Relevant bibliographies by topics / Cancer and invasion

Academic literature on the topic 'Cancer and invasion'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Cancer and invasion"

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Doak, Andrea E., Rose Qu, and Kevin J. Cheung. "Abstract A014: Transcriptional regulation of basal leader cell identity during collective breast cancer invasion." Cancer Research 83, no. 2_Supplement_2 (January 15, 2023): A014. http://dx.doi.org/10.1158/1538-7445.metastasis22-a014.

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Abstract An early step in breast cancer progression is invasion of tumor cells into surrounding tissues. In many breast cancers, particularly ductal carcinomas, this invasion is accomplished by tumor cells migrating as a cohesive group. This often involves cells that take on heterogeneous roles as either leader or follower cells. Studies in common mouse and human breast cancer models have established that leader cells express high levels of keratin-14 (K14) and other basal epithelial markers. The presence of these K14+ cells promote metastasis and predict poor prognosis. The molecular mechanisms regulating K14+ leader cell identity and the methods for targeted depletion of these cells remain obscure. Here we performed time-sampled single cell RNA-sequencing in 3D type I collagen-embedded tumor organoids isolated from the MMTV-PyMT luminal B model of breast cancer. 11 distinct cellular transcriptional states were identified, and through correlation with K14 expression and invasive strand formation we classified one of the states as leader cells. Having confirmed the leader cell cluster markers spatially localize to the invasive front, we next asked which transcription factors were enriched, reasoning that transcription factors could be master regulators of leader cell fate. Three different shRNAs targeting ten genes were systematically evaluated for their effects on collective invasion and keratin-14 transcription. Each transcription factor was designated as either an invasion promoter or invasion suppressor depending on the correlation between transcription factor expression and organoid invasion. Studies are ongoing investigating the impact of invasion-promoting and invasion-suppressing transcription factors on cellular transcriptional states and metastatic dissemination in-vivo. We propose that targeting invasion-suppressing pathways could be combined with therapies that specifically target and eliminate K14+ invasive cells. To this end, we have identified multiple candidate druggable targets and specific surface markers expressed in K14+ invasive cells. Citation Format: Andrea E. Doak, Rose Qu, Kevin J. Cheung. Transcriptional regulation of basal leader cell identity during collective breast cancer invasion [abstract]. In: Proceedings of the AACR Special Conference: Cancer Metastasis; 2022 Nov 14-17; Portland, OR. Philadelphia (PA): AACR; Cancer Res 2022;83(2 Suppl_2):Abstract nr A014.
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Hirano, Kazuki, Kosuke Nomura, Dan Nobuhiro, Masami Tanaka, Junichiro Sato, Akira Matsui, Shusuke Haruta, Daisuke Kikuchi, and Shu Hoteya. "A rare case of Helicobacter pylori–uninfected foveolar-type gastric cancer with submucosal invasion and lymph node metastasis." SAGE Open Medical Case Reports 10 (January 2022): 2050313X2211116. http://dx.doi.org/10.1177/2050313x221111673.

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Gastric cancer without Helicobacter pylori infection accounts for less than 1% of all gastric cancers, and is generally considered to be less invasive. This report describes a rare case of H. pylori–uninfected gastric cancer with deep submucosal invasion and lymph node metastasis. Endoscopic submucosal dissection was performed, and pathological examination revealed tubular adenocarcinoma with deep submucosal invasion. We diagnosed foveolar-type gastric adenocarcinoma. While many cases of foveolar-type gastric adenocarcinoma, especially of the white elevated type, are reported as early stage gastric cancer, this case is very rare because it showed submucosal invasion and lymph node metastasis.
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Carr, I., M. Levy, and P. Watson. "The invasive edge: invasion in colorectal cancer." Clinical & Experimental Metastasis 4, no. 2 (1986): 129–39. http://dx.doi.org/10.1007/bf00119079.

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Zhu, Shoumin, Abbes Belkhiri, and Wael El-Rifai. "Induction of MT1-MMP expression and enhancement of gastric cancer cells invasion by DARPP-32-CXCR4 interaction." Journal of Clinical Oncology 31, no. 4_suppl (February 1, 2013): 14. http://dx.doi.org/10.1200/jco.2013.31.4_suppl.14.

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14 Background: Dopamine and cAMP-regulated phosphoprotein, Mr 32000 (DARPP-32) is amplified and overexpressed in approximately 70% of gastric cancers. The prognosis for gastric cancer patients remains poor, especially in more advanced stages. Recently, it was suggested that CXCL-12 and its receptor, CXCR4, are involved in gastric cancer metastasis. However, the detailed mechanism of gastric cancer metastasis is still not completely understood. Methods: Cells invasive activity was determined by invasion assay and HUVEC invasion assay. The association between DARPP-32 and CXCR4 was evaluated by immunofluorescence and co-immunoprecipitation assays. CXCR4 degradation was analyzed by Ubiquitination Assay. Results: Overexpression of DARPP-32 in AGS cells increased cell invasion with about as three-fold invasive cells as the vector control (p<0.01). As measured by HUVEC invasion assay, overexpression of DARPP-32 in AGS cells also had a significant increase in the invasive activity (p<0.001). We found that DARPP-32 led to increased CXCR4 and MT1-MMP protein levels in DARPP-32 expressing AGS cells. The co-immunoprecipitation and immunofluorescence experiments demonstrated the existence of DARPP-32 and CXCR4 in the same protein complex. AGS cells expressing DARPP-32 displayed stable protein levels of CXCR4. IP-Western blot showed reduced ubiquitination of CXCR4 protein following the overexpression of DARPP-32 and treatment with CXCL-12, as compared to controls. Using AMD3100 (0.2 ng/ml) overnight blocked DARPP-32-induced cell invasion. The knockdown of endogenous DARPP-32 by lentiviral DARPP-32 shRNA in MKN-45 cell line reversed these signaling effects and decreased cell invasive activity, as measured by invasion and HUVEC invasion Assay (p<0.01, p<0.05). Conclusions: The in vitro studies indicate that DARPP-32 plays a role in invasion and metastasis; DARPP-32 promotes invasion and metastasis of gastric cancer cells by interacted with CXCR4, delaying CXCL-12-induced CXCR4 Ubiquitination and blocking CXCR4 degradation, activating MMP2 by increasing MT1-MMP expression. The in vivo experiments are ongoing to determine the efficacy of DARPP-32 in mediating CXCR4 overexpression and metastasis.
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Hansen, Malene Bredahl, Maria Postol, Siri Tvingsholm, Inger Ødum Nielsen, Tiina Naumanen Dietrich, Pietri Puustinen, Kenji Maeda, et al. "Identification of lysosome‐targeting drugs with anti‐inflammatory activity as potential invasion inhibitors of treatment resistant HER2 positive cancers." Cellular Oncology 44, no. 4 (May 3, 2021): 805–20. http://dx.doi.org/10.1007/s13402-021-00603-2.

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Abstract Purpose Most HER2 positive invasive cancers are either intrinsic non-responsive or develop resistance when treated with 1st line HER2 targeting drugs. Both 1st and 2nd line treatments of HER2 positive cancers are aimed at targeting the HER2 receptor directly, thereby strongly limiting the treatment options of HER2/ErbB2 inhibition resistant invasive cancers. Methods We used phenotypic high throughput microscopy screening to identify efficient inhibitors of ErbB2-induced invasion using 1st line HER2 inhibitor trastuzumab- and pertuzumab-resistant, p95-ErbB2 expressing breast cancer cells in conjunction with the Prestwick Chemical Library®. The screening entailed a drug’s ability to inhibit ErbB2-induced, invasion-promoting positioning of lysosomes at the cellular periphery, a phenotype that defines their invasiveness. In addition, we used high throughput microscopy and biochemical assays to assess the effects of the drugs on lysosomal membrane permeabilization (LMP) and autophagy, two features connected to cancer treatment. Using 2nd line HER2 inhibitor lapatinib resistant 3-dimensional model systems, we assessed the effects of the drugs on ErbB2 positive breast cancer spheroids and developed a high-throughput invasion assay for HER2 positive ovarian cancer organoids for further evaluation. Results We identified Auranofin, Colchicine, Monensin, Niclosamide, Podophyllotoxin, Quinacrine and Thiostrepton as efficient inhibitors of invasive growth of 2nd line HER2 inhibitor lapatinib resistant breast cancer spheroids and ovarian cancer organoids. We classified these drugs into four groups based on their ability to target lysosomes by inducing autophagy and/or LMP, i.e., drugs inducing early LMP, early autophagy with late LMP, late LMP, or neither. Conclusions Our results indicate that targetable lysosome-engaging cellular pathways downstream of ErbB2 contribute to invasion. They support lysosomal trafficking as an attractive target for therapy aiming at preventing the spreading of cancer cells. Since these drugs additionally possess anti-inflammatory activities, they could serve as multipurpose drugs simultaneously targeting infection/inflammation and cancer spreading.
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Rossi, Fabiana Alejandra, Ezequiel Hernán Calvo Roitberg, Juliana Haydeé Enriqué Steinberg, Molishree Umesh Joshi, Joaquín Maximiliano Espinosa, and Mario Rossi. "HERC1 Regulates Breast Cancer Cells Migration and Invasion." Cancers 13, no. 6 (March 15, 2021): 1309. http://dx.doi.org/10.3390/cancers13061309.

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Tumor cell migration and invasion into adjacent tissues is one of the hallmarks of cancer and the first step towards secondary tumors formation, which represents the leading cause of cancer-related deaths. This process is considered an unmet clinical need in the treatment of this disease, particularly in breast cancers characterized by high aggressiveness and metastatic potential. To identify and characterize genes with novel functions as regulators of tumor cell migration and invasion, we performed a genetic loss-of-function screen using a shRNA library directed against the Ubiquitin Proteasome System (UPS) in a highly invasive breast cancer derived cell line. Among the candidates, we validated HERC1 as a gene regulating cell migration and invasion. Furthermore, using animal models, our results indicate that HERC1 silencing affects primary tumor growth and lung colonization. Finally, we conducted an in silico analysis using publicly available protein expression data and observed an inverse correlation between HERC1 expression levels and breast cancer patients’ overall survival. Altogether, our findings demonstrate that HERC1 might represent a novel therapeutic target for the development or improvement of breast cancer treatment.
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Nagai, Tomoaki, Tomohiro Ishikawa, Yasuhiro Minami, and Michiru Nishita. "Tactics of cancer invasion: solitary and collective invasion." Journal of Biochemistry 167, no. 4 (January 11, 2020): 347–55. http://dx.doi.org/10.1093/jb/mvaa003.

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Abstract Much attention has been paid on the mechanism of cancer invasion from the viewpoint of the behaviour of individual cancer cells. On the other hand, histopathological analyses of specimens from cancer patients and of cancer invasion model animals have revealed that cancer cells often exhibit collective invasion, characterized by sustained cell-to-cell adhesion and polarized invasion as cell clusters. Interestingly, it has recently become evident that during collective invasion of cancer cells, the cells localized at invasion front (leader cells) and the cells following them (follower cells) exhibit distinct cellular characteristics, and that there exist the cells expressing representative proteins related to both epithelial and mesenchymal properties simultaneously, designated as hybrid epithelial-to-mesenchymal transition (EMT)-induced cells, in cancer tissue. Furthermore, the findings that cells adopted in hybrid EMT state form clusters and show collective invasion in vitro emphasize an importance of hybrid EMT-induced cells in collective cancer invasion. In this article, we overview recent findings of the mechanism underlying collective invasion of cancer cells and discuss the possibility of controlling cancer invasion and metastasis by targeting this process.
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Yanagisawa, Kiminori, Masamitsu Konno, Hao Liu, Shinji Irie, Tsunekazu Mizushima, Masaki Mori, Yuichiro Doki, Hidetoshi Eguchi, Michiya Matsusaki, and Hideshi Ishii. "A Four-Dimensional Organoid System to Visualize Cancer Cell Vascular Invasion." Biology 9, no. 11 (October 27, 2020): 361. http://dx.doi.org/10.3390/biology9110361.

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Vascular invasion of cancer is a critical step in cancer progression, but no drug has been developed to inhibit vascular invasion. To achieve the eradication of cancer metastasis, elucidation of the mechanism for vascular invasion and the development of innovative treatment methods are required. Here, a simple and reproducible vascular invasion model is established using a vascular organoid culture in a fibrin gel with collagen microfibers. Using this model, it was possible to observe and evaluate the cell dynamics and histological positional relationship of invasive cancer cells in four dimensions. Cancer-derived exosomes promoted the vascular invasion of cancer cells and loosened tight junctions in the vascular endothelium. As a new evaluation method, research using this vascular invasion mimic model will be advanced, and applications to the evaluation of the vascular invasion suppression effect of a drug are expected.
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Evans, Douglas M., and Kimberly Sloan-Stakleff. "Suppression of the Invasive Capacity of Human Breast Cancer Cells by Inhibition of Urokinase Plasminogen Activator via Amiloride and B428." American Surgeon 66, no. 5 (May 2000): 460–64. http://dx.doi.org/10.1177/000313480006600507.

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Inhibition of urokinase plasminogen activator (uPA) has been shown to suppress cancer cell invasion and metastasis in the laboratory setting by numerous investigators. Most studies have used murine cell lines implanted in syngeneic rodents or transfected human cell lines grown in immunocompromised laboratory hosts. In this study using Matrigel invasion chambers and two separate uPA inhibitors, amiloride and B428, the invasive capacity of unaltered human breast cancer cells was significantly suppressed. Cell proliferation was also suppressed to a lesser degree. These findings suggest that uPA inhibition may be a valid clinical approach to the control of the invasion and metastasis of human cancers.
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Cooper, Harry S. "Pathologic Issues in the Treatment of Endoscopically Removed Malignant Colorectal Polyps." Journal of the National Comprehensive Cancer Network 5, no. 9 (October 2007): 991–96. http://dx.doi.org/10.6004/jnccn.2007.0083.

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Endoscopically removed malignant colorectal polyps are early stage cancers for which treatment depends on histopathologic findings. For accurate pathologic evaluation, the polyps should be received in 1 piece because margins cannot be accurately assessed in fragmented polyps. Polyps with grade I or II cancer, no lymphovascular invasion, and a negative resection margin can be successfully treated with endoscopic polypectomy, whereas those with grade III cancer, lymphovascular invasion, or a positive or close margin require definitive surgical resection after endoscopic polypectomy. Potentially new significant parameters for patient management are depth of invasion and tumor budding. The pathology report must be clear and concise, indicating all relevant important parameters. The pathologist must differentiate invasive adenocarcinoma from intramucosal adenocarcinoma and pseudo-invasion.
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Dissertations / Theses on the topic "Cancer and invasion"

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Smith, Neil Jonathan. "Extramural vascular invasion in colorectal cancer." Thesis, Institute of Cancer Research (University Of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.510379.

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Ünlü, Ali. "Mechanism of invasion by prostate cancer." Thesis, University of Glasgow, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244438.

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Peng, Lu. "Multiscale mathematical modelling of cancer invasion." Thesis, University of Dundee, 2015. https://discovery.dundee.ac.uk/en/studentTheses/c0aec459-7953-4172-b1f9-5ad029aae9df.

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Invasion of the surrounding tissue is one of the hallmarks of cancer. Solid tumours have a reciprocal relationship with the surrounding microenvironment, a complex tissue composed of extracellular matrix and other multiple distinct cell types. Prote- olytic degradation and remodelling of the extracellular matrix is essential for cancer cells to be able to invade. Important matrix degrading enzymes include the matrix metalloproteases (MMP) and the urokinase plasminogen activator (uPA). This thesis has investigated the complex process of cancer growth and spread that occur across several different spatial scales, in order to gain a better understanding of the key processes involved during invasion. At first, we tested our modelling concept by applying a level-set method to a moving boundary problem. Later, a multi-scale mathematical model of cancer invasion was developed by coupling the urokinase plasminogen activation (uPA) system with a two-scale computational modelling technique. This approach allows us to investigate cancer invasion not only at the macroscopic tissue level, but also at the microscopic cellular level. Our computational simulation results demonstrate a range of heterogeneous dynamics which are qualitatively similar to the invasive growth patterns observed in a number of different types of cancer known as tumour infiltrative growth patterns (INF).
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Safuan, Sabreena. "Lymphovascular invasion in melanoma and breast cancer." Thesis, University of Nottingham, 2012. http://eprints.nottingham.ac.uk/12771/.

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The theory of metastatic cascade suggests that vasculature plays a central role in the metastatic processes by being the major route of spreading. Two main circulatory systems in the body are responsible for cancer cell dissemination; the blood vascular system and the lymphatic system. However, comparing between these circulatory systems, much less is known about lymphatic vessels, with few studies being conducted about the initial steps of metastasis. In the first part of this project, a series of 202 formalin fixed paraffin embedded (FFPE) cutaneous melanoma sections were stained with D2-40, CD34 and CD68 to identify lymphatics, blood vessels and macrophages respectively, to examine vessel distribution and the involvement of inflammatory infiltrate in mediating vascular invasion (VI). Sections were also stained by conventional haematoxylin and eosin (H&E), to assess VI, and results compared against those obtained by immunohistochemistry (IHC) that allow discrimination of lymphatic and blood vessel invasion. It was found that lymphatics are mainly located at the peritumoural area of the tumour but intratumoural lymphatics are present and appeared to be functional based on the presence of tumour emboli in the vessels. In addition, vascular invasion in melanoma is mainly lymphatic vessel invasion with H&E assessment underestimating its incidence. Lymphatic vessel invasion were significantly associated with markers of aggressive disease which suggest their importance in melanoma. Lymphatic vessel invasion was also associated with a high macrophage count, suggesting a role for macrophage in mediating the process of metastatic via lymphatic vessels. In the second part of this project, the adhesion pattern of melanoma and breast cancer cell lines to blood and lymphatic endothelial cell models; large vessel versus microvessel and primary versus immortalised cells were compared. In addition, the effect of macrophage secreted cytokines; TNF-α and IL-1β, tumour conditioned media and macrophage conditioned media on the adhesive process were also studied. Both melanoma and breast cancer cells exhibited a higher level of adhesion to blood compared to the lymphatic endothelial cells. IL-1β stimulation of endothelial cells, tumour cells or both together showed a significant increased in the percentage of adhered tumour cells to the endothelial cell models with a higher increased to the lymphatic endothelial cells. A significant increased tumour cell adhesion was also observed with macrophage conditioned media and this effect seemed to be associated with the amount of IL-1β present. Interestingly, the increased adhesion effect observed with this supernatant was removed with the use of interleukin-1 converting enzyme (ICE) inhibitor. Expression of adhesion molecules; CLEVER-1, ICAM-1 and VCAM-1 were examined to study which adhesion molecules might regulate the process of tumour-endothelial interactions. Stimulation of endothelial cell models with IL-1β did not show any significant altered CLEVER-1 expression suggesting that although CLEVER-1 is an important lymphatic specific adhesion molecule, it may not be the principle regulator of tumour-endothelial interactions. This process may be regulated by ICAM-1 and VCAM-1 in which the expression increased significantly upon stimulation with IL-1β. In the third part of this study, the effect of TNF-α, IL-1β, tumour conditioned media and macrophage conditioned media stimulation on melanoma and breast cancer cell migration were investigated using wound healing assays. Following exposure to TNF-α and IL-1β, a significant increase in the percentage of wound closure was observed and the increase was higher in IL-1β stimulated cells. Similarly, when tumour cells were exposed to macrophage conditioned media, there was an increase in the percentage of wound closure compared to control cells. The effect of IL-1β and macrophage conditioned media on breast cancer cell migration across blood and lymphatic endothelial cells were also studied using Boyden chamber transmigration assay. Significant increased in tumour cells transmigration was observed with IL-1β stimulation, with similar affinity across both endothelial cell types. However, when cells were stimulated with macrophage supernatant from lipopolysaccharide (LPS) stimulated macrophages, an increase transmigratory effect was notably observed to the lymphatic endothelial cells. Interestingly, the increased adhesion effect was removed with the used of ICE inhibitors. The last part of this study dealt with IL-1β expression in breast tissue samples. 1511 early stage breast cancer tissue microarray samples were stained with commercially available IL-1β antibody to examine the association with lymphatic vessel invasion, clinicopathological variables and clinical outcome. High IL-1β expression in tumour cells was significantly associated with the absence of both intra-tumoural and peri-tumoural lymphatic vessel invasion. A significant association was also observed between low IL-1β expression in tumour cells with breast cancer specific survival and disease free interval. In conclusion, lymphatic vessels have been found to play a significant role in breast cancer and melanoma cells progression by being the major route for vascular dissemination. In the in-vitro settings, this study has shown that IL-1β, with macrophages as the main producer, could regulate tumour cell invasion especially to the lymphatic circulation. This project has yielded some important results towards understanding of the lymphatic vasculature and modulation of lymphatic vessel invasion. However, more studies are needed to enable translation of research into clinical management of cancer.
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Starobinska, Ella. "Matrix Degradation and Invasion in Breast Cancer." Thesis, The University of Arizona, 2012. http://hdl.handle.net/10150/244788.

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In order to metastasize, cancer cells need to invade and degrade matrix. Previous research showed that Epidermal Growth Factor Receptor (EGFR) is an oncogene, a member of ErBb family, that is over-expressed in aggressive cancers. EGFR mediates cell survival, proliferation, and motility through different signaling pathways. Located on the basolateral membrane of the cell, EGFR can be either translocated to the nucleus, degraded by the lysosome or recycled. However, in cancerous cells, EGFR activity is altered by MUC1, which associates itself with EGFR. Research suggested that this pathway acts in a Met-dependent manner. We conducted matrix degradation and invasion assays to see whether MUC1/EGFR activity has affect on these processes. Matrix degradation assay showed that Muc1 and EGFR inhibit matrix degradation and PMIP promotes it. However, Muc1/EGFR regulated matrix degradation is not Met-dependant. Meanwhile, the transwell invasion assay provided variable and statistically insignificant results.
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Planchon, Damien. "Etude du rôle de la surexpression des flotillines dans l'invasion cellulaire." Thesis, Montpellier, 2017. http://www.theses.fr/2017MONTT056.

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L’invasion cellulaire est un phénomène pendant lequel les cellules présentent des changements importants dans leur forme et acquièrent la capacité à dégrader les structures qui les entourent afin de migrer au sein d’un organisme. L’invasion est cruciale pour la stabilité physiologique d’un organisme car elle intervient à différentes étapes de notre vie notamment lors du développement embryonnaire ou pendant une réaction immunitaire. Cependant ce mécanisme est également majeur lors de la progression tumorale. Dans nos organismes, les cellules sont entourées par la matrice extracellulaire (MEC) qui doit être remodelée ou dégradée lors du processus d’invasion. Cette dégradation est réalisée par des structures cellulaires spécialisées, les invadopodes, qui sont des sites où sont libérés les protéines spécialisées dans la dégradation de la MEC, parmi lesquelles MT1-MMP joue un rôle prépondérant. Les capacités à envahir et à dégrader la MEC d’une cellule dépendent donc fortement de la libération de MT1-MMP aux sites de dégradation. Les mécanismes qui permettent le transport de MT1-MMP aux zones d’intérêts sont encore mal compris. Dans ce contexte, nous avons mis en évidence que les Flotillines sont d’importants régulateurs de l’adressage et la libération de MT1-MMP à ces sites de dégradations. Les Flotillines 1 et 2 sont des protéines ubiquitaires très conservées. La quantité de Flotillines est augmentée dans de nombreux cancers invasifs et ceci est considéré comme un marqueur de mauvais pronostic. Lors de mon projet, nous avons mis en évidence que l’augmentation de la quantité de Flotillines dans des cellules normales de différentes origines, est suffisante pour induire une forte invasion cellulaire in vivo et in vitro (respectivement dans des modèles de xénogreffes chez le poisson zèbre dans modèles de sphéroïdes 3D dans des matrices de collagènes). De même, la suppression des Flotillines dans des cellules cancéreuses est associée à une diminution de leurs capacités invasives in vivo et in vitro. Ces résultats s’expliquent par le fait que les Flotillines régulent le trafic intracellulaire de MT1-MMP et augmentent sa libération aux sites de dégradation favorisant ainsi l’invasion cellulaire
Tumor cell invasion and consecutive metastasis formation are the main cause of death in cancer patients. Invading tumor cells are surrounded by stroma and extracellular matrix (ECM) that is remodeled or degraded during the metastatic process. ECM degradation is mediated by specialized organelles called invadosomes. Their function strongly depends on matrix metalloproteinases (MMPs) that degrade ECM. Among all the MMPs, MT1-MMP plays a major role the invasive behavior of metastatic cells.Flotillin 1 and 2 are two ubiquitous and highly conserved membrane proteins that can assemble in large oligomers, known to participate in membrane proteins clustering and endocytosis. Flotillins are overexpressed in many invasive cancers and considered as markers of poor prognosis, results we confirmed using several sarcoma and carcinoma models. During my project we identified Flotillins as regulators of MT1-MMP trafficking and cell invasion.We used a dual reciprocal approach consisting of the overexpression of Flotillins in non tumoral cells and of down-regulation of Flotillins in metastatic cells. We showed that flotillins downregulation in invasive cancer cells dramatically inhibit their invasive properties as monitored in vitro using a 3D-collagen invasion assay and in vivo using zebrafish xenografts. Reciprocally, ectopic overexpression of Flotillins in non-tumoral cells is sufficient to induce their invasive behavior in vitro and in vivo. This increase of invasion is mainly due to a higher ability to degrade the matrix in a MT1-MMP-dependent manner. Finally, we showed that Flotillins are critical regulators of the trafficking and the release of MT1-MMP at the degradation site
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Woodward, Julia Keren Lynda. "Adhesion and invasion studies of uveal melanoma." Thesis, University of Sheffield, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251213.

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García, de Albéniz Xabier. "Mechanisms of invasion and metastasis in colorectal cancer." Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/300900.

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We studied the mechanisms driving the metastatic spread in colorectal cancer (CRC), focusing in the MAPK pathway. We developed in vivo a highly metastatic cell line using a KRAS-mutated cell line (SW620) in an ortothopic xenograft mouse model and used both in vivo and in vitro experiments to evaluate the mechanisms of metastasis. We also used data from two large prospective cohorts of incident CRC to evaluate the association of an intronic variant of SMAD7 (rs4939827, 18q21) with the phenotype and molecular characterisitics of CRC. In the first project, we inoculated SW620 luciferase-expressing cells into portal circulation of immunodeficient mice via intrasplenic injection followed by splenectomy, in order to isolate cell populations that target the liver. Comparative transcriptomic analysis identified 194 genes differentially expressed between the parental and the highly metastatic cell line. We found pathways of nitrogen metabolism, cell adhesion molecules and mitogen-activated protein kinases (MAPKs). Downregulation of ERK2 (but not of ERK1) in the highly metastatic cell line reverted its metastatic capacity to the liver, but not to the lung in our mice model. We thus hypothesized that the ability to metastasize the lung by the highly metastatic derivative had to be driven by other mechanism. The expression of parathyroid hormone-like hormone (PTHLH) was upregulated in our highly metastatic derivative and was inversely correlated with the expression of MKK6. Downregulation of PHTLH in the highly metastatic derivative decreased its capacity to colonize the lung without decreasing its capacity to colonize the liver after intra portal inoculation. We evidenced that PTHLH induced apoptosis of human pulmonary endothelial cells via apoptosis-inducing factor mitochondrion-associated 1. In the second project we evaluated the association of the SMAD7 intronic variant with tumor phenotype and several CRC molecular characteristics. We used 1509 CRC cases and 2307 age-matched controls nested within the Nurses Health Study (NHS) and the Health Professionals Follow-up Study (HPFS). We randomly selected between one and three matched controls. Among the 1509 cases with blood or buccal samples in this study, we were able to successfully obtain tissue suitable for molecular analyses in 658 cases. We genotyped rs4939827 (TaqMan) successfully in 98% of the samples in NHS and 99.6% of the samples in HPFS. The phenotipic features evaluated were: TNM stage, grade of differentiation, location of the primary tumor (colon vs. rectum) and age at diagnosis. The evaluated molecular characteristics were DNA methylation of RUNX3 and LINE-1 (long interspersed nucleotide element-1), CpG island methylator phenotype (CIMP), microsatellite instability, TP53 expression by immunohistochemistry and the mutational status of BRAF, KRAS and PIK3CA. We found that the minor allele (G) in rs4939827 was associated with a lower risk of developing tumor stage pT1 or pT2 CRC [multivariate odds ratio (OR), 0.73; 95% confidence interval (CI) 0.62-0.87] but not tumor stage pT3 or pT4 (multivariate OR, 1.07; 95% CI 0.93-1.23, P for heterogeneity = 1.2 x 10-4). The association between rs4939827 and CRC also significantly differed by methylation of RUNX3 (P for heterogeneity = 0.005). Among those with CRC, the minor allele (G) in rs4939827 was significantly associated with poorer overall survival (hazards ratio, 1.20; 95% CI, 1.02-1.42). In conclusion, we provide clinical and molecular evidence showing that ERK2 activation provides colon cancer cells with the ability to seed and colonize the liver and reduced p38 MAPK signalling endows cancer cells with the ability to form lung metastasis from previously established liver lesions. We also show that patients with the rs4939827 CRC-susceptibility locus diagnosed with CRC tend to develop tumors with greater invasiveness (as measured by the pT stage).
Parte de esta investigación consiste en explorar los mecanismos involucrados en el patrón metastático de CCR. Asimismo usamos datos epidemiológicos donde evaluamos la asociación entre el polimorfismo intrónico de SMAD7 (rs4939827, 18q21) con el genotipo y características tumorales. En el primer proyecto usamos un modelo murino de metástasis hepáticas para crear un derivado celular con alto tropismo metastático a hígado y pulmón. Mediante análisis de expresión de genes usando chips de transcripción identificamos 194 genes diferencialmente expresados El análisis de muestras clínicas mostró que aquellos pacientes cuyo tumor presentaba bajos niveles de p38 sufrían una mayor frecuencia de metástasis al pulmón, pero no a otros órganos. Al tratar ratones que habían desarrollado metástasis hepáticas derivadas de la línea celular parental con un inhibidor específico de p38, vimos que se incrementaba la afinidad metastática al pulmón. Evidenciamos que p38, a través del silenciamiento de PTHLH, en el derivado celular altamente metastático disminuía su capacidad de colonizar el pulmón. Demostramos que PTHLH induce la apoptosis de células humanas de endotelio pulmonar a través del factor AIFM1, facilitando que las células metastáticas puedan extravasarse al pulmón. En el segundo proyecto evaluamos la asociación de un polimorfismo intrónico del gen SMAD7 con el fenotipo y varias características moleculares del tumor. Para ello empleamos 1509 casos de cáncer de colon y recto y 2307 controles emparejados anidados en las cohortes Nurses Health Study y Health Professionals Follow-up Study. Encontramos que el alelo de menor frecuencia de rs4939827 (G) se asociaba con un menor riesgo de desarrollar un CCR con un estadio pT1 o pT2 [razón de odds (OR) ajustada, 0.73; intervalo de confianza al 95\% (CI) 0.62-0.87] pero no con tumores con estadio pT3 o pT4 (OR ajustada, 1.07; 95\% CI 0.93-1.23, valor p de heterogeneidad = 1.2 x 10-4). La asociación entre el polimorfismo de rs4939827 y CCR también difería significativamente según la metilación de RUNX3 (valor p de heterogeneidad = 0.005). Entre aquellos pacientes diagnosticados con CCR, el alelo de menor frecuencia de rs4939827 (G) estaba significativamente asociado con peor supervivencia (hazards ratio, 1.20; 95\% CI, 1.02-1.42).
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Koo, V. S. W. "Bioimaging and quantitative analysis of bladder cancer invasion." Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.484961.

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TGF-beta1 is known to induce changes tumour morphology and motility which are associated with invasion and metastasis via the phenomenon of epithelial-mesenchymal transition (EMD. Although morphology and motility can be determined in vitro, tumour invasion and metastasis are best investigated in an animal model that can be monitored. The aim of this study was to quantify the effects ofTGF-bT;ta1 on AY-27 bladder tumour and to establish DsRed2 fluorescence monitoring in the AY-27/F344 Fisher rat bladder tumour model using IVIS®200 imaging system. Using cbnventional microscopic assessment, scratch wound and Matrigel assays, we showed that TGF-beta1 induces spindle-shape morphology and significantly increased the motility and invasion in AY-27 cells. Preliminary data showed decreased expression of cytokeratin 18 and polarised distribution of vimentin of TGF-beta1 treated cells, indicating the occurrence of EMT. We also developed the Spindle Index assay that objectively quantified morphology change; and invented a novel chemo-attractant based Koo Assay of Migration which quantified tumour motility. These novel assays concurred with the above reference assays and can serve as an adjunctive investigative tool. DsRed2 was transfected into AY-27 using Lipofectamine2000 and the fluorescent intensity and stability were quantified using IVIS®200 and phase-contrasUfluorescent microscopy. However. the DsRed2 fluorescence intensity was not bright or stable. In addition. the DsRed2 transfection has altered the. morphology and growth characteristics of the cell. Instead, we used tdTomato, a variant of DsRed, and found it superior to DsRed2 in the fluorescent intensity and stability and it did not alter the characteristics of AY-27 cells. We showed that fluorescence detection of SUbcutaneously injected AY-27/tdTomato in F344 rat was successful using IVIS®200. However. intravesical fluorescence detection was hampered due to the thick rat tissue overlying the bladder. We suggest that f1uorescently tagged bladder or other deep intra-abdominal tumour model in rats may not be suitable for monitoring using IVIS®200.
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Marchesin, Valentina. "Role of ARF6 in breast cancer cell invasion." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066297/document.

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La migration des cellules tumorales à travers la matrice extracellulaire dépend de l'activité d'une métalloprotéase matricielle, MT1-MMP, ancrée à la membrane plasmique. MT1-MMP accumule aux invadopodes, des protrusions membranaires à base d'actine responsables de la dégradation de la matrice. La petite protéine G ARF6 est impliquée dans la régulation du trafic membranaire et dans le remodelage du cytosquelette d'actine. Dans mon travail de thèse, j'ai montré qu'ARF6 et deux de ses protéines effectrices JIP3 et JIP4, sont nécessaires à l'exocytose de MT1-MMP au niveau des invadopodes et, par conséquent, à la capacité des cellules tumorales à remodeler la matrice extracellulaire et migrer à travers un environnement matriciel tridimensionnel. ARF6, à travers son interaction avec JIP3/4, contrôle négativement l'activité du complexe dynactine/dynéine, un moteur moléculaire qui se déplace en direction du bout (-) des microtubules, et donc la clairance des endosomes MT1-MMP à partir de la périphérie cellulaire. En plus dans des échantillons humaines ARF6 est accumulée au niveau de la membrane plasmique, avec MT1-MMP, dans un sous-groupe de carcinomes mammaires agressifs, en confirmant donc l'implication d'un axe ARF6-JIP3/JIP4-MT1-MMP dans le processus invasif du cancer du sein. Dans une deuxième étude, j'ai montré que l'hyperactivation d'ARF6 induit un réarrangement important du cytosquelette d'actine à la surface ventrale des cellules tumorales mammaires et contribue à l'activation et au ciblage de Rac1 au front cellulaire. Mon travail a permis d'identifier de nouveaux mécanismes moléculaires par lesquels ARF6 contribue au programme invasif des cellules tumorales mammaires
The ability of cancer cells to traffic through the extracellular matrix relies on the action of the membrane-anchored matrix metalloprotease MT1-MMP. MT1-MMP is exocytosed to invadopodia, the actin-based membrane protrusions responsible for matrix degradation. The small GTP-binding protein ARF6 is known to coordinate post-endocytic recycling and actin cytoskeletal organization at the plasma membrane and was shown to be up-regulated in breast cancer cells. In my PhD work I showed that ARF6 and two of its effectors JIP3 and JIP4 are required for MT1-MMP endosomes intracellular positioning and exocytosis at invadopodia and consequently for tumor cells ability to remodel the matrix and invade through a three-dimensional matrix environment. ARF6, through the interaction with JIP3/4, negatively controls the activity of the minus-end-directed microtubule motor dynactin/dynein, thus negatively regulating the clearance and inward movement of MT1-MMP endosomes from the cell periphery. In human samples ARF6 is accumulated at the plasma membrane, together with MT1-MMP, in a subset of highly aggressive breast carcinomas, thus corroborating the ARF6-JIP3/JIP4-MT1-MMP axis in breast cancer invasion. In a second study I addressed the contribution of ARF6 activation on actin cytoskeleton remodeling in breast cancer cells. ARF6 links epidermal growth factor receptor signaling to Rac1 activation and targeting to the leading edge where it activates the SCAR/WAVE complex and regulates ventral actin polymerization during lamellipodia extension. Collectively my work identifies novel molecular mechanisms through which ARF6 contributes to the invasive program of breast tumor cells
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Books on the topic "Cancer and invasion"

1

Leong, Stanley P. L., ed. From Local Invasion to Metastatic Cancer. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-087-8.

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Brunson, Kenneth W., ed. Local Invasion and Spread of Cancer. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-1093-5.

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Mareel, Marc M. Mechanisms of invasion and metastasis. Boca Raton: CRC Press, 1991.

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1959-, Mikkelsen Tom, ed. Brain tumor invasion: Biological, clinical, and therapeutic considerations. New York: Wiley-Liss, 1998.

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Brown, James Stephen. Invasion of the mandible in oral cancer. Birmingham: University of Birmingham, 1994.

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Kagan, A. Robert, and Richard J. Steckel, eds. Practical Approaches to Cancer Invasion and Metastases. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-84885-8.

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Wells, Alan, ed. Cell Motility in Cancer Invasion and Metastasis. Berlin/Heidelberg: Springer-Verlag, 2006. http://dx.doi.org/10.1007/b103440.

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Heino, Jyrki, and Veli-Matti Ka ha ri. Cell invasion. Georgetown, Tex: Landes Bioscience, 2002.

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S, Lakshmi M., ed. The genetics of cancer: Genes associated with cancer invasion, metastasis, and cell proliferation. San Diego: Academic Press, 1997.

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Mark, Scholz, ed. Invasion of the prostate snatchers: No more unnecessary biopsies, radical treatment or loss of sexual potency. New York: Other Press, 2010.

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Book chapters on the topic "Cancer and invasion"

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Gilcrease, Michael Z. "Invasion." In Encyclopedia of Cancer, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_3133-2.

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Gilcrease, Michael Z. "Invasion." In Encyclopedia of Cancer, 2344–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_3133.

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Gilcrease, Michael Z. "Invasion." In Encyclopedia of Cancer, 1904–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_3133.

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Mareel, M. M. "Invasion, Matrix Degradation, Angiogenesis, Motility." In Cancer Metastasis, 219–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74236-1_29.

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Xu, Ying, Juan Cui, and David Puett. "Understanding Cancer Invasion and Metastasis." In Cancer Bioinformatics, 253–78. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1381-7_10.

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Takahashi, Akiko. "Gastric Cancer: SM1 Invasion." In Endoscopic Diagnosis of Superficial Gastric Cancer for ESD, 85–90. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-54469-2_11.

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Wang, Fengqiang, and David A. Fishman. "Lysophosphatidic Acid and Invasion." In Cancer Treatment and Research, 269–96. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-98094-2_13.

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Gabbert, H. E. "In Vivo Observations on Tumor Invasion." In Cancer Metastasis, 55–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74236-1_8.

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Viapiano, Mariano S., and Sean E. Lawler. "Glioma Invasion: Mechanisms and Therapeutic Challenges." In CNS Cancer, 1219–52. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-553-8_49.

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Foulk, Russell, and Olga Genbacev. "Trophoblast Implantation Versus Tumor Invasion." In Cancer and Pregnancy, 267–76. London: Springer London, 2001. http://dx.doi.org/10.1007/978-1-4471-0707-1_21.

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Conference papers on the topic "Cancer and invasion"

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Zielinski, Rachel, Cosmin Mihai, and Samir Ghadiali. "Multi-Scale Modeling of Cancer Cell Migration and Adhesion During Epithelial-to-Mesenchymal Transition." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53511.

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Cancer is a leading cause of death in the US, and tumor cell metastasis and secondary tumor formation are key factors in the malignancy and prognosis of the disease. The regulation of cell motility plays an important role in the migration and invasion of cancer cells into surrounding tissues. The primary modes of increased motility in cancerous tissues may include collective migration of a group of epithelial cells during tumor growth and single cell migration of mesenchymal cells after detachment from the primary tumor site [1]. In epithelial cancers, metastasizing cells lose their cell-cell adhesions, detach from the tumor mass, begin expressing mesenchymal markers, and become highly motile and invasive, a process known as epithelial-to-mesenchymal transition (EMT) (Fig. 1) [2]. Although the cellular and biochemical signaling mechanisms underlying EMT have been studied extensively, there is limited information about the biomechanical mechanisms of EMT. In particular, it is not known how changes in cell mechanics (cell stiffness, cell-cell adhesion strength, traction forces) influence the detachment, migration and invasion processes that occur during metastasis.
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Al-Atieh, Noor, Salma Ahmad, Hanan Nazar, and Allal Ouhtit. "Anti-cancer properties of Microalgae (T1) Extract in Breast Cancer Cell Lines." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0154.

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Breast cancer (BC), a worldwide health issue, is the most common malignant cancer in women in Gulf region, including the State of Qatar. Unfortunately, malignant tumors has the capability to metastasis, which involves both migration and invasion of cancer cells which are the most threatening aspects of cancer (McSherry et al., 2007). Consequently, researchers have concentrated on Complementary and Alternative medicine (CAM) modalities, as conventional medicine has been facing various challenges such as; poor understanding of the mechanisms with BC proliferation and invasion within various groups of patients, drug resistance, and the failure of current therapies to completely cure the disease. A significant CAM method have been raised which is the treatment with herbs and extracts derived from seeds, leaves, fruits and roots of plants; each of these invariably represents a combination of several bioactive compounds. Our biofuel has provided us with a crude extract of a microalgae coded as T1 that consist of carotenoids, chlorophyll a, and chlorophyll b. Carotenoids is a bioactive molecule that inhibits the proliferation, migration, invasion and induce apoptosis to tumor cells.
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Ouldamer, L. "EP945 Lymphovascular invasion in ovarian cancer." In ESGO Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/ijgc-2019-esgo.991.

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Soucy, P., W. Ehringer, C. Klinge, H. Frieboes, and A. Gobin. "An Innovative Approach for Curcumin Delivery for Breast Cancer Using Albumin Nanoparticles." In ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93295.

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Triple-negative breast cancer (TNBC) accounts for ∼25% of breast cancer among premenopausal African-American and Latino women1. Curcumin (diferuloylmethane; CCM), a natural polyphenol extracted from turmeric, has chemopreventive and chemotherapeutic activity in various cancers 2,3 and inhibits growth and invasion of TNBC/basal-like MDA-MB-231 human breast cancer cells 4. CCM has been reported to affect all stages of tumor progression and metastases due to its interactions with multiple targets. We employ a novel approach utilizing both computational and experimental modeling to characterize and analyze TNBC and the 3D tumor microenvironment responses to albumin bound CCM particles (ACP) versus CCM alone.
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Ranade, Rohit Raghunath. "Preoperative and intraoperative assesment of myometrial invasion and histological grade in endometrial cancer: Role of MRI and frozen section." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685336.

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Introduction: The role of systematic lymphadenectomy in clinically early stage endometrial cancer is controversial. A number of factors can predict lymph node metastasis including myometrial invasion, tumor grade in endometrial cancers. The purpose of the present study is to evaluate the accuracy of preoperative MRI and intraoperative frozen section in determining the depth of myometrial invasion, cervical involvement, tumor size and lymph nodal status. We also studied the accuracy of preoperative endometrial biopsy and intraoperative frozen section in determining the grade of the tumor. Materials and Methods: Medical records of 235 consecutive cases of clinically early stage endometrial cancer were reviewed retrospectively. A record of depth of myometrial invasion, tumor size, cervical involvement and presence of enlarged lymph nodes was made on a preoperative MRI. Similarly depth of myometrial invasion, tumor size, cervical involvement and grade of the tumor were recorded on an intraoperative frozen section. The grade of the tumor was also recorded on a preoperative endometrial biopsy. Standard statistical calculations were used. Results: The sensitivity and specificity of MRI for myometrial invasion for the first 160 cases were 81.3 and 75%, respectively while that for frozen section were 80 and 96.2%, respectively. For tumor grade the sensitivity and specificity of preoperative endometrial biopsy were 60 and 95.6%, respectively while that of frozen section were 53.8 and 97.6%, respectively. For cervical involvement the sensitivity of MRI and frozen section was 62.5 and 98.4%, respectively. Updated results of the entire cohort of 235 cases will be presented at the conference if selected. Conclusion: Although the sensitivity of both frozen section and MRI for predicting deep myometrial invasion was similar (80 vs 81.3%) but the specificity (96.2 vs 75%) and negative predictive value (92.7 vs 88.2%) of frozen section were superior to MRI. Both preoperative biopsy and intraoperative frozen section had low sensitivity (60 vs 53.8%) for detecting a high grade lesion.
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Fouzat, Arij. "Elaeagnus Angustifolia extract inhabits cell invasion of human colorectal cancer cells and increases the survival rate of the Drosophila colon cancer model." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0103.

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Colorectal cancer (CRC), the third most common type of cancer in the world, is an aggressive type of cancer with high tendency to metastasize and invade to other tissues and distant organs. Traditional CRC treatment regimen includes 5-fluorouracil (5-FU); however, tumors develop a resistance against these drugs, apart from the severe side effects that develop upon these therapies. Nowadays, traditional medicinal plants are the focus of increased interest as a source for new potential drugs, particularly those that serve as anti-cancerous agents. Elaeagnus angustifolia (EA) is a medicinal plant that can be used traditionally to manage several human ailments including cancers especially oral and HER2-positive breast cancer as recently reported by our group. However, the effect of EA flower extract on human CRC has not been investigated yet. Therefore, EA effect was explored in vitro using KRAS CRC cell lines (HCT-116 and LoVo) and in vivo using transgenic Drosophila melanogaster model for KRAS gene, which is known to develop CRC. Our results from the in vitro investigations revealed that EA flower extract significantly inhibits cell motility and invasion in addition to colony formation. Moreover, we found that EA extract modulates the epithelial–mesenchymal transition (EMT) event and its related genes; EMT is a known hallmark of cancer invasion and metastasis. More significantly, our in vivo data pointed out that EA extract increases the survival rate of KRAS mutation D. melanogaster model. Our findings implicate that EA extract may possess chemo-preventive effects against human CRC.
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Moreno, Andre, Kimberly Masiero Cola, Larissa Heberle, and Marcelo Moreno. "RELATIONSHIP BETWEEN IMMUNOHISTOCHEMICAL CHARACTERIZATION AND FORM OF DIAGNOSIS OF BREAST CANCER." In Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1008.

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Introduction: Breast cancer is the most incident neoplasia among Brazilian women. According to immunogenetic characteristics, it is possible to verify that malignant breast neoplasms with greater biological activity would be those classified as luminary B, HER2+ and triple-negative, and that the one with the lowest biological activity would be the luminal subtype A. Thus, a mammography would be more likely to detect cancers with a low degree of biological characteristics such as “luminal A”. On the other hand, mammary carcinomas with greater potential for systemic dissemination show faster growth in the breast parenchyma and are detected predominantly by self-examination. Knowledge of this difference in the clinical behavior of mammary malignant neoplasms is important for the diagnosis of “interval” breast cancers, that is, breast cancer that appears in the period between the performance of annual screening mammograms. Objectives: Verify the relationship between immunohistochemical characterization of malignant breast neoplasms and the finding that motivated the medical consultation, in women with breast cancer and residents of Western Santa Catarina, Brazil. Methods: Observational, cross-sectional study, which included women diagnosed with breast cancer and treated at an oncology referral center in the city of Chapecó, state of Santa Catarina, Brazil, from January 2000 to December 2016. Patients that presented medical records whose main complaint was towards the diagnosis of breast cancer were included (example: nodule diagnosed by imaging exams, self-examination, clinical examination). Besides this, the breast injury related to this complaint should have been breast cancer diagnosed by an anatomopathological examination and an immunohistochemistry study. The project was developed in accordance to CEP/UNOCHAPECO no. 1819869. Results: Data from 209 patients were analyzed, from which 83 (39.7%) cases of breast cancer were detected by a mammography examination; 115 (55%) cases by breast self-examination and 11 (5.2%) cases by other forms of examination, which included clinical breast examination done by a doctor, magnetic resonance imaging and ultrasound. The luminal A immunohistochemical profile was more prevalent among patients who underwent breast cancer detection through mammography (62.6%). There was a correlation between lymph node invasion and the screening method, in which 78.6% of cancers detected by self-examination showed expansion to lymph nodes, while those detected by mammography presented an invasion rate of 45.7% (p=0.002). Conclusions: Breast cancer with immunohistochemical characterization, related to greater biological activity, were most often detected by self-examination, while neoplasms with indolent development were diagnosed predominantly by mammography.
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Mohamed, Islam, Ahmed Moahmed, Mennatallah Abdelkader, Alaaeldin Saleh, and Ala-Eddin Al-Moustafa. "Elaeagnus Angustifolia: a Promising Medicinal Plant for Cancer Theraby." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0124.

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Introduction: Elaeagnus angustifolia (EA) is a medicinal plant that has been used for centuries in treating many human diseases, in the Middle East, including fever, amoebic dysentery, gastrointestinal problems. However, the effect of EA plant extract on human cancer progression especially oral malignancy has not been investigated yet. Thus, first we examined the effect of EA flower extract on angiogenesis in ovo, and on selected parameters in human oral cancer cells. Materials and methods: Chorioallantoic membranes (CAMs) of chicken embryos at 3-7 days of incubation were used to assess the effect EAflower plant extract on angiogenesis. Meanwhile, cell proliferation, soft agar, cell cycle, cell invasion and cell wounding assays were performed to explore the outcome of EA plant extract on FaDu and SCC25 oral cancer cell lines. On the other hand, western blot analysis was carried out to evaluate E-cadherin and Erk1/Erk2 expression and activation, respectively, in FaDu and SCC25 under the effect of EA extract. Results: Our data show that EA extract inhibits cell proliferation and colony formation, in addition to the initiation of Scell cycle arrest and reductionof G1/G2 phases. In parallel, EA extract provokes differentiation to an epithelial phenotype “mesenchymal-epithelial transition: MET” which is the opposite of “epithelial-mesenchymal transition, EMT”: an important event in cell invasion and metastasis. Thus, EA extract causes a dramatic decrease in cell motility and invasion abilities of FaDu and SCC25 cancer cells in comparison with their controls. These changes are accompanied by an up-regulation of E-cadherin expression. The molecular pathway analysis of the EA flower extract reveals that it can inhibit the phosphorylation of Erk1/Erk2, which could be behind the inhibition of angiogenesis, the initiation of MET event and the overexpression of E-cadherin. Conclusions: Our findings indicate that EA plant extract can downgrade human oral cancer progression by the inhibition of angiogenesis and cell invasion via Erk1/Erk2 signaling pathways.
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Mohamed, Mai, and Patricia Kruk. "Abstract 5080: Amylase overexpression promotes ovarian cancer invasion." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-5080.

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Griggs, J., E. Gillespie, D. Hanauer, C. Jagielski, M. Sabel, and M. Sorbero. "Obesity and Angiolymphatic Invasion in Primary Breast Cancer." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-5151.

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Reports on the topic "Cancer and invasion"

1

Quaranta, Vito. Extracellular Matrix in Breast Cancer Invasion. Fort Belvoir, VA: Defense Technical Information Center, June 2001. http://dx.doi.org/10.21236/ada398487.

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Bowden, Emma. Collagen-Induced Invasion in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 1998. http://dx.doi.org/10.21236/ada358110.

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3

Covic, Lidija, Nga Nguyen, Athan Kuliopulos, and Roger A. Graham. Pepducin Based Intervention of Breast Cancer Invasion. Fort Belvoir, VA: Defense Technical Information Center, August 2006. http://dx.doi.org/10.21236/ada458458.

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4

Simpson, Kaylene J. RhoGTPase Involvement in Breast Cancer Migration and Invasion. Fort Belvoir, VA: Defense Technical Information Center, March 2008. http://dx.doi.org/10.21236/ada482256.

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Ying, Hongan, Jinfan Shao, Xijuan Xu, Wenfeng Yu, and Weiwen Hong. Perineural Invasion is an Indication of Adjuvant Chemotherapy in Node Negative Colorectal cancer. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2021. http://dx.doi.org/10.37766/inplasy2021.12.0103.

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Abstract:
Review question / Objective: Perineural invasion (PNI) is a possible route for metastatic spread in various cancer types, including colorectal cancer (CRC). PNI is linked to poor prognosis. For patients with lymph node positive colorectal cancer, a number of large-scale RCT studies have confirmed that they can benefit from chemotherapy, but there are still many controversies about whether colorectal patients with negative lymph nodes need adjuvant chemotherapy. At present, there is a general consensus that patients with stage II colorectal cancer who have risk factors such as PNI+ need chemotherapy. However, there are many recent literatures that show that patients with stage II colorectal cancer with nerve invasion risk factors can not prolong the OS and DFS of patients. At the same time, chemotherapy increases the toxicity, economic and mental burden of patients. Therefore, we hope to write this review to summarize the current research findings and provide some clinical guidance on whether patients with lymph node negative colon cancer who have perineural invasion should receive chemotherapy. Condition being studied: Patients with high-risk such as PNI+ stage II colon cancer (CC) are recommended to undergo adjuvant chemotherapy (ACT). However, whether such patients can benefit from ACT remains unclear. And recently studies shown that, ACT had no significant benefit among patients with PNI.
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Simpson, Kaylene J. Rho GTPase Involvement in Breast Cancer Migration and Invasion. Fort Belvoir, VA: Defense Technical Information Center, March 2005. http://dx.doi.org/10.21236/ada435395.

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Graves, David E. Toll Like Receptor-9 Mediated Invasion in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada567128.

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Selander, Katri. Toll Like Receptor-9 Mediated Invasion in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada567243.

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Eckert, Mark A. Mechanism of Twist1-Induced Invasion in Breast Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, January 2012. http://dx.doi.org/10.21236/ada588172.

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Graves, David E. Toll-Like Receptor-9-Mediated Invasion in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada549125.

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