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Berlin Brandenburg

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  • 1
    Language: English
    In: Annals of internal medicine, 19 June 2018, Vol.168(12), pp.893-904
    Keywords: Autoimmune Diseases -- Etiology ; Diet -- Adverse Effects ; Hydroxymethylglutaryl-Coa Reductase Inhibitors -- Adverse Effects ; Muscular Diseases -- Etiology ; Oryza -- Adverse Effects
    ISSN: 00034819
    E-ISSN: 1539-3704
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  • 2
    Language: English
    In: Cancer Research, 12/01/2015, Vol.75(23 Supplement), pp.A34-A34
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 3
    In: Neuropathology, August 2013, Vol.33(4), pp.424-430
    Description: Chordomas are tumors of notochordal differentiation of low to intermediate grade malignancy. These tumors are typically slow growing, with an indolent but progressive clinical course. We present a case of a highly proliferative chordoma arising in a 73‐year‐old woman with unusually rapid clinical growth and aggressive histologic and immunohistochemical features. This patient had an unusually brief preclinical course and within 1 month of developing headaches presented to medical attention with diplopia. The resected chordoma showed uncommonly elevated mitotic activity, without the histologic hallmarks of de‐differentiation. This proliferative activity correlated with elevated i67 staining (60%), B‐cell leukemia/lymphoma1 (1) expression (100%), and topoisomerase IIα staining (〉95%). E‐cadherin expression was also lost throughout the majority of the tumor. Other markers of epithelial mesenchymal transition () including vimentin, ‐cadherin, Slug and Twist, were also strongly expressed in this aggressive tumor. The sellar component of the tumor recurred within a 2‐month interval. The evaluation of the additional biomarkers, including makers of studied in this, case may allow for identification of aggressive chordomas in which the tempo of disease is significantly more rapid than in typical cases of chordoma.
    Keywords: ‐1 ; Brachyury ; Chordoma ; Epithelial Mesenchymal Transition ; I67
    ISSN: 0919-6544
    E-ISSN: 1440-1789
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  • 4
    Language: English
    In: Cancer Research, 03/15/2016, Vol.76(6 Supplement), pp.A17-A17
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 5
    Language: English
    In: Cancer Research, 12/01/2015, Vol.75(23 Supplement), pp.B35-B35
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 6
    Language: English
    In: Clinical cancer research : an official journal of the American Association for Cancer Research, 15 October 2013, Vol.19(20), pp.5711-21
    Description: Ficlatuzumab is a novel therapeutic agent targeting the hepatocyte growth factor (HGF)/c-MET pathway. We summarize extensive preclinical work using this agent in a mouse brain orthotopic model of glioblastoma. Sequential experiments were done using eight- to nine-week-old nude mice injected with 3 × 10(5) U87 MG (glioblastoma) cells into the brain. Evaluation of ficlatuzumab dose response for this brain tumor model and comparison of its response to ficlatuzumab and to temozolamide were conducted first. Subsequently, various small-animal imaging modalities, including bioluminescence imaging (BLI), positron emission tomography (PET), and MRI, were used with a U87 MG-Luc 2 stable cell line, with and without the use of ficlatuzumab, to evaluate the ability to noninvasively assess tumor growth and response to therapy. ANOVA was conducted to evaluate for significant differences in the response. There was a survival benefit with ficlatuzumab alone or in combination with temozolamide. BLI was more sensitive than PET in detecting tumor cells. Fluoro-D-thymidine (FLT) PET provided a better signal-to-background ratio than 2[(18)F]fluoro-2-deoxy-d-glucose (FDG) PET. In addition, both BLI and FLT PET showed significant changes over time in the control group as well as with response to therapy. MRI does not disclose any time-dependent change. Also, the MRI results showed a temporal delay in comparison to the BLI and FLT PET findings, showing similar results one drug cycle later. Targeting the HGF/c-MET pathway with the novel agent ficlatuzumab appears promising for the treatment of glioblastoma. Various clinically applicable imaging modalities including FLT, PET, and MRI provide reliable ways of assessing tumor growth and response to therapy. Given the clinical applicability of these findings, future studies on patients with glioblastoma may be appropriate.
    Keywords: Antibodies, Monoclonal ; Luminescent Measurements ; Magnetic Resonance Imaging ; Positron-Emission Tomography ; Glioma -- Diagnosis ; Hepatocyte Growth Factor -- Metabolism
    ISSN: 1078-0432
    E-ISSN: 15573265
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  • 7
    Language: English
    In: World Neurosurgery, July 2015, Vol.84(1), pp.189.e1-189.e5
    Description: Osteomalacia-inducing tumors (OIT) are mesenchymal tumors that characteristically secrete fibroblast growth factor 23, resulting in a paraneoplastic syndrome of hypophosphatemic osteomalacia. These tumors are known to occur in soft tissues and bones in various sites. It is very unusual for OITs to occur intracranially, with only 10 reported intracranial cases since their discovery in 1959. The most common intracrainal OITs are phosphaturic mesenchymal tumors and hemangiopericytomas. We report a case of hypophosphatemic osteomalacia caused by a tumor in the right anterior cranial fossa. We also hypothesize, based on our review of the literature, that this entity is underdiagnosed. A 49-year-old woman had a history of a nonhealing ankle fracture that required repeated surgery over 3 years. She subsequently was found to have severe hypophosphatemia and evidence of osteomalacia together with multiple occult fractures. A diagnosis of tumor-induced osteomalacia was suspected. An elevated serum fibroblast growth factor 23 level confirmed the diagnosis. An octreotide scan that was performed to locate the responsible tumor revealed an area of avid uptake in the right frontal lobe. Magnetic resonance imaging showed a large right anterior fossa extra-axial mass. The patient was referred for surgical intervention and was cured clinically after surgical removal of the tumor. Pathologic examination revealed a phosphaturic mesenchymal OIT. Her phosphate levels returned to normal 3 weeks after surgery. The diagnosis of OIT should be considered in a case of severe hypophosphatemia and metabolic bone disease that is not explained by any other metabolic or hereditary disease. These tumors can occur intracranially and may be confused with a meningioma or a hemangiopericytoma. Taking OIT into consideration in such cases could lead to a shorter time to diagnosis and management, which in our case took 4 years.
    Keywords: Oncogenic Osteomalacia ; Osteomalacia-Inducing Tumors ; Phosphaturic Mesenchymal Tumors ; Tumor-Induced Osteomalacia
    ISSN: 1878-8750
    E-ISSN: 1878-8769
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  • 8
    Language: English
    In: Journal of Neuro-Oncology, 2016, Vol.126(1), pp.69-75
    Description: Glioblastoma is the most common and deadly type of brain cancer. Over the past decade, several divergent genetic pathways have been implicated in the initiation, progression and clinical outcome of this disease. As our understanding of GBM expands and identifies actionable targets specific to individual tumors, there will be a pressing need for the development of new tools that will maximize the use of limited clinical samples to enable the employment of personalized care paradigms. We used PrimePCR validated assays to generate a custom real-time PCR screening panel, containing 74 previously published mRNA targets showing gene expression changes in glioblastoma, and five house-keeping genes. A cohort of 19 frozen brain specimens were analyzed, including WHO Grade II oligodendroglioma (n = 3), WHO Grade II astrocytoma (n = 2), WHO Grade III astrocytoma (n = 1), and glioblastoma (n = 13). Four normal brain samples were also analyzed. We performed RNA extraction, followed by cDNA synthesis, multiplexed pre-amplification and SYBR-based qPCR, to generate expression profiles on all samples. We demonstrated that the workflow shows high tolerance to variation in RNA quality (RIN 8.5-4) and high sensitivity in detection. cDNA input that is equivalent to 3 ng of starting RNA was sufficient to conduct accurate semiquantitative analysis of the panel of 79 assays. Using principal component analysis, we were able to accurately separate glioblastoma from low-grade glioma. The two WHO Grade III tumors analyzed clustered with glioblastoma, but showed more similarity to Grade II gliomas. In this study, we have shown the feasibility of consolidating high-throughput data into a single functional panel capable of accurately classifying glioma specimens based solely on semiquantitative gene expression profiling.
    Keywords: Glioblastoma ; Genomics ; PCR ; Molecular profiling ; Amplification
    ISSN: 0167-594X
    E-ISSN: 1573-7373
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  • 9
    In: Annals of Neurology, June 2018, Vol.83(6), pp.1089-1095
    Description: VPS13 protein family members VPS13A through VPS13C have been associated with various recessive movement disorders. We describe the first disease association of rare recessive variants including frameshift, missense, and partial duplication mutations with a novel complex, hyperkinetic neurological disorder....
    Keywords: Intellectual Disability -- Genetics ; Movement Disorders -- Genetics ; Muscle Spasticity -- Genetics ; Mutation -- Genetics ; Optic Atrophy -- Genetics ; Proteins -- Genetics ; Spinocerebellar Ataxias -- Genetics;
    ISSN: 0364-5134
    E-ISSN: 1531-8249
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  • 10
    Language: English
    In: JAMA neurology, October 2014, Vol.71(10), pp.1319-25
    Description: Over the past 4 years, our understanding of gliomagenesis and the practice of neuro-oncology have been radically changed by the discovery of mutations involving the isocitrate dehydrogenase (IDH) enzymes. IDH mutation has been found to be an inciting event in gliomagenesis and to have a profound effect on the molecular and genetic route of oncogenic progression and on clinical outcome. To review the role of IDH enzymes in normal physiology and describe aberrations in the IDH pathway that are associated with gliomagenesis, to review recent work examining the effect of IDH-targeted therapy in cancers harboring IDH mutation, and to determine how this work has expanded our understanding of the role of IDH in the development and progression of glioma. A systematic review of the literature dating from 2008, when IDH mutation was discovered to be clinically significant in glioma, to 2013 was performed using the PubMed database. The following search terms were used: IDH, IDH1, IDH2, and isocitrate dehydrogenase, in conjunction with glioma or leukemia. The search was limited to articles published in English. Further hand searching was performed using a review of the pertinent references from the identified publications. All identified original articles were investigated for content and critiqued by Z.T. and S.D. IDH mutation is an early event in gliomagenesis and has significant implications for glioma progression and tumor behavior. Early evidence suggests that IDH may be a therapeutic target in IDH-mutant gliomas. IDH mutation is a central and defining event in the development and progression of glioma and may be a key target for future therapies for these types of neoplasms.
    Keywords: Brain Neoplasms -- Genetics ; Glioma -- Genetics ; Isocitrate Dehydrogenase -- Genetics
    ISSN: 21686149
    E-ISSN: 2168-6157
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