scholarly journals A Histopathology Model of Astrocytoma

2021 ◽  
Author(s):  
Alireza Arabestanino ◽  
Arman Ai ◽  
Hastin Jalali
Keyword(s):  
Confounding Factor ◽  
Neoplastic Transformation ◽  
Cell Types ◽  
Low Grade ◽  
Pathological Findings ◽  
Biological Features ◽  
Molecular Events ◽  
The Face ◽  
Morphological Variants ◽  
Human Nervous System

Abstract Neoplastic transformation occurs in all glial cell types of the human nervous system, producing a wide variety of clinic-pathological entities and morphological variants. As the molecular events responsible for astrocytoma formation and progression are being clarified, it is becoming possible to correlate these alterations with the specific histopathological and biological features of astrocytoma, anaplastic astrocytoma and glioblastoma multiforme. Diagnosis, treatment, and prognostication in brain stem astrocytoma’s have been hindered by the occurrence in the same site of two distinct pathological entities-fibrillary and pilocytic astrocytoma. The small size of the specimens from this region adds an additional confounding factor in tumor classification. Nevertheless, histological assignment to either of these two prognostically different categories is often possible, especially if the importance of this distinction is recognized. In the face of a nonspecific histological diagnosis, e.g. "low-grade astrocytoma', certain radiographic and clinical features may, in combination with the pathological findings, be useful in tumor subclassification.

scholarly journals Extraneous E-Cadherin Engages the Deterministic Process of Somatic Reprogramming through Modulating STAT3 and Erk1/2 Activity

Cells ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 284
Author(s):  
Yu-Hao Liu ◽  
Chien-Chang Chen ◽  
Yi-Jen Hsueh ◽  
Li-Man Hung ◽  
David Hui-Kang Ma ◽  
...  
Keyword(s):  
Stochastic Process ◽  
Molecular Mechanism ◽  
Activity Ratio ◽  
Cell Types ◽  
Deterministic Process ◽  
Modes Of Action ◽  
Molecular Events ◽  
Different Cell Types ◽  
Selection Of ◽  
E Cadherin

Although several modes of reprogramming have been reported in different cell types during iPSC induction, the molecular mechanism regarding the selection of different modes of action is still mostly unknown. The present study examined the molecular events that participate in the selection of such processes at the onset of somatic reprogramming. The activity of STAT3 versus that of Erk1/2 reversibly determines the reprogramming mode entered; a lower activity ratio favors the deterministic process and vice versa. Additionally, extraneous E-cadherin facilitates the early events of somatic reprogramming, potentially by stabilizing the LIF/gp130 and EGFR/ErbB2 complexes to promote entry into the deterministic process. Our current findings demonstrated that manipulating the pSTAT3/pErk1/2 activity ratio in the surrounding milieu can drive different modes of action toward either the deterministic or the stochastic process in the context of OSKM-mediated somatic reprogramming.

scholarly journals CBIO-19. LOW GLOBAL HISTONE H4 ACETYLATION LEVELS REVEAL CANDIDATE QUIESCENT CELL POPULATIONS IN GLIOMA AND DISTINGUISH TUMORS BY GRADE

2020 ◽  
Vol 22 (Supplement_2) ◽  
pp. ii19-ii19
Author(s):  
Anca Mihalas ◽  
Heather Feldman ◽  
Anoop Patel ◽  
Patrick Paddison
Keyword(s):  
Cell Types ◽  
Strand Break ◽  
Cell Cycle Gene ◽  
Low Grade ◽  
Histone H4 ◽  
Current Standard ◽  
A Genome ◽  
Histone H4 Acetylation

Abstract Current standard of care therapy for glioblastoma (GBM) includes cytoreduction followed by ablative therapies that target rapidly dividing cell types. However, the presence of quiescent-like/G0 states, therefore, represents a natural reservoir of tumor cells that are resistant to current treatments. Quiescence or G0 phase is a reversible state of “stasis” cells enter in response to developmental or environmental cues. To gain insight into how glioblastoma cells might regulate G0-like states, we performed a genome-wide CRISPR-Cas9 screen in patient-derived GBM stem-like cells (GSCs) harboring a G0-reporter to identify genes that when inhibited trap GSCs in G0-like states. Among the top screen hits were members of the Tip60/KAT5 histone acetyltransferase complex, which targets both histones (e.g., H4) and non-histone proteins for acetylation. NuA4 functions as a transcriptional activator, whose activities are coordinated with MYC in certain contexts, and also participates in DNA double-strand break repair by facilitating chromatin opening. However, currently little is known about the roles for NuA4 complex in GBM biology. Through modeling KAT5 function in GSC in vitro cultures and in vivo tumors, we find that KAT5 inhibition causes cells to arrest in a G0-like state with high p27 levels, G1-phase DNA content, low protein synthesis rates, low rRNA rates, lower metabolic rate, suppression of cell cycle gene expression, and low histone H4 acetylation. Interestingly, partial inhibition of KAT5 activity slows highly aggressive tumor growth, while increasing p27hi H4-aclow populations. Remarkably, we that low grade gliomas have significantly higher H4-aclow subpopulations and generally lower H4-ac levels than aggressive grade IV tumors. Taken together, our results suggest that NuA4/KAT5 activity may play a key role in quiescence ingress/egress in glioma and that targeting its activity in high grade tumors may effectively “down grade” them, thus, increase patient survival.

microRNA-252 and FoxO repress inflammaging by a dual inhibitory mechanism on Dawdle mediated TGF-β pathway in Drosophila

Genetics ◽  
2021 ◽  
Author(s):  
Xiaofen Wu ◽  
Kongyan Niu ◽  
Xiaofan Wang ◽  
Jing Zhao ◽  
Han Wang ◽  
...  
Keyword(s):  
Cell Types ◽  
Innate Immune ◽  
Low Grade ◽  
Sequencing Analysis ◽  
Immune Genes ◽  
Healthy Longevity ◽  
Muscle Tissues ◽  
Distinct Cell ◽  
A Cell ◽  
Innate Immune Genes

Abstract Inflammaging refers to low-grade, chronically activated innate immunity that has deleterious effects on healthy lifespan. However, little is known about the intrinsic signaling pathway that elicits innate immune genes during aging. Here using Drosophila melanogaster, we profile the microRNA targetomes in young and aged animals, and reveal Dawdle (Daw), an activin-like ligand of the TGF-β pathway, as a physiological target of microRNA-252 (miR-252). We show that miR-252 cooperates with Forkhead box O (FoxO), a conserved transcriptional factor implicated in aging, to repress Daw. Unopposed Daw triggers hyper activation of innate immune genes coupled with a decline in organismal survival. Using adult muscle tissues, single-cell sequencing analysis describes that Daw and its downstream innate immune genes are expressed in distinct cell types, suggesting a cell non-autonomous mode of regulation. We further determine the genetic cascade by which Daw signaling leads to increased Kenny/IKKγ protein, which in turn activates Relish/NF-κB protein and consequentially innate immune genes. Finally, transgenic increase of miR-252 and FoxO pathway factors in wild-type Drosophila extends lifespan and mitigates the induction of innate immune genes in aging. Together, we propose that miR-252 and FoxO promote healthy longevity by cooperative inhibition on Daw mediated inflammaging.

T(11;18)(q21;q21) is associated with advanced mucosa-associated lymphoid tissue lymphoma that expresses nuclear BCL10

Blood ◽  
2001 ◽  
Vol 98 (4) ◽  
pp. 1182-1187 ◽  
Author(s):  
Hongxiang Liu ◽  
Hongtao Ye ◽  
Ahmet Dogan ◽  
Renzo Ranaldi ◽  
Rifat A. Hamoudi ◽  
...  
Keyword(s):  
Malt Lymphoma ◽  
Lymphoid Tissue ◽  
Fusion Transcript ◽  
Low Grade ◽  
Chain Reaction ◽  
Nuclear Expression ◽  
Molecular Events ◽  
Multistep Process ◽  
Polymerase Chain ◽  
H Pylori

The development of gastric mucosa-associated lymphoid tissue (MALT) lymphoma is a multistep process and can be clinico-pathologically divided into Helicobacter pylori-associated gastritis, low-grade tumors, and high-grade tumors. The molecular events underlying this progression are largely unknown. However, identification of the genes involved in MALT lymphoma-specific t(11;18)(q21;q21) and t(1;14)(p22;q32) has provided fresh insights into the pathogenesis of this disease. T(11;18)(q21;q21) results in a chimeric transcript between the API2 and theMALT1 genes, whereas t(1;14) (p22;q32) causes aberrant nuclear BCL10 expression. Significantly, nuclear BCL10 expression also occurs frequently in MALT lymphomas without t(1;14)(p22;q32), suggesting an important role for BCL10 in lymphoma development. Thirty-three cases of H pylori gastritis, 72 MALT lymphomas, and 11 mucosal diffuse large B-cell lymphomas (DLBCL) were screened for t(11;18)(q21;q21) by reverse transcription–polymerase chain reaction followed by sequencing. BCL10 expression in lymphoma cases was examined by immunohistochemistry. The API2–MALT1 fusion transcript was not detected in H pylorigastritis and mucosal DLBCL but was found in 25 of 72 (35%) MALT lymphomas of various sites. Nuclear BCL10 expression was seen in 28 of 53 (53%) of MALT lymphomas. Of the gastric cases, the largest group studied, the frequency of both t(11;18)(q21;q21) and nuclear BCL10 expression was significantly higher in tumors that showed dissemination to local lymph nodes or distal sites (14 of 18 = 78% and 14 of 15 = 93%, respectively) than those confined to the stomach (3 of 29 = 10% and 10 of 26 = 38%). Furthermore, t(11;18)(q21;q21) closely correlated with BCL10 nuclear expression. These results indicate that both t(11;18)(q21;q21) and BCL10 nuclear expression are associated with advanced MALT lymphoma and that their oncogenic activities may be related to each other.

scholarly journals The landscape of myeloid and astrocyte phenotypes in acute multiple sclerosis lesions

2019 ◽  
Author(s):  
Calvin Park ◽  
Gerald Ponath ◽  
Maya Levine-Ritterman ◽  
Edward Bull ◽  
Eric C. Swanson ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Myeloid Cells ◽  
Cell Types ◽  
Tissue Imaging ◽  
Low Grade ◽  
Cellular Interactions ◽  
Extrinsic Factors ◽  
Activation Markers ◽  
Powerful Approach ◽  
Study Heterogeneity

AbstractActivated myeloid cells and astrocytes are the predominant cell types in active multiple sclerosis (MS) lesions. Both cell types can adopt diverse functional states that play critical roles in lesion formation and resolution. In order to identify phenotypic subsets of myeloid cells and astrocytes, we profiled acute MS lesions with thirteen glial activation markers using imaging mass cytometry (IMC), a method for multiplexed labeling of histological sections. In a demyelinating lesion, we found multiple distinct myeloid and astrocyte phenotypes that populated separate lesion zones. In a post-demyelinating lesion, phenotypes were less distinct and more uniformly distributed. In both lesions cell-to-cell interactions were not random, but occurred between specific glial subpopulations and lymphocytes. Finally, we demonstrated that myeloid, but not astrocyte phenotypes were activated along a lesion rim-to-center gradient, and that marker expression in glial cells at the lesion rim was driven more by cell-extrinsic factors than in cells at the center. This proof-of-concept study demonstrates that highly multiplexed tissue imaging, combined with the appropriate computational tools, is a powerful approach to study heterogeneity, spatial distribution and cellular interactions in the context of MS lesions. Identifying glial phenotypes and their interactions at different lesion stages may provide novel therapeutic targets for inhibiting acute demyelination and low-grade, chronic inflammation.

scholarly journals Novel formulation approaches for wound healing

2020 ◽  
Vol 11 (SPL4) ◽  
pp. 937-948
Author(s):  
Tanaji D Nandgude ◽  
Syed Nateque Naser
Keyword(s):  
Wound Healing ◽  
Healing Process ◽  
Cell Types ◽  
Wound Management ◽  
Wound Healing Process ◽  
Anatomic Structure ◽  
Tissue Integrity ◽  
Molecular Events ◽  
Acute Injuries ◽  
Healing Wounds

A wound is damage to the typical anatomic structure. Wound healing is an immediate therapeutic response to injury. It is a creation of the combined response of some cell types towards injury. Wound healing takes place by a sequence of molecular events which cooperate to fix tissue integrity and cell work. In typical healthy individual under ordinary conditions, these physiological events take place smoothly. Though sometimes, these molecular events are arrested, this brings about in struggle to heal. There is an assortment of approaches for the way toward managing and controlling both acute injuries (acute wounds) and ceaseless non-mending wounds (chronic non-healing wounds). The principal objective of these two cases is to achieve better-wound healing. Ideal formulations of wound healing should not only enhance the healing process but also reduce pain, infection and loss of electrolytes, proteins and liquids from the injury. A broad scope of items typically introduced with target various parts of the wound healing process depends on numerous types of wounds and novel polymers utilised for the conveyance of medications to both acute and ceaseless injuries. These include alginate, hydrocolloids, hydrofibers, polyurethane, and hydrogels. This article gives particular importance to different novel approaches in the management of wound healing. This review draws out the data and hopes to provide understanding into traditional, current and imminent techniques and methods for wound management.

scholarly journals Current Status of Histogenetic and Morphogenetic Concepts of Salivary Gland Tumorigenesis

1993 ◽  
Vol 4 (5) ◽  
pp. 639-677 ◽  
Author(s):  
Irving Dardick ◽  
Aileen P. Burford-Mason
Keyword(s):  
Salivary Gland ◽  
Acinar Cells ◽  
Neoplastic Transformation ◽  
Cell Types ◽  
Salivary Gland Tumors ◽  
Current Status ◽  
Normal Gland ◽  
Routine Diagnosis ◽  
Diagnosis And Classification

Because of their complexity and relative infrequency, salivary gland tumors commonly result in diagnostic problems. Histogenetic and morphogenetic concepts of tumorigenesis in these glands are reviewed and their relevance to routine diagnosis and classification of salivary gland tumors evaluated. Evidence is presented from animal and human studies that under steady-state and pathophysiological conditions, all cell types present in the normal gland, including acinar cells, are capable of rapidly entering the cell cycle and are, therefore, possible targets for neoplastic transformation.

High incidence of lung, bone, and lymphoid tumors in transgenic mice overexpressing mutant alleles of the p53 oncogene

1989 ◽  
Vol 9 (9) ◽  
pp. 3982-3991
Author(s):  
A Lavigueur ◽  
V Maltby ◽  
D Mock ◽  
J Rossant ◽  
T Pawson ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Malignant Transformation ◽  
P53 Protein ◽  
P53 Gene ◽  
Cell Types ◽  
Molecular Events ◽  
High Incidence ◽  
Transgenic Lines ◽  
Functional Inactivation

We have investigated the role of the p53 gene in oncogenesis in vivo by generating transgenic mice carrying murine p53 genomic fragments isolated from a mouse Friend erythroleukemia cell line or BALB/c mouse liver DNA. Elevated levels of p53 mRNA were detected in several tissues of two transgenic lines tested. Increased levels of p53 protein were also detected in most of the tissues analyzed by Western blotting (immunoblotting). Because both transgenes encoded p53 proteins that were antigenically distinct from wild-type p53, it was possible to demonstrate that overexpression of the p53 protein was mostly, if not entirely, due to the expression of the transgenes. Neoplasms developed in 20% of the transgenic mice, with a high incidence of lung adenocarcinomas, osteosarcomas, and lymphomas. Tissues such as ovaries that expressed the transgene at high levels were not at higher risk of malignant transformation than tissues expressing p53 protein at much lower levels. The long latent period and low penetrance suggest that overexpression of p53 alone is not sufficient to induce malignancies and that additional events are required. These observations provide direct evidence that mutant alleles of the p53 oncogene have oncogenic potential in vivo and that different cell types show intrinsic differences in susceptibility to malignant transformation by p53. Since recent data suggest that p53 may be a recessive oncogene, it is possible that the elevated tumor incidence results from functional inactivation of endogenous p53 by overexpression of the mutant transgene. The high incidence of lung and bone tumors suggests that p53 transgenic mice may provide a useful model to investigate the molecular events that underlie these malignancies in humans.

Small Lymphoid Proliferations in Extranodal Locations

2007 ◽  
Vol 131 (3) ◽  
pp. 383-396
Author(s):  
Dinesh S. Rao ◽  
Jonathan W. Said
Keyword(s):  
B Cell ◽  
Medical Center ◽  
Correct Diagnosis ◽  
Cell Types ◽  
Correct Identification ◽  
Low Grade ◽  
Molecular Features ◽  
Mantle Cell ◽  
Ancillary Studies ◽  
Widespread Dissemination

Abstract Context.—Low-grade non-Hodgkin lymphomas frequently involve extranodal sites including the gastrointestinal tract, skin, and lung, either selectively or as part of widespread dissemination. Differentiation from inflammatory or infectious conditions requires knowledge of specific histologic characteristics of the various entities as well as ancillary techniques. Objective.—To describe the key features and provide diagnostic clues to the identification of specific extranodal low-grade lymphomas of T-cell and B-cell types including small lymphocytic lymphoma, follicular lymphoma, mantle cell lymphoma, extranodal marginal zone B-cell lymphomas of mucosal-associated lymphoid tissue, and hairy cell leukemia. Histologic and cytologic features are highlighted, as well as appropriate integration of results of ancillary diagnostic studies including flow cytometry, immunohistochemistry, molecular features, and cytogenetics. Data Sources.—The published literature as well as personal experience from a specialized hematopathology practice at a large university medical center. Conclusions.—Correct identification of extranodal low-grade lymphomas and differentiation from hyperplastic and inflammatory or infectious processes require the ability to distinguish each of the specific entities discussed. Ancillary studies are often indispensable in reaching a correct diagnosis.

Intraductal papillary neoplasm of bile duct: all rare in one

2020 ◽  
Vol 13 (11) ◽  
pp. e237001
Author(s):  
Aprajita Chaturvedi ◽  
Manjunath Maruti Pol ◽  
Kirti Jangra ◽  
Priyanka Singh
Keyword(s):  
Bile Duct ◽  
Histopathological Examination ◽  
Anatomical Variations ◽  
Small Lesion ◽  
Low Grade ◽  
Pathological Findings ◽  
Intraductal Papillary Neoplasm ◽  
Contrast Enhanced ◽  
Low Grade Dysplasia ◽  
Papillary Neoplasm

A 45-year-old woman was referred from Department of Dermatology to Surgery outpatient department with pruritus since 6 months and an episode of jaundice that lasted for 15 days about 6 months ago. She was referred with a contrast-enhanced MRI finding that showed a small lesion in the lower end of common bile duct. Endoscopy-guided biopsy was performed twice at our hospital, the second revealed low grade dysplasia. Consequently, she underwent pancreaticoduodenectomy. Intraoperatively, there were both vascular and biliary anatomical variations that were missed on preoperative images. On histopathological examination, it turned out to be a mixed variety of intraductal papillary neoplasm of bile duct (IPNB). As all findings were rare in one, hence, we present this case of IPNB that presented to us with variable clinical, radiological, surgical and pathological findings.

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