scholarly journals PATH-16. HISTOPATHOLOGICAL EPENDYMOMA VARIANTS ARE ASSOCIATED WITH DISTINCT CLINICAL PARAMETERS AND DNA METHYLATION PATTERNS

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi146-vi146 ◽  
Author(s):  
Julia E Neumann ◽  
Michael Spohn ◽  
Denise Obrecht ◽  
Martin Mynarek ◽  
Christian Thomas ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Growth Pattern ◽  
Who Classification ◽  
Clear Cell ◽  
Clinical Parameters ◽  
Tanycytic Ependymoma ◽  
Molecular Features ◽  
Papillary Growth Pattern ◽  
Methylation Patterns ◽  
Papillary Growth

Abstract According to the current WHO classification, ependymal tumors are classified as subependymomas, myxopapillary ependymomas, classic ependymomas, anaplastic ependymomas and RELA-fusion positive ependymoma (RELA-EPN). Among classic ependymomas, the WHO defines rare histological variants, i.e. the clear-cell, papillary, and tanycytic ependymoma. In parallel to this WHO classification scheme, DNA methylation patterns can distinguish nine distinct molecular ependymoma subgroups, some of which tightly overlap with certain histopathological subgroups, e.g. subependyomas or myxopapillary ependymomas. Since very little is known about the molecular background of histological classic ependymoma variants, we analyzed histomorphology, clinical parameters and global DNA methylation patterns of diagnosed tanycytic ependymomas (n=12), clear-cell ependymomas (n=14) and papillary ependymomas (n=19). Surprisingly, up to 42% of these variants did not match to ependymomas using a previously published DNA methylation-based classifier for brain tumors. Among the tumors with a match to one of the nine known ependymoma methylation classes, tanycytic ependymomas were predominantly located in the spine, but showed diverse molecular methylation patterns. Most clear-cell ependymomas showed a common histomorphology, were found supratentorially and fell into the methylation class of RELA-EPN. Papillary ependymomas showed a “papillary”, “trabecular” or “pseudo-papillary” growth pattern. Interestingly, a true papillary growth pattern was strongly associated with the molecular class B of posterior fossa ependymoma (PFB), but tumors displayed DNA methylation sites that were significantly different when compared to PFB ependymomas without papillary growth. Our results show that the diagnosis of classic histological ependymoma variants can be challenging. While clear-cell and papillary ependymomas harbor common molecular features, tanycytic ependymoma may not represent a molecularly distinct subgroup.

scholarly journals A case of clear cell adenocarcinoma with a predominantly papillary growth pattern in the uterine cervix

2004 ◽  
Vol 43 (3) ◽  
pp. 166-170
Author(s):  
Shizuko KOBAYASHI ◽  
Takashi KITAMURA ◽  
Masaaki JITSUHARA ◽  
Chiyuki KANEKO ◽  
Atsuko MASUNAGA ◽  
...  
Keyword(s):  
Uterine Cervix ◽  
Growth Pattern ◽  
Clear Cell ◽  
Clear Cell Adenocarcinoma ◽  
Papillary Growth Pattern ◽  
Papillary Growth

A case of angioglioma composed of astrocytoma with a papillary growth pattern: Immunohistochemical and ultrastructural studies

2002 ◽  
Vol 19 (2) ◽  
pp. 111-116 ◽  
Author(s):  
Hiroyoshi Suzuki ◽  
Hiroshi Uenohara ◽  
Akihiro Utsunomiya ◽  
Noriko Kurihara ◽  
Shinsuke Suzuki ◽  
...  
Keyword(s):  
Growth Pattern ◽  
Ultrastructural Studies ◽  
Papillary Growth Pattern ◽  
Papillary Growth

scholarly journals Cholangiocarcinoma with intraductal tubular growth pattern versus intraductal papillary growth pattern

2016 ◽  
Vol 29 (3) ◽  
pp. 293-301 ◽  
Author(s):  
Tetsuo Tsukahara ◽  
Yoshie Shimoyama ◽  
Tomoki Ebata ◽  
Yukihiro Yokoyama ◽  
Tsuyoshi Igami ◽  
...  
Keyword(s):  
Growth Pattern ◽  
Papillary Growth Pattern ◽  
Papillary Growth ◽  
Pattern Versus

Genome-Wide DNA Methylation Analysis of Patients with Myelodysplastic Syndrome After Azacitidine Treatment.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 600-600
Author(s):  
Hyang-Min Byun ◽  
Timothy Triche ◽  
Hyeoung-Joon Kim ◽  
Hee Nam Kim ◽  
Yeo-Kyeoung Kim ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Bone Marrow ◽  
Who Classification ◽  
Methylation Pattern ◽  
Methylation Analysis ◽  
Cpg Sites ◽  
Genome Wide ◽  
Methylation Patterns ◽  
Dna Methylation Analysis ◽  
Hypermethylated Genes

Abstract Abstract 600 Background: Azacitidine is hypothesized to exert its therapeutic effect in patients with myelodysplastic syndrome (MDS) through inhibition of DNA methylation. However to date no genomic DNA methylation pattern has been shown to predict response to azacitidine in patients with MDS, and no aberrantly silenced gene or group of genes has been shown to be reactivated by azacitidine that can be clearly linked to the beneficial clinical effect. We sought to identify the gene or group of aberrantly hypermethylated genes that are responsible for the therapeutic effect of azacitidine by retrospectively analyzing genome-wide DNA methylation profiles from bone marrow samples of a cohort of 113 patients with MDS treated with the DNA methylation inhibitor, azacitidine. Methods: Bone marrow aspirates were collected at time of diagnosis prior to treatment, after 4 cycles of azacitidine therapy and 8 cycles of therapy. DNA was isolated and bisulfite treated with the EZ-96 DNA Methylation-Gold Kit. DNA methylation analysis was performed on 27,578 CpG sites representing 14,475 genes (almost ¾ of known genes) using the Infinium Bead Array system for samples at the time of diagnosis, 4 and 8 cycles of therapy. Only 19,662 CpG sites were used for further analysis due to exclusion of CpG sites that were on the × chromosome, sites suspected of containing single nucleotide polymorphisms (SNP), and sites within DNA repeats. In total 91 samples were analyzed from 43 patients with MDS, which were selected to represent different disease classifications and responses to therapy, and bone marrow aspirates from 10 healthy control subjects without MDS. Results: Two-way hierarchical cluster analysis showed clear clustering of bone marrow samples taken from subjects without MDS. DNA methylation patterns from healthy controls clustered together, and pre and post azacitidine treatment samples from the same subject clustered together as well. Samples did not cluster by DNA methylation patterns for WHO classification, International Prognostic Scoring System (IPSS), cytogenetic abnormalities, or response to azacitidine. Supervised cluster analysis is ongoing. Global decreases in DNA methylation as measured by the average methylation for all 19,662 loci assayed did decrease with treatment and there was a trend for a larger decrease in DNA methylation in those patients who responded to azacitidine. Conclusion: In this pilot study of genome-wide DNA methylation analysis of MDS patients treated with azacitidine we find global decreases of DNA methylation. We were unable to identify a DNA methylation pattern or group of hypermethylated genes that would predict response to azacitidine. MDS samples did not cluster by WHO classification, IPSS or response to azacitidine. Larger translational studies are needed, but the possibility that DNA methylation decreases in patients treated with azacitidine serve as a pharmacological marker rather than a therapeutic target should also be considered Disclosures: Laird: Celgene: Consultancy. Yang:Celgene: Honoraria, Research Funding, Speakers Bureau.

Adenocarcinoma of the Uterine Cervix with Predominantly Villogladular Papillary Growth Pattern

1997 ◽  
Vol 64 (1) ◽  
pp. 147-152 ◽  
Author(s):  
Tsunehisa Kaku ◽  
Toshiharu Kamura ◽  
Toshiyuki Shigematsu ◽  
Kunihiro Sakai ◽  
Naoyuki Nakanami ◽  
...  
Keyword(s):  
Uterine Cervix ◽  
Growth Pattern ◽  
Papillary Growth Pattern ◽  
Papillary Growth

scholarly journals Challenging of frozen diagnoses of small sclerosing pneumocytoma

2021 ◽  
pp. jclinpath-2020-206729
Author(s):  
Zhanxian Shang ◽  
Yuchen Han ◽  
Jinchen Shao ◽  
Lei Zhu ◽  
Haohua Teng ◽  
...  
Keyword(s):  
Growth Pattern ◽  
Foam Cell ◽  
Frozen Section ◽  
Pulmonary Nodules ◽  
Clinical Information ◽  
Cell Populations ◽  
Cell Accumulation ◽  
Papillary Growth Pattern ◽  
Small Pulmonary Nodules ◽  
Papillary Growth

AimsAn increasing number of small pulmonary nodules are being screened by CT, and an intraoperative diagnosis is necessary for preventing excessive treatment. However, there is limited literature on the frozen diagnosis of small sclerosing pneumocytomas (SPs). In particular, tumours smaller than 1 cm are challenging for pathologists performing intraoperative frozen diagnosis.MethodsIn total, 230 cases of SP were surgically resected between January 2015 and March 2019 at Shanghai Chest Hospital, and of them, 76 cases were smaller than 1 cm. The histology and clinical information of these 76 cases (33.0%, 76/230) were reviewed retrospectively, 54 cases of which were diagnosed intraoperatively, and the pitfalls were summarised. All diagnoses were confirmed on permanent sections and immunohistochemical sections.ResultsHistologically, 78.9% (60/76) of the small SP was dominated by one growth pattern, and solid and papillary growth pattern were the most commonly misdiagnosed circumstances. The rate of intraoperative misdiagnosis of these SP smaller than 1 cm was 11.1% (6/54).ConclusionsThe main reason for misdiagnosis was failure to recognise the dual cell populations and the cellular atypia. Diagnostic clues include the gross morphology, the presence of dual-cell populations and a hypercellular papillary core, foam cell accumulation in glandular spaces and haemorrhage and haemosiderin on the periphery. In spite of awareness of pitfalls some cases may still be essentially impossible to diagnose on frozen section.

Examination of the dynamics of global DNA methylation pattern establishment during spermatogenesiss

2007 ◽  
Vol 30 (4) ◽  
pp. 90
Author(s):  
Kirsten Niles ◽  
Sophie La Salle ◽  
Christopher Oakes ◽  
Jacquetta Trasler
Keyword(s):  
Dna Methylation ◽  
Germ Cell ◽  
Germ Cells ◽  
Epigenetic Modification ◽  
Methylation Pattern ◽  
Chromosome 9 ◽  
Specific Gene ◽  
Global Methylation ◽  
Dna Methylation Pattern ◽  
Methylation Patterns

Background: DNA methylation is an epigenetic modification involved in gene expression, genome stability, and genomic imprinting. In the male, methylation patterns are initially erased in primordial germ cells (PGCs) as they enter the gonadal ridge; methylation patterns are then acquired on CpG dinucleotides during gametogenesis. Correct pattern establishment is essential for normal spermatogenesis. To date, the characterization and timing of methylation pattern acquisition in PGCs has been described using a limited number of specific gene loci. This study aimed to describe DNA methylation pattern establishment dynamics during male gametogenesis through global methylation profiling techniques in a mouse model. Methods: Using a chromosome based approach, primers were designed for 24 regions spanning chromosome 9; intergenic, non-repeat, non-CpG island sequences were chosen for study based on previous evidence that these types of sequences are targets for testis-specific methylation events. The percent methylation was determined in each region by quantitative analysis of DNA methylation using real-time PCR (qAMP). The germ cell-specific pattern was determined by comparing methylation between spermatozoa and liver. To examine methylation in developing germ cells, spermatogonia from 2 day- and 6 day-old Oct4-GFP (green fluorescent protein) mice were isolated using fluorescence activated cell sorting. Results: As compared to liver, four loci were hypomethylated and five loci were hypermethylated in spermatozoa, supporting previous results indicating a unique methylation pattern in male germ cells. Only one region was hypomethylated and no regions were hypermethylated in day 6 spermatogonia as compared to mature spermatozoa, signifying that the bulk of DNA methylation is established prior to type A spermatogonia. The methylation in day 2 spermatogonia, germ cells that are just commencing mitosis, revealed differences of 15-20% compared to day 6 spermatogonia at five regions indicating that the most crucial phase of DNA methylation acquisition occurs prenatally. Conclusion: Together, these studies provide further evidence that germ cell methylation patterns differ from those in somatic tissues and suggest that much of methylation at intergenic sites is acquired during prenatal germ cell development. (Supported by CIHR)

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