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hpa001906

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Angela N Viaene et al.
Brain pathology (Zurich, Switzerland), 31(1), 45-60 (2020-07-19)
Congenital brain tumors are rare accounting for 0.5%-1.9% of all pediatric brain tumors. While different criteria have been used to classify a tumor as congenital, those diagnosed prior to 6 months of age are considered to be "probably" congenital in origin.
Amber E Kerstetter-Fogle et al.
International journal of molecular sciences, 21(14) (2020-07-24)
Glioblastoma multiforme (GBM) is the most malignant primary brain cancer affecting adults. Therapeutic options for GBM have remained the same for over a decade with no significant improvement. Many therapies that are successful in culture have failed in patients, likely
Diana Cantero et al.
Neuro-oncology advances, 2(1), vdz059-vdz059 (2020-07-10)
Giant cell glioblastoma (gcGBM) is a rare morphological variant of IDH-wildtype (IDHwt) GBM that occurs in young adults and have a slightly better prognosis than "classic" IDHwt GBM. We studied 36 GBMs, 14 with a histopathological diagnosis of gcGBM and
ATRX Mutations in Pineal Parenchymal Tumors of Intermediate Differentiation.
Mart?-nez, et al.
Journal of Neuropathology and Experimental Neurology (2020)
Ramin A Morshed et al.
Journal of neuro-oncology, 141(2), 383-391 (2018-12-01)
WHO grade II gliomas are uncommon in patients over the age of 60, and there is a lack in consensus regarding their management. We present molecular tumor characteristics as well as clinical outcomes in patients over the age of 60
Mark Barszczyk et al.
Acta neuropathologica, 128(6), 863-877 (2014-08-15)
Pediatric ependymomas are highly recurrent tumors resistant to conventional chemotherapy. Telomerase, a ribonucleoprotein critical in permitting limitless replication, has been found to be critically important for the maintenance of tumor-initiating cells (TICs). These TICs are chemoresistant, repopulate the tumor from
Gerald F Reis et al.
Journal of neuropathology and experimental neurology, 74(5), 442-452 (2015-04-09)
Lower-grade (World Health Organization Grades II and III) gliomas vary widely in clinical behavior and are classified as astrocytic, oligodendroglial, or mixed. Anaplasia depends greatly on mitotic activity, with CDKN2A loss considered as the most common mechanism for cell cycle
N Leventoux et al.
Scientific reports, 10(1), 5504-5504 (2020-03-29)
IDH1-mutated gliomas are slow-growing brain tumours which progress into high-grade gliomas. The early molecular events causing this progression are ill-defined. Previous studies revealed that 20% of these tumours already have transformation foci. These foci offer opportunities to better understand malignant
Yavuz Oktay et al.
Scientific reports, 6, 27569-27569 (2016-06-11)
The single nucleotide polymorphism rs55705857, located in a non-coding but evolutionarily conserved region at 8q24.21, is strongly associated with IDH-mutant glioma development and was suggested to be a causal variant. However, the molecular mechanism underlying this association has remained unknown.
Arjen H G Cleven et al.
Clinical sarcoma research, 7, 8-8 (2017-05-10)
Mutations in isocitrate dehydrogenase (IDH)1 or -2 are found in ~50% of conventional central chondrosarcomas and in up to 87% of their assumed benign precursors enchondromas. The mutant enzyme acquires the activity to convert α-ketoglutarate into the oncometabolite d-2-hydroxyglutarate (d-2-HG), which
Michael W Ronellenfitsch et al.
Brain pathology (Zurich, Switzerland), 28(1), 94-102 (2016-12-10)
We report a novel CASP9 germline mutation that may increase susceptibility to the development of brain tumors. We identified this mutation in a family in which three brain tumors had developed within three generations, including two anaplastic astrocytomas occurring in
Kenta Masui et al.
BioMed research international, 2018, 7945845-7945845 (2018-04-26)
Telomerase reverse transcriptase (TERT) is important for the biology of diffuse gliomas. TERT promoter mutations are selectively observed among 1p/19q-codeleted oligodendrogliomas and isocitrate dehydrogenase gene- (IDH-) wildtype glioblastoma (GBM). However, TERT transcripts range widely in various cancers including gliomas, and
Saeko Hayashi et al.
Oncotarget, 6(18), 15871-15881 (2015-05-21)
The prognostic significance of 1p19q loss in astrocytic gliomas has been inconclusive.We collected 57 gliomas with total 1p19q loss from among 218 cases of WHO grade-II/III gliomas operated at Keio University Hospital between 1990 and 2010. These tumors were classified
Christopher M Heaphy et al.
Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 33(8), 1475-1481 (2020-03-24)
Telomeres are nucleoprotein complexes located at the termini of eukaryotic chromosomes that prevent exonucleolytic degradation and end-to-end chromosomal fusions. Cancers often have critically shortened, dysfunctional telomeres contributing to genomic instability. Telomere shortening has been reported in a wide range of
Terhi V Ahvenainen et al.
Cancer, 124(24), 4650-4656 (2018-11-14)
Uterine leiomyomas (ULs) are the most common gynecologic tumors and affect 3 of every 4 women by the age of 50 years. The majority of ULs are classified as conventional tumors, whereas 10% represent various histopathological subtypes with features that
Yuchen Jiao et al.
Oncotarget, 3(7), 709-722 (2012-08-08)
Mutations in the critical chromatin modifier ATRX and mutations in CIC and FUBP1, which are potent regulators of cell growth, have been discovered in specific subtypes of gliomas, the most common type of primary malignant brain tumors. However, the frequency
Doreen N Nguyen et al.
Brain pathology (Zurich, Switzerland), 23(3), 237-243 (2012-08-30)
Recent studies suggest that the telomere maintenance mechanism known as alternative lengthening of telomeres (ALT) is relatively more common in specific glioma subsets and strongly associated with ATRX mutations. We retrospectively examined 116 high-grade astrocytomas (32 pediatric glioblastomas, 65 adult
Meaghan Morris et al.
Journal of neuropathology and experimental neurology, 79(10), 1038-1043 (2020-09-22)
Mutations in histone H3 are key molecular drivers of pediatric and young adult high-grade gliomas. Histone H3 G34R mutations occur in hemispheric high-grade gliomas and H3 K27M mutations occur in aggressive, though histologically diverse, midline gliomas. Here, we report 2
Farzad Fereidouni et al.
Nature biomedical engineering, 1, 957-966 (2017-01-01)
Histologic examination of tissues is central to the diagnosis and management of neoplasms and many other diseases, and is a foundational technique for preclinical and basic research. However, commonly used bright-field microscopy requires prior preparation of micrometre-thick tissue sections mounted
Sabine A Hartlieb et al.
Nature communications, 12(1), 1269-1269 (2021-02-26)
Telomere maintenance by telomerase activation or alternative lengthening of telomeres (ALT) is a major determinant of poor outcome in neuroblastoma. Here, we screen for ALT in primary and relapsed neuroblastomas (n = 760) and characterize its features using multi-omics profiling. ALT-positive tumors
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Lauren Fishbein et al.
Nature communications, 6, 6140-6140 (2015-01-22)
Pheochromocytomas and paragangliomas (PCC/PGL) are the solid tumour type most commonly associated with an inherited susceptibility syndrome. However, very little is known about the somatic genetic changes leading to tumorigenesis or malignant transformation. Here we perform whole-exome sequencing on a
Harikleia Episkopou et al.
Molecular cell, 75(3), 469-482 (2019-07-07)
A significant fraction (∼10%) of cancer cells maintain their telomere length via a telomerase-independent mechanism known as alternative lengthening of telomeres (ALT). There are no known molecular, ALT-specific, therapeutic targets. We have identified TSPYL5 (testis-specific Y-encoded-like protein 5) as a
Aruna Nambirajan et al.
Brain tumor pathology, 38(1), 30-40 (2020-11-02)
The PFA molecular subgroup of posterior fossa ependymomas (PF-EPNs) shows poor outcome. H3K27me3 (me3) loss by immunohistochemistry (IHC) is a surrogate marker for PFA wherein its loss is attributed to overexpression of Cxorf67/EZH2 inhibitory protein (EZHIP), C17orf96, and ATRX loss.
Mi Jung Kwon et al.
Brain pathology (Zurich, Switzerland), 30(2), 235-245 (2019-08-23)
The extremely invasive phenotypes and genotypes related to progression of gliomatosis cerebri (GC) remain unclear although GC has been removed as an independent entity from the 2016 WHO classification. Hence, categorization of GC under the current WHO molecular classification is
Marta Mellai et al.
Cells, 9(6) (2020-07-01)
Neuron glial antigen 2 or chondroitin sulphate proteoglycan 4 (NG2/CSPG4) is expressed by immature precursors/progenitor cells and is possibly involved in malignant cell transformation. The aim of this study was to investigate its role on the progression and survival of
Junbo Liang et al.
FEBS letters, 594(1), 67-78 (2019-07-23)
α-Tthalassemia mental retardation X-linked (ATRX) is a chromatin remodeler frequently mutated in many cancers. Despite the binding pattern of ATRX in heterochromatin, ATRX-mediated epigenomic changes in cancer cells have not been profiled, especially for the heterochromatin regions. Here, we profiled
Christian Koelsche et al.
Acta neuropathologica, 126(6), 907-915 (2013-10-25)
Hot spot mutations in the promoter region of telomerase reverse transcriptase (TERT) have recently been described in several human tumor entities. These mutations result in an upregulation of the telomerase complex activity and thus constitute a relevant mechanism for immortalization
Seong-Ik Kim et al.
Journal of pathology and translational medicine, 52(1), 28-36 (2017-09-30)
Mixed gliomas, such as oligoastrocytomas (OA), anaplastic oligoastrocytomas, and glioblastomas (GBMs) with an oligodendroglial component (GBMO) are defined as tumors composed of a mixture of two distinct neoplastic cell types, astrocytic and oligodendroglial. Recently, mutations ATRX and TP53, and codeletion
Asa Bolander et al.
Cancer genomics & proteomics, 5(6), 293-300 (2009-03-17)
Patients with metastazing malignant melanoma have a poor outcome and determination of thickness of the primary tumor remains as the most important prognostic predictor. The aim of this study was to use an antibody-based proteomics strategy to search for new
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