that contained MDS and DKO mice with no overt disease. The transcriptome of DKO marrow cells was unique in that 152 suppressed and 687 activated gene products relative to WT samples were not found in either Fancc−/− or Fancg−/− samples. Furthermore, there are distinct transcriptomal differences between the DKO mice with MDS and those that do not have MDS. These data suggest that some of these changes may be adaptive and involved in the molecular pathogenesis of MDS. The DKO model provides the first preclinical platform to systematically evaluate the molecular pathogenesis of bone marrow failure and myelodysplasia in the setting of Fanconi anemia.
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Mori, Minako, Asuka Hira, Kenichi Yoshida, Hideki Muramatsu, Yusuke Okuno, Michiko Anmae, Kazuo Tamura, et al. "Characterization of Pathogenic Variants and Clinical Phenotypes in 117 Japanese Fanconi Anemia Patients." Blood 132, Supplement 1 (November 29, 2018): 3860. http://dx.doi.org/10.1182/blood-2018-99-110362.
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Abstract Objective: Fanconi anemia (FA) is the most common inherited bone marrow failure syndrome associated with multiple congenital abnormalities and predisposition to malignancies, resulting from mutations in one of the 22 known FA genes (FANCA to W). The proteins encoded by these genes participate in DNA repair pathway (the FA pathway) for endogenous aldehyde damage. Compared to the situation in the US or Europe, the number of Japanese FA patients with genetic diagnosis was relatively limited. In this study, we reveal the genetic subtyping and the characteristics of mutated FA genes in Japanese population and clarify the genotype-phenotype correlations. Results: We studied 117 Japanese FA patients from 103 families (1996 to 2018). The diagnosis of FA was confirmed on the basis of chromosomal breakage tests and clinical features. Molecular diagnosis was obtained in 107 (91.5%) of the 117 patients through direct sequencing of FANCA and FANCG, MLPA analysis for FANCA, targeted exome sequencing (targeted-seq), and whole exome sequencing (WES) analysis (Figure 1). To provide genetic subtyping for the 10 unclassified cases, we tried to apply various technologies. Array CGH revealed large deletions in two FA-B and one FA-T cases. Whole genome sequencing and RNA-sequencing analysis identified splicing site or aberrant splicing mutations among three cases (one FA-B, one FA-C, and one FA-N). Collectively, 113 (97%) of Japanese 117 FA patients were successfully subtyped and a total of 219 mutated alleles were identified. FA-A and FA-G accounted for the disease in 58% and 25% of FA patients, respectively, whereas each of the other complementation groups accounted for less than 5% of FA cases. FANCB was the third most common complementation group (n=4) and only one FA-C case was identified in Japanese FA patients. In the 68 FA-A patients, we identified 130 mutant alleles that included 55 different FANCA variants (17 nucleotide substitutions, 16 small deletions/insertions, 12 large deletions, 1 large duplication and 9 splice site mutation). FANCA c.2546delC was the most prevalent (41/130 alleles; 32%). In the 29 FA-G patients, 57 mutant alleles were identified and seven different FANCG variants were detected. FANCG c.307+1G>C and 1066C>T accounted for most of FANCG mutant alleles (49/57; 88%) in the Japanese FA-G patients. The three hotspot mutations (FANCA c.2546delC, FANCG c.307+1G>C and c.1066C>T) existed at low prevalence (0.04-0.1%) in the whole-genome reference panel of 3554 Japanese individuals (3.5KJPN, Tohoku Megabank). Consistent with the paucity of the FA-C patients as opposed to the previous report (Blood 2000), the FANCC IVS4+4A mutation was absent in the 3.5KJPN database. We were able to examine the hematological outcomes in a subset of our cases (52 FA-A and 23 FA-G). Interestingly, the FA-G patients developed bone marrow failure (BMF) at a significantly younger age than FA-A patients (median age at onset of BMF: 3.1 years vs 5 years). Furthermore, the patients with the FANCA c.2546delC mutation had an increased risk of developing myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML), compared to FA-A patients without the mutation. In the rare complementation groups of FA, two FA-B cases with complete loss of FANCB gene and one FA-I patient with N-terminal premature termination codons revealed severe somatic abnormalities, consistent with VACTERL-H association. Two FANCD1 (BRCA2) patients and one FANCN (PALB2) patients did not experience bone marrow failure but developed early-onset malignancies (immature teratoma, T-lymphoblastic lymphoma, adenosquamous lung carcinoma, Wilms tumor). Conclusion: This is the largest series of subtyped Japanese FA patients to date and the results would be useful for future clinical management. To provide molecular diagnosis for FA in Japan, we suggest to start with PCR-direct sequencing of the three common mutations (FANCA c.2546delC, FANCG c.307+1G>C and FANCG c.1066C>T) along with MLPA assay for FANCA. These analyses would enable the identification of about 50% of the mutant alleles. For the rest of the cases, WES or targeted-seq analysis should be useful, however, large deletions and aberrant splicing need to be kept in mind. Disclosures Takaori-Kondo: Pfizer: Honoraria; Novartis: Honoraria; Celgene: Honoraria, Research Funding; Bristol-Myers Squibb: Honoraria; Janssen Pharmaceuticals: Honoraria.
Dissertations / Theses on the topic "Fancg gene"
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Barroca, Vilma. "Renouvellement des cellules souches : plasticité des progéniteurs germinaux et rôle du gène Fancg dans la fonction des cellules souches hématopoïétiques." Phd thesis, Université d'Orléans, 2009. http://tel.archives-ouvertes.fr/tel-00461254.
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La préservation d'un stock de cellules souches fonctionnelles est indispensable pour le maintien de nombreux tissus chez l'adulte. Les cellules souches se multiplient pour s'auto-renouveller et entrent en différenciation donnant naissance à des progéniteurs puis à des cellules matures. Récemment, la possibilité pour les progéniteurs de se reprogrammer en cellules souches et de réacquérir un potentiel de régénération à long terme a été suggérée notamment dans le tissu germinal. Ainsi, l'auto-renouvellement et la reprogrammation des progéniteurs pourraient jouer un rôle dans le maintien du pool de cellules souches. Mon travail de thèse portait sur l'étude de ces deux mécanismes de régénération des cellules souches chez la souris. J'ai tout d'abord étudié la reprogrammation des progéniteurs germinaux au cours de la spermatogenèse. Ce travail montre la capacité des progéniteurs germinaux mâles, les spermatogonies différenciées, à modifier leur programme de différenciation et à générer de nouvelles cellules souches germinales après transplantation testiculaire. Les progéniteurs germinaux pourraient ainsi constituer une réserve de " cellules souches potentielles ". Le tissu germinal possède donc une certaine plasticité. La seconde partie de mon travail porte sur l'implication du gène Fancg de l'anémie de Fanconi, voie de réponse aux dommages à l'ADN, dans l'auto-renouvellement et la fonctionnalité des cellules souches hématopoïétiques au cours de l'hématopoïèse. L'intégrité génétique des cellules souches doit en effet être préservée tout au long de la vie de l'individu. Cette étude montre que l'invalidation du gène Fancg perturbe le processus de migration, la quiescence, et la régulation de l'expression de certains gènes clés des fonctions des cellules souches. Ces altérations participent au déficit fonctionnel des cellules souches hématopoïétiques observées dans le modèle murin Fancg-/-.
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Amstalden, Lucila Gobby. "Estudo das mutações do gene FANCG em pacientes com quadro clinico sugestivo de anemia de Fanconi." [s.n.], 2006. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308582.
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Orientador: Carmen Silvia BertuzzoDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: A Anemia de Fanconi (AF) é uma doença caracterizada por múltiplas anomalias congênitas, progressiva falha da medula óssea e alto risco para desenvolvimento de câncer. E denominada também de Síndrome da Instabilidade Cromossômica devido ao fato de suas células apresentarem hipersensibilidade a agentes indutores de quebras cromossômicas. A mais importante das características clínicas é a manifestação hematológica. A incidência da anemia aplástíca, Síndrome Mieloplásica e Leucemia Mielóide Aguda é a maior resposável pela morbidade e mortalidade na AF A incidência da AF em todo o mundo é de. aproximadamente, 3 por milhão. No Brasil não há dados sobre a prevalência da doença. Foram descobertos 12 grupos de complementação e descobertos, até o momento. 11 genes relacionados ao distúrbio. São eles: FANCA. B, C, Dl, D2, E. F G, I, J, L e M. O trabalho teve como objetivo geral a análise das mutações principais (IVS8+2A>G, IVS11+lOC, IVS3+1G>C e 1794J803dellO) do gene FANCG em pacientes com quadro clínico compatível com AF. Foram analisados 38 indivíduos por meio da técnica de PCR associada à digestão e triagem por SSCP e subseqüente seqüenciamento. Nós encontramos um homozigoto para a mutação IVS8+2A>G e uma variante neutra (H482H). Concluímos com nosso estudo que, há uma heterogeneidade molecular em nosso meio; o DEB teste não é 100% eficaz na detecção de indivíduos com AF; o Teste de Complementação deve ser introduzido o quanto antes em nosso país para auxiliar no direcionamento da pesquisa para um determinado gene e minimizar os casos em que não há a confirmação de diagnóstico e, por último, há a necessidade de um Registro Brasileiro para AF com o objetivo de recolher informações clinicas e genéticas de indivíduos com o distúrbio.
Abstract: Fanconi anaemia (FA) is an autosomal recessive disease characterised by congenital abnormalities, progressive bone marrow failure and high risk of developing cancer. It's called Chromosomal Instability Syndrome due to the fact of cells presents hipersensibility to DNA cross-linking agents like mitomycin C and diepoxybutane. The most important clinical feature is hematologic. The incidence of aplastic anemia, myelodysplastic syndrome and acute myeloide leukaemia is the most important cause of morbidity and mortality in FA. The incidence of FA is approximately three per million and the heterozygote frequency is estimated at 1 in 300 in Europe and United States. In Brazil there's not data about prevalence of FA. It was discovered at least 12 complementation groups and eleven gene have been cloned: FANCA, B, C, DJ, D2, E, F, G, I, J, L eM. The study had as general objective the analysis of the main mutation (IVS8-2A>G, TVSll+lOC, IVS3+1G>C e 1794J803dell0) of FANCG gene in patients with clinical features of FA. It was analysed 38 patients through the test polymerase chain reaction (PCR) associated with digestion and mutation screening by SSCP with posterior sequencing. Molecular analysis found a homozygote to rVS8+2A>G and a neutral variant (H482H). We concluded that there's a molecular heterogeneity in our region; it's necessary to introduce the use of complementary tests in Brazil, in order to address the molecular analysis and at last, it's necessary a Brazilian Fanconi Anemia Registry (BFAR) to receive clinical and genetics information of AF patients.
Mestrado
Ciencias Biomedicas
Mestre em Ciências Médicas
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Buwe, Andrea [Verfasser], and M. [Akademischer Betreuer] Schmid. "Geschlechts-chromosomale Kopplung der Fanconi Anämie Gene FANCC und FANCG im Hühnergenom und die geschlechtsspezifische Sensibilität der Hühnerzellen gegenüber Mitomycin C / Andrea Buwe. Betreuer: M. Schmid." Würzburg : Universitätsbibliothek der Universität Würzburg, 2013. http://d-nb.info/1034256610/34.
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Solyom, S. (Szilvia). "BRCA/Fanconi anemia pathway genes in hereditary predisposition to breast cancer." Doctoral thesis, Oulun yliopisto, 2011. http://urn.fi/urn:isbn:9789514294099.
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Abstract Two major genes are involved in hereditary predisposition to breast and ovarian cancer – BRCA1 and BRCA2. However, germline mutations in these tumor suppressors account for a maximum 20% of the familial breast cancer cases. A significant portion of the genes predisposing to this disease is unknown and therefore needs to be discovered. The aim of this study was to identify novel breast cancer susceptibility genes from the interweaving BRCA/Fanconi anemia (FA) pathway. Five candidate genes – MERIT40, ABRAXAS, BRIP1, CHK1, and FANCA – were screened for mutations by utilizing conformation-sensitive gel electrophoresis and sequencing, or with multiplex ligation-dependent probe amplification in blood DNA samples of Finnish familial breast cancer patients. Investigation of the MERIT40 gene revealed novel nucleotide changes, being the first report on mutation screening of this gene. None of the observed alterations, however, appeared to be disease related, suggesting that germline mutations in MERIT40 are rare or absent in breast cancer patients. A missense alteration (c.1082G>A, leading to Arg361Gln) was identified in ABRAXAS in 3 out of 125 Northern Finnish breast cancer families (2.4%), but not in any of the 867 healthy controls. The prevalence of the mutation between familial and control cases was statistically significantly different (p=0.002). ABRAXAS c.1082G>A appears to have pathological significance based on its exclusive occurrence in cancer cases, evolutionary conservation, disruption of a putative nuclear localization signal, reduced nuclear localization of the protein, and defective accumulation at DNA damage sites. The BRIP1 (FANCJ) and CHK1 genes were screened for large genomic rearrangements, but no abnormalities were detected, ruling out a significant contribution to breast cancer susceptibility in the Northern Finnish population. A novel large heterozygous deletion was identified in the FANCA gene in one out of 100 breast cancer families, removing the promoter and the first 12 exons. The deletion allele was not present in the tested controls, suggesting that it might contribute to breast cancer susceptibility. This is the first report on the association of a large-size germline deletion in a gene acting in the upstream part of the FA signaling pathway with familial breast cancerTiivistelmä BRCA1 ja BRCA2 ovat kaksi tärkeintä perinnöllisen rinta- ja munasarjasyövän alttiusgeeniä. Niissä esiintyvät ituradan muutokset selittävät kuitenkin vain noin 20 % familiaalisista rintasyöpätapauksista. Suurin osa alttiusgeeneistä on edelleen tunnistamatta ja näitä tekijöitä etsitään aktiivisesti. Tämän tutkimuksen tarkoituksena on ollut tunnistaa uusia alttiustekijöitä toisiinsa läheisesti liittyviltä BRCA/Fanconin anemia (FA) signaalinsiirtoreiteiltä. Viisi kandidaattigeeniä - MERIT40, ABRAXAS, BRIP1, CHK1 ja FANCA – kartoitettiin mutaatioiden suhteen suomalaisissa rintasyöpäperheissä käyttämällä konformaatiosensitiivistä geelielektroforeesia ja sekvensointia, tai multiplex ligation-dependent probe amplification- menetelmää. MERIT40-geenissä havaittiin useita aikaisemmin raportoimattomia nukleotidimuutoksia, mutta yhdenkään niistä ei havaittu liittyvän rintasyöpäalttiuteen. MERIT40-geenimuutosten mahdollista yhteyttä rintasyöpäalttiuteen ei ole tutkittu aikaisemmin. ABRAXAS-geenissä havaittiin missense-mutaatio (c.1082G>A, joka johtaa Arg361Gln aminohappokorvautumiseen) kolmessa pohjoissuomalaisessa rintasyöpäperheessä (3/125, 2.4 %). Muutosta ei havaittu terveissä kontrolleissa (N=867), ja ero mutaation esiintyvyydessä familiaalisten rintasyöpätapausten ja terveiden kontrollien välillä oli tilastollisesti merkitsevä (p=0.002). ABRAXAS c.1082G>A-muutos on todennäköisesti patogeeninen, sillä kyseinen aminohappopaikka on evolutiivisesti konservoitunut ja sijaitsee todennäköisellä tumaanohjaussignaalialueella. Funktionaaliset kokeet osoittivat, että mutatoitunut proteiinituote lokalisoitui villityypin proteiinia heikommin tumaan ja sen ohjautuminen DNA-vaurioalueille oli puutteellista. BRIP1- (FANCJ) ja CHK1-geeneistä etsittiin laajoja genomisia uudelleenjärjestelyjä, mutta niitä ei havaittu. Näin ollen kyseisillä muutoksilla ei ole merkittävää roolia perinnöllisessä rintasyöpäalttiudessa suomalaisessa väestössä. FANCA-geenissä havaittiin laaja heterotsygoottinen deleetio yhdessä tutkitusta 100 rintasyöpäperheestä. Deleetio poistaa geenin promoottorialueen lisäksi sen 12 ensimmäistä eksonia. Deleetioalleelia ei havaittu terveissä kontrolleissa, joten se mahdollisesti liittyy perinnölliseen rintasyöpäalttiuteen. Tutkimus on ensimmäinen, jossa raportoidaan laaja genominen deleetio FA-signaalinsiirtoreitin ylävirran geenissä familiaalisessa rintasyövässä
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Hira, Asuka. "Mutations in the gene encoding the E2 conjugating enzyme UBE2T cause Fanconi Anemia." Kyoto University, 2015. http://hdl.handle.net/2433/202672.
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Gonçalves, Claudia Estela 1970. "Estudo molecular do gene FANCA em pacientes com quadro clínico de Anemia de Fanconi." [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308602.
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Orientador: Carmen Sílvia BertuzzoTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: A Anemia de Fanconi (AF) é uma alteração genética caracterizada por múltiplas anomalias congênitas, anormalidades hematológicas e predisposição a uma variedade de tumores. A incidência mundial da AF em todo o mundo é de aproximadamente três por milhão e a frequência de heterozigotos é estimada em um para 300 na Europa e Estados Unidos. É uma doença causada por mutações em genes relacionados ao sistema de reparo. Até o momento foram descritos 16 genes que podem estar multados. São eles: FANCA, FANCB, FANCC, FNCD1, FANCD2, FANCE, FANCF, FANCG, FANCI, FANCJ, FANCL, FANCM, FANCN, FANCO, FANCP E PANCQ. Os grupos mais frequentes são o FANCA e FANCC. De qualquer modo devido a essa heterogeneidade gênica, o diagnóstico molecular dessa alteração é complexo. Com o intuito de testar uma estratégia diagnóstica, o presente trabalho se propôs a identificar as mutações mais frequentes no gene FANC por PCR e digestão enzimática e investigar mutações no gene FANCA, por meio da Reação em Cadeia da Polimerase seguida de digestão enzimática da mutação Brasileira e posterior sequenciamento dos 43 éxons em 60 pacientes portadores de Anemia de Fanconi DEB positivos. Foram detectados 19 pacientes (27,94%), como sendo do grupo C e 16 pacientes como grupo A (23,53%). A mutação ?3788-3790 do gene FANCA teve uma frequência alélica de 15,4%. Foram encontradas 3 mutações intrônicas, 1 mutação sinônima e 1 mutação de sentido trocado no gene FANCA. Não foram encontradas correlações com as manifestações hematológicas, renais, baixo peso, malformações congênitas de membros, machas e pigmentação de pele, sexo e idade
Abstract: The Fanconi Anemia (FA) is a genetic disorder characterized by multiple congenital and hematological abnormalities and predisposition to a variety of tumors. The worldwide incidence of AF is approximately three per million and the frequency of heterozygotes is estimated at one in 300 in Europe and the United States. It is a disease caused by mutations in genes involved in the repair system. So far have been described 16 genes that may be mutated. They are: FANCA , FANCB , FANCC , FNCD1 , FANCD2 , FANCE , FANCF , FANCG , FANCI , FANCJ , FANCL , FANCM , FANCN , FANCO , FANCP And PANCQ . The most common groups are the FANCA and FANCC. However due to this genetic heterogeneity, molecular diagnosis of this change is complex. In order to test a diagnostic strategy, the present study aimed to identify the most frequent mutations in the FANC gene by PCR and restriction enzyme digestion and investigate mutations in the FANCA gene, using the polymerase chain reaction followed by enzymatic digestion of the mutation Brazilian and subsequent sequencing of the 43 exons in 60 patients with Fanconi Anemia positive DEB. 19 patients (27.94%) were detected as group C and 16 patients as group A (23.53%). The ?3788 - 3790 mutation in the FANCA gene had an allelic frequency of 15.4%. Three intronic mutations, one synonymous mutation and one mutation changed direction in FANCA gene were found. No correlation with hematologic, renal, low weight manifestations of congenital malformations members, butches and skin pigmentation, age and sex were found
Doutorado
Clinica Medica
Doutora em Clínica Médica
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Gonçalves, Claudia Estela 1970. "Estudo das mutações do gene Fancc em pacientes com quadro clinico de anemia de Fanconi na região de Campinas." [s.n.], 2008. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308586.
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Orientador: Carmen Silvia BertuzzoDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: A Anemia de Fanconi (AF) é uma doença que apresenta herança autossômica recessiva. É caracterizada por múltiplas anomalias congênitas, progressiva falha da medula óssea e alto risco para desenvolvimento de câncer. A mais importante das características clínicas é a manifestação hematológica, responsável pelo grande número de morbidade e mortalidade em portadores de AF. Também é chamada de síndrome da instabilidade cromossômica por apresentar hipersensibilidade a agentes clastogênicos como a mitomicina C e diepoxibutano. A incidência da AF em todo o mundo é de aproximadamente, três por milhão e a frequência de heterozigotos é estimada em um para 300 na Europa e Estados Unidos. No Brasil não há dados sobre a prevalência da doença. Foram descobertos até o momento 13 grupos de complementação (FANCA, B, C, D1, D2, E, F, G, I, J, L, M e N), e os 13 genes foram clonados e pelo menos 11 genes estão relacionados ao distúrbio. O presente estudo teve como objetivo a análise das principais mutações (IVS4+4A>T, Q13X, W22X, DG322, R185X, L496R, L554P, e R548X) do gene FANCC em pacientes com quadro clínico de AF. Foram analisados 121 indivíduos com clínica compatível à AF e com DEB teste positivo. Na amostra encontramos 14% de indivíduos heterozigotos e 4% de indivíduos homozigotos para as mutações mais freqüentes do gene FANCC. As mutações mais prevalentes foram: IVS4+4A>T com 6,6% dos alelos analisados, com freqüência similar à encontrada na literatura, W22X com 2.47% dos cromossomos analisados e Q13X com 1.23% dos cromossomos analisados. Na triagem de mutações pela técnica de SSCP, encontramos alterações nos éxons 1, 4 e 6.
Abstract: Fanconi anaemia (FA) is an autosomal recessive disease characterized by congenital abnormalities, progressive bone marrow failure and high risk of developing cancer. The most important of the clinic feature is hematologic, and too the most important cause of morbidity and mortality in FA. It's also called Chromosomal Instability Syndrome to the fact of cells presents hipersensibility to DNA cross-linking agents like mitomycin C and diepoxybutane. The incidence of FA is approximately three per million and the heterozygote frequency is estimated at 1 in 300 in Europe and United States. In Brazil there's no data about prevalence of FA. It was discovered at least 13 complementation groups (FANCA, B, C, D1, D2, E, F, G, I, J, L, M e N), and 13 genes have been cloned and there are at least 11 that are related to the disease. The study had as general objective the analysis of the main mutations (IVS4+4A>T, Q13X, W22X, DG322, R185X, L496R, L554P, and R548X) of FANCC gene in patients with clinic compatible of FA. We analyzed 121 patients with compatible clinic and positive DEB test. In the sample we found 14% of individuals heterozygous and homozygous individuals of 4% for the most frequent mutations of the gene FANCC. Mutations were more prevalent: IVS4 4 A> T with 6.6% of alleles tested, often similar to that found in the literature, W22X with 2.47% of chromosomes analyzed and Q13X with 1.23% of chromosomes analyzed. In screening for mutations by the technique of SSCP, we found changes in exons 1, 4 and 6.
Mestrado
Mestre em Farmacologia
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Eirenschmalz, Margarethe. "Dreiecksverhältnisse im Schnee the socio-cultural evolution of the mountain film genre as illustrated by analysis of gender-nature relations in three films by Fanck, Riefenstahl, and Trenker /." abstract and full text PDF (free order & download UNR users only), 2008. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:1456412.
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Fach, Cornelia. "Selektive Amplifikation, Klonierung und Sequenzierung eines hypermutablen Bereiches des Fanconi-Anämie-A (FANCA)-Gens aus Fibroblasten-Kulturen unterschiedlicher Passagen und Genotypen." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=973119675.
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Buwe, Andrea. "Geschlechts-chromosomale Kopplung der Fanconi Anämie Gene FANCC und FANCG im Hühnergenom und die geschlechtsspezifische Sensibilität der Hühnerzellen gegenüber Mitomycin C." Doctoral thesis, 2013. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-77593.
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Fanconi Anämie ist eine seltene rezessiv vererbte Erkrankung, deren zu Grunde liegende Enzymdefekte in ein Netzwerk unterschiedlichster DNA-Reparaturproteine eingewoben sind. Phylogenetisch sind uns Vögel relativ nahe verwandt, was sie zu einem guten Modellorganismus jenseits der Säugetiermodelle macht. Eine von Hühnerzellen abgeleitete Zelllinie (DT40) wurde bereits schon breit eingesetzt um die Funktion des FA-Signalwegs zu erforschen. Nachdem auch das Hühnergenom vollständig entschlüsselt wurde, konnten zu fast allen FA-Genen Orthologe gefunden werden. Unter den zahlreichen FA-Genen sind für diese Arbeit vor allem FANCC und -G von Bedeutung, da beide Gene auf dem Z-Geschlechtschromosom des Huhns liegen und eine Inaktivierung des zweiten Z-Chromosoms beim Hahn äquivalent zur X-Inaktivierung beim Menschen nicht stattfindet. Somit sollte es ein ´natürliches´ Gendosisungleichgewicht zwischen den Geschlechtern geben. Im durchgeführten Southern Blot konnte keine geschlechtsspezifisch weibliche Bande (für FANCC und -G) gefunden werden. Somit ist davon auszugehen, dass die FA-Gene C und G ausschließlich auf dem Z-Chromosom lokalisiert sind. Dies wurde auch nochmals mittels FISH bestätigt - beide Gene fanden sich auf dem kurzen Arm des Z-Chromosoms (FANCC zentromernah, FANCG zentromerfern). Aus Studien mit DT40 Zellen ist bereits bekannt, dass FA defiziente Zellen ähnlich wie humane FA-Zellen eine Hypersensitivität gegenüber Substanzen zeigen, die DNA-crosslinks verursachen. In Anlehnung an die humane FA-Diagnostik wurden die neu etablierten embryonalen Fibroblasten mit unterschiedlichen Konzentrationen und Einwirkzeiten von MMC behandelt und die Schäden ausgewertet. In allen Untersuchungen trugen die weiblichen Zellen mehr Schäden davon als die männlichen. Bei niedrigen Konzentrationen zeigte sich dies nur als Trend, bei höheren MMC-Konzentrationen und längeren Einwirkzeiten fanden sich bei fast allen durchgeführten Untersuchungen auch statistisch signifikante Unterschiede. Somit ergibt sich aus dieser Arbeit ein deutlicher Hinweis auf ein funktionelles Ungleichgewicht zwischen Henne und Hahn was die DNA-Reparatur nach Schädigung durch MMC angehtFanconi anemia is a rare recessive disorder whose underlying enzyme deficiencies are woven into a network of various DNA repair proteins. Phylogenetically related birds are relatively close to us, which makes it a good model organism beyond the mammalian models. A cell line derived from chicken cells (DT40) has already been widely used to study the FA pathway. Even after the chicken genome was completely decoded, orthologs could be found for almost all FA genes. Among the numerous FA genes are mainly FANCC and G of importance since both genes are located on the Z sex chromosome of chicken. An inactivation of the second Z chromosome as the inactivation of the x chromosom in human does not take place. Thus there should be a 'natural' imbalance of the gen dose between the sexes. Southern blot showed no gender female band (for FANCC and G). Thus it can be assumed that the FA genes C and G are exclusively localized on the Z chromosome. This was also confirmed by FISH, both genes were located on the short arm of the Z chromosome. From studies in DT40 cells is already known that FA deficient cells, similar to a human FA cell show hypersensitivity to substances that cause DNA crosslinks. Based on the human FA diagnosis, newly established embryonic fibroblasts were treated with different concentrations of MMC and chromosomal the damage was evaluated. In all studies, the female cells contributed more damage than the male. At low concentrations, this was only shown as a trend, at higher MMC concentrations and longer exposure times there was a significant differences. Thus, results from this study, a clear indication of a functional imbalance between hen and rooster in terms of DNA repair after damage by MMC
Books on the topic "Fancg gene"
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Shen geng Taiwan, fang yan quan qiu. Taibei Shi: Taiwan jing ji yan jiu yuan, 2012.
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Na de qi, geng yao fang de xia. Taibei Shi: Yu he wen hua chu ban you xian gong si, 2008.
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Bi ming wang xing geng yuan de di fang. Taoyuan Shi: Dou dian wen chuang jie she, 2012.
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yan, Wang zhi. Ru he rang ni de hai zi geng you xiu. Bei jing: Zhong guo yan shi chu ban she, 2008.
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1963-, Yang Liling, ed. Duo dian si kao, geng neng fang song: Kaneiji jie ya fang cheng shi. Taibei Shi: Tian xia yuan jian chu ban gu fen you xian gong si, 2006.
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Dian hua ying xiao guan li: Dian hua ying xiao yao ji qiao, geng yao guan li. Nanjing: Feng huang chu ban she, 2010.
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Yikun, Peng, ed. Chen Geng da jiang zai jie fang zhan zheng zhong. Beijing: Jie fang jun chu ban she, 1985.
Find full textBook chapters on the topic "Fancg gene"
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Nanda, I., A. Buwe, A. Wizenman, M. Takata, T. Haaf, M. Schartl, and M. Schmid. "Fanconi Anemia Genes in Vertebrates: Evolutionary Conservation, Sex-Linkage, and Embryonic Expression of FANCC and FANCG in Avian Cells." In Fanconi Anemia, 183–99. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000102556.
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García-García, María J. "A History of Mouse Genetics: From Fancy Mice to Mutations in Every Gene." In Advances in Experimental Medicine and Biology, 1–38. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-2389-2_1.
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"FANC Genes." In Encyclopedia of Cancer, 1374. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2114.
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Nemunaitis, John, Donald Rao, and Neil Senzer. "FANG: bi-shRNAifurin and GMCSF DNA-Augmented Autologous Tumor Cell Vaccine: Clinical Results." In Gene and Cell Therapy, 1073–90. CRC Press, 2015. http://dx.doi.org/10.1201/b18002-51.
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Tu, C. H., and H. P. Huang. "RiverFlow2D with UAV to improve ecological corridor of wild creek in Taiwan- The case study in Geng-fang Nanshih creek." In River Flow 2020, 1816–23. CRC Press, 2020. http://dx.doi.org/10.1201/b22619-255.
Full textConference papers on the topic "Fancg gene"
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Fink, Andrew, Arjun Kalvala, Li Gao, Kathleen Dotts, Brittany Aguila, Shirley Tang, Gregory A. Otterson, Miguel A. Villalona-Calero, and Wenrui Duan. "Abstract 4438: Promoter hypermethylation status of Fanconi Anemia (FA) pathway genes FANCF, FANCL and FANCS in non-small cell lung cancer (NSCLC)." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4438.
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Solyom, Szilvia, Robert Winqvist, Jenni Nikkilä, and Katri Pylkäs. "Abstract 5599: Screening for large genomic rearrangements in the FANCA and FANCJ genes reveals extensive genomic FANCA deletion in a Finnish breast cancer family." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-5599.
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Duan, Wenrui, Tyler Rees, Kevin Vu, Brittany Barnwell, Li Gao, Arjun Kalvala, xin wu, Gregory A. Otterson, and Miguel A. Villalona-Calero. "Abstract 4246: Promoter hypermethylation and gene expression of FANCF in non-small cell lung cancer (NSCLC)." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4246.
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Takahashi, Junichi, Takaaki Masuda, Yosuke Kuroda, Akihiro Kitagawa, Yushi Motomura, Kensuke Koike, Dai Shimizu, et al. "Abstract 3173: Clinical significance of Fanconi anemia complementation group E(FANCE)DNA repair-related gene expression in hepatocellular carcinoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3173.
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Takahashi, Junichi, Takaaki Masuda, Yosuke Kuroda, Akihiro Kitagawa, Yushi Motomura, Kensuke Koike, Dai Shimizu, et al. "Abstract 3173: Clinical significance of Fanconi anemia complementation group E(FANCE)DNA repair-related gene expression in hepatocellular carcinoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3173.
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Fierheller, Caitlin, Wejdan M. Alenezi, Corinne Serruya, Timothée Revil, Javad Nadaf, Anne-Marie Mes-Masson, Diane Provencher, et al. "Abstract 2056: The genomic landscape of carriers of rare variants in FANCI, a new candidate ovarian cancer predisposing gene." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2056.
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