• IMMUNE NETWORK
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• v.13 no.5
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• pp.222-226
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• 2013

Translocations involving chromosome 21q22 are frequently observed in hematologic malignancies including acute myeloid leukemia (AML), most of which have been known to be involved in malignant transformation through transcriptional dysregulation of Runt-related transcription factor 1 (RUNX1) target genes. Nineteen RUNX1 translocational partner genes, at least, have been identified, but not Homeobox A (HOXA) genes so far. We report a novel translocation of RUNX1 into the HOXA gene cluster in a 57-year-old female AML patient who had been diagnosed with myelofibrosis 39 months ahead. G-banding showed 46,XX,t(7;21)(p15;q22). The involvement of RUNX1 and HOXA genes was confirmed by fluorescence in situ hybridization.

• Journal of Digestive Cancer Research
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• v.11 no.1
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• pp.30-34
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• 2023

Since the 1990s, serrated polyps have been established to contribute to intermediate cancer development, and their importance has begun to be recognized. Serrated polyps are morphologically difficult to detect through endoscopy, and an effective resection method has not been established. Among serrated polyps, studies on sessile serrated lesions, with a relatively high risk of colorectal cancer transformation and detected with difficulty, are in progress. Studies to date describe the endoscopic features as mucus cap, surface debris or stool, attenuation of underlying vasculature, cloud-like surface, dark spots in crypts, and ill-defined irregular border. Additionally, it is expected that relatively large serrated polyps can be safely removed through cold snare resection. A plan for an effective management of serrated polyps through continuous research in the future is warranted.

• International Journal of Computer Science & Network Security
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• v.21 no.2
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• pp.120-130
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• 2021

The spinal cord or CSF surgery is a very complex process. It requires continuous pre and post-surgery evaluation to have a better ability to diagnose the disease. To detect automatically the suspected areas of tumors and symptoms of CSF leakage during the development of the tumor inside of the brain. We propose a new method based on using computer software that generates statistical results through data gathered during surgeries and operations. We performed statistical computation and data collection through the Google Source for the UK National Cancer Database. The purpose of this study is to address the above problems related to the accuracy of missing hybrid KNN values and finding the distance of tumor in terms of brain cancer or CSF images. This research aims to create a framework that can classify the damaged area of cancer or tumors using high-dimensional image segmentation and Laplace transformation method. A high-dimensional image segmentation method is implemented by software modelling techniques with measures the width, percentage, and size of cells within the brain, as well as enhance the efficiency of the hybrid KNN algorithm and Laplace transformation make it deal the non-zero values in terms of missing values form with the using of Frobenius Matrix for deal the space into non-zero values. Our proposed algorithm takes the longest values of KNN (K = 1-100), which is successfully demonstrated in a 4-dimensional modulation method that monitors the lighting field that can be used in the field of light emission. Conclusion: This approach dramatically improves the efficiency of hybrid KNN method and the detection of tumor region using 4-D segmentation method. The simulation results verified the performance of the proposed method is improved by 92% sensitivity of 60% specificity and 70.50% accuracy respectively.

• Proceedings of the Ginseng society Conference
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• 1990.06a
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• pp.96-101
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• 1990

• Journal of Ginseng Research
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• v.14 no.2
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• pp.238-243
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• 1990

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.2
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• pp.669-672
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• 2013

Objective: To investigate the expression of Twist and E-cadherin in ovarian cancer tissues as well as the role of epithelial-mesenchymal transformation (EMT) in ovarian cancer metastasis. Method: The expressions of Twist and E-cadherin in 54 cases of ovarian cancer and paracancerous tissues were detected by Western blottin g and reverse transcriptase polymerase chain reaction. We used RNA interference to silence Twist expression in human ovarian cancer cell line, and detected E-cadherin expression using Western blotting. Results: There was an increase in the relative abundance of Twist proteins and a decrease in E-cadherin in ovarian cancer compared with normal ovary tissues (P < 0.05). The expression levels of Twist and E-cadherin mRNA were $1.49{\pm}0.53$ and $0.82{\pm}0.24$ in ovarian cancer, and $1.14{\pm}0.38$ and $1.08{\pm}0.19$ in paracancerous tissues, respectively. The difference between the indicators in ovarian cancer and in paracancerous tissues was statistically significant (P < 0.05). When the Twist expression was silenced in an ovarian cancer cell line, the expression of the E-cadherin protein increased (P<0.05). Conclusion: The expression of Twist is upregulated, whereas that of E-cadherin is downregulated in ovarian cancer. EMT, mediated by Twist, may be correlated with ovarian cancer metastasis.

• BMB Reports
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• v.51 no.7
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• pp.319-326
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• 2018

Increasing evidence suggests that cancer stem cell (CSC) theory represents an important mechanism underlying the observed failure of existing therapeutic modalities to fully eradicate cancers. In addition to their more established role in maintaining minimal residual disease after treatment and forming the new bulk of the tumor, CSCs might also critically contribute to tumor recurrence and metastasis. For this reason, specific elimination of CSCs may thus represent one of the most important treatment strategies. Emerging evidence has shown that CSCs have a different metabolic phenotype to that of differentiated bulk tumor cells, and these specific metabolic activities directly participate in the process of CSC transformation or support the biological processes that enable tumor progression. Exploring the role of CSC metabolism and the mechanism of the metabolic plasticity of CSCs has become a major focus in current cancer research. The targeting of CSC metabolism may provide new effective therapies to reduce the risk of recurrence and metastasis. In this review, we summarize the most significant discoveries regarding the metabolism of CSCs and highlight recent approaches in targeting CSC metabolism.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.2
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• pp.455-461
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• 2016

Galectins are ${\beta}$-galactoside binding lectins that contain one or more carbohydrate recognition domains. As a consequence of sugar-binding properties, galectins exhibit a variety of interactions with glycoproteins, thus playing important roles in various pathological processes. A number of studies have shown roles of galectins in cancer. Galectin-7 is a prototype member of the galectin family implicated in epithelial stratification and cell migration. It can act as a potent dual regulator in different types of cancer. Galectin-7 may contribute either to neoplastic transformation and tumour progression through regulation of cell growth, cell cycle, angiogenesis, apoptosis and cell migration or may have a protective effect in cancer depending on the tissue type. A perusal of the literature indicates particular roles of galectin-7 in carcinomas and melanomas, while contributions await greater exploration in other types of cancers including sarcomas and leukemia. This review collectively summarizes available literature on expression and roles of galectin-7 in different cancers.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.6
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• pp.2429-2435
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• 2012

Methyl isocyanate may have a role in cancer etiology, although the link is unclear. There is evidence in the literature that it can induce cancer in animals but the carcinogenic potency is weak. Pheochromocytoma of adrenal medulla and acinar cell tumors of pancreas have been observed in methyl isocyanate exposed animals. Conversely, emerging data from population-based epidemiological studies are contradictory since there is no evidence of such cancers in methyl isocyanate exposed humans. Recently, we reported a high prevalence of breast and lung cancers in such a population in Bhopal. In vitro findings appearing in the latest scientific literature suggest that genomic instability is caused by methyl isocyanate analogs in lung, colon, kidney, ovary epithelial cells, and that hepatocytes may undergo oncogenic transformation, have obvious implications. The conflicting information prompted us to present this update over the last three decades on methyl isocyanate-induced cancers after an extensive literature search using PubMed. While the pertinent literature remains limited, with a scarcity of strong laboratory analyses and field-epidemiological investigations, our succinct review of animal and human epidemiological data including in vitro evidences, should hopefully provide more insight to researchers, toxicologists, and public health professionals concerned with validation of the carcinogenicity of methyl isocyanate in humans.

• Archives of Pharmacal Research
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• v.28 no.1
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• pp.1-15
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• 2005

Cancer is still a major global health concern even after an everlasting strive in conquering this dread disease. Emphasis is now given to chemoprevention to reduce the risk of cancer and also to improve the quality of life among cancer afflicted individuals. Recent progress in molecular biology of cancer has identified key components of the cellular signaling network, whose functional abnormality results in undesired alterations in cellular homeostasis, creating a cellular microenvironment that favors premalignant and malignant transformation. Multiple lines of evidence suggest an elevated expression of cyclooxygenase-2 (COX-2) is causally linked to cancer. In response to oxidative/pro-inflammatory stimuli, turning on unusual signaling arrays mediated through diverse classes of kinases and transcription factors results in aberrant expression of COX-2. Population-based as well as laboratory studies have explored a broad spectrum of chemopreventive agents including selective COX-2 inhibitors and a wide variety of anti-inflammatory phytochemicals, which have been shown to target cellular signaling molecules as underlying mechanisms of chemoprevention. Thus, unraveling signaling pathways regulating aberrant COX-2 expression and targeted blocking of one or more components of those signal cascades may be exploited in searching chemopreventive agents in the future.