Tumor Cell Mechanosensing During Incorporation into the Brain Microvascular Endothelium

A member of a population who is at risk of becoming infected by disease is a susceptible individual. Finding disease susceptibility and generating an alert in advance, is valuable for an individual. The aim of the work presented a feature vector using different statistical texture analyses of brain tumors from an MRI image. The statistical feature texture is computed using GLCM (Gray Level Co-occurrence Matrices) of brain tumor cell structure. For this paper, the brain tumor cell segmented using the strip method to implement hybrid Assured Convergence Particle Swarm Optimization (ACPSO) - Fuzzy C-means clustering (FCM). Furthermore, the four angles 0o, 45o, 90o, and 135o have calculated the segmented brain image in GLCM. The four angular directions are calculated using texture features are correlation, energy, contrast and homogeneity. The texture analysis is performed on different types of images using past years. So, the algorithm proposed statistical texture features are calculated for iterative image segmentation. The algorithm FETC (Feature Extraction Tumor Cell) extracts statistical features of GLCM. These results show that MRI images can be implemented in a system of brain cancer detection.

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Capturing Changes in the Brain Microenvironment during Initial Tumor Cell Invasion.

10.1158/0008-5472.sabcs-09-4162 ◽

2009 ◽

Author(s):

M. Lorger ◽

B. Felding-Habermann

Keyword(s):

Tumor Cell ◽

Cell Invasion ◽

Tumor Cell Invasion ◽

Initial Tumor ◽

The Brain

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IMMU-26. VISUALIZING TUMOR CELL - LYMPHOCYTE INTERACTIONS IN THE BRAIN METASTATIC CASCADE USING IN VIVO TWO PHOTON MICROSCOPY

Neuro-Oncology ◽

10.1093/neuonc/noy148.529 ◽

2018 ◽

Vol 20 (suppl_6) ◽

pp. vi126-vi127

Author(s):

Manuel Piechutta ◽

Anna Berghoff ◽

Matthia Karreman ◽

Katharina Gunkel ◽

Wolfgang Wick ◽

...

Keyword(s):

Tumor Cell ◽

Metastatic Cascade ◽

Two Photon Microscopy ◽

Two Photon ◽

The Brain

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Vascular Genomics of the Human Brain

Journal of Cerebral Blood Flow & Metabolism ◽

10.1097/00004647-200203000-00001 ◽

2002 ◽

Vol 22 (3) ◽

pp. 245-252 ◽

Cited By ~ 36

Author(s):

Eric V. Shusta ◽

Ruben J. Boado ◽

Gary W. Mathern ◽

William M. Pardridge

Keyword(s):

Gene Expression ◽

Human Brain ◽

Differential Gene Expression ◽

Molecular Transport ◽

Brain Diseases ◽

Microvascular Endothelium ◽

Whole Brain ◽

Differential Gene ◽

Brain Microvasculature ◽

The Brain

The microvasculature of the human brain plays an important role in the development and maintenance of the central nervous system and in the pathogenesis of brain diseases, and is the site of differential gene expression within the brain. However, human brain microvascular-specific genes may not be detected in whole-brain gene microarray because the volume of the brain microvascular endothelium is relatively small (0.1%) compared with the whole brain. Therefore, the differential gene expression within the human brain microvasculature was evaluated using suppression subtractive hybridization with RNA isolated from human brain microvessels. Gene identification was restricted to the first 71 clones that were differentially expressed at the brain microvasculature. Twenty of these were genes encoding proteins with known function that were involved in angiogenesis, neurogenesis, molecular transport, and maintenance of endothelial tight junctions or the cytoskeleton. Eighteen genes coding for proteins of an unknown function were identified, including five genes containing satellite DNA sequences. The results provide the initial outline of the genomics of the human brain microvasculature, and have implications for the identification of both targets for brain-specific drug transport and changes in microvascular gene expression in brain diseases.

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Mechanisms of Brain Aging Regulation by Insulin: Implications for Neurodegeneration in Late-Onset Alzheimer's Disease

ISRN Neurology ◽

10.5402/2011/306905 ◽

2011 ◽

Vol 2011 ◽

pp. 1-9 ◽

Cited By ~ 21

Author(s):

Artur F. Schuh ◽

Carlos M. Rieder ◽

Liara Rizzi ◽

Márcia Chaves ◽

Matheus Roriz-Cruz

Keyword(s):

Alzheimer’S Disease ◽

Insulin Resistance ◽

Alzheimer's Disease ◽

Brain Aging ◽

Late Onset ◽

Energy Deficit ◽

Insulin Degrading Enzyme ◽

Microvascular Endothelium ◽

Chronic Hyperglycemia ◽

The Brain

Insulin and IGF seem to be important players in modulating brain aging. Neurons share more similarities with islet cells than any other human cell type. Insulin and insulin receptors are diffusely found in the brain, especially so in the hippocampus. Caloric restriction decreases insulin resistance, and it is the only proven mechanism to expand lifespan. Conversely, insulin resistance increases with age, obesity, and sedentarism, all of which have been shown to be risk factors for late-onset Alzheimer's disease (AD). Hyperphagia and obesity potentiate the production of oxidative reactive species (ROS), and chronic hyperglycemia accelerates the formation of advanced glucose end products (AGEs) in (pre)diabetes—both mechanisms favoring a neurodegenerative milieu. Prolonged high cerebral insulin concentrations cause microvascular endothelium proliferation, chronic hypoperfusion, and energy deficit, triggering β-amyloid oligomerization and tau hyperphosphorylation. Insulin-degrading enzyme (IDE) seems to be the main mechanism in clearing β-amyloid from the brain. Hyperinsulinemic states may deviate IDE utilization towards insulin processing, decreasing β-amyloid degradation.

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Pathological Investigation of Meningioma Capsule with respect to Tumor Cell Invasion

10.21203/rs.3.rs-945497/v1 ◽

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.

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PTEN and Autism With Macrocepaly

10.1093/med/9780199744312.003.0010 ◽

2013 ◽

Author(s):

Craig M. Powell

Keyword(s):

Tumor Cell ◽

Signaling Pathways ◽

Intracellular Signaling ◽

Clinical Phenotype ◽

Model Systems ◽

Tumor Cell Lines ◽

Gene Encoding ◽

Increased Risk ◽

The Brain

Phosphatase and Tensin homolog deleted on chromosome 10 (PTEN) is a gene encoding an intracellular signaling molecule. PTEN was originally discovered as the gene responsible for a subset of familial hamartoma (tumor) syndromes associated with increased risk for certain cancers (Nelen et al., 1997) and as a gene often mutated in human cancers and tumor cell lines (Li et al., 1997; Steck et al., 1997). More recently, mutations in PTEN have been linked genetically to the clinical phenotype of autism or developmental delay with macrocephaly (Boccone et al., 2006; Butler et al., 2005; Buxbaum et al., 2007; Goffin, Hoefsloot, Bosgoed, Swillen, & Fryns, 2001; Herman, Butter, et al., 2007; McBride et al., 2010; Orrico et al., 2009; Stein, Elias, Saenz, Pickler, & Reynolds, 2010; Varga, Pastore, Prior, Herman, & McBride, 2009; Zori, Marsh, Graham, Marliss, & Eng, 1998). This chapter examines the role of PTEN in intracellular signaling, the link between PTEN signaling pathways and other autism-related genes and signaling pathways, the genetic relationship between PTEN and autism, model systems in which effects of Pten deletion on the brain have been studied, and promising preclinical data identifying therapeutic targets for patients with autism/macrocephaly associated with PTEN mutations.

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TAMI-21. TUMOR-ASSOCIATED MICROGLIA GUIDE GBM INFILTRATION VIA PLEXIN-B2

Neuro-Oncology ◽

10.1093/neuonc/noab196.805 ◽

2021 ◽

Vol 23 (Supplement_6) ◽

pp. vi202-vi202

Author(s):

Sangjo Kang ◽

Anirudh Sattiraju ◽

Yuhuan Li ◽

Shalaka Wahane ◽

Theo Hanna ◽

...

Keyword(s):

Tumor Cell ◽

Close Contact ◽

Primary Brain Tumor ◽

Physical Interaction ◽

Wide Field ◽

Cell Alignment ◽

Ecm Remodeling ◽

Underlying Mechanisms ◽

Cellular Alignment ◽

The Brain

Abstract Glioblastoma (GBM) is the most common malignant primary brain tumor. The nature of invasiveness of GBM makes complete surgical resection difficult. However, how GBM cells achieve wide infiltration in the brain is poorly understood. Microglia, the resident immune cells in the brain can support GBM growth and invasion, but the underlying mechanisms remain elusive. Here, we show that microglia are activated in a wide field away from tumor boundaries, ahead of tumor cell infiltration. Invading GBM cells are in close contact with microglia, progressively aligned with one another in the direction of tumor invasion. Moreover, ECM is also aligned with the infiltrating tumor and microglia, which may serve as invasion tracks in the brain. Mechanistically, we demonstrate that microglia direct cellular alignment and ECM remodeling in the invasion tracks through an axon guidance receptor Plexin-B2. Myeloid-specific ablation of Plexin-B2 perturbs microglia and tumor cell alignment, microglia migration, ECM organization, and GBM invasiveness. Together, our data reveal a hitherto under-appreciated role of microglia in providing directional cues for GBM invasion through physical interaction and alignment of ECM and tumor cells, thus providing new insights and novel molecular targets in curbing GBM invasion.

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