• Asian Pacific Journal of Cancer Prevention
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• v.17 no.8
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• pp.4013-4017
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• 2016

Background: To compare the pathological findings and oncologic outcomes of stage IA cervical carcinoma patients, between adenocarcinoma and squamous cell carcinoma cases. Materials and Methods: A total of 151 medical records of stage IA cervical carcinoma patients undergoing primary surgical treatment during 2006-2013 were reviewed. Information from pathological diagnosis and recurrence rates were compared with descriptive statistical analysis. The Kaplan-Meier method and Cox proportional hazards model were used for survival analysis. Results: The median age was 48.9 years. There was no significant difference in rates of lymph node, parametrium, uterine, vaginal, or ovarian metastasis, when comparing adenocarcinoma with squamous cell carcinoma. Overall recurrence rates of adenocarcinoma (5.7%) and squamous cell carcinoma (2.6%) were not statistically significant different, even when stratified by stage. When comparing progression free survival with squamous cell carcinoma, adenocarcinoma had an HR of 0.448 (0.073-2.746), p=0.386. Conclusions: Microinvasive adenocarcinoma of cervix has similar rate of extracervical involvement and oncologic outcomes to squamous cell carcinoma.

• BMB Reports
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• v.45 no.10
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• pp.554-559
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• 2012

Oligosaccharide modification by N-acetylglucosaminyltransferase-V (GnT-V), a glycosyltransferase encoded by the Mgat5 gene that catalyzes the formation of ${\beta}1$,6GlcNAc (N-acetylglucosamine) branches on N-glycans, is thought to be associated with cancer growth and metastasis. Overexpression of GnT-V in cancer cells enhances the signaling of growth factors such as epidermal growth factor by increasing galectin-3 binding to polylactosamine structures on receptor N-glycans. In contrast, GnT-V deficient mice are born healthy and lack ${\beta}1$,6GlcNAc branches on N-glycans, but develop immunological disorders due to T-cell dysfunction at 12-20 months of age. We have developed Mgat5 transgenic (Tg) mice (GnT-V Tg mice) using a ${\beta}$-actin promoter and found characteristic phenotypes in skin, liver, and T cells in the mice. Although the GnT-V Tg mice do not develop spontaneous cancers in any organs, there are differences in the response to external stimuli between wild-type and GnT-V Tg mice. These changes are similar to those seen in cancer progression but are unexpected in some aspects. In this review, we summarize what is known about GnT-V functions in skin and liver cells as a means to understand the physiological roles of GnT-V in mice.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.11
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• pp.6215-6220
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• 2013

Kisspeptins (KPs) encoded by the KiSS-1 gene are C-terminally amidated peptide products, including KP-10, KP-13, KP-14 and KP-54, which are endogenous agonists for the G-protein coupled receptor-54 (GPR54). Functional analyses have demonstrated fundamental roles of KiSS-1 in whole body homeostasis including sexual differentiation of brain, action on sex steroids and metabolic regulation of fertility essential for human puberty and maintenance of adult reproduction. In addition, intensive recent investigations have provided substantial evidence suggesting roles of Kisspeptin signalling via its receptor GPR54 in the suppression of metastasis with a variety of cancers. The present review highlights the latest studies regarding the role of Kisspeptins and the KiSS-1 gene in tumor progression and also suggests targeting the KiSS-1/GPR54 system may represent a novel therapeutic approach for cancers. Further investigations are essential to elucidate the complex pathways regulated by the Kisspeptins and how these pathways might be involved in the suppression of metastasis across a range of cancers.

• Radiation Oncology Journal
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• v.34 no.3
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• pp.209-215
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• 2016

Purpose: We sought to determine if organ preservation (OP) with neoadjuvant chemoradiation (CRT) was feasible in patients with sinonasal cancer determined to require exenteration. Materials and Methods: Twenty patients were determined to require exenteration for definitive treatment from 2005 to 2014. Fourteen patients underwent OP and 6 patients received exenteration with adjuvant CRT. Exenteration free survival (EFS), locoregional control (LRC), progression-free survival (PFS), and overall survival (OS) were estimated. Results: Five patients (36%) receiving OP had complete disease response at time of surgery. With a median follow-up of 18.8 months, EFS was 62% at 2 years for patients undergoing OP. At 2 years, there were no significant differences in LRC, PFS or OS (all all p > 0.050) between the groups. Less grade 3 or greater toxicity was seen in patients undergoing OP (p = 0.003). Visual function was preserved in all patients undergoing OP. Conclusion: For patients with sinonasal cancer, OP may avoid exenteration, offering similar disease control and improved toxicity.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.5
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• pp.2021-2023
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• 2012

Purpose: DBC2 (Deleted in Breast Cancer 2) has been indicated to be a tumor suppressor gene in many cancers including lung adenocarcinoma recently. In this study, we aimed to explore the expression status of DBC2 in different subtypes of lung adenocarcinoma (from pre-invasive to invasive lesions), and to determine if downregulation becomes more marked with pathological progression. Methods: We collected 172 tissue samples from different subtypes of lung adenocarcinoma and investigated the frequency of DBC2 loss by immunohistochemistry. Results: Our results indicated that DBC2 downregulation is a relatively frequent event in lung adenocarcinoma. Moreover, as the adenocarcinoma subtype turns to be more invasive, more downregulation occurred. Conclusion: We conclude that loss of DBC2 expression is an early and progressive event in the pathogenesis of lung adenocarcinoma. Positive DBC2 immunohistochemistry may become an indicator for early stage disease and better prognosis of lung adenocarcinomas.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.5
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• pp.3315-3318
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• 2013

Gall bladder carcinoma is the most common cancer of biliary tree, characterized by rapid progression and a very high mortality rate. Detection at an early stage, however, is indicative of a very good prognosis and prolonged survival. The practice of histopathological examination of gall bladder specimens removed for clinically benign conditions and its usefulness has been a subject of controversy. The present prospective study was carried out over a period of four years in order to find out the incidence of unsuspected gallbladder carcinoma in cholecystectomy specimens received in our histopathology laboratory and to analyze their clinico-pathological features. A total of 4,115 cases were examined. Incidentally detected cases comprised 0.44%, which accounted for 72% of all gall bladder carcinomas detected. The majority were in an early, surgically resectable stage. From the results of this study we recommend that in India and other countries with relatively high incidences of gall bladder carcinoma, all cholecystectomy specimens should be submitted to histopathology laboratory, as this is the only means by which malignancies can be detected at an early, potentially curable stage.

• Korean Journal of Head & Neck Oncology
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• v.33 no.1
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• pp.1-5
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• 2017

Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer globally with high morbidity and mortality. Immune surveillance is well recognized as an important mechanism to prevent development or progression of HNSCC. HNSCC can escape the immune system through multiple mechanisms including development of tolerance in T cells and inhibition of T-cell-related pathways, generally referred to as checkpoint inhibitors. Recent clinical trials have demonstrated a clear advantage in advanced HNSCC patients treated with immune checkpoint blockade. Right at the front of the new era of immunotherapy, we will review current knowledge of immune escape mechanisms and clinical implication for HNSCC.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.35 no.4
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• pp.199-204
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• 2009

Purpose: The purpose of this study is to investigate the epithelial-mesenchymal transition (EMT) induced by Snail transcription factor and Snail-transfected in vivo tumors with histopathological features. Materials and methods: We induced in vivo xenografted tumorigenesis in the oral vestibules of nude mice by a Snail transfected HaCaT cell line and investigated morphological and immunohistochemical features in Snail expressive tumors. Results: We identified tumor masses in 14 out of 15 nude mice in the HaCaT-Snail cell inoculation group, but no tumors were present in any of the HaCaT cell inoculation group. Induced tumors showed features of poorly differentiated carcinoma with invasion to neighboring muscles and bones. The HaCaT-Snail tumors showed decreased expressions of E-cadherin and cytokeratin, but showed increased expressions of vimentin and N-cadherin. Discussion: The Snail transfected xenograft can improve productivity of malignant tumors, show various histopathological features including invasive growth, and aid in the investigation of tumor progression and the interaction with surrounding tissues.

• Molecules and Cells
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• v.37 no.4
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• pp.286-294
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• 2014

Mammalian polo-like kinase 1 (Plk1) has been studied intensively as a key regulator of various cell cycle events that are critical for proper M-phase progression. The polobox domain (PBD) present in Plk1's C-terminal noncatalytic region has been shown to play a central role in targeting the N-terminal kinase domain of Plk1 to specific subcellular locations. Subsequent studies reveal that PBD binds to a phosphorylated motif generated by one of the two mechanisms - self-priming by Plk1 itself or non-self-priming by a Pro-directed kinase, such as Cdc2. Here, we comparatively review the differences in the biochemical steps of these mechanisms and discuss their physiological significance. Considering the diverse functions of Plk1 during the cell cycle, a better understanding of how the catalytic activity of Plk1 functions in concert with its cisacting PBD and how this coordinated process is intricately regulated to promote Plk1 functions will be important for providing new insights into different mechanisms underlying various Plk1-mediated biological events that occur at the multiple stages of the cell cycle.

• Radiation Oncology Journal
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• v.36 no.3
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• pp.172-181
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• 2018

Successful anticancer strategies require a differential response between tumor and normal tissue (i.e., a therapeutic ratio). In fact, improving the effectiveness of a cancer therapeutic is of no clinical value in the absence of a significant increase in the differential response between tumor and normal tissue. Although radiation dose escalation with the use of intensity modulated radiation therapy has permitted the maximum tolerable dose for most locally advanced cancers, improvements in tumor control without damaging normal adjacent tissues are needed. As a means of increasing the therapeutic ratio, several new approaches are under development. Drugs targeting signal transduction pathways in cancer progression and more recently, immunotherapeutics targeting specific immune cell subsets have entered the clinic with promising early results. Radiobiological research is underway to address pressing questions as to the dose per fraction, irradiated tumor volume and time sequence of the drug administration. To exploit these exciting novel strategies, a better understanding is needed of the cellular and molecular pathways responsible for both cancer and normal tissue and organ response, including the role of radiation-induced accelerated senescence. This review will highlight the current understanding of promising biologically targeted therapies to enhance the radiation therapeutic ratio.