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Dissertations / Theses on the topic 'Cadherins'

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Published: 4 June 2021

Last updated: 25 January 2023

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1

Munro, Sandra Bronwen. "An investigation of the cadherins expressed in mouse thymocytes and testis, utilizing the polymerase chain reaction, identification of two novel cadherins, t1-cadherin and t2-cadherin." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0005/NQ30347.pdf.

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2

Munro, Sandra Bronwen. "An investigation of the cadherins expressed in mouse thymocytes and testis, utilizing the polymerase chain reaction : identification of two novel cadherins, T1-cadherin and T2-cadherin." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=42105.

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The cadherins are calcium-dependent cell adhesion molecules. I have used a polymerase chain reaction (PCR) strategy to identify the cadherins expressed in mouse CD4$ sp+$ CD8$ sp+$ thymocytes and testis. Two novel cadherins (designated T1-cadherin and T2-cadherin) were discovered utilizing this approach. cDNAs containing partial coding regions for T1-cadherin and T2-cadherin were used as molecular probes in Northern blot and in situ hybridization protocols to determine the tissue- and cell-specific expression patterns of T1- and T2-cadherin. A T1-cadherin mRNA transcript of 3 kb was detected in adult mouse testes extracts. An mRNA transcript of 3.5 kb was detected for T2-cadherin in mouse brain and testes extracts. In situ hybridization analysis suggested that T2-cadherin is expressed by the Sertoli cells in the seminiferous epithelium. In addition to T1-cadherin and T2-cadherin, five other cadherins (E-cadherin, N-cadherin, P-cadherin, K-cadherin, and OB-cadherin) were found to be expressed at various stages during testicular development. The relative levels of each testicular cadherin mRNA transcript were determined in fetal, newborn, 7-day-old, 21-day-old, and adult mouse testes by semi-quantitative PCR. N-cadherin mRNA was expressed at all stages of testicular development, with maximal levels being present in the testes of 21-day-old mice. E-cadherin, P-cadherin, K-cadherin, OB-cadherin, and T2-cadherin mRNA transcripts were expressed in the fetal gonad. The testicular levels of these cadherin mRNA transcripts decreased dramatically after birth. Conversely, T1-cadherin mRNA was not detected in the fetal, newborn, and 7-day-old testes, but was present in 21-day-old and adult testes. T1-cadherin levels were 10-fold higher in the testes of adult mice, compared to the levels found in the testes of 21-day-old mice. As well, the N-cadherin, T1-cadherin, and T2-cadherin mRNA levels were examined in the estrogen receptor knockout (ERKO) mouse. T1-cadherin mRNA levels

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3

Zhang, Wentao. "IQGAP1 knockdown enhances the endothelial barrier in vitro." Morgantown, W. Va. : [West Virginia University Libraries], 2006. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=4740.

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Thesis (Ph. D.)--West Virginia University, 2006.
Title from document title page. Document formatted into pages; contains viii, 114 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 101-114).

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4

Uglow, Elizabeth. "The role of cadherins in vascular disease." Thesis, University of Bristol, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268829.

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5

McEvoy, Katherina Yasmin. "The role of desmosomal cadherins in colorectal tumourigenesis." Thesis, University of Birmingham, 2012. http://etheses.bham.ac.uk//id/eprint/3466/.

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In cancer, loss of intercellular contact contributes to tumour progression and invasion. Desmosomal cadherins are essential constituents of desmosomes – intercellular junctions that confer significant adhesive strength to epithelial tissues and cardiac muscle. Although changes in desmosomal components have been noted in a variety of cancers previously, this investigation has shown for the first time altered desmocollin expression in colorectal cancer. Real-time PCR and western blotting were used to assess desmocollin expression in a series of colorectal cancer and matched normal tissue samples. Loss of desmocollin 2 expression was observed in the cancer samples. In addition, de novo expression of desmocollins 1 and 3, which are not normally expressed in the colon, was observed. Desmoglein gene expression was also altered in the cancer samples. Although classical cadherin switching is a hallmark of the epithelial-mesenchymal transition, desmocollin switching has not previously been reported. Further experiments, to investigate the effect of loss of desmocollin 2 and desmoglein 2 on the behaviour of cultured cells were performed. In addition, experiments were carried out to identify those transcription factors that regulate desmosomal cadherin gene expression in the colon. Transcription factors of the CCAAT/enhancer-binding proteins family act as transcriptional activators of desmosomal cadherin promoters in colonic cells.

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6

Xu, Mei. "Cellular mechanisms of effects of sphingosine 1-phosphate on vascular endothelial barrier." Morgantown, W. Va. : [West Virginia University Libraries], 2008. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5586.

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Thesis (Ph. D.)--West Virginia University, 2008.
Title from document title page. Document formatted into pages; contains ix, 109 p. : ill. (some col.). Includes abstract. Includes bibliographical references.

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7

Chan, Wai-man Vivian. "Functional characterization of liver intestine-cadherin (CDH17) in hepatocellular carcinoma." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B37424671.

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8

Pon, Yuen-lam. "Regulation of cadherins and catenins in ovarian surface epithelium and ovarian cancer." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39634231.

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9

Lim, Foon Lian. "Role of cadherin 2 in the intervertebral disc." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hdl.handle.net/10722/198869.

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Intervertebral disc (IVD) degeneration could lead to many serious complications including low back pain and disc herniation. However, the mechanism of disc degeneration is not fully understood, hindering the development of the therapeutics to cure this disease. The integrity of the nucleus pulposus (NP), which is derived from the notochord and situated in the core of the IVD, has long been implicated in the function and homeostasis of the IVD. Previous puncture-induced disc degeneration mouse model showed segregation of NP cell mass during the early stage of disc degeneration, indicating that an alteration in the cell adhesion molecule activities is involved in this process. By microarray analysis, our group have revealed specific expression of Cdh2 gene, encoding cadherin 2/N-cadherin, a subtype of cadherins in the NP cells, suggesting a regulatory role of cadherin 2 in the IVD. Cadherins are single transmembrane glycoproteins mediating calcium-dependent intercellular adhesions. Cadherin 2 is involved in chondrogenesis and skeletogenesis, suggesting that it is important in skeletal development and function. This study hypothesized that cadherin 2 is required in the normal IVD development and homeostasis. The purposes of this project is firstly to fully characterize changes in cadherin 2 expression in the normal and degenerative discs in rodent and human, and secondly to examine the effect of loss of function of cadherin 2 on IVD homeostasis by functional blocking of the protein in the rodent NP and conditional knock out of cadherin 2 from the murine NP. The rodent adult NP is similar to human fetal NP, where cadherin 2 is homogeneously expressed in the cell membranes of the notochordal (NC) cells, suggesting that cadherin 2 is a potential NC cell marker. The rodent degenerative NP is similar to human adult NP, where down-regulation of cadherin 2 is observed, the NC cells are replaced by small round cells, and the cell-cell contact is lost. Blocking cadherin 2 function in the rodent NP and conditional knock out of cadherin 2 in the notochord and consequently the NP will lead to transformation of NC cells into small cells, loss of cell-cell contact and a change in the extracellular matrix (ECM), suggesting that cadherin 2 is important in the maintenance of the phenotype and intercellular adhesion of the NC cells. In conclusion, this study indicates that cadherin 2 is mainly expressed in the NC cells of the NP and serves as a potential NC cell marker. It plays a regulatory role in the IVD homeostasis through the maintenance of the NC cell phenotype by intercellular adhesions. This study contributes to the knowledge about the role of cadherin 2 in the disc homeostasis and the early mechanism of disc degeneration, and this would help in developing a therapeutic method to intervene or even reverse the disease process of disc degeneration.
published_or_final_version
Orthopaedics and Traumatology
Doctoral
Doctor of Philosophy

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10

Modak, Debadrita. "Structural and biochemical studies of non-clustered protocadherins." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1595567250446369.

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11

Jakab, Karoly Robert. "Physical mechanisms of cell rearrangements from tissue liquidity to artificial organ structures /." Diss., Columbia, Mo. : University of Missouri-Columbia, 2006. http://hdl.handle.net/10355/4426.

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Thesis (Ph.D.)--University of Missouri-Columbia, 2006.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on March 25, 2009) Vita. Includes bibliographical references.

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12

Chung, Man-fai Yvonne. "Investigation of biomarkers in esophageal squamous cell carcinoma." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43704025.

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13

Zhu, Rui. "Liver-intestine cadherin (CDH17) in hepatocellular carcinoma molecular analysis and clinical implications /." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43703793.

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14

Koutsouki, Evgenia. "The role of cadherins in vascular smooth muscle cell apoptosis." Thesis, University of Bristol, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.420910.

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15

Goel, Aviva J. "Niche Regulation of Muscle Stem Cell Quiescence by Classical Cadherins." Thesis, Icahn School of Medicine at Mount Sinai, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10743988.

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Many adult stem cells are characterized by prolonged quiescence, promoted by cues from their niche. Upon tissue damage, a coordinated transition to the activated state is necessary for successful repair. Non-physiological breaks in quiescence often lead to stem cell depletion and impaired tissue restoration. Here, I identify cadherin-mediated adhesion and signaling between muscle stem cells (satellite cells; SCs) and their myofiber niche as a mechanism that orchestrates the quiescence-to-activation transition. Conditional removal of N-cadherin and M-cadherin in mice leads to a break in SC quiescence with long-term expansion of a regeneration-proficient SC pool. These SCs have an incomplete disruption of the myofiber-SC adhesive junction, and maintain niche residence and cell polarity, yet show properties of SCs in a state of transition from quiescence towards full activation. Among these properties is nuclear localization of b- catenin, which is necessary for this phenotype. These findings are consistent with the conclusion that injury-induced perturbation of niche adhesive junctions is a first step in the quiescence-to-activation transition.

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16

Symonds, James Matthew. "Expression of cadherins in human lymphocytes and skeletal muscle cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ50890.pdf.

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17

Symonds, James Matthew. "Expression of cadherins in human lymphocytes and skeletal muscle cells." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=21649.

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Cadherins are a family of membrane glycoproteins involved in calcium-dependent cell-cell adhesion. The expression of cadherins in two human cell types, lymphocytes and skeletal myoblasts, was examined. Human peripheral lymphoid tissue lymphocytes were analysed for N-cadherin expression. A specific population of B lymphocytes was shown to express N-cadherin. Further, N-cadherin was shown to be expressed in a distinct pattern within the germinal centers of lymph nodes by immunohistochemical techniques. N-cadherin was also detected in a B cell population from human bone marrow and peripheral blood lymphocytes from B-cell chronic lymphocytic leukemia patients. These results suggest that N-cadherin may play a role in the development, differentiation and cell survival of B lymphocytes. Human myogenic cells were studied for cadherin expression before and after the induction of myoblast fusion. Polymerase chain reaction identified two cadherins, N-cadherin and OB-cadherin, in human myoblasts. These two cadherins were shown to be developmentally regulated during myogenesis. Collectively, these studies point to a role for cadherins in human myogenesis and lymphocyte differentiation.

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18

De, la Huerta Irina. "Expression and Role of Cadherins in the Mammalian Visual System." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10252.

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The complex circuitry of the visual system contains around one hundred functionally distinct neuronal types that become specified and connect with the appropriate synaptic partners during development. Previous studies have indicated that immature retinal ganglion cells already express subset-specific molecules that guide them to make precise synaptic choices. In the mammalian retina, members of the cadherin family of adhesion molecules are attractive candidates for this role. To test this idea I began by investigating the expression of cadherins 1-26 in the mouse retina and superior colliculus using in situ hybridization. I then studied the connectivity of cadherin-expressing neurons by analyzing mouse lines in which a marker was inserted after the start codon of each of six cadherin genes of interest. In this way, I identified functional circuits in the visual system that are marked by cadherins. One such circuit is formed of direction-selective retinal ganglion cells (DSGCs), which fire in response to objects moving in one (preferred) direction, and their synaptic partners, the starburst amacrine cells. There are four DSGC subsets, distinguished by their preference for dorsal, ventral, nasal, or temporal motion on the retina. I determined that cadherin 6 is selectively expressed by the two DSGCs subtypes that respond to dorsal or to ventral movement. In collaboration with other lab members I used in situ hybridization and gene expression profiling to identify other molecular markers that distinguish between the four DSGC subsets and that distinguish DSGCs from other retinal ganglion cells. Finally, I used birthdating and lineage tracing methods to ask when DSGCs become molecularly specified. I determined that at least two subsets of DSGCs are specified at or shortly after their birth. For cadherin 6-positive DSGCs, I went on to show that they are specified even before their birth, and that they arise from committed retinal progenitors. Globally, my experiments aimed not only to examine cadherin expression and function in the visual system, but also to demonstrate a method of using molecular signatures to probe the mechanisms of neural circuit assembly in the central nervous system.

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19

Prakash, Saurabh Clandinin Thomas R. "Classical cadherins and target selection in the Drosophila visual system /." May be available electronically:, 2009. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.

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20

Phillips, Kelli R. "Characterization of myosin I in the inner ear." Morgantown, W. Va. : [West Virginia University Libraries], 2007. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5140.

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Thesis (Ph. D.)--West Virginia University, 2007.
Title from document title page. Document formatted into pages; contains vii, 114 p. : ill. (some col.). Includes abstract. Includes bibliographical references.

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21

Pon, Yuen-lam, and 潘婉琳. "Regulation of cadherins and catenins in ovarian surface epithelium andovarian cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39634231.

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22

Zhu, Alan Jian. "Role of integrins and cadherins in regulating keratinocyte growth and differentiation." Thesis, Imperial College London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300439.

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23

Prasad, Tuhina Weiner Joshua A. "The role of gamma-protocadherins in interneuron survival and circuit formation in the developing spinal cord." [Iowa City, Iowa] : University of Iowa, 2009. http://ir.uiowa.edu/etd/423.

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24

Tam, Hok-nang Alex. "Epigenetic inactivation of protocadherin PCDH10 in esophageal cancer /." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36586390.

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25

Kuhn, Axel. "Synthese und Konformationsanalyse von Glycopeptiden aus der homophilen Erkennungsregion des LI-Cadherins." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=975967142.

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26

Brasch, Julia [Verfasser]. "Structural and biophysical studies of adhesive binding by classical cadherins / Julia Brasch." Hannover : Technische Informationsbibliothek und Universitätsbibliothek Hannover (TIB), 2011. http://d-nb.info/1013288424/34.

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27

Michels, Christian [Verfasser]. "Role of classical cadherins in epidermal junction and barrier formation / Christian Michels." Köln : Universitäts- und Stadtbibliothek Köln, 2010. http://d-nb.info/1013736311/34.

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28

Aiga, Mytyl. "Understanding the spatial and functional relationship between cadherins and neuroligins at synapses." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/27814.

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Cadherins and Neuroligins (NLs) are two of the most extensively studied cell adhesion molecules (CAMs) at synapses and have previously been shown to localize to synapses and exert a key role during their development. Despite this, their spatial and functional relationship with respect to one another has not been studied to date. In the present study, we examine the spatial and functional relationship of cadherin and NL isoforms at glutamatergic and GABAergic synapses in cultured hippocampal neurons. Analysis of the synaptic distribution of N-cadherin and NL1 and NL2 in hippocampal cultures, confirm previous studies demonstrating the enrichment of NL2 at GABAergic synapses and enrichment of NL1 and N-cadherin at glutamatergic synapses. We have also observed subsets of GABAergic synapses that express both N-cadherin and NL2 as well as glutamatergic synapses that only express either NL1 or N-cadherin. These groups of glutmatergic and GABAergic synapses may represent a specific subtype of synapse, or may reflect the differential localization of these adhesion molecules during synapse formation. Moreover, using a combination of overexpression and knockdown analysis we demonstrate that NL1 and N-cadherin promote the formation of synapses, in part, by a common pathway. Indeed, knocking down these proteins individually results in approximately 50% reduction in glutamatergic synapse density with a similar reduction upon combined knockdown. In addition, functional compensation assays demonstrate that NL1 expression can fully rescue synapse loss that is due to knockdown of N-cadherin expression. Furthermore, N-cadherin expression can partially rescue synapse loss that is due to knockdown of NL1 expression. Together this work demonstrates that these two cell adhesion proteins act in concert to regulate excitatory synapse formation. Specifically, we show that N-cadherin acts upstream of NL1 to promote synapse formation and that NL1 is a limiting factor in this pathway.

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29

Leong, Cheng-Mee, and n/a. "Human papillomavirus E6 regulation of E-cadherin : a mechanistic and functional study." University of Otago. Department of Microbiology & Immunology, 2007. http://adt.otago.ac.nz./public/adt-NZDU20070601.143218.

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The majority of human papillomavirus (HPV) types cause cutaneous and mucosal disease. Persistent infection with high-risk HPV types is the primary risk factor for the development of cervical cancer. The ability of the virus to persist is contributed to by numerous immune evasion mechanisms. We previously demonstrated that the HPV type 16 (HPV16) E6 protein, down-regulates epithelial (E)-cadherin expression and that the associated Langerhans cells (LC) depletion may contribute to impaired immune recognition by the host. The aims of this study were firstly to establish if E6 down-regulation of E-cadherin is conserved amongst all HPV types, secondly to determine if the reduced E-cadherin expression correlates with reduced LC density in HPV-infected tissues, thirdly, to identify a region of E6 responsible in E-cadherin regulation and fourthly to establish if down-regulation of cell surface E-cadherin also occurs in another DNA tumour virus, adenovirus (Ad). E6 protein from a range of HPV types representing the α, β and γ genera was expressed in HCT116 cells and the effect on cell surface E-cadherin expression was measured by flow cytometry. In addition, a series of tissues infected with HPV types representative of HPV of α, β, [nu] and γ genera were stained to confirm E-cadherin regulation in vivo and to determine the functional significance of E-cadherin expression in relation to LC localisation. In order to identify the region of the E6 protein that was important for E-cadherin regulation, a series of HPV16 E6 mutants were tested for their ability to regulate E-cadherin. Finally, the effects of Ad on cell surface E-cadherin were examined by measuring E-cadherin expression in Ad infected HCT116 cells. E6 down-regulation of E-cadherin was conserved in α, [nu] and γ genera but was lost in β-HPV types, correlating with the ability of the virus to persist. In vivo analysis of patient tissues confirmed this pattern of E-cadherin regulation by E6 types and showed a direct association between loss of E-cadherin and LC depletion, suggesting that E-cadherin regulation by E6 is the cause of depletion of LC in infected tissue. Mutational analysis of HPV16 E6 led to the identification of a putative E-cadherin regulatory region with a conserved motif, H/L/V-[phi]-X-X-X-X-R. A potential mechanism used by E6 to regulate cell surface E-cadherin involved down-regulation of p21[waf1/cip1] (p21) via a p53-independent pathway. Finally, study of Ad showed a similar ability of the virus to regulate E-cadherin, indicating conservation in another DNA tumour virus. This research shows that E-cadherin regulation by E6 is directly associated with LC depletion and viral persistence. The data presented here suggest that LC depletion by HPV is widely conserved in HPV types that cause persistent disease. E-cadherin regulation contributes to this effect through a specific regulatory region of the protein and manipulation of levels of cellular p21. These data may provide a foundation for the development of therapeutics for HPV that aim to overcome immune evasion by the virus.

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30

Chan, Wai-man Vivian, and 陳慧雯. "Functional characterization of liver intestine-cadherin (CDH17) in hepatocellular carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B38891116.

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31

Chung, Man-fai Yvonne, and 鍾文暉. "Investigation of biomarkers in esophageal squamous cell carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43704025.

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32

Zhu, Rui, and 朱睿. "Liver-intestine cadherin (CDH17) in hepatocellular carcinoma: molecular analysis and clinicalimplications." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43703793.

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33

Sampaio, JoÃo Paulo Aguiar. "ImunoexpressÃo de Caderina-E no cÃncer colorretal primÃrio e nas metÃstases linfonodais." Universidade Federal do CearÃ, 2013. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=11260.

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A Caderina-E estÃ intimamente relacionada com a transiÃÃo epitelial-mesenquimal e com a progressÃo tumoral em muitos tipos de cÃncer, inclusive no cÃncer colorretal. O objetivo deste trabalho foi avaliar a imunoexpressÃo de Caderina-E no cÃncer colorretal primÃrio e nas respectivas metÃstases linfonodais, na mucosa colÃnica normal, e investigar possÃveis correlaÃÃes desta expressÃo com parÃmetros clÃnicopatolÃgicos. Setenta e sete casos de colectomias por carcinoma colorretal e dez casos de linfonodos metastÃticos, dos arquivos do Departamento de Patologia e Medicina Legal/Universidade Federal do CearÃ, foram utilizados. Realizou-se o Tissue Microarray e imunohistoquÃmica, com anticorpo monoclonal anti-Caderina-E. Foram avaliados os seguintes escores: 0 = ausÃncia de expressÃo; 1 = expressÃo citoplasmÃtica; 2 = expressÃo mista (citoplasmÃtica e membranar); 3 = expressÃo membranar pura. Foi utilizada tanto a classificaÃÃo proposta por Jawhari et al., agrupando os casos em expressÃo anormal (escores 0, 1 e 2) e expressÃo normal (escore 3), como os critÃrios propostos por Almeida et al., agrupando os casos como expressÃo nÃo-membranar (escores 0 e 1) e expressÃo membranar (escores 2 e 3). Os tumores primÃrios tiveram mais casos de expressÃo de Caderina-E anormal em comparaÃÃo com a mucosa normal (p < 0.0001). NÃo houve diferenÃa significante entre expressÃo de Caderina-E no tumor intestinal e em metÃstases linfonodais, embora nestas a expressÃo membranar tenha sido mais freqÃente do que no sÃtio primÃrio. Tumores de cÃlulas agrupadas apresentaram maior expressÃo de Caderina-E membranar do que os de cÃlulas isoladas, tanto utilizando a classificaÃÃo de Jawhari et al. (p = 0.0230), como os critÃrios propostos por Almeida et al. (p = 0.0043). Em conclusÃo, a expressÃo anormal de Caderina-E no tumor primÃrio, com persistÃncia freqÃente da imunomarcaÃÃo membranar associada Ã marcaÃÃo citoplasmÃtica (marcaÃÃo anormal heterogÃnea ou mista), reforÃa as evidÃncias de que esta alteraÃÃo no cÃncer Ã mais qualitativa do que propriamente quantitativa. O predomÃnio da expressÃo membranar no sÃtio primÃrio da neoplasia e na metÃstase, com ou sem expressÃo citoplasmÃtica associada, principalmente em tumores de cÃlulas agrupadas, sugere que a presenÃa da Caderina-E Ã essencial para a invasÃo local e progressÃo tumoral, em oposiÃÃo ao clÃssico paradigma de que a progressÃo tumoral se exacerba com a perda desta molÃcula de adesÃo.
E-cadherin is closely related to epitelial-mesenchymal transition and tumor progression in many cancers, including colorectal cancer. The aim of this study is to evaluate the expression of E-cadherin in primary colorectal cancer as well as in lymph node metastasis, establishing also a comparison with the expression of E-cadherin in normal colonic mucosa. We utilized 77 cases of colectomies for colorectal carcinoma and 10 cases of metastatic lymph nodes from the files of the Department of Pathology and Forensic Medicine/Federal University of Ceara. Tissue microarray and immunohistochemistry were performed with monoclonal anti-E-cadherin, evaluated using the following scores: 0 = no staining; 1 = cytoplasmic staining; 2 = mixed staining (cytoplasmic and membranous); 3 = membranous staining. It was used the classification proposed by Jawahri et al. which includes cases of abnormal expression (0, 1 and 2 scores) and cases of normal expression (3 score), and was also used the classification proposed by Almeida et al. which includes cases of non-membranous expression (0 and 1 scores) and membranous expression (2 and 3 scores). Primary tumors presented more cases of abnormal E-cadherin expression in comparison to normal colonic mucosa (p < 0.0001). There were no differences between E-cadherin expression in the primary tumor in comparison to lymph node metastasis. The grouped cell tumors showed increased expression of E-cadherin in comparison to isolated cell tumors, either using the classification proposed by Jawhari et al. (p = 0.0230) and the classification proposed by Almeida et al. (p = 0.0043). In conclusion, abnormal expression of E-cadherin in the primary tumor, with frequent membranar immunostaining associated with the cytoplasmic marking (abnormal heterogeneous or mixed staining), reinforces the evidence that E-cadherin expression change in cancer is more qualitative than quantitative. The predominance of membranar expression in primary tumor and lymph node metastasis, with or without associated cytoplasmatic expression, particularly in cell-grouped tumors, suggests that E-cadherin presence is essential for local invasion and tumor progression, as opposed to the classical paradigm that tumor progression is exacerbated by the loss of this adhesion molecule.

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34

Huseynov, Inga [Verfasser]. "Analyse des löslichen E-Cadherins im Serum von Patienten mit malignem Melanom / Inga Huseynov." Köln : Deutsche Zentralbibliothek für Medizin, 2013. http://d-nb.info/1034150057/34.

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Chen, Pei-Ling. "The role of atypical cadherins in regulating photoreceptor synaptic specificity and maintenace in drosophila /." May be available electronically:, 2007. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.

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Willecke, Maria. "Regulation of organ size by the atypical cadherins fat and dachsous through the hippo pathway /." Tübingen, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253071.

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Machell, Naomi Haruko. "The expression and distribution of cadherins during rat ovarian development, folliculogenesis, luteinization, and oocyte maturation /." Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=82926.

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The cadherins are a superfamily of transmembrane glycoproteins that mediate calcium-dependent cell adhesion. Cadherins have several functions including roles in cell sorting and polarity, tissue morphogenesis, and embryogenesis. The study of cadherins in ovarian cells has thus far revealed important roles for them in ovarian cell survival, differentiation, and function. The ovary has a structured topology that undergoes organized and cyclical tissue remodeling events. It is our contention that cadherin expression influences ovarian structure and morphogenesis.
We have undertaken a series of studies to examine the expression of several cadherins in the rat ovary during the perinatal, prepubertal, and adult developmental periods. The studies focus on the ovarian topology and tissue remodeling processes in the ovary, such as folliculogenesis and corpus luteum formation. The results of our studies show that cadherin expression in the rat ovary is present at all stages of development and that their expression patterns are specific, but often overlapping. The patterns of cadherin expression correlate with the organization of the ovarian cell types into tissues. The distribution of E-, N-, P-, K- and OB-cadherin expression depends on age or the developmental stage of follicles, corpora lutea, and/or oocytes. We have observed changes in E- and P-cadherin expression during important developmental events such as initiation of follicle growth and antrum formation, and E- and N-cadherin expression during preovulatory follicle development, corpus luteum formation, and oocyte meiotic maturation. Our findings establish that ovarian cadherin expression is pervasive throughout its development, and in addition, the distribution and variation in expression patterns that we have observed, support the hypothesis that cadherins are involved in the organization and morphogenesis of the rat ovary.

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Dewitz, Carola [Verfasser]. "Dissecting classical cadherins roles in motor neuron nuclear organization in the spinal cord / Carola Dewitz." Berlin : Freie Universität Berlin, 2019. http://d-nb.info/1187244104/34.

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Bello, S. M. "The role of cadherins and catenins in the segregation and migration of spinal motor neurons." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1393502/.

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During development Spinal motor neurons are generated from their point of origin in the ventricular zone and migrate to reach their final settling position (motor pools) in the ventral spinal cord. The formation of motor pools depends on early motor column segregation; cadherins cell adhesive proteins have been implicated in the segregation of motor neurons in the spinal cord but the exact role for these cell-cell adhesion molecules in the organisation and migration of spinal motor neurons during development is not established. I show that during development expression of cadherins contribute to the organisation and migration of spinal lateral motor column (LMC) motor neurons to their final settling positions and there is close association between spinal motor neuron and radial glia. Misexpression of a dominant negative cadherin results in abnormal migration of spinal motor neurons and columnar desegregation. Similarly, expression of a dominant negative catenin (a major cytoplasmic binding partner to cadherins) results in columnar desegregation and arrest of motor neuron along their migratory route. Perturbations of Wnt signalling have no effect on motor neurons migration indicating that the results are due to perturbation of cadherin adhesive function. Our observation that cadherin and catenins but not Wnt signalling contributes to normal migration and segregation of spinal motor neurons, suggest that cadherin may act in close association with radial glia in directing the migration of spinal motor neurons similar to the establish role of radial glia in cortical neuronal migration.

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Wu, Jiahn-Chun. "The expression of cadherins and catenins in the developing rat and mouse testis and ovary /." The Ohio State University, 1994. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487858417981845.

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Lisowska, Justyna. "Control by CCM complex of the dialog between integrins and cadherins for the vascular stability." Thesis, Grenoble, 2014. http://www.theses.fr/2014GRENV065.

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Les interactions cellule-cellule et cellule-matrice extracellulaire (MEC) sont cruciales pour entretenir la cohésion tissulaire. Ces deux types d'adhésions sont fonctionnellement interconnectés par un dialogue permanent qui met en jeu des voies de signalisation convergentes régulant notamment l'architecture et la contractilité du cytosquelette d'acto-myosine sous-jacent. Ce dialogue permet d'établir un équilibre de forces intracellulaires en réponse à la tension appliquée par le milieu extérieur. L'endothélium des vaisseaux sanguins est un tissu soumis à des conditions mécaniques particulières. En plus des compressions intercellulaires subies par tout épithélium, les cellules endothéliales (CEs) doivent également subir et résister aux forces hémodynamiques du flux sanguin et à la rigidité de la lame basale – deux signaux mécaniques agissant de part et d'autre de l'endothélium. Les Cerebral Cavernous Maformations (CCM) ou encore angiomes caverneux sont des lésions vasculaires hémorragiques d'origine génétique qui se développent au niveau des capillaires du système nerveux central et qui se caractérisent par des défauts dans l'environnement proche des CEs. La perte des jonctions intercellulaires et du recouvrement par les cellules murales, l'organisation aberrante de la membrane basale aussi que la stagnation du flux sanguin sont les caractéristiques des CCM. C'est pourquoi nous avons choisi cette pathologie comme modèle intéressant de mécanotransduction mettant en jeu le dialogue entre les intégrines et les cadhérines. En effet, les trois gènes indifféremment mutés dans cette pathologie codent pour des protéines, CCM1-3, qui s'associent en un complexe ternaire et qui sont reconnues comme des acteurs importants de la régulation des jonctions adhérentes. Des études moléculaires et protéomiques montrant que le complexe CCM interagit avec la protéine ICAP-1, un régulateur négatif de l'intégrine β1, nous ont conduit à formuler l'hypothèse selon laquelle ce complexe jouerait un rôle pivot dans la signalisation croisée entre ces intégrines et cadhérines. Les études effectuées pendant ma thèse ont démontré que les protéines CCM régulent l'homéostasie tensionnelle médiée par les structures d'adhérence intercellulaires et à la MEC par leur action inhibitrice sur l'intégrine β1 et en controlant une balance d'activité entre les deux isoformes de ROCK, ROCK1 et ROCK2. Nous avons montré que, suite à la perte des protéines CCMs, la suractivation de l'intégrine β1 augmente la sensibilité des CEs aux signaux mécaniques comme la rigidité de la MEC ou les forces hémodynamiques du flux sanguin. Il en résulte une suractivation de la contractilité cellulaire dépendante de ROCK1 déclenchant une boucle de rétrocontrôle mécanique conduisant à l'amplification des tensions intra- et extracellulaire et brisant ainsi l'homéostasie tensionnelle pour favoriser le phénotype malin
Cell-cell or cell-matrix interactions have crucial roles in the maintenance of the physical cohesion of any tissue. In addition, growing body of evidence indicates that these two adhesion systems do not act independently, but rather are functionally interconnected by a permanent crosstalk. This dialog usually operates via common molecules that trigger convergent signaling as well as by actomyosin network which, by providing physical link, contributes to establishment of intracellular force counterbalancing tension applied by extracellular surrounding. Blood vessels endothelium is a particular tissue in term of mechanical conditions. Apart from intracellular compression, endothelial lining needs to resist hemodynamic forces as well as rigidity of the basal membrane - two mechanical inputs acting from opposite sides of the endothelial layer. Cerebral Cavernous Malformation (CCM) is a sporadically acquired or inherited disease of venous capillaries within neuro-vascular unit characterized by defects in all aspects of local microenvironment. Loss of intra-endothelial junctions and mural cell coverage, aberrant organization of basal lamina as well as stagnant blood flow are features of CCM lesions. Thereby, CCM became for us an interesting model to study mechanotrasduction process and in this context, the cross-talk between integrin and cadherin mediated adhesion structures. Indeed, CCM proteins are well recognized players involved in a control of VE-cadherin mediated intracellular junctions. In addition, CCM1 was found to interact with ICAP-1, a negative regulator of β1 integrin, raising the possibility that this complex most likely acts as molecular node regulating β1 integrin/ VE-cadherin convergent signaling pathways.Studies performed during this thesis have demonstrated that CCM complex coordinates cadherin- and integrin-mediated tensional homeostasis by repressing β1 integrin activation and maintaining a balance of activity between the two isoforms of RhoA-associated kinases ROCK1 and ROCK2. We have found that β1 integrin sustained over-activation upon CCM proteins loss contributes to increased ECs sensitivity to mechanical cues, such as ECM physical reorganization or hemodynamic force that in turn activates ROCK1-dependent contractility. This establishes a positive feedback mechanical loop that breaks tensional homeostasis and switches on the malignant phenotype

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Patricio, Flavia Rezende Pereira. "E-caderina e B-catenina : analise da expressão e relação com a evolução e prognostico nos tumores do cortex de adrenal em crianças." [s.n.], 2009. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308380.

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Orientador: Antonio Gonçalves de Oliveira Filho
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-08-13T04:54:32Z (GMT). No. of bitstreams: 1 Patricio_FlaviaRezendePereira_M.pdf: 2174141 bytes, checksum: 0011ea137b3f271896d984e54bb4f4d6 (MD5) Previous issue date: 2009
Resumo: Tumores do córtex da supra-renal (TCSR) em crianças são raros e correspondem a 0,2% dos tumores da infância. Estes tumores são endocrinologicamente ativos, causando na maioria das vezes, virilização do paciente associada, ou não, a um aumento de cortisol. O tratamento dos TCSR é principalmente cirúrgico, sendo a cirurgia com o procedimento de ressecção completa do tumor e sem ruptura a principal modalidade terapêutica. No entanto, a distinção entre tumores benignos e malignos, baseada exclusivamente na histologia, pode ser difícil de ser realizada. Os fatores prognósticos são baseados quase exclusivamente no estadiamento da doença, o qual leva em conta o peso e volume tumoral e a disseminação metastática do tumor. Estudos clínicos e experimentais sugerem que a propagação metastática em alguns tumores está relacionada aos níveis de E-caderina e ?-catenina, que são moléculas presentes no tecido epitelial normal, estando envolvidas diretamente na adesão intercelular. A análise da expressão destas moléculas pode fornecer dados que permite identificar grupos de pacientes mais propensos à evolução tumoral desfavorável, proporcionando, assim, um tratamento mais adequado e individualizado a estes pacientes. Com o objetivo de analisar a expressão da E-caderina e ?-catenina em crianças com TCSR e sua correlação com a evolução da doença, foi realizada uma revisão retrospectiva dos prontuários de 33 crianças com diagnóstico de TCSR tratadas no Centro Infantil Boldrini (Janeiro de 1998 a Janeiro de 2005). Foram coletados e analisados dados referentes ao sexo, idade, manifestações clínicas, estadiamento, tratamento e evolução dos pacientes. Para a análise imunoistoquímica, foi empregada a técnica de multitissue array com anticorpos específicos para E-caderina e ?-catenina em 30 tumores de crianças com TCSR e uma adrenal normal. Houve predominância do sexo feminino na amostra e a apresentação clínica mais freqüente foi a virilização. Nesta série, observou-se que crianças com idade inferior a dois anos apresentaram melhor prognóstico e, também que a ruptura e recidiva tumoral apresentaram influência negativa na sobrevida dos pacientes. A análise imunoistoquímica mostrou expressão da E-caderina em 73,3% e ?-catenina em 83,3% das crianças que apresentavam TCSR. Além disso, não foi verificada sua expressão na glândula adrenal normal. Quando avaliada a relação da expressão da E-caderina e ?-catenina com os estádios evolutivos da doença, não foi verificada associação significativa entre as variáveis. A positividade da E-caderina e ?-catenina na membrana celular, citoplasma ou núcleo, verificou-se que a expressão na membrana celular mostrou associação significativa com mau prognóstico
Abstract: Adrenal cortical tumor (ACT) in children are rare and they correspond to 0,2% of the tumors of the childhood. They are usually active, causing mainly virilization of patient associate or not with increased levels of corticoids. The treatment of the TCSR is mainly surgical, being the surgery with complete resection of the tumor without spillage the therapeutic mainstay. The distinction between benign and malignant tumors based exclusively on the histology can be difficult and very often uncertain. The prognostic factors are based almost exclusively on the staging of the disease, who takes into account the weight and volume tumoral and the metastatic dissemination. Clinical and experimental studies suggest that metastatic dissemination in some tumors is related with the levels of E-cadherin and ?-catenin. These molecules are found in the normal epithelial tissues and are strongly related with intercellular adhesion. The analysis of the expression of these molecules maybe can allow identifying groups of patients with higher risk of presenting unfavorable outcomes and ensuing appropriate and individualized treatment. With the objective of analyzing the expression of E-cadherin and ?-catenin in children with ACT and its correlation with the evolution of the disease, a retrospective chart review of 33 children with diagnosis of ACT treated at Centro Infantil Boldrini (January of 1998 through January of 2005). Data regarding sex, age, clinical presentation, staging, treatment and outcome were collected and analyzed. Multitissue array technique using specific antibodies for E-cadherin and ?-catenin was done in 30 tumors from children with ACT and 1 normal adrenal tissue. There was predominance of the feminine sex and the most frequent clinical presentation was virilization. In these series children with age bellow two years had a better outcome and tumoral spillage and relapse have had negative influence in the survival of the patients. Immunohistochemical analysis showed expression of E-cadherin in 73,3 % and ?-catenin in 83,3 % of the children who had ACT but showed no expression in the normal adrenal tissue. When the relationship between the expression of E-cadherin and ?-catenin with the stages of the disease was analyzed, no significant association was found. When analyzed the expression of E-cadherin and ?-catenin in the cellular membrane, cytoplasm or nucleus, its presence in the membrane of the cell was found as associated with poor outcome. As far we know, this is the first study to evaluate the expression of E-cadherin and ?-catenin in children with ACT and, although with small number of patients due to the rarity of the disease, it apparently shows some relationship with prognosis. When the relationship between the expression of E-cadherin and ?-catenin with the stages of the disease was analyzed, no significant association was found. When analyzed the expression of E-cadherin and ?-catenin in the cellular membrane, cytoplasm or nucleus, its presence in the membrane of the cell was found as associated with poor outcome. As far we know, this is the first study to evaluate the expression of E-cadherin and ?-catenin in children with ACT and, although with small number of patients due to the rarity of the disease, it apparently shows some relationship with prognosis
Mestrado
Cirurgia
Mestre em Cirurgia

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43

Chan, Wing-san. "Curcumin inhibits cell migration of nasopharyngeal carcinoma through reactivation of e-cadherin expression." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B4189697X.

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Vosnidou, Nancy Carol Hoffman. "Computational analysis of cadherins : sequence analysis of dimerization properties and quantum caculations of calcium coordination characteristics /." free to MU campus, to others for purchase, 2002. http://wwwlib.umi.com/cr/mo/fullcit?p3060154.

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Graff, Gretchen Melaine. "Cadherin-Based Adhesion Molecules for Classification of Melanoma with Aqua Technology." Yale University, 2008. http://ymtdl.med.yale.edu/theses/available/etd-08092007-132245/.

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Cadherin and catenin-family proteins regulate adhesion in malignant melanoma. Using AQUA (Automated Quantitative Analysis) to quantitate the levels of alpha-catenin, beta-catenin, p120-catenin, N-cadherin, E-cadherin, and P-cadherin in melanoma on tissue microarrays (TMAs), we classified 513 patients by protein expression using hierarchical clustering and regression analysis. The dendrogram supported positive correlations seen upon Spearman rho analysis of P-cadherin and beta-catenin (r=0.5238, p<0.0001) and negative, weak association of N-cadherin with other markers. Patients with high expression of N-cadherin had the highest 20-year survival rate (p=0.0003). Our adherens protein molecular classification of melanoma defines at least two distinctive sub-populations of melanoma patients, those with high expression of N-cadherin and those with low expression who have decreased survival. These findings extend previous cDNA array-based findings of an epithelioid class and neural crest class of melanomas.

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Arulanandam, Rozanne. "Novel mechanisms of Stat3 activation." Thesis, Kingston, Ont. : [s.n.], 2010. http://hdl.handle.net/1974/5442.

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Eriksson, Malin. "Manipulating neural stem cells." Stockholm, 2010. http://diss.kib.ki.se/2010/978-91-7409-853-2/.

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Tam, Hok-nang Alex, and 譚學能. "Epigenetic inactivation of protocadherin PCDH10 in esophageal cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B45011011.

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Callegaro, Clarissa Freitas. "Expressão de citoqueratinas, filagrina, involucrina, E-caderina e p63 em lesões de molusco contagioso." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/5/5133/tde-16032009-110633/.

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Introdução: O molusco contagioso (MC) é um vírus da família Poxviridae que infecta os queratinócitos epidérmicos levando a hiperplasia e formação de inclusões eosinofílicas intracitoplasmáticas os corpos de molluscum. Poucos estudos analisam as alterações induzidas por este Mollucipox vírus nas estruturas que compõem o citoesqueleto e a adesão celular dos queratinócitos. Objetivos: Verificar o padrão de expressão de citoqueratinas, filagrina, involucrina, E-caderina e p63 pela técnica de imuno-histoquímica em lesões de MC e compará-las com a epiderme adjacente aparentemente normal (EAAN). Método: Através de técnica de imuno-histoquímica, estudou-se a expressão de K1, K10, K14, K16, filagrina, involucrina, E-caderina e p63 em lesões de MC de 41 pacientes imunocompetentes. Os padrões de expressão nas lesões de MC foram comparados com a EAAN. Resultados: A expressão de K1/K10 ocorreu como o habitual nas camadas suprabasais da epiderme. A marcação de K14 foi observada nas camadas epidérmicas basal e suprabasal nas lesões de MC e EAAN. A K16, que é expressa somente em processos hiperproliferativos, foi demonstrada na camada espinhosa tanto nos focos de MC como na EAAN. Filagrina e involucrina expressaram-se nas camadas granulosa, espinhosa e em alguns casos até mesmo na camada basal na epiderme infectada e EAAN. A E-caderina esteve presente até a porção inferior dos corpos de molusco enquanto na EAAN apresentou-se nas camadas basal e espinhosa. A expressão nuclear do p63 ocorreu nas camadas basal e espinhosa tanto no MC como EAAN. Conclusão: A infecção pelo Molluscipox vírus parece interferir no processo de diferenciação terminal dos queratinócitos. A expressão tardia de K14 e p63 na camada espinhosa, assim como a expressão precoce de filagrina e involucrina, associada ao estado hiperproliferativo demonstrado pela presença aberrante de K16, refletem um distúrbio no processo de maturação dos queratinócitos infectados. As alterações observadas na EAAN podem representar evento precoce no distúrbio de queratinização induzido pelo vírus na pele infectada.
Background: Molluscum contagiosum (MC) is a Molluscipox virus infection of the epidermal keratinocytes with hyperplasia and intracytoplasmic inclusions the molluscum bodies (MB). Few studies address cytokeratins (K) profile in MC, mainly focusing the terminal epidermal keratinization process. Methods: In order to verify K1, K10, K14, K16, involucrin, filaggrin, E-cadherin and p63 expression in MC, 41 lesions were subjected to immunohistochemical technique. The immunolabeling pattern of MC was compared to adjacent normal appearing epidermis (ANAE). Results: K1 and K10 were expressed in supra basal layers of MC and ANAE. K14 was expressed in basal and suprabasal layers in MC and also in ANAE. K16 was expressed in MC and ANAE, through all spinous layers. Involucrin and filaggrin were observed in granular, spinous and even in basal layer of ANAE and MC. E-cadherin was present up to the first layers of epidermis with MB while ANAE exhibited E-cadherin labeling at basal and spinous layers. Basal and spinous layers keratinocytes nuclei, in both MC and ANAE, express p63. Conclusion: Infection by Molluscipox virus may noticeably alter keratinocyte differentiation status and cell adhesion. The presence of K14 and p63 in spinous layer, as well as early expression of involucrin and filaggrin, associated to a hyperproliferative state disclosed by the presence of K16, may be a result of a disruption in keratinocytes maturation process. The changes observed at ANAE may represent early events in keratinization disturbance.

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Barcelos, Andrezza Camarinha Napolitano. "Análise comparativa da expressão de citoqueratinas, involucrina, filagrina e e-caderina em verrugas planas e em lesões do tipo verruga plana na Epidermodisplasia Verruciforme." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5133/tde-30102008-153151/.

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Epidermodisplasia verruciforme (EV) é uma genodermatose rara, com susceptibilidade para infecção pelo vírus do papiloma humano, considerada modelo de oncogênese viral. Comparou-se a expressão epidérmica das citoqueratinas (K) 1, 10, 14, 4, 16, involucrina, filagrina e e-caderina, em lesões de verrugas planas e nas verrugas planas da EV através de método imunohistoquímico. Na EV houve ausência ou retardo de expressão (queratinócitos mais superficias) de K1/10, com substituição pela K14. Houve expressão basal e suprabasal de K14 em ambos os grupos, bem como positividade para K4 e 16, e expressão de involucrina nas camadas mais inferiores da epiderme. A expressão de filagrina não foi alterada, e a de e-caderina apresentou-se diminuída nas células coilocitóticas superficiais na EV
Epidermodisplasia verruciforme (EV) is a rare genodermatosis with susceptibility to human papillomavirus infection, considered a model of viral oncogenesis. We compared epidermal expression of cytokeratins (K) 1, 10, 14, 4, 16, involucrin, filaggrin and e-cadherin in plane warts and plane wart-type lesions in EV by immunohistochemical technique. In EV there was absent or retarded expression (more superficial keratinocytes) of K1/10, being substituted by K14. There was basal and suprabasal expression of K14 in both groups, as well as positivity for K4 and K16, and involucrin expression in more inferior layers of epidermis. Filaggrin expression was not altered, and e-cadherin was diminished in superficial koilocytotic cells in EV

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