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Berlin Brandenburg

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  • 1
    Language: English
    In: International journal of oncology, July 2015, Vol.47(1), pp.106-14
    Description: Leupaxin belongs to the group of paxillin proteins and was reported to play a major role in the invasion and migration of prostate cancer cells. In the present study we were able to show by using a cDNA cancer profiling array that leupaxin is upregulated in breast and endometrial cancer, whereas downregulation of leupaxin was observed in lung cancer. In addition, immunohistochemical studies using a leupaxin-specific antibody on human breast cancer specimens (n=127) revealed that leupaxin is expressed mainly in invasive ductal carcinomas and ductal carcinoma in situ (40 and 49% respectively), and only in a minority of lobular mammary carcinomas. To further investigate the role of leupaxin in the progression of breast cancer the expression of leupaxin was analysed in six breast cancer cell lines. The estrogen receptor α (ERα)-positive HCC70 and the ERα-negative MDA-MB‑231 cells showed leupaxin expression on the RNA and protein level. Leupaxin localizes in these mammary carcinoma cells at focal adhesion sites and shuttles between membrane and nucleus via its LD4 motif as major nuclear export signal. Interaction partners of leupaxin in the nucleus represent the estrogen receptors ERα and ERβ. Both ERα and ERβ bind to the LIM domains of leupaxin via their AF-1/DNA binding domains. Furthermore, leupaxin is able to induce transcriptional activity of ERα independent of the presence of estradiol. The specific downregulation of leupaxin expression using siRNAs in mammary carcinoma cells resulted in reduced migratory capability and diminished invasiveness whereas no effect on proliferation was observed. Collectively, these results show that leupaxin has particular influence on the progression and invasion of breast cancer cells and may therefore represent an interesting candidate protein for diagnosis and therapeutic interventions.
    Keywords: Breast Neoplasms -- Pathology ; Cell Adhesion Molecules -- Genetics ; Estrogen Receptor Alpha -- Genetics ; Phosphoproteins -- Genetics
    ISSN: 10196439
    E-ISSN: 1791-2423
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  • 2
    Language: English
    In: Cancer Research, 04/15/2011, Vol.71(8 Supplement), pp.2508-2508
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 3
    Language: English
    In: The Journal of Pediatrics, 2009, Vol.155(1), pp.140-143
    Description: ( ) mutations cause Rett syndrome in females. Here we report on a male infant with neonatal encephalopathy, myoclonic jerks, and irregular breathing patterns caused by a novel frameshift mutation in the gene. In addition he has facial dysmorphisms previously not described in these patients.
    Keywords: Medicine
    ISSN: 0022-3476
    E-ISSN: 1097-6833
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  • 4
    Language: English
    In: International Journal of Radiation Oncology, Biology, Physics, 2010, Vol.78(4), pp.1184-1192
    Description: The standard treatment of patients with locally advanced rectal cancers comprises preoperative 5-fluorouracil–based chemoradiotherapy followed by standardized surgery. However, tumor response to multimodal treatment has varied greatly, ranging from complete resistance to complete pathologic regression. The prediction of the response is, therefore, an important clinical need. To establish models for studying the molecular basis of this heterogeneous tumor response, we exposed 12 colorectal cancer cell lines to 3 μM of 5-fluorouracil and 2 Gy of radiation. The differences in treatment sensitivity were then correlated with the pretherapeutic gene expression profiles of these cell lines. We observed a heterogeneous response, with surviving fractions ranging from 0.28 to 0.81, closely recapitulating clinical reality. Using a linear model analysis, we identified 4,796 features whose expression levels correlated significantly with the sensitivity to chemoradiotherapy ( 〈.05), including many genes involved in the mitogen-activated protein kinase signaling pathway or cell cycle genes. These data have suggested a potential relevance of the insulin and Wnt signaling pathways for treatment response, and we identified , , and as potential therapeutic targets. The microarray measurements were independently validated for a subset of these genes using real-time polymerase chain reactions. We are the first to report a gene expression signature for the chemoradiosensitivity of colorectal cancer cells. We anticipate that this analysis will unveil molecular biomarkers predictive of the response of rectal cancers to chemoradiotherapy and enable the identification of genes that could serve as targets to sensitize resistant primary tumors.
    Keywords: Colorectal Cancer ; Chemoradiotherapy ; Response ; Resistance ; Gene Expression Profiling ; Medicine
    ISSN: 0360-3016
    E-ISSN: 1879-355X
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  • 5
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 09 July 1996, Vol.93(14), pp.7263-7268
    Description: Prostate carcinoma is the second leading cause of death from malignancy in men in the United States. Prostate cancer cells express type I insulin-like growth factor receptor (IGF-IR) and prostate cancer selectively metastazises to bone, which is an environment rich in insulin-like growth factors (IGFs), thereby supporting a paracrine action for cancer cell proliferation. We asked whether the IGF-IR is coupled to tumorigenicity and invasion of prostate cancer. When rat prostate adenocarcinoma cells (PA-III) were stably transfected with an antisense IGF-IR expression construct containing the ZnSO〈sub〉4〈/sub〉-inducible metallothionein-1 transcriptional promoter, the transfectants expressed high levels of IGF-IR antisense RNA after induction with ZnSO〈sub〉4〈/sub〉, which resulted in dramatically reduced levels of endogenous IGF-IR mRNA. A significant reduction in expression both of tissue-type plasminogen activator and of urokinase-type plasminogen activator occurred in PA-III cells accompanying inhibition of IGF-IR. Subcutaneous injection of either nontransfected PA-III or PA-III cells transfected with vector minus the IGF-IR insert into nude mice resulted in large tumors after 4 weeks. However, mice injected with IGF-IR antisense-transfected PA-III cells either developed tumors 90% smaller than controls or remained tumor-free after 60 days of observation. When control-transfected PA-III cells were inoculated over the abraded calvaria of nude mice, large tumors formed with invasion of tumor cells into the brain parenchyma. In contrast, IGF-IR antisense transfectants formed significantly smaller tumors with no infiltration into brain. These results indicate an important role for the IGF/IGF-IR pathway in metastasis and provide a basis for targeting IGF-IR as a potential treatment for prostate cancer.
    Keywords: Biological sciences -- Biology -- Cytology -- Lymphocytes ; Health sciences -- Medical conditions -- Diseases -- Lymphocytes ; Health sciences -- Medical conditions -- Diseases -- Lymphocytes ; Physical sciences -- Chemistry -- Chemical compounds -- Lymphocytes ; Biological sciences -- Biology -- Genetics -- Lymphocytes ; Physical sciences -- Chemistry -- Chemical compounds -- Lymphocytes ; Biological sciences -- Biology -- Physiology -- Lymphocytes ; Biological sciences -- Biology -- Physiology -- Lymphocytes ; Biological sciences -- Biology -- Cytology -- Lymphocytes ; Biological sciences -- Biology -- Anatomy -- Lymphocytes
    ISSN: 00278424
    E-ISSN: 10916490
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  • 6
    Language: English
    In: European Journal of Medical Genetics, August 2012, Vol.55(8-9), pp.480-484
    Description: We report on monochorionic diamniotic male twins discordant for the trisomy 12p syndrome. Trisomy 12p mosaicism with a supernumerary der(12)(pter 〉 q12) was detected in approximately 50% of lymphocytes in both children. Fluorescence in situ hybridisation (FISH) revealed a high grade mosaicism of approximately 77% trisomy 12p cells in buccal smear and 85% in hair follicles in the affected twin, while in the normal developing brother an additional 12p chromosome fragment could not be detected in those tissues. Instead, in 3% of buccal smear and hair follicle cells a minute supernumerary marker chromosome comprising central portions of chromosome 12 was observed. Trisomy 12p mosaicism, confined to the lymphocytes of the unaffected twin, may be due to prenatal twin-to-twin transfusion, explaining the conspicuously discordant clinical phenotype. We discuss the possible sequence of events leading to the cytogenetic findings and compare the clinical phenotype presented in the affected twin with other cases of trisomy 12p and tetrasomy 12p (Pallister-Killian syndrome). ► Monozygotic twins with mosaic trisomy 12p in lymphocytes and discordant phenotype. ► High grade mosaicism of trisomy 12p cells in the affected twin. ► Low grade mosaicism of a minute supernumerary marker in the normal developing twin. ► Lymphocytes analysis is not adequate for mosaicism detection in monocygotic twins.
    Keywords: Trisomy 12p ; Monozygotic Twins ; Mosaicism ; Discordant Phenotype ; Medicine
    ISSN: 1769-7212
    E-ISSN: 1878-0849
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  • 7
    Language: English
    In: Molecular Cytogenetics, Dec 29, 2018, Vol.11(1)
    Description: Background Down syndrome, typically caused by trisomy 21, may also be associated by duplications of the Down syndrome critical region (DSCR) on chromosome 21q22. However, patients with small duplications of DSCR without accompanying deletions have rarely been reported. Case presentation Here we report a 51/2-year-old boy with clinical features of Down syndrome including distinct craniofacial dysmorphism and sandal gaps as well as developmental delay. Conventional karyotype was normal, whereas interphase FISH analysis revealed three signals for DSCR in approximately 40% of lymphocytes and 80% of buccal mucosa cells. Array-CGH analysis confirmed a 2.56 Mb duplication of chromosome 21q22.13q22.2 encompassing DYRK1A. Conclusion This presents one of the smallest duplications within DSCR leading to a Down syndrome phenotype. Since the dosage sensitive gene DYRK1A is the only duplicated candidate DSCR gene in our patient, this finding supports the hypothesis that DYRK1A contributes to dysmorphic and intellectual features of Down syndrome even in a mosaic state. Keywords: Down syndrome, Down syndrome critical region, Microduplication, Mosaicism, DYRK1A
    Keywords: Instrument Industry (Equipment) – Analysis ; Down Syndrome – Research ; Dysmorphology – Research
    ISSN: 1755-8166
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  • 8
    Language: English
    In: Molecular cytogenetics, 23 January 2014, Vol.7(1), pp.7
    Description: Reported cases of "pure" duplication of the entire short arm of chromosome 16 (16p) are rare, with only 7 patients described in the literature. We report on a female infant with de novo 16p duplication localized to the short arm of chromosome 6, detected by chromosomal analysis and characterized by array CGH and fluorescence in situ hybridization. This baby girl presented with clinical symptoms characteristic of patients with duplications of the short arm of chromosome 16: psychomotor retardation, constitutional growth delay and specific dysmorphic features, including proximally placed hypoplastic thumbs. In addition, she exhibited evidence of neonatal hemochromatosis as shown by direct hyperbilirubinemia, iron overload and elevated liver enzyme levels. To our knowledge, this is the first report of signs of neonatal hemochromatosis in a patient with 16p duplication.
    Keywords: Instrument Industry (Equipment) ; Newborn Infants ; Hemochromatosis ; Cytogenetics ; Liver ; Liver Diseases;
    ISSN: 1755-8166
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  • 9
    Language: English
    In: Molecular cytogenetics, 2014, Vol.7(1), pp.74
    Description: Kleefstra syndrome is characterized by intellectual disability, muscular hypotonia in childhood and typical facial features. It results from either a microdeletion of or a deleterious sequence variant in the gene euchromatic histone-lysine N-methyltransferase 1 (EHMT1) on chromosome 9q34. We report on a 3-year-old girl with characteristic symptoms of Kleefstra syndrome. Array comparative genomic hybridization analysis revealed a 145 kilobases duplication spanning exons 2 to 10 of EHMT1. Sequence analysis characterized it as an intragenic tandem duplication leading to a frame shift with a premature stop codon in EHMT1. This is the first description of an intragenic duplication of EHMT1 resulting in Kleefstra syndrome.
    Keywords: Array Cgh ; Ehmt1 ; Haploinsufficiency ; Intragenic Duplication ; KS ; Kleefstra Syndrome
    ISSN: 1755-8166
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  • 10
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 09 July 1996, Vol.93(14), pp.7263-7268
    Description: Prostate carcinoma is the second leading cause of death from malignancy in men in the United States. Prostate cancer cells express type I insulin-like growth factor receptor (IGF-IR) and prostate cancer selectively metastazises to bone, which is an environment rich in insulin-like growth factors (IGFs), thereby supporting a paracrine action for cancer cell proliferation. We asked whether the IGF-IR is coupled to tumorigenicity and invasion of prostate cancer. When rat prostate adenocarcinoma cells (PA-III) were stably transfected with an antisense IGF-IR expression construct containing the ZnSO〈sub〉4〈/sub〉-inducible metallothionein-1 transcriptional promoter, the transfectants expressed high levels of IGF-IR antisense RNA after induction with ZnSO〈sub〉4〈/sub〉, which resulted in dramatically reduced levels of endogenous IGF-IR mRNA. A significant reduction in expression both of tissue-type plasminogen activator and of urokinase-type plasminogen activator occurred in PA-III cells accompanying inhibition of IGF-IR. Subcutaneous injection of either nontransfected PA-III or PA-III cells transfected with vector minus the IGF-IR insert into nude mice resulted in large tumors after 4 weeks. However, mice injected with IGF-IR antisense-transfected PA-III cells either developed tumors 90% smaller than controls or remained tumor-free after 60 days of observation. When control-transfected PA-III cells were inoculated over the abraded calvaria of nude mice, large tumors formed with invasion of tumor cells into the brain parenchyma. In contrast, IGF-IR antisense transfectants formed significantly smaller tumors with no infiltration into brain. These results indicate an important role for the IGF/IGF-IR pathway in metastasis and provide a basis for targeting IGF-IR as a potential treatment for prostate cancer.
    ISSN: 00278424
    Source: Archival Journals (JSTOR)
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