The Experts below are selected from a list of 84 Experts worldwide ranked by ideXlab platform
Takashi Saku - One of the best experts on this subject based on the ideXlab platform.
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Keratin Pearl degradation in oral squamous cell carcinoma reciprocal roles of neutrophils and macrophages
Journal of Oral Pathology & Medicine, 2014Co-Authors: Ahmed Essa, Manabu Yamazaki, Satoshi Maruyama, Tatsuya Abe, Hamzah Babkair, Jun Cheng, Takashi SakuAbstract:Background We have reported that neutrophilic infiltration was associated with round-shaped dyskeratosis foci, a kind of Keratin Pearl, of oral carcinoma in situ and that those inflammatory cells are recruited from intra-epithelially entrapped blood vessels. Based on these lines of evidence, we have formulated a hypothesis that Keratin Pearls are terminally degraded by neutrophils. To confirm this hypothesis, we investigated immunohistochemically stepwise degradation of Keratin Pearls in oral squamous cell carcinoma (SCC) to clarify any other type scavenger cells in addition to neutrophils are involved in this particular degradation process. Methods Neutrophils (neutrophil elastase) and macrophage subpopulations (CD68, CD163 and CD204) were immunohistochemically localized in 30 cases of oral SCC with typical round-shaped Keratin Pearls. SCC cells were revealed by immunohistochemistry for Keratin (K) 17, and blood vessels were demonstrated by CD31. Results Keratin Pearl degradation process was divided into four steps: (i) intact stage: no macrophage infiltration but minimal neutrophils were found in Keratin Pearls; (ii) neutrophil recruit stage: no macrophage infiltration but focal neutrophilic infiltration within the Pearls; (iii) neutrophil predominant stage: dense neutrophil infiltration with minimal macrophages and segregated Keratinized cancer cells strongly positive for K17; and (iv) macrophage predominant stage: dense infiltration of CD68-, CD163 (mononuclear)- and CD204 (multinucleated)-positive macrophages engulfing detached Keratinized SCC cells. Conclusion Keratin Pearl degradation in oral SCC is strictly regulated by two types of scavenger cells: neutrophils, which perform initial tasks, and macrophages, which reciprocally take over from neutrophils the role to finalize the degradation processes.
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hemophagocytosis mediated Keratinization in oral carcinoma in situ and squamous cell carcinoma a possible histopathogenesis of Keratin Pearls
Journal of Cellular Physiology, 2013Co-Authors: Kamal Aleryani, Ahmed Essa, Manabu Yamazaki, Satoshi Maruyama, Tatsuya Abe, Hamzah Babkair, Jun Cheng, Masayuki Tsuneki, Takashi SakuAbstract:Although the histopathogenetic process of Keratin Pearls is still poorly understood, acceleration of Keratinization in squamous cell carcinoma (SCC) cells may represent one possible therapeutic avenue. Based on our histopathological observations, we have hypothesized that SCC cells are Keratinized by phagocytosis of extravasated erythrocytes. To confirm this hypothesis, we firstly examined immature Keratin Pearls in oral carcinoma in situ (CIS) and mature ones in SCC by immunohistochemistry. Concentric dyskeratotic cells in CIS Keratin Pearls became positive for Keratin (K) 10, K17, heme oxygenase-1 (HO-1), or protease activated receptor-2 (PAR-2), a candidate regulator for hemophagocytosis. When ZK-1 cells, an SCC cell system, were incubated with human peripheral blood erythrocytes, or with crude and purified hemoglobins (Hbs), their erythro-hemophagocytotic activities were confirmed by immunofluorescence. Immunofluorescence signals for K10, K17, and HO-1 were enhanced due to hemophagocytosis in time-dependent manners. mRNA expression levels for the three molecules were most enhanced by purified Hb, followed by crude Hb and erythrocytes. K17/K10 mRNA expression levels were more elevated when PAR-2 was activated in ZK-1 cells. The results indicated that immature and mature Keratin Pearls in CIS and SCC were generated by oxidative stresses derived from erythro-hemophagocytosis, which might mediate HO-1 expression and be regulated by PAR-2. Thus, hemorrhage from the rupture of blood vessels can be one of the triggers for Keratin Pearl formation in oral CIS and SCC. J. Cell. Physiol. 228: 1977–1988, 2013. © 2013 Wiley Periodicals, Inc.
Ahmed Essa - One of the best experts on this subject based on the ideXlab platform.
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Keratin Pearl degradation in oral squamous cell carcinoma reciprocal roles of neutrophils and macrophages
Journal of Oral Pathology & Medicine, 2014Co-Authors: Ahmed Essa, Manabu Yamazaki, Satoshi Maruyama, Tatsuya Abe, Hamzah Babkair, Jun Cheng, Takashi SakuAbstract:Background We have reported that neutrophilic infiltration was associated with round-shaped dyskeratosis foci, a kind of Keratin Pearl, of oral carcinoma in situ and that those inflammatory cells are recruited from intra-epithelially entrapped blood vessels. Based on these lines of evidence, we have formulated a hypothesis that Keratin Pearls are terminally degraded by neutrophils. To confirm this hypothesis, we investigated immunohistochemically stepwise degradation of Keratin Pearls in oral squamous cell carcinoma (SCC) to clarify any other type scavenger cells in addition to neutrophils are involved in this particular degradation process. Methods Neutrophils (neutrophil elastase) and macrophage subpopulations (CD68, CD163 and CD204) were immunohistochemically localized in 30 cases of oral SCC with typical round-shaped Keratin Pearls. SCC cells were revealed by immunohistochemistry for Keratin (K) 17, and blood vessels were demonstrated by CD31. Results Keratin Pearl degradation process was divided into four steps: (i) intact stage: no macrophage infiltration but minimal neutrophils were found in Keratin Pearls; (ii) neutrophil recruit stage: no macrophage infiltration but focal neutrophilic infiltration within the Pearls; (iii) neutrophil predominant stage: dense neutrophil infiltration with minimal macrophages and segregated Keratinized cancer cells strongly positive for K17; and (iv) macrophage predominant stage: dense infiltration of CD68-, CD163 (mononuclear)- and CD204 (multinucleated)-positive macrophages engulfing detached Keratinized SCC cells. Conclusion Keratin Pearl degradation in oral SCC is strictly regulated by two types of scavenger cells: neutrophils, which perform initial tasks, and macrophages, which reciprocally take over from neutrophils the role to finalize the degradation processes.
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hemophagocytosis mediated Keratinization in oral carcinoma in situ and squamous cell carcinoma a possible histopathogenesis of Keratin Pearls
Journal of Cellular Physiology, 2013Co-Authors: Kamal Aleryani, Ahmed Essa, Manabu Yamazaki, Satoshi Maruyama, Tatsuya Abe, Hamzah Babkair, Jun Cheng, Masayuki Tsuneki, Takashi SakuAbstract:Although the histopathogenetic process of Keratin Pearls is still poorly understood, acceleration of Keratinization in squamous cell carcinoma (SCC) cells may represent one possible therapeutic avenue. Based on our histopathological observations, we have hypothesized that SCC cells are Keratinized by phagocytosis of extravasated erythrocytes. To confirm this hypothesis, we firstly examined immature Keratin Pearls in oral carcinoma in situ (CIS) and mature ones in SCC by immunohistochemistry. Concentric dyskeratotic cells in CIS Keratin Pearls became positive for Keratin (K) 10, K17, heme oxygenase-1 (HO-1), or protease activated receptor-2 (PAR-2), a candidate regulator for hemophagocytosis. When ZK-1 cells, an SCC cell system, were incubated with human peripheral blood erythrocytes, or with crude and purified hemoglobins (Hbs), their erythro-hemophagocytotic activities were confirmed by immunofluorescence. Immunofluorescence signals for K10, K17, and HO-1 were enhanced due to hemophagocytosis in time-dependent manners. mRNA expression levels for the three molecules were most enhanced by purified Hb, followed by crude Hb and erythrocytes. K17/K10 mRNA expression levels were more elevated when PAR-2 was activated in ZK-1 cells. The results indicated that immature and mature Keratin Pearls in CIS and SCC were generated by oxidative stresses derived from erythro-hemophagocytosis, which might mediate HO-1 expression and be regulated by PAR-2. Thus, hemorrhage from the rupture of blood vessels can be one of the triggers for Keratin Pearl formation in oral CIS and SCC. J. Cell. Physiol. 228: 1977–1988, 2013. © 2013 Wiley Periodicals, Inc.
Edna Cukierman - One of the best experts on this subject based on the ideXlab platform.
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the functional interplay between egfr overexpression htert activation and p53 mutation in esophageal epithelial cells with activation of stromal fibroblasts induces tumor development invasion and differentiation
Genes & Development, 2007Co-Authors: Takaomi Okawa, Carmen Z Michaylira, Jiri Kalabis, Douglas B Stairs, Hiroshi Nakagawa, Claudia D Andl, Cameron N Johnstone, Andres J P Kleinszanto, Wafik S Eldeiry, Edna CukiermanAbstract:Esophageal cancer is a prototypic squamous cell cancer that carries a poor prognosis, primarily due to presentation at advanced stages. We used human esophageal epithelial cells as a platform to recapitulate esophageal squamous cell cancer, thereby providing insights into the molecular pathogenesis of squamous cell cancers in general. This was achieved through the retroviral-mediated transduction into normal, primary human esophageal epithelial cells of epidermal growth factor receptor (EGFR), the catalytic subunit of human telomerase (hTERT), and p53 R175H , genes that are frequently altered in human esophageal squamous cell cancer. These cells demonstrated increased migration and invasion when compared with control cells. When these genetically altered cells were placed within the in vivo-like context of an organotypic three-dimensional (3D) culture system, the cells formed a high-grade dysplastic epithelium with malignant cells invading into the stromal extracellular matrix (ECM). The invasive phenotype was in part modulated by the activation of matrix metalloproteinase-9 (MMP-9). Using pharmacological and genetic approaches to decrease MMP-9, invasion into the underlying ECM could be suppressed partially. In addition, tumor differentiation was influenced by the type of fibroblasts within the stromal ECM. To that end, fetal esophageal fibroblasts fostered a microenvironment conducive to poorly differentiated invading tumor cells, whereas fetal skin fibroblasts supported a well-differentiated tumor as illustrated by Keratin “Pearl” formation, a hallmark feature of well-differentiated squamous cell cancers. When inducible AKT was introduced into fetal skin esophageal fibroblasts, a more invasive, less-differentiated esophageal cancer phenotype was achieved. Invasion into the stromal ECM was attenuated by genetic knockdown of AKT1 as well as AKT2. Taken together, alterations in key oncogenes and tumor suppressor genes in esophageal epithelial cells, the composition and activation of fibroblasts, and the components of the ECM conspire to regulate the physical and biological properties of the stroma.
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the functional interplay between egfr overexpression htert activation and p53 mutation in esophageal epithelial cells with activation of stromal fibroblasts induces tumor development invasion and differentiation
Genes & Development, 2007Co-Authors: Takaomi Okawa, Carmen Z Michaylira, Jiri Kalabis, Douglas B Stairs, Hiroshi Nakagawa, Claudia D Andl, Cameron N Johnstone, Andres J P Kleinszanto, Wafik S Eldeiry, Edna CukiermanAbstract:Esophageal cancer is a prototypic squamous cell cancer that carries a poor prognosis, primarily due to presentation at advanced stages. We used human esophageal epithelial cells as a platform to recapitulate esophageal squamous cell cancer, thereby providing insights into the molecular pathogenesis of squamous cell cancers in general. This was achieved through the retroviral-mediated transduction into normal, primary human esophageal epithelial cells of epidermal growth factor receptor (EGFR), the catalytic subunit of human telomerase (hTERT), and p53 R175H , genes that are frequently altered in human esophageal squamous cell cancer. These cells demonstrated increased migration and invasion when compared with control cells. When these genetically altered cells were placed within the in vivo-like context of an organotypic three-dimensional (3D) culture system, the cells formed a high-grade dysplastic epithelium with malignant cells invading into the stromal extracellular matrix (ECM). The invasive phenotype was in part modulated by the activation of matrix metalloproteinase-9 (MMP-9). Using pharmacological and genetic approaches to decrease MMP-9, invasion into the underlying ECM could be suppressed partially. In addition, tumor differentiation was influenced by the type of fibroblasts within the stromal ECM. To that end, fetal esophageal fibroblasts fostered a microenvironment conducive to poorly differentiated invading tumor cells, whereas fetal skin fibroblasts supported a well-differentiated tumor as illustrated by Keratin “Pearl” formation, a hallmark feature of well-differentiated squamous cell cancers. When inducible AKT was introduced into fetal skin esophageal fibroblasts, a more invasive, less-differentiated esophageal cancer phenotype was achieved. Invasion into the stromal ECM was attenuated by genetic knockdown of AKT1 as well as AKT2. Taken together, alterations in key oncogenes and tumor suppressor genes in esophageal epithelial cells, the composition and activation of fibroblasts, and the components of the ECM conspire to regulate the physical and biological properties of the stroma.
John D Gottsch - One of the best experts on this subject based on the ideXlab platform.
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surgical management of anterior chamber epithelial cysts
American Journal of Ophthalmology, 2003Co-Authors: Julia A Haller, Walter J Stark, Amr Azab, Robert W Thomsen, John D GottschAbstract:Abstract Purpose To review management strategies for treatment of anterior chamber epithelial cysts. Design Retrospective review of consecutive interventional case series. Methods Charts of patients treated for epithelial ingrowth over a 10-year period by a single surgeon were reviewed. Cases of anterior chamber epithelial cysts were identified and recorded, including details of ocular history, preoperative and postoperative acuity, intraocular pressure (IOP), and ocular examination, type of surgical intervention, and details of further procedures performed. Results Seven eyes with epithelial cysts were identified. Patient age ranged from 1.5 to 53 years at presentation. Four patients were children. In four eyes, cysts were secondary to trauma, one case was presumably congenital, one case developed after corneal perforation in an eye with Terrien’s marginal degeneration, and one case developed after penetrating keratoplasty (PK). Three eyes were treated with vitrectomy, en bloc resection of the cyst and associated tissue, fluid–air exchange and cryotherapy. The last four eyes were treated with a new conservative strategy of cyst aspiration (three cases) or local excision (one Keratin “Pearl” cyst), and endolaser photocoagulation of the collapsed cyst wall/base. All epithelial tissue was successfully eradicated by clinical criteria; one case required repeat excision (follow-up, 9 to 78 months, mean 45). Two eyes required later surgery for elevated IOP, two for cataract extraction and one for repeat PK. Final visual acuity ranged from 20/20 to hand motions, depending on associated ocular damage. Best-corrected visual results were obtained in the more conservatively managed eyes. Conclusions Anterior chamber epithelial cysts can be managed conservatively in selected cases with good results. This strategy may be particularly useful in children’s eyes, where preservation of the lens, iris, and other structures may facilitate amblyopia management.
Hamzah Babkair - One of the best experts on this subject based on the ideXlab platform.
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Keratin Pearl degradation in oral squamous cell carcinoma reciprocal roles of neutrophils and macrophages
Journal of Oral Pathology & Medicine, 2014Co-Authors: Ahmed Essa, Manabu Yamazaki, Satoshi Maruyama, Tatsuya Abe, Hamzah Babkair, Jun Cheng, Takashi SakuAbstract:Background We have reported that neutrophilic infiltration was associated with round-shaped dyskeratosis foci, a kind of Keratin Pearl, of oral carcinoma in situ and that those inflammatory cells are recruited from intra-epithelially entrapped blood vessels. Based on these lines of evidence, we have formulated a hypothesis that Keratin Pearls are terminally degraded by neutrophils. To confirm this hypothesis, we investigated immunohistochemically stepwise degradation of Keratin Pearls in oral squamous cell carcinoma (SCC) to clarify any other type scavenger cells in addition to neutrophils are involved in this particular degradation process. Methods Neutrophils (neutrophil elastase) and macrophage subpopulations (CD68, CD163 and CD204) were immunohistochemically localized in 30 cases of oral SCC with typical round-shaped Keratin Pearls. SCC cells were revealed by immunohistochemistry for Keratin (K) 17, and blood vessels were demonstrated by CD31. Results Keratin Pearl degradation process was divided into four steps: (i) intact stage: no macrophage infiltration but minimal neutrophils were found in Keratin Pearls; (ii) neutrophil recruit stage: no macrophage infiltration but focal neutrophilic infiltration within the Pearls; (iii) neutrophil predominant stage: dense neutrophil infiltration with minimal macrophages and segregated Keratinized cancer cells strongly positive for K17; and (iv) macrophage predominant stage: dense infiltration of CD68-, CD163 (mononuclear)- and CD204 (multinucleated)-positive macrophages engulfing detached Keratinized SCC cells. Conclusion Keratin Pearl degradation in oral SCC is strictly regulated by two types of scavenger cells: neutrophils, which perform initial tasks, and macrophages, which reciprocally take over from neutrophils the role to finalize the degradation processes.
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hemophagocytosis mediated Keratinization in oral carcinoma in situ and squamous cell carcinoma a possible histopathogenesis of Keratin Pearls
Journal of Cellular Physiology, 2013Co-Authors: Kamal Aleryani, Ahmed Essa, Manabu Yamazaki, Satoshi Maruyama, Tatsuya Abe, Hamzah Babkair, Jun Cheng, Masayuki Tsuneki, Takashi SakuAbstract:Although the histopathogenetic process of Keratin Pearls is still poorly understood, acceleration of Keratinization in squamous cell carcinoma (SCC) cells may represent one possible therapeutic avenue. Based on our histopathological observations, we have hypothesized that SCC cells are Keratinized by phagocytosis of extravasated erythrocytes. To confirm this hypothesis, we firstly examined immature Keratin Pearls in oral carcinoma in situ (CIS) and mature ones in SCC by immunohistochemistry. Concentric dyskeratotic cells in CIS Keratin Pearls became positive for Keratin (K) 10, K17, heme oxygenase-1 (HO-1), or protease activated receptor-2 (PAR-2), a candidate regulator for hemophagocytosis. When ZK-1 cells, an SCC cell system, were incubated with human peripheral blood erythrocytes, or with crude and purified hemoglobins (Hbs), their erythro-hemophagocytotic activities were confirmed by immunofluorescence. Immunofluorescence signals for K10, K17, and HO-1 were enhanced due to hemophagocytosis in time-dependent manners. mRNA expression levels for the three molecules were most enhanced by purified Hb, followed by crude Hb and erythrocytes. K17/K10 mRNA expression levels were more elevated when PAR-2 was activated in ZK-1 cells. The results indicated that immature and mature Keratin Pearls in CIS and SCC were generated by oxidative stresses derived from erythro-hemophagocytosis, which might mediate HO-1 expression and be regulated by PAR-2. Thus, hemorrhage from the rupture of blood vessels can be one of the triggers for Keratin Pearl formation in oral CIS and SCC. J. Cell. Physiol. 228: 1977–1988, 2013. © 2013 Wiley Periodicals, Inc.
