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  • American Association for Cancer Research (AACR)  (81)
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  • 1
    Online Resource
    Online Resource
    Abstract 1718: Favorable clinical outcomes of pemetrexed treatment in anaplastic lymphoma kinase positive non-small-cell lung cancer patients were associated with low expression of thymidylate synthase in tumor
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 1718-1718
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 1718-1718
    Abstract: Introduction The purpose of this study was to investigate the clinical characteristics and treatment outcomes of patients with anaplastic lymphoma kinase (ALK)-positive non-small-cell lung cancer (NSCLC) to conventional chemotherapy in the pre-ALK inhibitor era Patients and Methods We retrospectively screened 381 consecutive NSCLC patients without known epidermal growth factor receptor (EGFR) or KRAS mutation who were diagnosed between 2007 and 2008 at a single center, and identified ALK rearrangements by fluorescence in situ hybridization Additional 44 ALK-positive patients from other period were included for the analysis of clinical outcomes Results Of the 381 tumors screened, four were excluded because the samples were unevaluable Twenty-one (5 6%) showed ALK rearrangements, with twenty adenocarcinomas and one pleomorphic carcinoma Of the entire 65 ALK-positive patients, 32 patients received pemetrexed as a second- or further-line therapy, in whom response rate was 34 4% (11/32) and median progression-free survival (PFS) was 4 0 months Among these 31 patients, 20 specimens were available for thymidylate synthase (TS) expression analysis Low expression of TS were found in 80% (16/20), with a trend toward longer PFS than TS-positive patients (median PFS 4 0 vs 1 0 months, P = 0 095) Conclusions The prevalence of ALK rearrangement was 5 6% among EGFR and/or KRAS wild-type/unknown NSCLC population Low TS protein expression might be associated with better clinical outcomes in ALK-positive NSCLC patients after pemetrexed given as a second- or further-line therapy Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1718. doi:1538-7445.AM2012-1718
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-1718
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
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  • 2
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    Online Resource
    Erythropoietin Induces Lymph Node Lymphangiogenesis and Lymph Node Tumor Metastasis
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 13 ( 2011-07-01), p. 4506-4517
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 13 ( 2011-07-01), p. 4506-4517
    Abstract: Cancer therapy often produces anemia, which is treated with erthropoietin (EPO) to stimulate erythrocyte production. However, concerns have recently arisen that EPO treatment may promote later tumor metastasis and mortality. The mechanisms underlying such effects are unknown, but it is clear that EPO has pleiotropic effects in cell types other than hematopoietic cells. In this study, we investigated how EPO affects lymphangiogenesis and lymph node tumor metastasis in mouse models of breast cancer and melanoma. In these models, EPO increased lymph node lymphangiogenesis and lymph node tumor metastasis in a manner associated with increased migration, capillary-like tube formation, and dose- and time-dependent proliferation of human lymphatic endothelial cells. EPO increased sprouting of these cells in a thoracic duct lymphatic ring assay. These effects were abrogated by cotreatment with specific inhibitors of phosphoinositide 3-kinase or mitogen-activated protein kinase, under conditions in which EPO increased Akt and extracellular signal–regulated kinase 1/2 phosphorylation. Intraperitoneal administration of EPO stimulated peritoneal lymphangiogenesis, and systemic treatment of EPO increased infiltration of CD11b+ macrophages in tumor-draining lymph nodes. Finally, EPO increased VEGF-C expression in lymph node–derived CD11b+ macrophages as well as in bone marrow–derived macrophages in a dose- and time-dependent manner. Our results establish that EPO exerts a powerful lymphangiogenic function and can drive both lymph node lymphangiogenesis and nodal metastasis in tumor-bearing animals. Cancer Res; 71(13); 4506–17. ©2011 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-10-3787
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 3
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    Online Resource
    Abstract LB-172: A randomized phase II study of S-1 versus capecitabine as first-line chemotherapy in the elderly metastatic gastric cancer patients with/without poor performance status: clinical and pharmacogenetic results.
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 8_Supplement ( 2013-04-15), p. LB-172-LB-172
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 8_Supplement ( 2013-04-15), p. LB-172-LB-172
    Abstract: Introduction: This study investigated the efficacy and safety of S-1 vs. capecitabine in elderly patients (pts) with metastatic gastric cancer (MGC) with/without poor performance status (PS), and examined the association between CYP2A6 polymorphisms and treatment outcomes. Methods: Eligibility criteria included MGC, measurable lesion(s), no prior chemotherapy for MGC, and age of 70-85 yrs with ECOG PS 0-2 or age ≥ 65 and & lt; 70 yrs with PS 2. Pts were randomized to receive S-1 40 mg/m2 bid or capecitabine 1250 mg/m2 bid on days 1-14 every 3 weeks. The primary endpoint was overall response rate (ORR) with time to progression (TTP), overall survival (OS), quality of life (QOL), safety, and the association between CYP2A6 genotypes (*1, *4, *7, *9, *10) and treatment outcomes as secondary endpoints. Results: From May 2007 to July 2010, 107 pts were randomized to receive either S-1 (n=53) or capecitabine (n=54). Baseline characteristics were well balanced between the two arms (S-1:capecitabine): median age, 72 yrs (range, 64-81):71 yrs (65-78); male, 74%:81%; and PS 0/1, 85%:83%. The median number of cycles was 4 (range, 1-26) in S-1 arm and 5 (1-32) in capecitabine arm. The incidence of G3/4 neutropenia was 3.8% in each arm, and the most common G3/4 non-hematological toxicities included anorexia (21.2% with S-1 vs. 7.5% with capecitabine), fatigue (13.5% vs. 15.1%), and nausea (7.7% vs. 1.9%). S-1 arm had higher incidences of vomiting (40.4% vs. 17.0%; P=0.010) and tearing (51.9% vs. 28.3%; P=0.017), and lower incidence of HFS (25.0% vs. 58.5%; P=0.001) than capecitabine arm. Of the 49 pts assessable for response in each arm, the ORR was 28.6% (95% CI, 15.9-41.3%) in S-1 arm and 26.5% (95% CI, 14.1-38.9%) in capecitabine arm. The median TTP was 3.2 months (95% CI, 1.6-4.8 months) in S-1 arm and 3.4 months (95% CI, 2.5-4.3 months) in capecitabine arm (P=0.825), and median OS was 8.5 months (95% CI, 6.1-10.9 months) and 10.3 months (95% CI, 7.1-13.5 months), respectively (P=0.691). CYP2A6 polymorphisms were associated with the efficacy of S-1. Pts having two variant alleles (V/V) had inferior efficacy to those having no or one variant allele (W/W or W/V): median TTP 2.3 vs. 4.1 months (P=0.062), and median OS 6.4 vs. 11.5 months (P=0.034). However, the efficacy of capecitabine did not differ according to CYP2A6 genotypes: median TTP was 3.6 months in V/V pts vs. 3.3 in W/W or W/V (P=0.257), and median OS was 11.6 vs. 10.2 months (P=0.756), respectively. In pts with V/V genotype, capecitabine arm had better TTP (median, 3.6 vs. 2.3 months; P=0.062) and OS (median, 11.6 vs. 6.5 months; P=0.090) than S-1 arm. Conclusions: Both S-1 and capecitabine were active and tolerable for elderly MGC pts with/without poor PS with different toxicity profiles. Genotyping for CYP2A6 might provide useful information for treatment selection. Citation Format: Sook Ryun Park, Sun-Young Kong, Mi-Jung Kim, Min Kyeong Kim, Byung-Ho Nam, Mihee Choi, Young-Iee Park. A randomized phase II study of S-1 versus capecitabine as first-line chemotherapy in the elderly metastatic gastric cancer patients with/without poor performance status: clinical and pharmacogenetic results. [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 LB-172. doi:10.1158/1538-7445.AM2013-LB-172
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2013-LB-172
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
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    detail.hit.zdb_id: 410466-3
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  • 4
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    Online Resource
    Abstract 1913: FGFR1 amplification as a druggable target in lung squamous cell carcinoma.
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 8_Supplement ( 2013-04-15), p. 1913-1913
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 8_Supplement ( 2013-04-15), p. 1913-1913
    Abstract: Background: Focal gene amplification is a potential target for diagnosis and therapy in cancer. Fibroblast growth factor receptor-type 1 (FGFR1) may play a role in the pathogenesis of lung squamous cell carcinoma (LSCC) and amplification of the FGFR1 gene is considered a candidate target for treatment of LSCC. The aim of this study was to simultaneously explore copy number changes of FGFR1 and 23 other genes by multiplex ligation-dependent probe amplification (MLPA), to compare the results with fluorescent in situ hybridization (FISH) data, and determine the clinicopathological significance of gene amplification. Methods: This study included 81 resected LSCC specimens obtained between 2008 and 2010, and 14 lung cancer cell lines. MLPA was performed using fresh tumor samples and cell lines and FISH was applied to formalin-fixed, paraffin-embedded tissues. Results: MLPA showed amplification/gain of MYC (48.1% of LSCCs), AURKA (44.4%), MET (29.6%), KIT (21.0%), and FGFR1 (14.8%). FISH showed FGFR1 amplification in 22 LSCCs (27.2%) using a cut-off value of ≥5. There was high concordance between FISH and MLPA (85.2%). No association between FGFR1 amplification and any clinicopathological variables was observed; however, associations were identified between EGFR and FGFR1 FISH-amplified tumors; PDGFRA and poor differentiation; KDR, ABL1, and MET and age; and SMO and CCND2 and pT stages. Conclusions: Our MLPA and FISH data showed that FGFR1 amplification is a common event, occurring in 15-27.2% of LSCCs. Other amplified genes may be also candidate targets for the treatment of LSCC. Citation Format: Mi Jung Kwon, Seung Eun Lee, Joungho Han, Jin Seok Ahn, Keunchil Park, Jhingook Kim, Myung-Ju Ahn, Yoon-La Choi. FGFR1 amplification as a druggable target in lung squamous cell carcinoma. [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 1913. doi:10.1158/1538-7445.AM2013-1913
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2013-1913
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
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  • 5
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    Online Resource
    Abstract PS11-39: Phase II pilot study of trastuzumab biosimilar (herzuma®) plus gedatolisib in patients with HER-2 positive metastatic breast cancer who progressed after 2 or more HER-2 directed chemotherapy [KM-10A/KCSG18-13 interim analysis]
    American Association for Cancer Research (AACR) ; 2021
    In:  Cancer Research Vol. 81, No. 4_Supplement ( 2021-02-15), p. PS11-39-PS11-39
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 81, No. 4_Supplement ( 2021-02-15), p. PS11-39-PS11-39
    Abstract: Background: Prognosis of patients with HER-2 positive metastatic breast cancer (MBC) has been revolutionized with the development of dual antibodies targeting HER-2 and antibody-drug conjugate, but resistance to anti-HER-2 therapy is inevitable ultimately. PI3K-AKT-mTOR pathway aberration is known to be one of the resistance mechanisms. This randomized phase 2 pilot study evaluated safety and efficacy of Herzuma® (trastuzumab biosimilar) plus Gedatolisib (dual PI3K/mTORC inhibitor) in patients with HER-2 positive MBC who progressed after multiple lines of therapy. Methods: Patients with HER-2 positive MBC with known PIK3CA pathologic mutation or amplification whose disease progressed after more than two HER-2 directed therapy were enrolled in the study. They received Herzuma® (8mg/kg IV for 1st cycle loading dose, and then 6mg/kg IV every 3 weeks) plus Gedatolisib (180mg on D1, 8, 15 of every 21 days). We evaluated efficacy of the combination treatment as interim analysis. The data cutoff of this interim analysis was Aug 4, 2020. Results: As a pilot study, 15 patients were enrolled and followed for a median of 2.3 months. At data cutoff, 11 patients were eligible for response assessment. All patients were confirmed to have pathologic PIK3CA aberrations: H1047R, H1047L, E542Q, E542K, E453K, N345K, and PIK3CA amplification. Five patients reached partial response (PR) as their best response, three were stable disease (SD), and three had progressive disease (PD). All patients who have reached PR remain on investigational treatment at the data cutoff point, and the longest one is on treatment for 7.8 months. One of the SD patients ended treatment due to disease progression, and the other two have been undergoing treatment. Overall, response rate was 45.5% and disease control rate was 72.7%. No fatal adverse events related to trial medication were reported. Conclusion: In this phase 2 pilot study, Trastuzumab biosimilar plus Gedatolisib presented 45.5% of response rate with manageable toxicity in patients with HER-2 positive MBC with PIK3CA aberration. Clinical trial information: NCT03698383 Acknowledgement: this research was supported by a grant of the Korea Health Technology R & D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (Grant number: HI17C2206). Citation Format: Ju Won Kim, Hee Kyung Ahn, Jong Gwon Choi, Yee Soo Chae, Gyeong Won Lee, Keon Uk Park, Eun Mi Lee, Sung Hoon Sim, Jee Hyun Kim, Yeon Hee Park, Mi So Kim, Jin Hyun Park, Jeong Eun Kim, Han Jo Kim, Mi Sun Ahn, So Yeon Oh, Min Hwan Kim, Su-Jin Koh, Kyoung Eun Lee, Myoung Joo Kang, Jae Ho Byun, Joo young Ha, Jung Hye Kwon, Joo Young Jung, Su Ee Lee, In Hae Park, Kyong Hwa Park. Phase II pilot study of trastuzumab biosimilar (herzuma®) plus gedatolisib in patients with HER-2 positive metastatic breast cancer who progressed after 2 or more HER-2 directed chemotherapy [KM-10A/KCSG18-13 interim analysis] [abstract] . In: Proceedings of the 2020 San Antonio Breast Cancer Virtual Symposium; 2020 Dec 8-11; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2021;81(4 Suppl):Abstract nr PS11-39.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.SABCS20-PS11-39
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
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    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 6
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    Online Resource
    Inhibition of 15-Hydroxyprostaglandin Dehydrogenase by Helicobacter pylori in Human Gastric Carcinogenesis
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Prevention Research Vol. 6, No. 4 ( 2013-04-01), p. 349-359
    Details
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 6, No. 4 ( 2013-04-01), p. 349-359
    Abstract: Helicobacter pylori (H. pylori) infection induces a chronic inflammatory response, which promotes gastric carcinogenesis. 15-Hydroxyprostaglandin dehydrogenase (15-PGDH) plays a key role as a tumor suppressor in gastrointestinal cancers. The aim of this study was to elucidate the role of 15-PGDH in gastric carcinogenesis associated with H. pylori. 15-PGDH expression in gastric biopsies from H. pylori–infected (n = 25) and noninfected (n = 15) subjects was analyzed by quantitative real-time PCR, Western blot analysis, and immunohistochemistry. 15-PGDH DNA methylation was evaluated by methylation-specific PCR and pyrosequencing. The expression of 15-PGDH, Snail, extracellular signal–regulated kinase (ERK)1/2, TLR4, and MyD88 in response to H. pylori infection was assessed by immunoblot analysis. Compared with negative specimens, H. pylori–positive specimens had 2-fold lower 15-PGDH mRNA levels and significantly less 15-PGDH protein. In four H. pylori–infected subjects with longitudinal follow-up, the suppression of 15-PGDH expression was reversed by H. pylori eradication therapy. In parallel with suppressing 15-PGDH expression, H. pylori infection activated expression of TLR4 and MyD88 expression, increased levels of phospho-ERK1/2, and increased expression of EGF receptor (EGFR)-Snail. Inhibition of Snail and MyD88 reversed suppression of 15-PGDH expression, and siMyD88 reduced phosphorylated ERK1/2. Similarly, treatment with an ERK1/2 and EGFR inhibitor also restored 15-PGDH expression. H. pylori appeared to promote gastric carcinogenesis by suppressing15-PGDH. This process is mediated by the TLR4/MyD88 pathway via ERK1/2 or EGFR-Snail transcriptional regulation. 15-PGDH may be a useful marker and a potential therapeutic target in H. pylori–induced gastric carcinogenesis. Cancer Prev Res; 6(4); 349–59. ©2013 AACR.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.CAPR-12-0389
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
    detail.hit.zdb_id: 2422346-3
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  • 7
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    Abstract P5-16-03: Phase II study of trastuzumab biosimilar (Herzuma®) plus gedatolisib in patients with HER-2 positive metastatic breast cancer who progressed after 2 or more HER-2 directed chemotherapy (BR 18-13, KM-10A): Interim analysis
    American Association for Cancer Research (AACR) ; 2022
    In:  Cancer Research Vol. 82, No. 4_Supplement ( 2022-02-15), p. P5-16-03-P5-16-03
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 82, No. 4_Supplement ( 2022-02-15), p. P5-16-03-P5-16-03
    Abstract: Background: Prognosis of patients with HER-2 positive metastatic breast cancer (MBC) has been revolutionized with the development of monoclonal antibodies targeting HER-2 and antibody-drug conjugate, but resistance to anti-HER-2 therapy is inevitable ultimately. PI3K-AKT-mTOR pathway aberration is known to be one of the key resistance mechanisms. BR18-13(KM-10A) study is a phase 2 clinical trial evaluating efficacy and safety of Herzuma® (trastuzumab biosimilar) plus Gedatolisib (dual PI3K/mTORC inhibitor) in patients with HER-2 positive MBC who progressed after multiple lines of therapy. Methods: Patients with HER-2 positive MBC with known PIK3CA pathologic mutation or amplification whose disease progressed after more than 2 HER-2 directed therapy were enrolled in the study. They received Herzuma® (8mg/kg IV for 1st cycle loading dose, and then 6mg/kg IV every 3 weeks) plus Gedatolisib (180mg on D1, 8, 15 of every 21 days). We evaluated efficacy of the combination treatment as interim analysis. The data cutoff of this interim analysis was June 8, 2021. Results: 17 patients were enrolled and followed for a median of 6.2 months. At data cutoff, 17 patients were eligible for response assessment. All patients were confirmed to have pathologic PIK3CA aberrations: 9 kinase mutations (H1047X), 5 helical mutations (E545X), 2 other point mutations, and 1 amplification. Overall, response rate was 64.7% and disease control rate was 82.4%. Eleven patients reached partial response (PR) as their best response, three were stable disease (SD), and three had progressive disease (PD). Two patients who have reached PR remain on investigational treatment until the data cutoff point, and the longest one is on treatment for 12.0 months. The median progression-free survival assessed in data cutoff time was 5.9 months. One patient ended treatment due to CNS disease progression, but her visceral metastatic lesions were decreased with experimental treatment. No fatal adverse events related to trial medication were reported. Conclusion: In this phase 2 study, Trastuzumab biosimilar plus Gedatolisib presented 64.7% of response rate with manageable toxicity in patients with HER-2 positive MBC with PIK3CA mutation. Clinical trial information: NCT03698383 Acknowledgement: this research was supported by a grant of the Korea Health Technology R & D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (Grant number: HI17C2206). Citation Format: Ju Won Kim, Hee Kyung Ahn, Jong Gwon Choi, Yee Soo Chae, Gyeong-Won Lee, Keon Uk Park, Eunmi Lee, Sung Hoon Sim, Jee Hyun Kim, Yeon Hee Park, Miso Kim, Jin Hyun Park, Jeong Eun Kim, Han Jo Kim, Mi Sun Ahn, So Yeon Oh, Min Hwan Kim, Su-Jin Koh, Kyoung Eun Lee, Myoung Joo Kang, Jae Ho Byun, Joo Young Ha, Jung Hye Kwon, Joo Young Jung, Su Ee Lee, Inhae Park, Kyong Hwa Park. Phase II study of trastuzumab biosimilar (Herzuma®) plus gedatolisib in patients with HER-2 positive metastatic breast cancer who progressed after 2 or more HER-2 directed chemotherapy (BR 18-13, KM-10A): Interim analysis [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P5-16-03.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.SABCS21-P5-16-03
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
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  • 8
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    RhoGDI2 Expression Is Associated with Tumor Growth and Malignant Progression of Gastric Cancer
    American Association for Cancer Research (AACR) ; 2009
    In:  Clinical Cancer Research Vol. 15, No. 8 ( 2009-04-15), p. 2612-2619
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 15, No. 8 ( 2009-04-15), p. 2612-2619
    Abstract: Purpose: Rho GDP dissociation inhibitor 2 (RhoGDI2) has been identified as a regulator of Rho family GTPase. However, there is currently no direct evidence suggesting whether RhoGDI2 activates or inhibits Rho family GTPase in vivo (and which type), and the role of RhoGDI2 in tumor remains controversial. Here, we assessed the effects of RhoGDI2 expression on gastric tumor growth and metastasis progression. Experimental Design: Proteomic analysis was done to investigate the tumor-specific protein expression in gastric cancer and RhoGDI2 was selected for further study. Immunohistochemistry was used to detect RhoGDI2 expression in clinical samples of primary gastric tumor tissues which have different pathologic stages. Gain-of-function and loss-of-function approaches were done to examine the malignant phenotypes of the RhoGDI2-expressing or RhoGDI2-depleting cells. Results: RhoGDI2 expression was correlated positively with tumor progression and metastasis potential in human gastric tumor tissues, as well as cell lines. The forced expression of RhoGDI2 caused a significant increase in gastric cancer cell invasion in vitro, and tumor growth, angiogenesis, and metastasis in vivo, whereas RhoGDI2 depletion evidenced opposite effects. Conclusion: Our findings indicate that RhoGDI2 is involved in gastric tumor growth and metastasis, and that RhoGDI2 may be a useful marker for tumor progression of human gastric cancer.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-08-2192
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2009
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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  • 9
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    Overexpression of High-Mobility Group Box 2 Is Associated with Tumor Aggressiveness and Prognosis of Hepatocellular Carcinoma
    American Association for Cancer Research (AACR) ; 2010
    In:  Clinical Cancer Research Vol. 16, No. 22 ( 2010-11-15), p. 5511-5521
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 16, No. 22 ( 2010-11-15), p. 5511-5521
    Abstract: Purpose: We investigated the expression of high-mobility group box 2 (HMGB2) in patients with hepatocellular carcinoma (HCC) and its clinical effects with underlying mechanisms. Experimental Design: HMGB2 mRNA levels were measured in 334 HCC patients by real-time reverse transcription-PCR and HMGB2 protein levels in 173 HCC patients by immunohistochemical studies. The HMGB2 expression level was measured by Western blotting for three HCC cell lines. To clarify the precise role of HMGB2 on cell proliferation, we did in vitro analysis with expression vectors and small interfering RNAs. Results: HMGB2 mRNA and protein expression were significantly higher in HCC than in noncancerous surrounding tissues (P & lt; 0.0001) and showed a positive correlation (ρ = 0.35, P & lt; 0.001). HMGB2 overexpression was significantly correlated with shorter overall survival time, both at mRNA (P = 0.0054) and protein level (P = 0.023). Moreover, HMGB2 mRNA level was an independent prognostic factor for overall survival in a multivariate analysis (P = 0.0037). HMGB2 knockdown by small interfering RNAs decreased cell proliferation, and overexpression of HMGB2 by expression vectors diminished cisplatin- and etoposide-induced cell death. Conclusions: Our clinical and in vitro data suggest that HMGB2 plays a significant role in tumor development and prognosis of HCC. These results can partly be explained by altered cell proliferations by HMGB2 associated with the antiapoptotic pathway. Clin Cancer Res; 16(22); 5511–21. ©2010 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-10-0825
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 1225457-5
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  • 10
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    EPB41L5 Mediates TGFβ-Induced Metastasis of Gastric Cancer
    American Association for Cancer Research (AACR) ; 2019
    In:  Clinical Cancer Research Vol. 25, No. 12 ( 2019-06-15), p. 3617-3629
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 25, No. 12 ( 2019-06-15), p. 3617-3629
    Abstract: Because of disease heterogeneity, limited studies on effective chemotherapies and therapeutic agents for advanced gastric cancer are available. Erythrocyte membrane protein band 4.1-like 5 (EPB41L5) has critical roles in renal and breast cancer metastasis. However, its role in metastatic gastric cancer remains unknown. Experimental Design: The specimens of 78 gastric cancer patients were analyzed by oligonucleotide microarray and survival analysis. In vitro experiments and metastatic mice models were used to assess the effects of EPB41L5 on gastric cancer metastasis. Results: Gastric cancer patients with high EPB41L5 levels had poor prognosis and low survival rate. Further, TGFβ1-induced EPB41L5 expression promoted gastric cancer cell migration and invasion by Smad-dependent TGFβ signaling. Phospho-Smad3 recruitment to the EPB41L5 promoter was significantly inhibited by a TGFβ inhibitor. EPB41L5 overexpression increased lung metastasis of gastric cancer cells in nude mice, which was completely reversed by anti-EPB41L5 monoclonal antibody treatment. Importantly, p120-catenin knockdown abolished EPB41L5-enhanced gastric cancer cell metastasis. Anti-EPB41L5 monoclonal antibody treatment blocked the association of EPB41L5 with p120-catenin. Conclusions: TGFβ/EPB41L5/p120-catenin axis regulates gastric cancer cell metastasis, and EPB41L5 is a promising therapeutic target for advanced gastric cancer.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-18-2959
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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