Relevant bibliographies by topics / Invasive phenotype

Academic literature on the topic 'Invasive phenotype'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Invasive phenotype"

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Golmohammadi, Rahim, Mohammad Reza Mohajeri, Alireza Mosavi Jarrahi, Ali Reza Moslem, Akbar Pejhan, and Ali Gohari. "Histopathologic Characteristics of Invasive and Non-invasive Ductal Tumors have Relationship with Different Phenotypes of ER / PR Receptors in Breast Cancer Patients." Asian Pacific Journal of Cancer Biology 6, no. 3 (July 9, 2021): 181–85. http://dx.doi.org/10.31557/apjcb.2021.6.3.181-185.

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Objective: Contradictory reports have been published regarding the expression levels of the hormone receptors of estrogen and progesterone (ER / PR) and theirclinical importance in diagnosis of breast cancer. The aim of this study was to evaluate the relationship between pathological features of invasive and non-invasive ductal tumors by different ER / PR phenotypes. Methods: This descriptive-analytical study was performed on 74 specimens of breast cancer referred to Isfahan Hospitals for diagnosis between 2015 - 2018. After fixation of the specimens in formalin, tissue passage, cross section and H / E staining, the specimens were divided into two groups: non- invasive and Invasive ductal Carcinoma. After removing of mask, expression of different ER / PR phenotypes was performed using primary monoclonal antibody and immunohistochemically methods. Results: From 74 malignant specimens, 61 (82.4%) were in the category of invasive ductal tumors and 13 cases (17.6%) were in the category of non-invasive ductal tumors. Out of 73 patients with positive ER or PR phenotype 47 samples (63.5%) had ER + / PR +phenotypes, 6 samples had (8.1%) ER+ / PR –phenotype, 20 samples (27%) had ER- / PR + phenotype and only one sample (1.4%) had the ER- / PR- phenotype and was in the category of invasive ductal tumors. There was not detected ER- / PR- phenotype expression in non-invasive ductal tumor. Further analysis showed that there were not significant difference between ER / PR phenotype and tumor stage (p =0.36) or with tumor Grade (P=0.38), high age of menopause or post menopause (P> 0.05). Conclusion: Our data shows that expression of ER- / PR- phenotype only was detected in invasive ductal tumor. It is thought that the tumor type maybe affects the expression of different types of ER / PR hormone receptor phenotypes in breast cancer patients.
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Akeda, Yukihiro, Kenichi Nagayama, Koichiro Yamamoto, and Takeshi Honda. "Invasive Phenotype ofVibrio parahaemolyticus." Journal of Infectious Diseases 176, no. 3 (September 1997): 822–24. http://dx.doi.org/10.1086/517312.

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Márquez, A., H. J. Fino, M. Correa, P. Tonino, and L. Sosa. "Ultrastructure of Leiomyosarcoma Invasive Phenotype." Microscopy and Microanalysis 3, S2 (August 1997): 19–20. http://dx.doi.org/10.1017/s143192760000698x.

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Malignant tumors are known to have an heterogeneous cell population. Metastases are supposed to be formed by subpopulations with high metastatic capability. These metastatic cells constitute the so called invasive phenotype. In that order of ideas, metastases could be pathologically different from their parent tumors if the invasive phenotype had distinct morphological features. The similarities or differences between primary tumors and their metastases have not been adequately studied at the ultrastructural level. In this work we report an electron microscopic study of liver leiomyosarcoma metastases which shows alterations not described in primary tumors of that kind.Biopsies of liver metastases from a colon leiomyosarcoma were surgically obtained. Samples were processed with routine techniques for transmission electron microscopy and observed in a Hitachi H-500 electron microscope.Some alterations usually observed in primary leiomyosarcomas were seen. They were presence of myofilaments with focal densities, nuclear changes, swollen mitochondria, and abundance of rough endoplasmic reticulum (Fig. 1).
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Čermák, Vladimír, Aneta Škarková, Ladislav Merta, Veronika Kolomazníková, Veronika Palušová, Stjepan Uldrijan, Daniel Rösel, and Jan Brábek. "RNA-seq Characterization of Melanoma Phenotype Switch in 3D Collagen after p38 MAPK Inhibitor Treatment." Biomolecules 11, no. 3 (March 17, 2021): 449. http://dx.doi.org/10.3390/biom11030449.

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Melanoma phenotype plasticity underlies tumour dissemination and resistance to therapy, yet its regulation is incompletely understood. In vivo switching between a more differentiated, proliferative phenotype and a dedifferentiated, invasive phenotype is directed by the tumour microenvironment. We found that treatment of partially dedifferentiated, invasive A375M2 cells with two structurally unrelated p38 MAPK inhibitors, SB2021920 and BIRB796, induces a phenotype switch in 3D collagen, as documented by increased expression of melanocyte differentiation markers and a loss of invasive phenotype markers. The phenotype is accompanied by morphological change corresponding to amoeboid–mesenchymal transition. We performed RNA sequencing with an Illumina HiSeq platform to fully characterise transcriptome changes underlying the switch. Gene expression results obtained with RNA-seq were validated by comparing them with RT-qPCR. Transcriptomic data generated in the study will extend the present understanding of phenotype plasticity in melanoma and its contribution to invasion and metastasis.
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Shelley, Greg, Jinlu Dai, Jill M. Keller, and Evan T. Keller. "Pheno-SELEX: Engineering Anti-Metastatic Aptamers through Targeting the Invasive Phenotype Using Systemic Evolution of Ligands by Exponential Enrichment." Bioengineering 8, no. 12 (December 13, 2021): 212. http://dx.doi.org/10.3390/bioengineering8120212.

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Multiple methods (e.g., small molecules and antibodies) have been engineered to target specific proteins and signaling pathways in cancer. However, many mediators of the cancer phenotype are unknown and the ability to target these phenotypes would help mitigate cancer. Aptamers are small DNA or RNA molecules that are designed for therapeutic use. The design of aptamers to target cancers can be challenging. Accordingly, to engineer functionally anti-metastatic aptamers we used a modification of systemic evolution of ligands by exponential enrichment (SELEX) we call Pheno-SELEX to target a known phenotype of cancer metastasis, i.e., invasion. A highly invasive prostate cancer (PCa) cell line was established and used to identify aptamers that bound to it with high affinity as opposed to a less invasive variant to the cell line. The anti-invasive aptamer (AIA1) was found to inhibit in vitro invasion of the original highly invasive PCa cell line, as well as an additional PCa cell line and an osteosarcoma cell line. AIA1 also inhibited in vivo development of metastasis in both a PCa and osteosarcoma model of metastasis. These results indicate that Pheno-SELEX can be successfully used to identify aptamers without knowledge of underlying molecular targets. This study establishes a new paradigm for the identification of functional aptamers.
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van de Merbel, Arjanneke F., Onno van Hooij, Geertje van der Horst, Cindy C. M. van Rijt-van de Westerlo, Maaike H. van der Mark, Henry Cheung, Jan Kroon, et al. "The Identification of Small Molecule Inhibitors That Reduce Invasion and Metastasis of Aggressive Cancers." International Journal of Molecular Sciences 22, no. 4 (February 8, 2021): 1688. http://dx.doi.org/10.3390/ijms22041688.

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Transformed epithelial cells can activate programs of epithelial plasticity and switch from a sessile, epithelial phenotype to a motile, mesenchymal phenotype. This process is linked to the acquisition of an invasive phenotype and the formation of distant metastases. The development of compounds that block the acquisition of an invasive phenotype or revert the invasive mesenchymal phenotype into a more differentiated epithelial phenotype represent a promising anticancer strategy. In a high-throughput assay based on E-cadherin (re)induction and the inhibition of tumor cell invasion, 44,475 low molecular weight (LMW) compounds were screened. The screening resulted in the identification of candidate compounds from the PROAM02 class. Selected LMW compounds activated E-cadherin promoter activity and inhibited cancer cell invasion in multiple metastatic human cancer cell lines. The intraperitoneal administration of selected LMW compounds reduced the tumor burden in human prostate and breast cancer in vivo mouse models. Moreover, selected LMW compounds decreased the intra-bone growth of xenografted human prostate cancer cells. This study describes the identification of the PROAM02 class of small molecules that can be exploited to reduce cancer cell invasion and metastases. Further clinical evaluation of selected candidate inhibitors is warranted to address their safety, bioavailability and antitumor efficacy in the management of patients with aggressive cancers.
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Schuster, A., V. Neirinckx, E. Klein, P. V. Nazarov, A. Oudin, A. Muller, F. Azuaje, C. Herold-Mende, B. Klink, and S. P. Niclou. "P11.26 Genome-wide shRNA screen identifies candidate genes driving glioblastoma invasion." Neuro-Oncology 21, Supplement_3 (August 2019): iii48. http://dx.doi.org/10.1093/neuonc/noz126.172.

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Abstract BACKGROUND A major hallmark of glioblastoma (GBM) is its highly invasive capacity, contributing to its aggressive behaviour. Since invasive cells cannot be easily removed by surgery or irradiation, they are left behind and eventually result in lethal recurrence. Therefore, a better understanding of the invasion process and of the key molecular players underlying the invasive capacities of GBM may lead to the identification of new therapeutic targets for GBM patients. MATERIAL AND METHODS To identify candidate genes responsible for invasion, a genome-wide shRNA screen was performed in patient-derived GBM sphere cultures. The phenotype of the most promising candidate was validated in in vitro invasion assays, ex vivo brain slice cultures and in vivo orthotopic xenografts in mice. Gene knockdown in invasive GBM cell lines was compared with overexpression in non-invasive cells. RNA sequencing of knockdown cells, along with the generation of deletion constructs were applied to uncover the mechanisms regulating invasion. RESULTS Through a whole genome shRNA screen, a zinc-finger containing protein was identified as an invasion essential candidate gene. Knockdown of this gene confirmed a strong decrease in invasion capacity in two highly invasive GBM cell lines. In contrast, gene overexpression switched non-invasive GBM cells to an invasive phenotype. Deletion of either one or both zinc-finger motifs led to decreased invasion indicating that the two zinc-finger motifs are essential for regulating invasion. Mutation of the nuclear localisation signal resulted in retention of the protein in the cytoplasm and loss of the invasion phenotype demonstrating that the protein activity is required in the nucleus. Gene expression analyses revealed that invasion-related genes are significantly regulated by the candidate gene once it is localized in the nucleus. CONCLUSION We identified a zinc-finger containing protein as a novel driver of GBM invasion, presumably through a transcription factor activity resulting in the induction of an invasive transcriptional program. This protein and its downstream pathway may represent a novel promising target to overcome invasive capacities in GBM.
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Mukhopadhyay, Utpal K., Patrick Mooney, Lilly Jia, Robert Eves, Leda Raptis, and Alan S. Mak. "Doubles Game: Src-Stat3 versus p53-PTEN in Cellular Migration and Invasion." Molecular and Cellular Biology 30, no. 21 (August 23, 2010): 4980–95. http://dx.doi.org/10.1128/mcb.00004-10.

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ABSTRACT We have recently shown that Src induces the formation of podosomes and cell invasion by suppressing endogenous p53, while enhanced p53 strongly represses the Src-induced invasive phenotype. However, the mechanism by which Src and p53 play antagonistic roles in cell invasion is unknown. Here we show that the Stat3 oncogene is a required downstream effector of Src in inducing podosome structures and related invasive phenotypes. Stat3 promotes Src phenotypes through the suppression of p53 and the p53-inducible protein caldesmon, a known podosome antagonist. In contrast, enhanced p53 attenuates Stat3 function and Src-induced podosome formation by upregulating the tumor suppressor PTEN. PTEN, through the inactivation of Src/Stat3 function, also stabilizes the podosome-antagonizing p53/caldesmon axis, thereby further enhancing the anti-invasive potential of the cell. Furthermore, the protein phosphatase activity of PTEN plays a major role in the negative regulation of the Src/Stat3 pathway and represses podosome formation. Our data suggest that cellular invasiveness is dependent on the balance between two opposing forces: the proinvasive oncogenes Src-Stat3 and the anti-invasive tumor suppressors p53-PTEN.
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Gajić, Ina, Miloš Marković, Dušan Kekić, Sunčica Popović, Vera Mijač, Lazar Ranin, and Nataša Opavski. "Serotypes and antimicrobial susceptibility of invasive 'Streptococcus pneumoniae' isolated in Serbia in 2012-2013." Medicinska istrazivanja 50, no. 2 (2016): 49–53. http://dx.doi.org/10.5937/medist1602049g.

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The aim of this study was to: determine susceptibility patterns of invasive Streptococcus pneumoniae to antimicrobial agents, evaluate macrolide resistance phenotypes and genotypes and identify capsular serotypes among invasive isolates of S. pneumoniae circulating in Serbia. The total of 85 invasive pneumococcal strains, collected during 2012 and 2013, were sent from regional laboratories to the National Reference Laboratory. Susceptibility testing was performed by disk diffusion and E test, while phenotypes and genotypes of macrolide resistant strains were determined by double-test and PCR, respectively. Serotyping was performed by Quelling reaction. The overall penicillin and erythromycin non-susceptibility rates were 14.12% and 28.23%, respectively. Resistance rates were significantly higher in children than in adults and (p<0,01). Co-resistance to penicillin and erythromycin was detected in 7.06% strains. Resistance rates to tetracycline and chloramphenicol were 29.41% and 15.29%, respectively. The rate of multi resistance was 27.06%. cMLS phenotype was detected in 62.5% of all macrolide resistant isolates, while 37.5% expressed M phenotype. All 15 isolates with cMLS phenotype harbored ermB gene and all M isolates harbored mefA. The most common resistant serotypes were 3, 9A and 23F. This study revealed that penicillin and macrolide resistance among invasive pneumococcal isolates is high. Obtained results emphasize the need for continuous monitoring of invasive pneumococcal disease in Serbia.
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Akeda, Yukihiro, Toshio Kodama, Takashige Kashimoto, Vlademir Cantarelli, Yasuhiko Horiguchi, Kenichi Nagayama, Tetsuya Iida, and Takeshi Honda. "Dominant-Negative Rho, Rac, and Cdc42 Facilitate the Invasion Process of Vibrio parahaemolyticus into Caco-2 Cells." Infection and Immunity 70, no. 2 (February 2002): 970–73. http://dx.doi.org/10.1128/iai.70.2.970-973.2002.

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ABSTRACT To clarify the invasive process of Vibrio parahaemolyticus, an invasion assay was performed using cells expressing dominant negative small GTPases of the Rho family. This assay showed that the dominant negative host phenotype facilitates bacterial invasion, suggesting that the mechanism of V. parahaemolyticus invasion differs from that reported for other invasive bacteria.
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Dissertations / Theses on the topic "Invasive phenotype"

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Okoro, Chinyere Kyna. "Invasive Salmonella typhimurium : linking phenotype to genotype." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607714.

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Bloomfield, Kelly Louise, and n/a. "Investigation of the Role of Thioredoxin in the Invasive Phenotype and its Interaction with the Transcription Factor Sp1." Griffith University. School of Biomolecular and Biomedical Science, 2003. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20031021.120018.

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Thioredoxin is a small ubiquitous oxido-reductase found in all species. The highly conserved active site, which facilitates thioredoxins redox activity, contains two redox active cysteine residues. Thioredoxin has numerous protein substrates to which it donates H+ ions and it can also function as a free radical scavenger. Through these activities thioredoxin is able to influence the redox state of not only its protein targets, but also the entire cellular environment. Thioredoxin has been implicated in many biological functions, and one mechanism by which it influences these functions is through interactions with a number of transcription factors including NF-kappa-B and p53. Thioredoxin also has numerous extracellular biological roles. It has been shown that thioredoxin is actively secreted from a number of normal and transformed cell lines including fibroblasts and activated B and T cells. This study investigates the role of thioredoxin in embryonic implantation and cancer cell metastasis, two physiological functions which rely on the same basic processes. Thioredoxin expression has previously been shown to be increased in many cancers. However it has not yet been established whether this increase is a causative or a side effect of the cancerous phenotype. Similarly thioredoxin expression has previously been shown to be increased during different phases of the oestrus cycle and pregnancy. This thesis describes the role of thioredoxin in embryonic implantation using a marmoset model. A thioredoxin cDNA was isolated and subsequently sequenced. Preliminary antibody experiments indicated that the anti human thioredoxin monoclonal antibodies available in our laboratory would recognise marmoset thioredoxin. Subsequently immunocytochemistry using anti human thioredoxin antibodies was carried out on sectioned marmoset uterus and embryonic tissue. The results indicated that thioredoxin is expressed by cells at the embryonic-maternal interface of early implantation sites. Further studies demonstrated that thioredoxin is also expressed and secreted by cultured blastocysts in vitro. This thesis also describes the role of thioredoxin in cancer cell metastasis. Results of this study indicate that thioredoxin is actively involved in facilitating the invasive phenotype of breast cancer cells. The two cell lines utilised were MCF-7, a well differentiated, relatively non-invasive breast cancer cell line; and MDA-MB-231, a poorly differentiated, highly invasive breast cancer cell line. The cell lines were transfected with thioredoxin sense, antisense and 1SS (encodes thioredoxin with both active cysteine residues mutated to serine residues and is thus redox inactive) constructs. The results demonstrate that when endogenous thioredoxin levels are increased, i.e. transfected with a sense thioredoxin construct, the invasive breast cancer cell line MDA-MB-231 becomes more invasive, conversely when endogenous levels are decreased, i.e. transfected with antisense or 1SS constructs, the invasive capacity of these cells decreases. However, when the endogenous level of thioredoxin was manipulated in the relatively non-invasive cell line MCF-7 very little effect was observed. Results also indicate that thioredoxin has the ability to act as a chemoattractant for actively invading breast cancer cells. Both of these functions appear to be dependent on thioredoxin's redox activity. Additional studies described in this thesis have shown that thioredoxin is involved in the regulation of Sp1 in vitro. Sp1 is a transcription factor known to regulate the transcription of a number of genes whose products are intimately involved in the invasive phenotype. The results in this study suggest that Sp1 DNA binding is regulated by thioredoxin such that when reduced by the enzyme its binding to DNA is facilitated. Results also indicate that Sp1 may regulate the transcription of thioredoxin by binding to Sp1 sites within the thioredoxin promoter.
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Bloomfield, Kelly Louise. "Investigation of the Role of Thioredoxin in the Invasive Phenotype and its Interaction with the Transcription Factor Sp1." Thesis, Griffith University, 2003. http://hdl.handle.net/10072/366170.

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Thioredoxin is a small ubiquitous oxido-reductase found in all species. The highly conserved active site, which facilitates thioredoxins redox activity, contains two redox active cysteine residues. Thioredoxin has numerous protein substrates to which it donates H+ ions and it can also function as a free radical scavenger. Through these activities thioredoxin is able to influence the redox state of not only its protein targets, but also the entire cellular environment. Thioredoxin has been implicated in many biological functions, and one mechanism by which it influences these functions is through interactions with a number of transcription factors including NF-_B and p53. Thioredoxin also has numerous extracellular biological roles. It has been shown that thioredoxin is actively secreted from a number of normal and transformed cell lines including fibroblasts and activated B and T cells. This study investigates the role of thioredoxin in embryonic implantation and cancer cell metastasis, two physiological functions which rely on the same basic processes. Thioredoxin expression has previously been shown to be increased in many cancers. However it has not yet been established whether this increase is a causative or a side effect of the cancerous phenotype. Similarly thioredoxin expression has previously been shown to be increased during different phases of the oestrus cycle and pregnancy. This thesis describes the role of thioredoxin in embryonic implantation using a marmoset model. A thioredoxin cDNA was isolated and subsequently sequenced. Preliminary antibody experiments indicated that the anti human thioredoxin monoclonal antibodies available in our laboratory would recognise marmoset thioredoxin. Subsequently immunocytochemistry using anti human thioredoxin antibodies was carried out on sectioned marmoset uterus and embryonic tissue. The results indicated that thioredoxin is expressed by cells at the embryonic-maternal interface of early implantation sites. Further studies demonstrated that thioredoxin is also expressed and secreted by cultured blastocysts in vitro. This thesis also describes the role of thioredoxin in cancer cell metastasis. Results of this study indicate that thioredoxin is actively involved in facilitating the invasive phenotype of breast cancer cells. The two cell lines utilised were MCF-7, a well differentiated, relatively non-invasive breast cancer cell line; and MDA-MB-231, a poorly differentiated, highly invasive breast cancer cell line. The cell lines were transfected with thioredoxin sense, antisense and 1SS (encodes thioredoxin with both active cysteine residues mutated to serine residues and is thus redox inactive) constructs. The results demonstrate that when endogenous thioredoxin levels are increased, i.e. transfected with a sense thioredoxin construct, the invasive breast cancer cell line MDA-MB-231 becomes more invasive, conversely when endogenous levels are decreased, i.e. transfected with antisense or 1SS constructs, the invasive capacity of these cells decreases. However, when the endogenous level of thioredoxin was manipulated in the relatively non-invasive cell line MCF-7 very little effect was observed. Results also indicate that thioredoxin has the ability to act as a chemoattractant for actively invading breast cancer cells. Both of these functions appear to be dependent on thioredoxin's redox activity. Additional studies described in this thesis have shown that thioredoxin is involved in the regulation of Sp1 in vitro. Sp1 is a transcription factor known to regulate the transcription of a number of genes whose products are intimately involved in the invasive phenotype. The results in this study suggest that Sp1 DNA binding is regulated by thioredoxin such that when reduced by the enzyme its binding to DNA is facilitated. Results also indicate that Sp1 may regulate the transcription of thioredoxin by binding to Sp1 sites within the thioredoxin promoter.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
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Thorn, Christopher Charles. "The molecular characteristics of the invasive phenotype in colorectal cancer." Thesis, University of Leeds, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493284.

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The infiltrative growth pattern in colorectal cancer has been demonstrated to confer a poor prognosis particularly in early stage disease. The phenotype demonstrates histological features of aggression and with reference to the contrasting pushing phenotype provides an in vivo model for invasive behaviour which has hitherto not been exploited in the context of molecular biology.
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Casillas, Andrea Lee, Jaime M. C. Gard, and Anne E. Cress. "DNA Damage Response to Ionizing Radiation Defective in the Invasive Cancer Phenotype." Thesis, The University of Arizona, 2015. http://hdl.handle.net/10150/578566.

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The purpose of this study was to determine the differences in DNA damage responses (DDRs) between immortalized normal prostate epithelial cells (PrEC) and prostate cancer cells (DU145). To study the DDRs, two protein markers were used. The first, phosphorylated KRAB Associated Protein 1 (pKAP-1) activates target genes involved in the DDR. The second, phosphorylated H2AX (pH2AX) is required for the assembly of damaged chromatin as well as for activation of checkpoints proteins. Ionizing Radiation (IR) was used to induce DNA damage. Flow Cytometry and Western Blot analyses were used to measure the levels of the proteins when exposed to various doses of IR (0, 2, 4, 8 Gy). In both cell lines, there was a clear dose dependent increase in pH2AX and pKAP-1, however error bars showed that with the pH2AX protein, only the later doses showed significant differences. Fluorescence staining was used to examine the localization of the proteins. Both cell lines showed punctate staining of pH2AX in the nuclei at 8Gy and no staining in unirradiated cells. With pKAP-1, the PrEC cells had punctate staining in the nuclei with 8Gy of radiation whereas the DU145 cells had a diffuse pattern in the nuclei.
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Bradley, Conor Aidan. "c-MET as a key regulator of an invasive and migratory phenotype in colorectal cancer." Thesis, Queen's University Belfast, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.695258.

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In the current study, we initially investigated the molecular mechanisms driving tumour cell migration and invasion in vitro using in-house generated invasive CRC cell line models, with which we reported an association between HGF-independent overexpression and hyper-phosphorylation of c-MET with a mesenchymal, migratory and invasive phenotype. Upon identification of this association, we subsequently demonstrated that RNAi-mediated ablation of c-MET abolished the basal migratory and invasive potential of CRC cell lines, illustrating a key role for c- MET expression in regulation of these phenotypes. Using a molecular pathology based methodology incorporating RNAscope®, a novel quantitative mRNA in situ hybridisation technique, we translated our observations in vivo, whereby we demonstrated that the MET transcript is significantly upregulated in tumour budding foci at the invasive edge of stage III CRC tumours. Upon evaluation of the role of the TME in dictating tumour cell phenotype using an in vitro coculture methodology, we highlighted a role for colonic myofibroblasts in promoting a migratory and invasive phenotype, and minor resistance to MEK1/2 inhibition in KRASMT CRC cell lines. Importantly, subsequent molecular characterisation revealed HG F as a major fibroblast-derived factor that was promoting these phenotypes through phosphorylation of c-MET, whereby neutralisation of HGF could partially abolish the pro-invasive fibroblast-derived signal. Finally, in attempting to assess the role of c-MET as a prognostic biomarker in early stage CRC, we demonstrated an apparent disparity between the prognostic value of MET gene expression and cMET protein expression, whereby only the former could predict poor outcome. Collectively, our study provides pre-clinical rationale for further investigation of therapeutic inhibition of the HGF/cMET pathway in the adjuvant setting to circumvent metastasic dissemination and therefore halt recurrence.
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Frye, Catherine Anne. "Rheumatoid arthritis synovial fibroblasts: Cytokine-induced invasive phenotype and associated mechanism(s) of tissue destruction." Diss., The University of Arizona, 1994. http://hdl.handle.net/10150/186719.

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The invasive and destructive properties of pannus tissue contribute to the loss of cartilage and bone in rheumatoid arthritis (RA). To further analyze the process of cartilage degradation, we have developed an in vitro model which allows for observations of cellular degradation and invasion of a cartilage matrix isolated from porcine knee joints. This matrix contains collagen type II, proteoglycans and glycosaminoglycans, and is similar in composition to human cartilage. Synovial fibroblasts isolated from the pannus tissue of patients with aggressive RA, based on clinical evaluation, demonstrated a highly invasive phenotype in this in vitro model; whereas synovial fibroblasts isolated from pannus tissue of less aggressive RA, based on clinical evaluation, showed a less invasive phenotype. Further characterization of cell-cartilage matrix interactions reveal that RA and normal synovial fibroblasts adhere to a similar degree to cartilage matrix, but this adhesion can be inhibited with arginine-glycine-aspartic acid (RGD) peptides, thus implicating integrins in this attachment process. During the subsequent process of spreading on cartilage matrix, highly invasive RA synovial fibroblasts maintained a round phenotype for a longer duration than normal synovial fibroblasts. Furthermore, with respect to the degradative ability of these cells, the level of expression and secretion of key metalloproteinases was measured, and interstitial collagenase activity was shown to correlate with the RA phenotype, while no expression was detected in normal synovial fibroblasts. By comparison, there was no differential expression of stromelysin, gelatinase A and gelatinase B found in normal synovial fibroblasts versus RA synovial fibroblasts. Normal synovial fibroblast invasion was augmented by culturing these cells in the presence of 5 U/ml IL-1β or 18 U/ml TGFβ whereas, PDGF at 100 ng/ml did not affect normal synovial fibroblast invasion. In addition, normal synovial fibroblasts cultured in 150 U/ml TNFα demonstrated a significant decrease in their ability to invade cartilage matrix. Collectively, these in vitro data suggest that highly invasive synovial fibroblasts correlate with advanced RA clinical disease. Moreover, this invasive phenotype may be due, in part, to decreased spreading ability on the cartilage matrix in addition to interstitial collagenase activity. This model allows for further molecular characterization of the invasive properties of the synovial fibroblast.
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McGarry, Lynn C. "Mediation of transformation by the v-fos oncogene : regulation of the invasive phenotype by histone deacetylases." Thesis, Open University, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403835.

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Longbrake, A. Christina W. "Ecology and invasive potential of Paulownia tomentosa (Scrophulariaceae) in a hardwood forest landscape." Ohio : Ohio University, 2001. http://www.ohiolink.edu/etd/view.cgi?ohiou992358342.

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Meistertzheim, Anne-Leila. "Capacité d'adaptation d'une espèce invasive, l'huître creuse du Pacifique Crassostrea gigas, en région Bretagne." Brest, 2008. http://www.theses.fr/2008BRES2030.

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L’huître creuse du Pacifique Crassostrea gigas est une espèce d’intérêt économique en France. L’extension de cette espèce pendant le dernier siècle a rapidement conduit au développement de populations sauvages. C. Gigas est, à présent, considérée comme une espèce invasive dans de nombreuses régions du globe. L’objectif principal de ce travail est de comprendre les capacités adaptatives de cette espèce, à l’aide d’une approche génétique et physiologique à différentes échelles spatiales et temporelles. A macro-échelle (le long des côtes françaises) et à micro-échelle (bas et haut d’estran), une différenciation génétique significative a été observée entre les population adultes à l’aide de marqueurs exoniques et allozymiques. A contrario, cette différence n’a pas décelée par les microsatellites. Dans trois sites bretons, une structuration génétique significative a été observée entre les adultes et les jeunes recrues des années 2005 et 2006, e également entre ces recrues et des naissains cultivés. Dans la seconde partie de cette étude, plusieurs indicateurs physiologiques de santé et de la « fitness » ont été estimés sur des adultes des trois sites cités précédemment. De fortes différences significatives ont été observées entre des individus de sexe et de stade de gamétogenèse différent, au cours de l’année 2005. Cependant, aucune différence majeure des performances physiologiques n’a été révélée entre les adultes à micro- et macro-échelles spatiales. En conclusion, l’ensemble de ces résultats suggère un fort potentiel invasif de C. Gigas, résultant d’une plasticité phénotypique et surtout d’une sélection locale appliquée sur sa forte diversité génétique
The Pacific oyster Crassostrea gigas is an important commercial species in France. The wide distribution of this species during the last decade quickly led to the developmeht of “wild” populations mainly in rocky intertidal areas. C. Gigas is now considered an invasive species in various parts of the world. The main objective of this work was to characterize the adaptative capabilities of C. Giqas in Brittany using genetic and physiological approaches at different spatial and temporal scales. Using exonic markers, significant genetic structures were observed between populations of adult oysters along the French coasts. In contrast, this difference was not observed using microsatellites. The study at the micro-scale, demonstrated no significant difference in allelic frequencies between oysters at high and low tidal heights, except at the MPI locus via allozymes analysis. At three sites f rom Brittany, significant genetic structure was observed between adult and juvenile oysters recruited in 2005 and 2006 and also between these same juveniles and cultivated spat. In the second part of this study, several physiological indicators of health and fitness-related traits were assessed on adults from the three sites described above. Strong significant differences were found between sex and gametogenesis stages throughout the year 2005. In contras no differential physiological performance was illustrated between adults at macro and micro-spatial scales. In conclusion, aIl of these results suggest a high potential of invasion for as that correspond to the compound of phenotypic plasticity and all above local selection applied to its high genetic diversity
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Books on the topic "Invasive phenotype"

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Singhi, Pratibha, Karthi Nallasamy, and Sunit Singhi. Fungal Infections of the Central Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0162.

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Fungal infections of the central nervous system are important because of their increasing incidence and the growing population of at-risk individuals. CNS spread is usually hematogenous but rarely can be due to direct invasion from adjacent structures. Morphology of the infecting fungus may predict the regions affected and the lesion phenotype. Meningitis and mass lesions are the most frequent. This chapter reviews the current understanding of the neuropathogenesis of fungal infections with mention of histopathological and imaging correlations. Important aspects of management are also discussed. Diagnosis requires strong clinical suspicion. Treatment is often multimodal with prolonged drug therapy, surgery, and supportive care.
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McGrath, Joanne C. A comparison of phenotypic plasticity in lythrum salicaria l., an invasive hydrophyte, and lythrum alatum pursh., its noninvasive congener: A thesis in Biology. 1995.

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Rice, Kelly C. regulation of the colonization and invasive phenotypes by protease activity in staphylococcus aureus: Analysis of fibronectin-binding protein (FNBP) and V8 protease as paradigms of this concept. 2001.

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Ritchie, James, Darren Green, Constantina Chrysochou, and Philip A. Kalra. Renal artery stenosis. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0215.

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In fibromuscular disease (FMD), renal artery occlusion seems to be rare. Balloon angioplasty appears moderately successful in the medium term in controlling hypertension, at least in younger patients. In more complicated circumstances, medical therapy may be preferred. Similar approaches have been used in Takayasu disease but with less information about lasting outcomes.In atherosclerotic renal disease, the risk of renal artery occlusion and loss of renal function seems higher, but so are the complications of invasive management. Randomized clinical studies have not shown better blood pressure control or renal outcomes between medical therapy and percutaneous revascularization. As a consequence, modern management of atherosclerotic renovascular disease is primarily pharmacological, with interventional techniques reserved for selected presentations such as rapidly declining therapy, acute occlusion, or characteristic ‘flash’ pulmonary oedema.Whilst this approach is widely accepted, long-term outcome data are scant and there is ongoing research interest into specific disease phenotypes, refined interventional techniques, and novel treatment strategies aimed at preserving the renal microcirculation.
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Machado, Pedro M. Inclusion body myositis. Edited by Hector Chinoy and Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0011.

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Sporadic inclusion body myositis (IBM) is an acquired muscle disorder associated with ageing, for which there is no effective treatment. It is characterized by a typical early clinical phenotype with (often asymmetric) weakness of the knee extensors and finger flexors, potential involvement of pharyngeal and upper-oesophageal muscles (which may contribute to malnutrition and aspiration), and progressive and slow deterioration, which may lead to severe disability and loss of quality of life. Muscle biopsy shows chronic myopathic features, lymphocytic infiltration with invasion of non-necrotic fibres, rimmed vacuoles, mitochondrial changes, and pathological accumulation of proteins in the muscle tissue. It remains uncertain whether IBM is primarily an immune-mediated inflammatory myopathy or a degenerative myopathy with an associated inflammatory component. This chapter will describe the clinical features, natural history, investigations, current pathogenic concepts, outcome measures, and therapeutic approaches in IBM. Despite recent clues, in many respects IBM remains an unsolved mystery.
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Geri, Guillaume, and Jean-Paul Mira. Host–pathogen interactions in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0306.

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Infection by a pathogenic micro-organism triggers a coordinated activation of both innate and adaptive immune responses. The innate immune response quickly triggers an antimicrobial response that will initiate development of a pathogen-specific, long-lasting adaptive immune response. Accurate recognition of microbial-associated molecular patterns by pattern-recognition receptors (PRRs) is the cornerstone of this immediate response. Most studied PRRs are Toll-like receptors (TLRs) and their kinase signalling cascades that activate nuclear transcription factors, and induce gene expression and cytokine production. Deficiencies or genetic variability in these different signalling pathways may lead to recurrent pyogenic infections and severe invasive diseases. After initial contact between the host and pathogen, numerous factors mediate the inflammatory response, as pro-inflammatory cytokines and chemokines. Apart from host genetic variability, pathogen diversity also influences the phenotypic features of various infectious diseases. Genomic analysis may assist in the development of targeted therapies or new therapeutic strategies based on both patient and microorganism genotype.
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Bass, Cristina, Barbara Bauce, and Gaetano Thiene. Arrhythmogenic right ventricular cardiomyopathy: diagnosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0360.

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Arrhythmogenic cardiomyopathy is a heart muscle disease clinically characterized by life-threatening ventricular arrhythmias and pathologically by an acquired and progressive dystrophy of the ventricular myocardium with fibrofatty replacement. The clinical manifestations of arrhythmogenic cardiomyopathy vary according to the ‘phenotypic’ stage of the underlying disease process. Since there is no ‘gold standard’ to reach the diagnosis of arrhythmogenic cardiomyopathy, multiple categories of diagnostic information have been combined. Different diagnostic categories include right ventricular morphofunctional abnormalities (by echocardiography and/or angiography and/or cardiovascular magnetic resonance imaging), histopathological features on endomyocardial biopsy, electrocardiogram, arrhythmias, and family history, including genetics. The diagnostic criteria were revised in 2010 to improve diagnostic sensitivity, but with the important prerequisite of maintaining diagnostic specificity. Quantitative parameters have been put forward and abnormalities are defined based on the comparison with normal subject data. A definite diagnosis of arrhythmogenic cardiomyopathy is achieved when two major, or one major and two minor, or four minor criteria from different categories are met. The main differential diagnoses are idiopathic right ventricular outflow tract tachycardia, myocarditis, sarcoidosis, dilated cardiomyopathy, right ventricular infarction, congenital heart diseases with right ventricular overload, and athlete’s heart. Among diagnostic tools, contrast-enhanced cardiovascular magnetic resonance is playing a major role in detecting subepicardial-midmural left ventricular free wall involvement, even preceding morphofunctional abnormalities. Moreover, electroanatomical mapping is an invasive tool able to detect early right ventricular free wall involvement in terms of low-voltage areas. Both techniques are increasingly used in the diagnostic work-up although are not yet part of diagnostic criteria.
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Book chapters on the topic "Invasive phenotype"

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Vinchure, Omkar, and Ritu Kulshreshtha. "MicroRNA Regulation of Invasive Phenotype of Glioblastoma." In MicroRNA, 173–200. Boca Raton : Taylor & Francis, 2018. | “A CRC title, part of the Taylor & Francis imprint, a member of the Taylor & Francis Group, the academic division of T&F Informa plc.”: CRC Press, 2018. http://dx.doi.org/10.1201/b22195-9.

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MacMillan, Connor D., Ann F. Chambers, and Alan B. Tuck. "Progression of Early Breast Cancer to an Invasive Phenotype." In Breast Cancer Metastasis and Drug Resistance, 143–59. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5647-6_8.

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Wang, Haizhen, and Xiangwei Wu. "Detection and Enumeration of Circulating Tumor Cells with Invasive Phenotype." In Advances in Experimental Medicine and Biology, 133–41. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55947-6_7.

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Pierleoni, Paola, Alberto Belli, Roberto Concetti, Lorenzo Palma, Federica Pinti, Sara Raggiunto, Simone Valenti, and Andrea Monteriù. "A Non-invasive Method for Biological Age Estimation Using Frailty Phenotype Assessment." In Lecture Notes in Electrical Engineering, 81–94. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-05921-7_7.

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Moortgat, Peter, Mieke Anthonissen, Ulrike Van Daele, Jill Meirte, Tine Vanhullebusch, and Koen Maertens. "Shock Wave Therapy for Wound Healing and Scar Treatment." In Textbook on Scar Management, 485–90. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44766-3_55.

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AbstractShock Wave Therapy (SWT) meets all the requirements for the ideal non-invasive scar treatment. It is safe, well tolerated by patients, cost-effective, easy to apply, has low complication rates, and can be used in an outpatient setting. The overall effect of SWT is an improvement of tissue homeostasis, accompanied by an improvement of the tissue self-healing abilities, and it seems to focus on inducing tissue regeneration and matrix remodeling in vivo by means of mechanotransduction.SWT has a beneficial effect on wound healing and is characterized by an upregulation of the angio-active factors as nitric oxide (NO) and vascular endothelial growth factor (VEGF) leading to induced angiogenesis. A downregulation of alpha-SMA expression, myofibroblast phenotype, TGF-β1 expression, fibronectin, and collagen type I are measured after SWT on scars, leading to improvement of several relevant scar parameters like height, pliability, vascularity, and pigmentation, and thus ameliorating function.For a full treatment outline, the energy flux density (EFD), the number of pulses, the pulse frequency, and the number and interval of treatments are the most relevant parameters. The EFD for soft tissue indications is typically in the range of 0.08–0.25 mJ/mm2, while scars and fibrosis are treated with an EFD ranging between 0.15 and 0.33 mJ/mm2. These settings seem to be ideal to induce the optimal cell responses for each indication.All the presented findings are fundamental knowledge for further investigation of SWT to reduce the fibrous component in regenerating and remodeling tissues. However, the full potential of SWT in wound healing and scar treatment needs further unraveling.
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Lande, Russell. "EVOLUTION OF PHENOTYPIC PLASTICITY IN COLONIZING SPECIES." In Invasion Genetics, 165–74. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781119072799.ch9.

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DeLosh, René M., and Robert H. Shoemaker. "Evaluation of Real-Time In Vitro Invasive Phenotypes." In Methods in Molecular Biology, 165–80. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1350-4_12.

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Blows, Mark W., and Katrina McGuigan. "THE DISTRIBUTION OF GENETIC VARIANCE ACROSS PHENOTYPIC SPACE AND THE RESPONSE TO SELECTION." In Invasion Genetics, 187–205. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781119072799.ch11.

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Thorn, Christopher C., Deborah Williams, and Thomas C. Freeman. "Oligonucleotide Microarray Expression Profiling of Contrasting Invasive Phenotypes in Colorectal Cancer." In Methods in Molecular Biology, 203–21. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-163-5_17.

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Bei, Amy Kristine, and Manoj T. Duraisingh. "Measuring Plasmodium falciparum Erythrocyte Invasion Phenotypes Using Flow Cytometry." In Malaria Vaccines, 167–86. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2815-6_14.

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Conference papers on the topic "Invasive phenotype"

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Schlesinger, Saundra, Catherine Buell, William Parks, and Peter Chen. "Lung Cancer Loss Of Syndecan-1 Promotes A More Invasive Phenotype." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6359.

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Watanabe, Takafumi, Steve Goodison, Charles J. Rosser, and Virginia Urquidi. "Abstract 436: Cell surface HSPA8/HSc70 influences invasive tumor cell phenotype." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-436.

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Stark, Mitchell S., Sabrina Hammerlindl, Lisa Tom, Kasturee Jagirdar, Jean-Marie Tan, Helmut Schaider, Richard A. Sturm, et al. "Abstract 5861: BOP1 expression contributes to the proliferative/invasive phenotype in melanoma." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-5861.

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Kosir, Mary A., and Donghong Ju. "Abstract 307: Acquisition of the invasive phenotype and EMT profile by CXCL7 transfection." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-307.

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Li, Yuejuan, Dianhua Jiang, Jiurong Liang, Eric B. Meltzer, Alice Gray, Lise Wogensen, Yu Yamaguchi, and Paul W. Noble. "Unrelenting Lung Fibrosis Requires An Invasive Myofibroblast Phenotype Regulated By Hyaluronan And CD44." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1977.

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Veerakumarasivam, Abhimanyu, Kasra Saeb-Parsy, Helen E. Scott, David E. Neal, and John D. Kelly. "Abstract 1191: Flotillin-2 overexpression is associated with an invasive urothelial cell carcinoma phenotype." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1191.

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Karnevi, Emelie, Ann H. Rosendahl, Moin A. Saleem, and Roland Andersson. "Abstract B17: Tumor-associated stellate cells promote an invasive phenotype of pancreatic cancer cells." In Abstracts: AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.panca2014-b17.

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Heyking, Kristina von, Annette Fasan, Stefan Burdach, and Günther H. Richter. "Abstract 3973: BRICHOS genes CHM1 and ITM2A maintain an undifferentiated, invasive phenotype in Ewing sarcoma." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3973.

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Pond, Erika D., Thomas C. Sroka, Jaime MC Gard, Sangita C. Pawar, Raymond B. Nagle, and Anne E. Cress. "Abstract 4345: Inadequate repair of ionizing radiation damage: A consequence of the invasive tumor phenotype." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4345.

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Mohapatra, Gayatry, Junko Kikuchi, and Michael J. Birrer. "Abstract 2997: SOX2 contributes towards invasive phenotype of serous ovarian cancer by up-regulating MMP2." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-2997.

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Reports on the topic "Invasive phenotype"

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Watson, Peter. Identification of Markers of the Invasive Phenotype in Human Breast Cancer (96 Cancer). Fort Belvoir, VA: Defense Technical Information Center, October 1999. http://dx.doi.org/10.21236/ada382826.

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Kelley, Amanda. The Effect of Temperature on Phenotypes of the Invasive European Green Crab: Physiologic Mechanisms that Facilitate Invasion Success. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1004.

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Corscadden, Louise, and Anjali Singh. Grip Strength Test In Rodents. ConductScience, January 2023. http://dx.doi.org/10.55157/cs2023109.

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The grip strength test is one of the most commonly applied tests in animal laboratories to measure neuromuscular functions or disorders. It was first developed in the 1970s. Today a wide range of techniques are available to study muscle strength in rodents. These methods are categorized into two categories:[2] Invasive method: In situ and in vitro measurements of muscle force are invasive methods. Non-invasive method: This method only includes in vivo measurement tests to analyze muscle force such as treadmill tests, wire hang tests, swimming endurance, vertical pole test, and grip strength tests. The most convenient technique of all tests is the grip strength test. It’s most convenient and causes less stress to animals. The grip test has been widely used in order to investigate the phenotypes of transgenic mice with neuromuscular disease and evaluate potential compounds involved in the motor functioning of organisms. The tests have been serving the purpose for 30 years either alone or in combination with other tests.
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Hunter, Martha S., and Einat Zchori-Fein. Rickettsia in the whitefly Bemisia tabaci: Phenotypic variants and fitness effects. United States Department of Agriculture, September 2014. http://dx.doi.org/10.32747/2014.7594394.bard.

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The sweet potato whitefly, Bemisia tabaci (Hemiptera: Aleyrodidae) is a major pest of vegetables, field crops, and ornamentals worldwide. This species harbors a diverse assembly of facultative, “secondary” bacterial symbionts, the roles of which are largely unknown. We documented a spectacular sweep of one of these, Rickettsia, in the Southwestern United States in the B biotype (=MEAM1) of B. tabaci, from 1% to 97% over 6 years, as well as a dramatic fitness benefit associated with it in Arizona but not in Israel. Because it is critical to understand the circumstances in which a symbiont invasion can cause such a large change in pest life history, the following objectives were set: 1) Determine the frequency of Rickettsia in B. tabaci in cotton across the United States and Israel. 2) Characterize Rickettsia and B. tabaci genotypes in order to test the hypothesis that genetic variation in either partner is responsible for differences in phenotypes seen in the two countries. 3) Determine the comparative fitness effects of Rickettsia phenotypes in B. tabaci in Israel and the United States. For Obj. 1, a survey of B. tabaci B samples revealed the distribution of Rickettsia across the cotton-growing regions of 13 sites from Israel and 22 sites from the USA. Across the USA, Rickettsia frequencies were heterogeneous among regions, but were generally at frequencies higher than 75% and close to fixation in some areas, whereas in Israel the infection rates were lower and declining. The distinct outcomes of Rickettsia infection in these two countries conform to previouslyreported phenotypic differences. Intermediate frequencies in some areas in both countries may indicate a cost to infection in certain environments or that the frequencies are in flux. This suggests underlying geographic differences in the interactions between bacterial symbionts and the pest. Obj. 2, Sequences of several Rickettsia genes in both locations, including a hypervariableintergenic spacer gene, suggested that the Rickettsia genotype is identical in both countries. Experiments in the US showed that differences in whitefly nuclear genotype had a strong influence on Rickettsia phenotype. Obj. 3. Experiments designed to test for possible horizontal transmission of Rickettsia, showed that these bacteria are transferred from B. tabaci to a plant, moved inside the phloem, and could be acquired by other whiteflies. Plants can serve as a reservoir for horizontal transmission of Rickettsia, a mechanism that may explain the occurrence of phylogenetically-similarsymbionts among unrelated phytophagous insect species. This plant-mediated transmission route may also exist in other insect-symbiont systems, and since symbionts may play a critical role in the ecology and evolution of their hosts, serve as an immediate and powerful tool for accelerated evolution. However, no such horizontal transmission of Rickettsia could be detected in the USA, underlining the difference between the interaction in both countries, or between B. tabaci and the banded wing whitefly on cotton in the USA (Trialeurodes sp. nr. abutiloneus) and the omnivorous bug Nesidiocoristenuis. Additionally, a series of experiments excluded the possibility that Rickettsia is frequently transmitted between B. tabaci and its parasitoid wasps Eretmocerusmundus and Encarsiapergandiella. Lastly, ecological studies on Rickettsia effects on free flight of whiteflies showed no significant influence of symbiont infection on flight. In contrast, a field study of the effects of Rickettsia on whitefly performance on caged cotton in the USA showed strong fitness benefits of infection, and rapid increases in Rickettsia frequency in competition population cages. This result confirmed the benefits to whiteflies of Rickettsia infection in a field setting.
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Horwitz, Benjamin A., and Barbara Gillian Turgeon. Fungal Iron Acquisition, Oxidative Stress and Virulence in the Cochliobolus-maize Interaction. United States Department of Agriculture, March 2012. http://dx.doi.org/10.32747/2012.7709885.bard.

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Our project focused on genes for high affinity iron acquisition in Cochliobolus heterostrophus, a necrotrophic pathogen of maize, and their intertwined relationship to oxidative stress status and virulence of the fungus on the host. An intriguing question was why mutants lacking the nonribosomal peptide synthetase (NRPS) gene (NPS6) responsible for synthesis of the extracellular siderophore, coprogen, are sensitive to oxidative stress. Our overall objective was to understand the mechanistic connection between iron stress and oxidative stress as related to virulence of a plant pathogen to its host. The first objective was to examine the interface where small molecule peptide and reactive oxygen species (ROS) mechanisms overlap. The second objective was to determine if the molecular explanation for common function is common signal transduction pathways. These pathways, built around sensor kinases, response regulators, and transcription factors may link sequestering of iron, production of antioxidants, resistance to oxidative stress, and virulence. We tested these hypotheses by genetic manipulation of the pathogen, virulence assays on the host plant, and by following the expression of key fungal genes. An addition to the original program, made in the first year, was to develop, for fungi, a genetically encoded indicator of redox state based on the commercially available Gfp-based probe pHyper, designed for animal cell biology. We implemented several tools including a genetically encoded indicator of redox state, a procedure to grow iron-depleted plants, and constructed a number of new mutants in regulatory genes. Lack of the major Fe acquisition pathways results in an almost completely avirulent phenotype, showing how critical Fe acquisition is for the pathogen to cause disease. Mutants in conserved signaling pathways have normal ability to regulate NPS6 in response to Fe levels, as do mutants in Lae1 and Vel1, two master regulators of gene expression. Vel1 mutants are sensitive to oxidative stress, and the reason may be underexpression of a catalase gene. In nps6 mutants, CAT3 is also underexpressed, perhaps explaining the sensitivity to oxidative stress. We constructed a deletion mutant for the Fe sensor-regulator SreA and found that it is required for down regulation of NPS6 under Fe-replete conditions. Lack of SreA, though, did not make the fungus over-sensitive to ROS, though the mutant had a slow growth rate. This suggests that overproduction of siderophore under Fe-replete conditions is not very damaging. On the other hand, increasing Fe levels protected nps6 mutants from inhibition by ROS, implying that Fe-catalyzed Fenton reactions are not the main factor in its sensitivity to ROS. We have made some progress in understanding why siderophore mutants are sensitive to oxidative stress, and in doing so, defined some novel regulatory relationships. Catalase genes, which are not directly related to siderophore biosynthesis, are underexpressed in nps6 mutants, suggesting that the siderophore product (with or without bound Fe) may act as a signal. Siderophores, therefore, could be a target for intervention in the field, either by supplying an incorrect signal or blocking a signal normally provided during infection. We already know that nps6 mutants cause smaller lesions and have difficulty establishing invasive growth in the host. Lae1 and Vel1 are the first factors shown to regulate both super virulence conferred by T-toxin, and basic pathogenicity, due to unknown factors. The mutants are also altered in oxidative stress responses, key to success in the infection court, asexual and sexual development, essential for fungal dissemination in the field, aerial hyphal growth, and pigment biosynthesis, essential for survival in the field. Mutants in genes encoding NADPH oxidase (Nox) are compromised in development and virulence. Indeed the triple mutant, which should lack all Nox activity, was nearly avirulent. Again, gene expression experiments provided us with initial evidence that superoxide produced by the fungus may be most important as a signal. Blocking oxidant production by the pathogen may be a way to protect the plant host, in interactions with necrotrophs such as C. heterostrophus which seem to thrive in an oxidant environment.
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Ficht, Thomas, Gary Splitter, Menachem Banai, and Menachem Davidson. Characterization of B. Melinensis REV 1 Attenuated Mutants. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7580667.bard.

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Brucella Mutagenesis (TAMU) The working hypothesis for this study was that survival of Brucella vaccines was directly related to their persistence in the host. This premise is based on previously published work detailing the survival of the currently employed vaccine strains S19 and Rev 1. The approach employed signature-tagged mutagenesis to construct mutants interrupted in individual genes, and the mouse model to identify mutants with attenuated virulence/survival. Intracellular survival in macrophages is the key to both reproductive disease in ruminants and reticuloendothelial disease observed in most other species. Therefore, the mouse model permitted selection of mutants of reduced intracellular survival that would limit their ability to cause reproductive disease in ruminants. Several classes of mutants were expected. Colonization/invasion requires gene products that enhance host-agent interaction or increase resistance to antibacterial activity in macrophages. The establishment of chronic infection requires gene products necessary for intracellular bacterial growth. Maintenance of chronic infection requires gene products that sustain a low-level metabolism during periods characterized little or no growth (1, 2). Of these mutants, the latter group was of greatest interest with regard to our originally stated premise. However, the results obtained do not necessarily support a simplistic model of vaccine efficacy, i.e., long-survival of vaccine strains provides better immunity. Our conclusion can only be that optimal vaccines will only be developed with a thorough understanding of host agent interaction, and will be preferable to the use of fortuitous isolates of unknown genetic background. Each mutant could be distinguished from among a group of mutants by PCR amplification of the signature tag (5). This approach permitted infection of mice with pools of different mutants (including the parental wild-type as a control) and identified 40 mutants with apparently defective survival characteristics that were tentatively assigned to three distinct classes or groups. Group I (n=13) contained organisms that exhibited reduced survival at two weeks post-infection. Organisms in this group were recovered at normal levels by eight weeks and were not studied further, since they may persist in the host. Group II (n=11) contained organisms that were reduced by 2 weeks post infection and remained at reduced levels at eight weeks post-infection. Group III (n=16) contained mutants that were normal at two weeks, but recovered at reduced levels at eight weeks. A subset of these mutants (n= 15) was confirmed to be attenuated in mixed infections (1:1) with the parental wild-type. One of these mutants was eliminated from consideration due to a reduced growth rate in vitro that may account for its apparent growth defect in the mouse model. Although the original plan involved construction of the mutant bank in B. melitensis Rev 1 the low transformability of this strain, prevented accumulation of the necessary number of mutants. In addition, the probability that Rev 1 already carries one genetic defect increases the likelihood that a second defect will severely compromise the survival of this organism. Once key genes have been identified, it is relatively easy to prepare the appropriate genetic constructs (knockouts) lacking these genes in B. melitensis Rev 1 or any other genetic background. The construction of "designer" vaccines is expected to improve immune protection resulting from minor sequence variation corresponding to geographically distinct isolates or to design vaccines for use in specific hosts. A.2 Mouse Model of Brucella Infection (UWISC) Interferon regulatory factor-1-deficient (IRF-1-/- mice have diverse immunodeficient phenotypes that are necessary for conferring proper immune protection to intracellular bacterial infection, such as a 90% reduction of CD8+ T cells, functionally impaired NK cells, as well as a deficiency in iNOS and IL-12p40 induction. Interestingly, IRF-1-/- mice infected with diverse Brucella abortus strains reacted differently in a death and survival manner depending on the dose of injection and the level of virulence. Notably, 50% of IRF-1-/- mice intraperitoneally infected with a sublethal dose in C57BL/6 mice, i.e., 5 x 105 CFU of virulent S2308 or the attenuated vaccine S19, died at 10 and 20 days post-infection, respectively. Interestingly, the same dose of RB51, an attenuated new vaccine strain, did not induce the death of IRF-1-/- mice for the 4 weeks of infection. IRF-1-/- mice infected with four more other genetically manipulated S2308 mutants at 5 x 105 CFU also reacted in a death or survival manner depending on the level of virulence. Splenic CFU from C57BL/6 mice infected with 5 x 105 CFU of S2308, S19, or RB51, as well as four different S2308 mutants supports the finding that reduced virulence correlates with survival Of IRF-1-/- mice. Therefore, these results suggest that IRF-1 regulation of multi-gene transcription plays a crucial role in controlling B. abortus infection, and IRF-1 mice could be used as an animal model to determine the degree of B. abortus virulence by examining death or survival. A3 Diagnostic Tests for Detection of B. melitensis Rev 1 (Kimron) In this project we developed an effective PCR tool that can distinguish between Rev1 field isolates and B. melitensis virulent field strains. This has allowed, for the first time, to monitor epidemiological outbreaks of Rev1 infection in vaccinated flocks and to clearly demonstrate horizontal transfer of the strain from vaccinated ewes to unvaccinated ones. Moreover, two human isolates were characterized as Rev1 isolates implying the risk of use of improperly controlled lots of the vaccine in the national campaign. Since atypical B. melitensis biotype 1 strains have been characterized in Israel, the PCR technique has unequivocally demonstrated that strain Rev1 has not diverted into a virulent mutant. In addition, we could demonstrate that very likely a new prototype biotype 1 strain has evolved in the Middle East compared to the classical strain 16M. All the Israeli field strains have been shown to differ from strain 16M in the PstI digestion profile of the omp2a gene sequence suggesting that the local strains were possibly developed as a separate branch of B. melitensis. Should this be confirmed these data suggest that the Rev1 vaccine may not be an optimal vaccine strain for the Israeli flocks as it shares the same omp2 PstI digestion profile as strain 16M.
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