scholarly journals Pathological Investigation of Meningioma Capsule with respect to Tumor Cell Invasion

2021 ◽  
Author(s):  
Takashi Sugawara ◽  
Daisuke Kobayashi ◽  
Taketoshi Maehara
Keyword(s):  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Invasion ◽  
Tumor Invasion ◽  
Recurrence Risk ◽  
Tumor Cell Invasion ◽  
Brain Surface ◽  
Eloquent Cortex ◽  
The Brain

Abstract OBJECTIVE No previous study has pathologically investigated whether the meningioma capsule presents with tumor cells. We investigated which types of tumor capsules include tumor cells to help decide the kind of capsules which can be left intraoperatively without recurrence risk. METHODS We investigated 22 specimens of 14 newly diagnosed meningiomas between February 2011 and June 2021. Capsules were classified into three types: tumor capsule (TC), capsule-like thickened arachnoid membrane (CAM), and extended membrane (EM). Capsule properties were scored as hardness (soft = 1, medium = 2, hard = 3) and transparency (high = 1, medium = 2, low = 3). Hardness, transparency, and score sum was compared between capsules with/without tumor invasion in CAM and EM types. RESULTS The mean follow-up duration was 28.1 months, and there was only one recurrence in a remote location from the residual capsule. Nine capsules were classified as TC, seven as CAM, and six as EM. 88.9% of TCs, 42.9% of CAMs, and 50% of EMs were invaded by tumor cells. Hardness, transparency, and score sum in CAM with tumor invasion was lower than in CAM without, but not significant (p = 0.114, p = 0.114, p = 0.057). CONCLUSION Thickened TC or soft and highly transparent CAM imply a high risk of tumor cell invasion, thus such cases should be followed up long and carefully. The hard and low transparent residual CAMs may have low risk of tumor invasion, thus these kinds of residual capsules might not increase the recurrence risk. Thus, leaving such capsules tightly adhered to the eloquent cortex is theoretically justified to avoid damaging the brain surface.

scholarly journals Aspirin inhibits platelets from reprogramming breast tumor cells and promoting metastasis

2019 ◽  
Vol 3 (2) ◽  
pp. 198-211 ◽  
Author(s):  
Kelly E. Johnson ◽  
Julia R. Ceglowski ◽  
Harvey G. Roweth ◽  
Jodi A. Forward ◽  
Mason D. Tippy ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Invasion ◽  
Breast Tumor ◽  
Tumor Metastasis ◽  
Tumor Cell Invasion ◽  
Akt Pathway ◽  
Breast Tumor Cells ◽  
Invasive Capacity ◽  
Platelet Releasate

Abstract It is now recognized that compounds released from tumor cells can activate platelets, causing the release of platelet-derived factors into the tumor microenvironment. Several of these factors have been shown to directly promote neovascularization and metastasis, yet how the feedback between platelet releasate and the tumor cell affects metastatic phenotype remains largely unstudied. Here, we identify that breast tumor cells secrete high levels of interleukin 8 (IL-8, CXCL8) in response to platelet releasate, which promotes their invasive capacity. Furthermore, we found that platelets activate the Akt pathway in breast tumor cells, and inhibition of this pathway eliminated IL-8 production. We therefore hypothesized inhibiting platelets with aspirin could reverse the prometastatic effects of platelets on tumor cell signaling. Platelets treated with aspirin did not activate the Akt pathway, resulting in reduced IL-8 secretion and impaired tumor cell invasion. Of note, patients with breast cancer receiving aspirin had lower circulating IL-8, and their platelets did not increase tumor cell invasion compared with patients not receiving aspirin. Our data suggest platelets support breast tumor metastasis by inducing tumor cells to secrete IL-8. Our data further support that aspirin acts as an anticancer agent by disrupting the communication between platelets and breast tumor cells.

scholarly journals P11.65 Insights into the mechanisms of primary brain tumor invasion

2019 ◽  
Vol 21 (Supplement_3) ◽  
pp. iii58-iii59
Author(s):  
A Bikfalvi ◽  
T Daubon ◽  
C Billottet
Keyword(s):  
Extracellular Matrix ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Conformational Changes ◽  
Cell Invasion ◽  
Immune Cell ◽  
Tumor Cell Invasion ◽  
Migration And Invasion ◽  
Matricellular Proteins

Abstract We have made progress in unravelling the mechanisms of tumor cell invasion by focusing the attention on two molecular pathways including chemokines and extracellular matrix molecules. Chemokines are important mediators of cell signaling that operate both on normal cells and tumor cells and in the immune-cell compartment (Billottet et al, 2013). Among the chemokine receptors, CXCR3 mediate diverse biological functions and comes in two major isoforms the A and B isoform. We found that ligand affinities and conformational changes are very different for the A and B form. We have recently elucidated the role and mechanism of CXCR3A in GBM invasion (Boyé et al, 2017b). We demonstrated that agonist stimulation enhances in vitro cell migration and invasion in GBM cells. A major finding was that CXCR3A forms a complex with the trafficking receptor Lipoprotein-related receptor-1 (LRP1). Silencing of LRP1 leads to an increase in the magnitude of ligand-induced conformational change with CXCR3-A focalized at the cell membrane, leading to sustained receptor activity and increase in the migration. This was also clinically validated. Our study defines LRP1 as a new regulator of CXCR3 and indicates that targeting CXCR3-A in GBM may constitute a promising strategy to halt tumor cell invasion. The extracellular matrix (ECM) has morphogenic roles in tumors. Important ECM components are the matricellular proteins, called thrombospondins(THBS1-5) (Adams and Lawler 2011). We recently elucidated the complex role of THSB1 in GBM invasion (Daubon et al.2019). Global expression analysis revealed that THBS1 is up-regulated in GBMs and associated with a poor prognosis. We, furthermore, demonstrated that THBS1 did not activate TGFβ in GBM but that TGFβ1 induced the expression of THBS1 via SMAD3. Furthermore, GBM invasion is compromised when THBS1 is silenced in tumor cells. Thus, our data clearly show that THBS1 is not only involved in the regulation of angiogenesis in GBM, but also impacts the invasive behaviour of glioma cells by interacting with a molecule called CD47 expressed on the surface of GBM cells. RNA-sequencing after microdissection of central and peripheral tumour areas in a human PDX model demonstrated that THBS1 was the gene with the highest connectivity in the peripheral invasive tumour areas. Taken together, these data indicate that THBS1 plays important role in the infiltrative process in GBM. REFERENCES: Adams JC, Lawler J. Cold Spring Harb Perspect Biol. 2011;3:a009712 Billottet C, Quemener C, Bikfalvi A. Biochim Biophys Acta. 2013;1836:287- Boyé K et al. Sci Rep. 2017;7:10703 Boyé K et al. Nat Commun. 2017;8:1571 Daubon T et al, Nature Communications. Nat Commun. 2019 Mar 8;10(1):1146 Murphy-Ullrich JE, Poczatek M. Cytokine Growth Factor Rev. 2000 11:59

scholarly journals Dynamin 2 interacts with α-actinin 4 to drive tumor cell invasion

2020 ◽  
Vol 31 (6) ◽  
pp. 439-451 ◽  
Author(s):  
Kevin M. Burton ◽  
Hong Cao ◽  
Jing Chen ◽  
Li Qiang ◽  
Eugene W. Krueger ◽  
...  
Keyword(s):  
Cell Migration ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Invasion ◽  
Tumor Cell Invasion ◽  
Related Protein ◽  
Invasive Tumor ◽  
Invasive Cell ◽  
Dynamin 2

Dyn2 and α-actinin 4 interact directly to regulate invasive cell migration and the stabilization of invadopodia. Intriguingly, this is specific for α-actinin 4, and not the highly related protein α-actinin 1. These findings elucidate a novel mechanism of regulating cell migration, with important implications for invasive tumor cells.

scholarly journals Latrunculin A and Its C-17-O-Carbamates Inhibit Prostate Tumor Cell Invasion and HIF-1 Activation in Breast Tumor Cells⊥

2008 ◽  
Vol 71 (3) ◽  
pp. 396-402 ◽  
Author(s):  
Khalid A. El Sayed ◽  
Mohammad A. Khanfar ◽  
Hassan M. Shallal ◽  
A. Muralidharan ◽  
Bhushan Awate ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Invasion ◽  
Breast Tumor ◽  
Prostate Tumor ◽  
Tumor Cell Invasion ◽  
Breast Tumor Cells ◽  
Latrunculin A ◽  
Prostate Tumor Cell

scholarly journals Morphological features of invasion of tumor cells of invasive ductal breast cancer

Morphologia ◽  
2021 ◽  
Vol 15 (3) ◽  
pp. 119-124
Author(s):  
L.A. Naleskina ◽  
T.V. Zadvornyi ◽  
L.M. Kunska ◽  
N.Y. Lukianova
Keyword(s):  
Breast Cancer ◽  
Connective Tissue ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Invasion ◽  
Tumor Cell Invasion ◽  
Invasive Front ◽  
Invasive Ductal Breast Cancer ◽  
Pathological Characteristics ◽  
Ductal Breast Cancer

Background. Nowadays, it has been proven that along with the invasion of individual tumor cells, their group migration occurs in the invasive front of the tumor, and this is an important factor in tumor progression. Objective: to determine the features of tumor cell invasion in the invasive front (IF) of invasive ductal breast cancer (BCa) without special specific features (IC NST) and to establish associative links between them and the clinical and pathological characteristics of the disease. Methods. The study was performed on BCa samples (after hematoxylin and eosin stained) from 120 patients with invasive ductal BCa I-II stage with G2 grade of tumor differentiation that didn’t receive neoadjuvant chemotherapy. Results. Tumors were divided into 3 groups: with predominance of parenchymal component (PC), with the larger component of connective tissue, and relatively equivalent ratio of these components. Within the IF of the studied tumors of patients with ІІ stage of the tumor process, group invasion of tumor structures was mainly determined, both separately and in combination. In particular, an increase in solid structures in tumors with a predominance of the PC, and in neoplasms with expressed desmoplastic changes in connective tissue and their advantage, - alveolar, tubular, discrete. Conclusion. In tumors of patients with invasive ductal BCa in the invasive front is dominated by collective migration of tumor cells, which is the starting mechanism of tumor progression and the first step of the metastatic process. Defined associative links between the features of tumor cell invasion and the clinical and pathological characteristics of the tumor process in BCa patients can be used in predicting this form of cancer.

scholarly journals Role of the Endothelium during Tumor Cell Metastasis: Is the Endothelium a Barrier or a Promoter for Cell Invasion and Metastasis?

2008 ◽  
Vol 2008 ◽  
pp. 1-13 ◽  
Author(s):  
Claudia Tanja Mierke
Keyword(s):  
Mechanical Properties ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Invasion ◽  
Primary Tumor ◽  
Tumor Cell Invasion ◽  
Metastasis Formation ◽  
Cancer Disease ◽  
Cell Mechanical Properties

The malignancy of cancer disease depends on the ability of the primary tumor to metastasize to distant organs. The process of the metastasis formation has largely been analyzed, but still main pathways regarding the extravasation step at the end of the metastasis formation process are controversially discussed. An agreement has been reached about the importance of the endothelium to promote metastasis formation either by enhancing the growth of the primary tumor or by homing (targeting) the tumor cells to blood or lymph vessels. The mechanical properties of the invading tumor cells become the focus of several studies, but the endothelial cell mechanical properties are still elusive. This paper describes the different roles of the endothelium in the process of metastasis formation and focuses on a novel role of the endothelium in promoting tumor cell invasion. It discusses how novel biophysical tools and in vivo animal models help to determine the role of the endothelium in the process of tumor cell invasion. Evidence is provided that cell mechanical properties, for example, contractile force generation of tumor cells, are involved in the process of tumor cell invasion.

Prostaglandin E2, Collagenase, and Protease Levels in Culture of Rat Tumor

1981 ◽  
Vol 89 (4) ◽  
pp. 564-568 ◽  
Author(s):  
Cheng Chun Huang
Keyword(s):  
Connective Tissue ◽  
Tumor Cell ◽  
Prostaglandin E2 ◽  
Tumor Cells ◽  
Cell Invasion ◽  
Leucine Aminopeptidase ◽  
Tumor Cell Invasion ◽  
Prostaglandin E ◽  
Growth Of Tumor ◽  
Rat Tumor

The production of collagenase, protease, leucine aminopeptidase, and prostaglandin E2 by rat tumor increased with the growth of tumor. The syntheses of collagenase, protease, and leucine aminopeptidase were significantly inhibited by indomethacin. Inhibition of collagenase, protease, and leucine aminopeptidase syntheses was overcome by the addition of prostaglandin E2 at a concentration equivalent to the endogeneous level of prostaglandin E2 in rat tumor. These findings suggested that prostaglandin E2, possibly derived from tumor cells, was involved in stimulating the tumor connective tissue stroma to produce collagenase, protease, and leucine aminopeptidase, which promoted tumor cell invasion.

TAMI-24. INHIBITION OF GBM INVASION BY THE Α-AMINO-3-HYDROXY-5-METHYL-4-ISOXAZOLEPROPIONIC ACID (AMPA) GLUTAMATE RECEPTOR ANTAGONIST PERAMPANEL

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi203-vi203
Author(s):  
Katharina Sarnow ◽  
Georgia Kanli ◽  
Olivier Keunen ◽  
Rolf Bjerkvig
Keyword(s):  
Tumor Cell ◽  
Receptor Antagonist ◽  
Single Cell ◽  
Glutamate Receptor ◽  
Cell Invasion ◽  
Brain Parenchyma ◽  
Adult Brain ◽  
Tumor Cell Invasion ◽  
Glutamate Receptor Antagonist ◽  
The Brain

Abstract BACKGROUND Extensive tumor cell invasion within the brain represents a major problem for effective treatment of glioblastomas (GBMs). The invasive processes can be divided into three types: Collective cell invasion, perivascular infiltration, and single-cell invasion into the brain parenchyma. GBM cells can form synapses with neural cells pointing at an extensive communication network between brain and GBM cells which can be mediated via the metabolites Glutamine and Glutamate both needed for GBM cell proliferation. In this context, it has been shown in preclinical models that Perampanel, an antiepileptic agent, functioning as non-competitive α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptor antagonist, has an inhibitory effect on GBM growth. To delineate how Perampanel affects GBM invasion, we utilised a highly characterized 3D GBM-brain organoid invasion model where single-cell invasion was studied in real-time following Perampanel treatment. METHODS A brain coculture model, consisting of rat brain organoids expressing various markers of the human adult brain, where confronted with GFP-labelled tumor cells. By using time-lapse confocal microscopy, we quantified single-cell invasion patterns and speed of invasion using two glioma stem cell models (BG5 and BG7). RESULTS Perampanel treatment significantly reduces tumor cell invasion into the brain organoids with the strongest effect seen in the most invasive GBM (BG5). The single-tumor cell invasion ratio was reduced by 72 % compared to the control (p= 0.0033). In contrast, collective cell invasion was reduced by 19 % (p= 0.028). Statistical analysis was performed using an unpaired sample t-test. CONCLUSION The AMPA glutamate receptor antagonist Perampanel significantly inhibits GBM invasion, suggesting an important role of the glutamate-glutamine cycle between the GBM cells and neurons in the invasion process. Moreover, this communication and exchange of metabolites seem to be more prominent where single GBM cells invade into the brain parenchyma compared to areas where collective invasion take place.

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