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  • 1
    Online Resource
    Online Resource
    Abstract 5476: CIP2A can be a therapeutic target of rapamycin in radioresistant head and neck cancer with P53 mutation
    American Association for Cancer Research (AACR) ; 2017
    In:  Cancer Research Vol. 77, No. 13_Supplement ( 2017-07-01), p. 5476-5476
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 77, No. 13_Supplement ( 2017-07-01), p. 5476-5476
    Abstract: The presence of p53 mutation was associated with poor survival in various tumors. The involvement of p53 in apoptosis and cell-cycle control makes it a plausible biomarker of prognosis . Classifying TP53 mutations in HNSCC described disruptive TP53 mutation in either the L2 or L3 loop of the DNA binding domain, resulting in polarity change within the protein, or stop cordon. Disruptive TP53 mutation in HNSCC tumors predicts for locoregional recurrence, due to increased radioresistance via the inhibition of senescence. Senescence induction contributes to cancer therapy responses and is crucial for p53-mediated tumor suppression. However, whether p53 inactivation actively suppresses senescence induction has been unclear. Here, we found that overexpression CIP2A (cancerous inhibitor of protein phosphatase 2A) positively correlated with presence of p53 mutation in head and neck cancer and mediates radioresistance through suppression of radiation induced senescence. And we demonstrated that rapamycin could induce senescence via CIP2A downregulation and increase radiosensitivity in p53 disruptive mutation cell line. This is the first investigation to analyze the role of CI2A in resistance to the radiotherapy of head and neck cancer. As a consequence, a greater understanding of radioresistance mechanisms through our results in head and neck cancer with p53 mutation will enable the rational design of combination regimens and sequential treatment algorithms to improve clinical outcomes and points to the usefulness of CIP2A as a biomarker to predict clinical response to rapamycin in head and neck cancer. Citation Format: Song Hee Kim, Won hyeok Lee, Myung Jin Lee, Hyo Won Chang, Ji Won Kim, Mi Ra Kim, Jung Je Park, Myung Woul Han, Sang Yoon Kim. CIP2A can be a therapeutic target of rapamycin in radioresistant head and neck cancer with P53 mutation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 5476. doi:10.1158/1538-7445.AM2017-5476
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2017-5476
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
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  • 2
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    Online Resource
    Homotypic Interaction of Stabilin-2 Plays a Critical Role in Lymph Node Metastasis of Tongue Cancer
    Anticancer Research USA Inc. ; 2016
    In:  Anticancer Research Vol. 36, No. 12 ( 2016-12-1), p. 6611-6618
    Details
    In: Anticancer Research, Anticancer Research USA Inc., Vol. 36, No. 12 ( 2016-12-1), p. 6611-6618
    Type of Medium: Online Resource
    ISSN: 0250-7005 , 1791-7530
    URL: Journal
    URL: Article
    DOI: 10.21873/anticanres
    DOI: 10.21873/anticanres.11267
    RVK:
    XA 10000
    Language: Unknown
    Publisher: Anticancer Research USA Inc.
    Publication Date: 2016
    detail.hit.zdb_id: 2145376-7
    detail.hit.zdb_id: 604549-2
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  • 3
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    Abstract 2278: Tumor microenvironment might be more important than pro-angiogenic chemotactic factors for tumor angiogenesis
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 2278-2278
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 2278-2278
    Abstract: During angiogenesis, many different tumor cytokines have been known to be involved in the regulation of chemotactic endothelial cell migration. Among those, a vascular endothelial growth factor (VEGF) is one of the most essential pro-angiogenic factors and the blockage of VEGF action through competitive inhibition on its receptor or by using of neutralizing antibody such as avastin has been considered as a promising anti-cancer approach to treat several solid tumors. However, despite their ability of releasing VEGF, some cancers show scarce angiogenesis and resistance to avastin treatment. To explore key factors deciding tumor angiogenesis apart from well-known pro-angiogenic cytokines, we compared the pro-angiogenic capability of the AMC-HN9 head and neck cancer cell line (HN9) which has a low degree of angiogenesis in vivo and are reluctant to avastin treatment with that of the highly angiogenic AMC-HN3 cancer cell line (HN3). Of interest, in vitro cytokine assay of HN9 culture media revealed no difference in the secretion profile of pro-angiogenic cytokines such as VEGF, PlGF, FGF2 and PDGF compared with those of HN3. In addition, HN9 media could strongly promoted tubular formation of HUVECs and migration of fibroblasts in vitro as much as HN3 could. Next, we proceeded to HN9 xenograft co-injected with ECM molecules including fibronectin, collagen III or matrigel. In the co-injected xenografts, density of CD34 positivity significantly increased and the tumor growth exceeded that of HN9 alone-injected ones. Moreover, prominent fibroblast infiltration adjacent to tumor vessels was detected in the co-injected xenografts. Taken together, these results imply that the formation of extracellular matrix surrounding tumor cells and the presence of activated fibroblasts are pre-requisites and more decisive in angiogenesis than tumor secreted pro-angiogenic cytokine per se. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2278.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM10-2278
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 4
    Online Resource
    Online Resource
    Quantitative Shear Wave Elastography in the Evaluation of Metastatic Cervical Lymph Nodes
    Elsevier BV ; 2013
    In:  Ultrasound in Medicine & Biology Vol. 39, No. 6 ( 2013-06), p. 935-940
    Details
    In: Ultrasound in Medicine & Biology, Elsevier BV, Vol. 39, No. 6 ( 2013-06), p. 935-940
    Type of Medium: Online Resource
    ISSN: 0301-5629
    URL: Article
    DOI: 10.1016/j.ultrasmedbio.2012.12.009
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2013
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    SSG: 12
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  • 5
    Online Resource
    Online Resource
    Importance of HPV involvement and FOXP3+ T-cell status as prognostic factors in tonsilar squamous cell carcinoma.
    American Society of Clinical Oncology (ASCO) ; 2012
    In:  Journal of Clinical Oncology Vol. 30, No. 15_suppl ( 2012-05-20), p. 5586-5586
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 30, No. 15_suppl ( 2012-05-20), p. 5586-5586
    Abstract: 5586 Background: Human papillomavirus (HPV) status is a strong and independent favorable prognostic factor for survival in tonsilar squamous cell cancer (TSCC). The reason for the improved survival in HPV associated TSCC is unclear. Recently, activation of immune surveillance mechanism against non-self Ag is postulated to one of reasonable causes as favorable prognosis of HPV associated with TSCC. Methods: We reviewed the medical records of histologically confirmed locally advanced TSCC patients, curatively treated in Asan Medical Center from January 2000 to December 2008. The immunohistochemistry (IHC) assays for p16 and FOXP3 were done in TSCC pafaffin-embedded samples. Results: We identified 79 patients who met the inclusion criteria. The median age was 54 years (range 32-76) and 16 (20%) patients were stage III and the others were all stage IV. With the median follow up of 62.9 months (95% CI, 59.2 - 66.7), sixty three (80%) were HPV-positive with p16 overexpression, and 38 (48%) were Treg-positive with FOXP3. Treg involvement was significantly related to HPV positive status (P=0.011). The result was the same after adjustment of age, T & N stage, smoking exposure and alcohol consumption. (Odd ratio = 6.54, 95% CI 1.58-27.1, P=0.01) Five-year overall survival (OS) rate in HPV-positive group was significantly higher than that of HPV-negative group (78% and 63%, Hazard Ratio (HR)=0.347, 95% CI 0.14-0.87, P=0.025), and 5-year OS of Treg-positive group was also higher than that of Treg-negative group (89% and 61%, HR=0.158, 95% CI 0.05-0.53, P=0.003). In multivariate analysis, the Treg status was an independent prognostic factor (HR=0.11, 95% CI 0.03-0.40, P=0.001), as well as HPV status. (HR=0.28, 95% CI 0.10 - 0.78, P=0.016). Conclusions: HPV positivity was associated with Treg positivity in TSCC and both were found to be favourable prognostic factors for survival.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/jco.2012.30.15_suppl.5586
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2012
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  • 6
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    Radioresistant Cancer Cells Can Be Conditioned to Enter Senescence by mTOR Inhibition
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 14 ( 2013-07-15), p. 4267-4277
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 14 ( 2013-07-15), p. 4267-4277
    Abstract: Autophagy is frequently activated in radioresistant cancer cells where it provides a cell survival strategy. The mTOR inhibitor rapamycin activates autophagy but paradoxically it also enhances radiosensitivity. In this study, we investigated the mechanisms of these opposing actions in radiation-resistant glioma or parotid carcinoma cells. Radiation treatment transiently enhanced autophagic flux for a period of 72 hours in these cells and treatment with rapamycin or the mTOR inhibitor PP242 potentiated this effect. However, these treatments also increased heterochromatin formation, irreversible growth arrest, and premature senescence, as defined by expression of senescence-associated β-galactosidase activity. This augmentation in radiosensitivity seemed to result from a restoration in the activity of the tumor suppressor RB and a suppression of RB-mediated E2F target genes. In tumor xenografts, we showed that administering rapamycin delayed tumor regrowth after irradiation and increased senescence-associated β-galactosidase staining in the tumor. Our findings suggest that a potent and persistent activation of autophagy by mTOR inhibitors, even in cancer cells where autophagy is occurring, can trigger premature senescence as a method to restore radiosensitivity. Cancer Res; 73(14); 4267–77. ©2013 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-12-3516
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
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  • 7
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    Online Resource
    Obesity Can Contribute to Severe Persistent Allergic Rhinitis in Children through Leptin and Interleukin-1β
    S. Karger AG ; 2021
    In:  International Archives of Allergy and Immunology Vol. 182, No. 6 ( 2021), p. 546-552
    Details
    In: International Archives of Allergy and Immunology, S. Karger AG, Vol. 182, No. 6 ( 2021), p. 546-552
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Obesity/overweight is associated with a higher risk of allergic rhinitis (AR) in children. 〈 b 〉 〈 i 〉 Objective: 〈 /i 〉 〈 /b 〉 This study aimed at exploring the mechanisms by which obesity affects the severity of AR through leptin and interleukin (IL)-1β were investigated. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 In all, 210 subjects with AR and 82 subjects without AR were included in this study. The levels of leptin and inflammatory biomarkers were measured in the serum to investigate the correlation with the severity of AR. Additionally, we analyzed whether changes in BMI regulate the severity of AR through serial follow-up of obese children. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 IL-1β, which is a biomarker of active inflammation in AR, was significantly higher in individuals with AR than in those without and higher in subjects in the obesity group than in those in the normal weight group. A regression analysis showed that the leptin level was associated with increased IL-1β expression in children with AR. In the multivariate analysis, only parental AR (9.2-fold increase in risk), elevated leptin (11.3-fold increase in risk), and high expression of IL-1β (5.8-fold increase in risk) emerged as significant risk factors of moderate to severe persistent allergic rhinitis. We also found that children with an increase or decrease in BMI showed changes in IL-1β and AR symptoms, which these changes were dependent on leptin and BMI. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 These results suggest that obesity is an important risk factor for the exacerbation of symptoms and leptin can exacerbate inflammation as well as severe and persistent symptoms through IL-1β in AR.
    Type of Medium: Online Resource
    ISSN: 1018-2438 , 1423-0097
    URL: Article
    DOI: 10.1159/000512920
    RVK:
    XA 49650
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2021
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  • 8
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    Online Resource
    Abstract 81: Rapamycin increases radiosensitivity of cancer cells by induction of premature senescence.
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 8_Supplement ( 2013-04-15), p. 81-81
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 8_Supplement ( 2013-04-15), p. 81-81
    Abstract: Autophagy is frequently activated in radioresistant cancer cells. Rapamycin, mammalian target of rapamycin (mTOR) inhibitor, activates autophagy but enhances radiosensitivity. The mechanism of these actions by which such opposing functions coexist was investigated on radiation-resistant cancer cell lines (AMC-HN-9 and U-87) and the antitumor activity was evaluated in mice bearing xenografts of the cancer cells. Enhanced autophagic flux induced by radiation returned to untreated control levels. Treatment of the cancer cells with rapamycin leads to the potentiation and prolongation of radiation-induced autophagy, the increases in senescence-associated β-galactosidase activity, heterochromatin formation, and irreversible growth arrest. Furthermore, rapamycine resulted in a tumor regrowth delay and increased the level of β-galactosidase staining and the expression of heterochromatin markers in irradiated xenografts. These results suggest that even though autophagy is a survival mechanism in radioresistant cells, a persistent activation of autophagy by mTOR inhibitor induces premature senescence in these cells, eventually making the cells radiosensitive. Our data suggest a novel mechanism by which an inhibition of mTOR pathway increases autophagy but paradoxically increases radiosensitivity in radioresistant cancer cells. Citation Format: Hae Yun Nam, Myung Woul Han, Hyo Won Chang, Yoon Sun Lee, Myungjin Lee, Mi Ra Kim, Hyang Ju Lee, Ji Yung Jeoung, So Young Moon, Hyo Jung Kim, Sang Yoon Kim, Seong Who Kim. Rapamycin increases radiosensitivity of cancer cells by induction of premature senescence. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 81. doi:10.1158/1538-7445.AM2013-81
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2013-81
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
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  • 9
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    Online Resource
    Abstract 144: Src leads to a novel mechanism of resistance to PI3K inhibitors through regulation of PI3K/p85 activation
    American Association for Cancer Research (AACR) ; 2017
    In:  Cancer Research Vol. 77, No. 13_Supplement ( 2017-07-01), p. 144-144
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 77, No. 13_Supplement ( 2017-07-01), p. 144-144
    Abstract: Activation of the PI3K pathway is commonly observed and is correlated with tumor development, progression, poor prognosis, and resistance to cancer therapies, such as radiotherapy, in most cancers. As a central node of this pathway, PI3K is an attractive target for PI3K-addicted cancer therapy and PI3K inhibitors may thus restore sensitivity to other treatments when administered as part of combination regimens. Here, we found that PI3K/p85 was expressed predominantly in the radioresistant head and neck cancer cell line (HN31 cell line). And then, we investigated whether PI3K modulation was crucial for the development of novel treatment strategies for radioresistant cancer cell line. Interestingly, we found that head and neck cancer cell lines with PI3K/p85 activation showed the resistance to PI3K inhibitors and the resistance mechanism was associated with Src activation which is a member of a superfamily of membrane-associated nonreceptor protein tyrosine kinases. Src inhibitor improves the efficacy of PI3K inhibitor treatment through suppression of Src and PI3K/p85 activation in HN31 cell line. Collectively, our study highlights the role of p85 and Src activation in the resistance for PI3K inhibition and the potential clinical application of combination regimens of Src and PI3K inhibitors in head and neck cancers. This is the first investigation to analyze the role of Src in resistance to the PI3K inhibitors of head and neck cancer. As a consequence, a greater understanding of resistance mechanisms through our results will enable the rational design of combination regimens and sequential treatment algorithms to improve clinical outcomes. Citation Format: Gui Chul Kim, Hae Yun Nam, Hyang Ju Lee, Min Kyung Kim, Geun Hee Lee, Myung Woul Han, Seong Who KIM, Sang Yoon Kim. Src leads to a novel mechanism of resistance to PI3K inhibitors through regulation of PI3K/p85 activation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 144. doi:10.1158/1538-7445.AM2017-144
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2017-144
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 10
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    Online Resource
    Abstract 1170: EphA3 maintains radioresistance in head and neck cancers
    American Association for Cancer Research (AACR) ; 2016
    In:  Cancer Research Vol. 76, No. 14_Supplement ( 2016-07-15), p. 1170-1170
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 76, No. 14_Supplement ( 2016-07-15), p. 1170-1170
    Abstract: Radiotherapy is a well-established therapeutic modality used in treatment of many cancers. However, radioresistance remains a serious obstacle to successful treatment. Radioresistance can cause local recurrence and distant metastases in some patients after treatment by radiation. Thus, special emphasis has been given to the discovery of effective radiosensitizers. EphA3 receptors functions contribute to tumor development, modulating cell-cell adhesion, invasion, neo-angiogenesis, tumor growth and metastasis. However, the role of EphA3 in radioresistance remains to be elucidated. Here, we established the stable radioresistant head and neck cancer cell line (AMC HN3R cell line) and identified that EphA3 was overexpressed predominantly in the AMC HN3R cancer cell line through DNA microarray, real time PCR and Western blotting. Additionally, we identified that EphA3 was overexpressed in recurred laryngeal cancer specimen after radiation therapy. And we found that EphA3 mediated the tumor invasiveness and migration and EMT (epithelial mesenchymal transition) related protein expression in AMC HN3R cancer cell line. To investigate the role of EphA3 in modulating the radiosensitivity, we observed the change of survival fraction after transfection EphA3 siRNA. And we found that inhibition of EphA3 enhances radiosensitivity in AMC HN 3R cell line. In conclusion, these results suggest that EphA3 is overexpressed in radioresistant head and neck cancer and can play a crucial role in development radioresistance in head and neck cancers through regulation of EMT pathway. Citation Format: Myung Woul Han, Song Hee Kim, Hyo Won Chang, Hae Yun Nam, Myungjin Lee, Gui Chul Kim, Yoon sun Lee, Mi Ra Kim. EphA3 maintains radioresistance in head and neck cancers. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1170.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2016-1170
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
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    detail.hit.zdb_id: 410466-3
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