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  • American Association for Cancer Research (AACR)  (12)
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  • American Association for Cancer Research (AACR)  (12)
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  • 1
    Online Resource
    Online Resource
    Caffeine-Mediated Inhibition of Calcium Release Channel Inositol 1,4,5-Trisphosphate Receptor Subtype 3 Blocks Glioblastoma Invasion and Extends Survival
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 3 ( 2010-02-01), p. 1173-1183
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 3 ( 2010-02-01), p. 1173-1183
    Abstract: Calcium signaling is important in many signaling processes in cancer cell proliferation and motility including in deadly glioblastomas of the brain that aggressively invade neighboring tissue. We hypothesized that disturbing Ca2+ signaling pathways might decrease the invasive behavior of giloblastoma, extending survival. Evaluating a panel of small-molecule modulators of Ca2+ signaling, we identified caffeine as an inhibitor of glioblastoma cell motility. Caffeine, which is known to activate ryanodine receptors, paradoxically inhibits Ca2+ increase by inositol 1,4,5-trisphospate receptor subtype 3 (IP3R3), the expression of which is increased in glioblastoma cells. Consequently, by inhibiting IP3R3-mediated Ca2+ release, caffeine inhibited migration of glioblastoma cells in various in vitro assays. Consistent with these effects, caffeine greatly increased mean survival in a mouse xenograft model of glioblastoma. These findings suggest IP3R3 as a novel therapeutic target and identify caffeine as a possible adjunct therapy to slow invasive growth of glioblastoma. Cancer Res; 70(3); 1173–83
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-09-2886
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 2
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    Nucleoporin 210 Serves a Key Scaffold for SMARCB1 in Liver Cancer
    American Association for Cancer Research (AACR) ; 2021
    In:  Cancer Research Vol. 81, No. 2 ( 2021-01-15), p. 356-370
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 81, No. 2 ( 2021-01-15), p. 356-370
    Abstract: The roles of chromatin remodelers and their underlying mechanisms of action in cancer remain unclear. In this study, SMARCB1, known initially as a bona fide tumor suppressor gene, was investigated in liver cancer. SMARCB1 was highly upregulated in patients with liver cancer and was associated with poor prognosis. Loss- and gain-of-function studies in liver cells revealed that SMARCB1 loss led to reduced cell proliferation, wound healing capacity, and tumor growth in vivo. Although upregulated SMARCB1 appeared to contribute to switch/sucrose nonfermentable (SWI/SNF) complex stability and integrity, it did not act using its known pathways antagonism with EZH2 or association between TP53 or AMPK. SMARCB1 knockdown induced a mild reduction in global H3K27 acetylation, and chromatin immunoprecipitation sequencing of SMARCB1 and acetylated histone H3K27 antibodies before and after SMARCB1 loss identified Nucleoporin210 (NUP210) as a critical target of SMARCB1, which bound its enhancer and changed H3K27Ac enrichment and downstream gene expression, particularly cholesterol homeostasis and xenobiotic metabolism. Notably, NUP210 was not only a putative tumor supporter involved in liver cancer but also acted as a key scaffold for SMARCB1 and P300 to chromatin. Furthermore, SMARCB1 deficiency conferred sensitivity to doxorubicin and P300 inhibitor in liver cancer cells. These findings provide insights into mechanisms underlying dysregulation of chromatin remodelers and show novel associations between nucleoporins and chromatin remodelers in cancer. Significance: This study reveals a novel protumorigenic role for SMARCB1 and describes valuable links between nucleoporins and chromatin remodelers in cancer by identifying NUP210 as a critical coregulator of SMARCB1 chromatin remodeling activity.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-20-0568
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
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  • 3
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    Abstract 4991: Hyleukin-7, the Fc-fused interleukin-7, generates anti-tumor activity by modulating both adaptive and innate immune cells in the tumor microenvironment
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Research Vol. 79, No. 13_Supplement ( 2019-07-01), p. 4991-4991
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 79, No. 13_Supplement ( 2019-07-01), p. 4991-4991
    Abstract: Interleukine-7 (IL-7), a strong candidate for a novel immunotherapeutic agent, plays important roles in the development and homeostasis of T lymphocytes. Recombinant IL-7 has shown positive effects in various models by increasing T cells in both mice and humans; however, the short half-life and stability of recombinant IL-7 has remained a challenge for its clinical application to cancer immunotherapy. Here, we investigated anti-tumor effects of a long-acting form of recombinant human IL-7 fused with hybrid Fc (rhIL-7-hyFc; Hyleukin-7) in mice. rhIL-7-hyFc administration in tumor-free mice generated the cytokine-induced CD8+ T cell proliferation, which altering CD8+ T cell homeostasis by expanding largely the TCM-phenotype CD8+ T cells displaying activation-induced attributes, such as Eomes, Granzyme B, CXCR3, and IFN-γ. When injected into mice with syngeneic tumor graft, rhIL-7-hyFc induced anti-tumor activity in a dose-dependent manner. rhIL-7-hyFc dramatically expands CD8+ T cells in the periphery and recruits effector CD8+ T cells in the tumor, yielding a high CD8+ T/Treg cell ratio in the tumor microenvironment (TME). rhIL-7-hyFc increases Ki-67 and granzyme-B expression but decreases expression levels of immune checkpoint molecules on CD8+ tumor-infiltrating lymphocytes (TILs). Surprisingly, rhIL-7-hyFc reduced myeloid-derived suppressor cells (MDSCs) in the TME, yielding the high CD8+ T/MDSC ratio. Collectively, rhIL-7-hyFc treatment confers anti-cancer activity by inducing a “CD8+ T cell infiltrated-inflamed-immune favorable” TME. The combination treatment of rhIL-7-hyFc with cyclophosphamide and immune checkpoint blockades showed enhanced anti-tumor efficacy in an advanced tumor model. Furthermore, we found that the anti-tumor activity of rhIL-7-hyFc was achieved under lymphopenic conditions by normalizing CD8+ T cell homeostasis. In sum, rhIL-7-hyFc generates an effective anti-tumor response through reconstructing CD8+ T lymphocytes; this activity was highly enhanced by combination therapies with the chemotherapeutics and immune checkpoint blockades. Our data suggests that rhIL-7-hyFc can be applied to various cancer immunotherapy regimens as a monotherapy or in combination partner with conventional and other immunotherapies. Citation Format: Ji-Hae Kim, Sung-Wook Hong, Young-Min Kim, Saet-byeul Jo, Man Kyu Ji, Yeon Kyung Oh, Han Wook Park, Sora Kim, Donghoon Choi, Byung Ha Lee, Se Hwan Yang, Young Chul Sung, Seung-Woo Lee. Hyleukin-7, the Fc-fused interleukin-7, generates anti-tumor activity by modulating both adaptive and innate immune cells in the tumor microenvironment [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 4991.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2019-4991
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
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  • 4
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    Abstract 2862: Novel immune checkpoint protein CNTN4 and the preclinical efficacy of affinity matured anti-CNTN4 antibody GENA-104A16
    American Association for Cancer Research (AACR) ; 2022
    In:  Cancer Research Vol. 82, No. 12_Supplement ( 2022-06-15), p. 2862-2862
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 82, No. 12_Supplement ( 2022-06-15), p. 2862-2862
    Abstract: The immunotherapeutic treatment has profoundly improved the clinical outcomes in patients with advanced cancers. However, most patients still have not responded to immune checkpoint inhibitor (ICI) treatment. Thus, it is still urgent to find novel treatments for patients who have no response to ICI and acquire ICI resistance. We previously suggested that contactin 4 (CNTN4), known initially to act as an axon guidance molecule during neural development, is a novel inhibitory immune checkpoint protein. In addition, we confirmed that CNTN4 is highly expressed on the various types of human tumor tissue, and anti-CNTN4 antibodies, GENA-104A07 and GENA-104A11, show the anti-tumor efficacy by enhancing T cell activity. In the present study, we describe the role of amyloid precursor protein (APP) expressed on T cells as a binding partner of CNTN4 and the preclinical characterization of GENA-104A16 as an immune-oncology drug candidate targeting CNTN4. Firstly, we investigated the APP expression on T cells and found that APP was detected in T cells' membrane and cytosolic fraction. Its expression level was higher on activated T cells. In addition, we observed that the immune-suppressive activity of CNTN4 on APP KO T cells was significantly decreased compared with APP WT T cells, which means APP as a binding partner of CNTN4 is a core molecule for transmitting immunosuppressive signal of CNTN4 to T cells. GENA-104A16 is a humanized antibody and binds to human and mouse CNTN4 with high binding affinity, which is matured from GENA-104A07 and GENA-104A11. In the in vitro functional assays, GENA-104A16 showed the improved effects on the restoration of T cell proliferation and activation (i.e., inflammatory cytokine releases from T cells and T cell activity-related signaling cascade) suppressed by CNTN4 and on CTL (cytotoxic T lymphocytes)-mediated killing for human cancer cell lines expressing CNTN4. In line with these effects, GENA-104A16 produced higher anti-tumor effects than GENA-104A11 in the CT26 syngeneic mouse colon cancer model. To identify the in vivo immune modulatory function of GENA-104A16, we analyzed the proportion of tumor-infiltrated T cells, Treg cells, and T cell subsets expressing perforin and granzyme B in CT26 tumor tissues. As a result, the population of CD4+ T cells, CD8+ T cells, and cytotoxic CD8+ T cells expressing perforin or granzyme B tended to increase in the tumors of GENA-104A16 treated mice while decreasing the FoxP3+CD25+ Treg population. Interestingly, GENA-104A16 treatment showed better anti-tumor effects together with the elevated level of CD8+ T cells expressing perforin and granzyme B than atezolizumab treatment. Overall, these preclinical studies demonstrate that GENA-104A16 is a promising blocking antibody for CNTN4-mediated immune suppression and can serve as an effective immune-oncology drug for patients with cancer that highly express CNTN4. Citation Format: Mi Young Cha, Hnkyung yu, Bu-Nam Jeon, Hyunuk Kim, Youngeun Ha, Yunyeon Kim, Joo-Yeon Chung, Soojung Moon, Hyunseong Youn, Han-sol Kim, Kyung Mi Park, Hansoo Park. Novel immune checkpoint protein CNTN4 and the preclinical efficacy of affinity matured anti-CNTN4 antibody GENA-104A16 [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2862.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2022-2862
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
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  • 5
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    Abstract 1731: Preclinical evaluation of the anti-tumor activity of Fc-fused interleukin-7 in both monotherapy and combination therapy
    American Association for Cancer Research (AACR) ; 2018
    In:  Cancer Research Vol. 78, No. 13_Supplement ( 2018-07-01), p. 1731-1731
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 78, No. 13_Supplement ( 2018-07-01), p. 1731-1731
    Abstract: A remarkable progress of cancer immunotherapy in a recent decade, including immune checkpoint blockades (ICB), has shed a new light on the medical treatment of cancer patients. These successes of immunotherapies affirm the notion that modulation of immune-related environment, although not directly targeting a tumor cell, might lead to a better efficacy for cancer treatment. Interleukine-7 (IL-7), a member of the common γ chain family cytokine, plays important roles in the development and homeostasis of lymphocytes in both mouse and human, in particular T lymphocytes. Positive effects of recombinant IL-7 on anti-tumor activity in preclinical models have placed IL-7 as a strong candidate for a novel immunotherapeutic agent in clinics; however, a short half-life of recombinant protein has remained a challenge. Here, we investigated anti-tumor effects in mice of the long-acting form of recombinant human IL-7 fused with hybrid Fc (IL-7-hyFc) in syngeneic tumor models. A dramatic inhibition of tumor growth was achieved when IL-7-hyFc is given in a single subcutaneous injection with palpable tumor burdens. IL-7-hyFc administration significantly enhanced the expression level of CXCR3 on T cells and the frequency of CD8+ tumor-infiltrating lymphocytes (TILs). Of interest, the fraction of PD-1+CD8+ TILs was decreased by IL-7-hyFc, with the cell surface level of PD-1 being diminished. Therefore, IL-7-hyFc is able to expand tumor antigen specific CD8+ effector T cells, resulting in the enhanced infiltration and functional recuperation of TILs. Nonetheless, the tumor growth inhibition by IL-7-hyFc was not observed in mice with large tumor burdens. To increase the therapeutic efficacy of IL-7-hyFc in this model, we combined single injection of the conventional chemotherapeutics cyclophosphamide (CTX) with a moderate dose in which CTX confers immunogenic tumor cell death without severely depleting immune compartment. The combinatorial treatment with IL-7-hyFc and CTX augmented the infiltration of CD8+ TILs, leading to an increased survival in a large established tumor model. In sum, IL-7-hyFc confers the effective anti-tumor responses through reconstructing CD8+ T lymphocytes; this activity was limited when the tumor burden was high but restored along with combination with the chemotherapeutics. Thus, these results imply that IL-7-hyFc can be applied to various cancer immunotherapy regimens as monotherapy or a combination partner with conventional and other immunotherapy, like ICB. Citation Format: Ji-Hae Kim, Donghoon Choi, Man Kyu Ji, Seat-byeul Jo, Han Wook Park, Yeon Kyung Oh, Youngmin Kim, Hyekang Kim, Byung Ha Lee, Se Hwan Yang, Young Chul Sung, Seung-Woo Lee. Preclinical evaluation of the anti-tumor activity of Fc-fused interleukin-7 in both monotherapy and combination therapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 1731.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2018-1731
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
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  • 6
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    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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  • 7
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    Abstract 2968: Development of anti-APP antibody targeting APP/CNTN4 axis as a novel cancer immunotherapy
    American Association for Cancer Research (AACR) ; 2023
    In:  Cancer Research Vol. 83, No. 7_Supplement ( 2023-04-04), p. 2968-2968
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 83, No. 7_Supplement ( 2023-04-04), p. 2968-2968
    Abstract: Immunotherapeutic treatment has profoundly improved the clinical outcomes in patients with advanced cancers. However, most patients still have not responded to immune checkpoint inhibitor (ICI) treatment. Thus, it is still urgent to find novel treatments for patients who have no response to ICI and acquire ICI resistance. Amyloid precursor protein (APP) is a type I transmembrane protein expressed in various cell types. It has primarily been known as a key molecule in brain-related diseases such as Alzheimer’s. However, the function of APP in regulating T cell activity has yet to be elucidated. Previously, we identified that APP expressed in T cells is a binding partner protein of a novel immune checkpoint protein contactin 4 (CNTN4), and APP is a central molecule for conveying immunosuppressive signal of CNTN4 to T cells through the investigation using APP knocked-out T cells. Here we further confirmed that APP had a mechanism of action to weaken TCR signaling by reducing adhesion capacity to cancer cells even with extracellular domain regardless of intracellular domain. When APP was knocked out on CD4+ or CD8+ T cells, the conjugation of T cells with CT26 murine colorectal cancer cells was maintained better than APP WT T cells, and the increased conjugation induced improved T cell-mediated cytotoxicity on CT26 cancer cells. With the anti-APP monoclonal antibody generated by single B cell screening using rabbits, we also explored APP as a potential cancer immunotherapeutic target like CNTN4. Anti-APP antibody bound explicitly to APP recombinant protein without off-target binding and strongly bound to HEK293 overexpressing APP. Moreover, the anti-APP antibody, which inhibited the interaction between APP and CNTN4 more, showed better anti-tumor efficacy in the syngeneic mice model. However, the anti-APP antibody did not affect tumor growth in the immune-deficient mice model, suggesting that the anti-APP antibody shows anti-tumor activity by immunomodulation. To further investigate the immune modulatory function of T cell subsets in tumor-infiltrating lymphocytes by anti-APP antibody treatment, we analyzed the proportion of T cells, Treg cells, and CD8+ T cells expressing granzyme B and perforin in tumor tissues. Collectively, an anti-APP antibody, a therapeutic monoclonal antibody targeting the APP/CNTN4 axis, has the potential for a significant breakthrough in anticancer therapy. Citation Format: Mi Young Cha, Youngeun Ha, Bu-Nam Jeon, Hyunuk Kim, Yunyeon Kim, Jiyeong Lee, Han-Sol Kim, A-Reum Jeong, Hyunkyung Yu, Kyung Mi Park, Hansoo Park. Development of anti-APP antibody targeting APP/CNTN4 axis as a novel cancer immunotherapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 2968.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2023-2968
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
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  • 8
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    Abstract B26: Expression of the KLF4 and SOX10 predicting for survival in colorectal cancer.
    American Association for Cancer Research (AACR) ; 2011
    In:  Molecular Cancer Therapeutics Vol. 10, No. 11_Supplement ( 2011-11-12), p. B26-B26
    Details
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 10, No. 11_Supplement ( 2011-11-12), p. B26-B26
    Abstract: The zinc finger transcription factor Krüppel-like factor 4 (KLF4) is involved in many important cellular processes such as growth, development, differentiation, proliferation, and apoptosis. A loss of KLF4 expression has been observed in human tumors, particularly in the gastrointestinal tract. Sry box 10 (SOX10) is a transcription factor expressed in nerve cell and melanocytes. SOX10 is believed to be essential for neural crest fate determination and to maintain the multipotency of neural crest cells. Here, to investigate the roles of KLF4 and SOX10 in colorectal cancers (CRC), we examined the expression of KLF4 and SOX10 in tumor tissues and paired normal tissues in 125 CRC patients by real-time reverse transcription-polymerase chain (real-time RT-PCR). CRC had significantly lower KLF4 and SOX10 levels compared with matched normal tissues (KLF4: 2007±1531 Copies/ul in CRC, 6585±2833 Copies/ul in normal tissues, SOX10: 60±100 Copies/ul in CRC, 399±215 Copies/ul in normal tissues) (P & lt;0.0001). Statistically, KLF4 and SOX10 expression was not associated with age, sex, stage, lymph node metastasis, differentiation, tumor location. However, in univariate analyses, KLF4 and SOX10 were significant predictors of survival (P=0.002, P=0.039) and in multivariate analyses, KLF4 was significantly predictor of survival (P=0.045). Therefore, these findings suggest that KLF4 and SOX10 might have a potent oncogenic role in CRC tumorigenesis and prognostic value in predicting survival of CRC patients. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2011 Nov 12-16; San Francisco, CA. Philadelphia (PA): AACR; Mol Cancer Ther 2011;10(11 Suppl):Abstract nr B26.
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    URL: Article
    DOI: 10.1158/1535-7163.TARG-11-B26
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
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  • 9
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    Abstract 4590: Genome-wide identification of possible methylation markers chemosensitive to targeted regimens in colorectal cancers
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 4590-4590
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 4590-4590
    Abstract: Purpose Few efficient methylation markers of chemosensitivity have been discovered. The genome-wide analysis of methylation markers is needed to identify chemosensitive candidates to targeted therapy. Methods This study describes a two-step process to select chemosensitive candidates of methylation genes. A genome-wide screening of methylation genes was performed using a beadarray and an in vitro chemosensitivity assay of 119 colorectal cancers (CRCs). Results Ten candidate genes identified during the initial screening were verified by biological utility assessment using cell viability assays of transfected CRC cells. Five methylation genes related to sensitivity to bevacizumab regimens (RASSF1, MMP25, KCNQ1, ESR1, and GALR2) or cetuximab regimens (SCL18A2, GPX7, NID2, IGFBP3, and ALX4) were chosen during the first step. A viability assay revealed that GALR2-overexpressing HCT116 cells were significantly more chemosensitive to bevacizumab regimens than control cells (P = 0.022 and 0.019 for bevacizumab with FOLFIRI and FOLFOX, respectively), concurrently verified on a caspase-3 activity assay. GPX7- or ALX4-overexpressed RKO cells were significantly less viable to cetuximab regimens compared to control cells (GPX7: P = 0.027 each for cetuximab with FOLFIRI and FOLFOX; ALX4: P = 0.049 and 0.003 for cetuximab with FOLFIRI and FOLFOX, respectively), but caspase-3 activity was not prominent in GPX7-overexpressed RKO cells. Conclusions Two novel genes, GALR2 and ALX4, have been identified as chemosensitive methylation candidates to bevacizumab and cetuximab regimens, respectively. As our study did not include a clinical association study, the two candidates should be validated in large clinical cohorts, hopefully predicting responsive patients to targeted regimens. 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 4590. doi:1538-7445.AM2012-4590
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-4590
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
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  • 10
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    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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    detail.hit.zdb_id: 410466-3
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