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  • American Association for Cancer Research (AACR)  (69)
  • 1
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    Posttraumatic Stress Disorder and Likelihood of Hormone Therapy Use among Women in the Nurses' Health Study II: A 26-Year Prospective Analysis
    American Association for Cancer Research (AACR) ; 2021
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 30, No. 3 ( 2021-03-01), p. 492-498
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 30, No. 3 ( 2021-03-01), p. 492-498
    Abstract: Posttraumatic stress disorder (PTSD) is associated with higher risk of certain chronic diseases, including ovarian cancer, but underlying mechanisms remain unclear. Although prior work has linked menopausal hormone therapy (MHT) use with elevated ovarian cancer risk, little research considers PTSD to likelihood of MHT use. We examined whether PTSD was prospectively associated with greater likelihood of initiating MHT use over 26 years. Methods: Using data from the Nurses' Health Study II, with trauma and PTSD (symptoms and onset date) assessed by screener in 2008 and MHT assessed via biennial survey (from 1989), we performed Cox proportional regression models with women contributing person-years from age 36 years. Relevant covariates were assessed at biennial surveys. We considered potential effect modification by race/ethnicity, age at baseline, and period (1989–2002 vs. 2003–2015). Results: Over follow-up, 22,352 of 43,025 women reported initiating MHT use. For example, compared with women with no trauma, the HR for initiating MHT was 1.18 for those with trauma/1–3 PTSD symptoms [95% confidence interval (CI), 1.13–1.22] and 1.31 for those with trauma/4–7 PTSD symptoms (95% CI, 1.25–1.36; P trend & lt; 0.001), adjusting for sociodemographic factors. Associations were maintained when adjusting for reproductive factors and health conditions. We found evidence of effect modification by age at baseline. Conclusions: Trauma and number of PTSD symptoms were associated with greater likelihood of initiating MHT use in a dose–response manner. Impact: MHT may be a pathway linking PTSD to altered chronic disease risk. It is important to understand why women with PTSD initiate MHT use.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1055-9965.EPI-20-1227
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
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  • 2
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    Abstract 5517: Pre-existing medical conditions and risk of breast cancer in Korea: A hospital based case-control study
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 5517-5517
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 5517-5517
    Abstract: Objective: To estimate the effect of highly prevalent medical conditions in Korean population on breast cancer risk in a large case-control study conducted in Korea. Methods: Cases were 3,358 women with incident, histologically confirmed breast cancer in two major hospitals interviewed between 2000 and 2007. Controls were 1820 women admitted to the same hospital and one another hospital for a variety of non-neoplastic conditions. Information of each disease was obtained from standardized questionnaire by trained personnel. Odds ratio(OR) for each disease were derived from multiple logistic regression adjusted for age, hospital, enrollment year, body mass index, age of menarche, age of first pregnancy and family history of breast or other cancer. Results: Among all incident breast cancer patients, pre-existing gastroduodenal diseases and asthma reduced the risk of breast cancer (OR=0.48; 95% confidence interval (C.I.)=0.35-0.67 and OR=0.39; 95% C.I.=0.24-0.64), whereas pre-existing ovarian disease increased the risk(OR=1.63; 95% C.I.=1.12-2.36) when other factors adjusted. Among premenopausal and postmenopausal women, the results of pre-existing gastroduodenal diseases and asthma were similar to those in all cases. But only among postmenopausal women, pre-existing diabetes and hypertension increased the risk of breast cancer significantly (OR=1.66; 95% C.I.=1.01-2.70, OR=1.41; 95% C.I.=1.03-1.92). Conclusion: There had been many studies indicating the association between diabetes and breast cancer development, and our results present the possibility of other disease to effect breast cancer development which can be differed by the menopausal status of women. Also, our study indicates other possible correlation for pre-existing diseases such as asthma, gastroduodenal disease and hypertension with altered breast cancer risk. 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 5517. doi:1538-7445.AM2012-5517
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-5517
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
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  • 3
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    Abstract CT171: Combinatorial allogeneic NK cell therapy with Pembrolizumab for cholangiocarcinoma; interim report of open label Phase1/2a study
    American Association for Cancer Research (AACR) ; 2021
    In:  Cancer Research Vol. 81, No. 13_Supplement ( 2021-07-01), p. CT171-CT171
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 81, No. 13_Supplement ( 2021-07-01), p. CT171-CT171
    Abstract: Combinatorial allogeneic NK cell therapy with Pembrolizumab for cholangiocarcinoma; interim report of open label Phase1/2a study Background: There are several things needed to be resolved for successful efficacy when NK cell therapy is applied for solid tumor; improvement of NK cell invasion into tumor, activation and production of a large number of NK cells, etc. Basically, in human, NK cell number is relatively small compared to other immune cells such as T cell and the number becomes severely low when NK cell is obtained from cancer patients. For these reasons, allogeneic NK cell has been used for clinical studies against various cancer types. Recently, we also have finished a phase1 study of allogeneic NK cell therapy for cholangiocarcinoma, enrolling 9 patients at inoperable and no chemotherapy favorable stage due to side effects. Four of nine patients (44%) showed SD (stable disease) after six NK cell injections and no severe AE (adverse event) was found. In this following phase 2a study, to bring out immuno-synergetic effect of NK cell therapy against the inoperably advanced bile duct cancer, we have designed a combinatorial protocol with using Pembrolizumab. Methods: Enrollment of 40 bile duct cancer patients has been finished for a combinatorial study of allogeneic NK cell therapy with Pembrolizumab at two different sites in Korea (ClinicalTrials gov, NCT03937895). Patients were eligible for the enrollment when they were inoperable and no chemotherapy favorable stage due to side effects, and also when they had PD-L1-positive score. For treatment, the most favorable method for highly activated allogeneic NK cell production has been determined from our previous study, resulting that 3x106 NK cells per kg are injected for each dose along with Pembrolizumab injection. Pembrolizumab (200mg) was given every 3 weeks for up to 9 times and NK cell injection was given for up to 18 times during the maximum injection period of Pembrolizumab. Results: Six patients (pts) were first enrolled for the pilot combinatorial study, dosing 6 times of NK cells and 3 times of Pembrolizumab. The result showed no severe AE from the injections. Among the five pts finished the injections, 2 pts showed SD (Stable Disease) and continued the treatment, being enrolled into the Phase 2a in which 34 more pts were enrolled. Among the 20 pts finished 6 NK cell and 3 Pembrolizumab injections (1st RECIST), 65% of pts showed SD. When 12 NK cell and 6 Pembrolizumab injections finished (2nd RECIST), pts had 40% and 20% of SD and PR (Partial remission). Of the 3 pts at 3rd RECIST (18 NK cell and 9 Pembrolizumab), 1 and 2 pts showed SD and PR, respectively. Finding pts experienced AE, a total of 6 AEs has been reported: no treatment-related AE, one grade 3 (Encephalopathy), and five grade 1-2 with common AE. In a recent safety and efficacy study of pembrolizumab alone (10mg/kg, every 2 weeks for up to 2 years) with 28 pts of advanced bile duct cancer showing PD-L1 expression, 17% pts showed PR, 17% pts and 52% had SD and PD (progressive disease), respectively. Although our study is still ongoing, continuing the combinatorial treatment gives rise to PR, suggesting that NK cell therapy with Pembrolizumab shows an immuno-synergetic effect for the cancer. Biomarker experiments with the injected NK cells supports our finding and we will discuss this at presentation. Citation Format: Yong Yoon Chung, Seung Woo Park, Jung-Min Im, Da-Kyung Yoo, Hyo-Cheon Cheon, Jae-Eun Kim, Kyeong-Pill Lim, Eun-Hee Yang, Hye-Jin choi, Hyo-Sun Chung, Seo-Yeon Kim, Ju-Yong Lee, In-Hye Jung, Seung Min Bang, Moon Jae Chung, Sung Ill Jang, Jae Hee Cho, Hee Seung Lee, Jung Youp Park, Jung Hyun Jo. Combinatorial allogeneic NK cell therapy with Pembrolizumab for cholangiocarcinoma; interim report of open label Phase1/2a study [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr CT171.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2021-CT171
    RVK:
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    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
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  • 4
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    Abstract P3-10-04: A open-label, randomized, parallel, phase III trial to evaluate the efficacy and safety of Genexol®-PM compared to Genexol®(conventional paclitaxel with cremorphor EL) in recurrent or metastatic breast cancer patients
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 9_Supplement ( 2015-05-01), p. P3-10-04-P3-10-04
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 9_Supplement ( 2015-05-01), p. P3-10-04-P3-10-04
    Abstract: Background: The rationale for developing an alternative paclitaxel formulation concerns Cremophor EL-related side effects, and a novel paclitaxel delivery system might augment its therapeutic efficacy. Genexol-PM is a novel polymeric micelle formulated paclitaxel free of Cremophor. The polymeric micelle formulation is composed of hundreds of low molecular weight, non-toxic, and biodegradable amphiphilic diblock copolymers which include monomethoxy poly (ethylene glycol)-block-poly (D,L-lactide). This multicenter phase III study was designed to evaluate the non-inferiority of efficacy of Genexol-PM compared to conventional CrEL-based paclitaxel. Methods: In this phase III study, 213 patients were enrolled onto the study and randomly assigned (1:1) to treatment group according to prior recurrent or metastatic breast cancer chemotherapy. The study evaluated the objective response rate for the primary objective, and others including overall survival (OS), progression free survival (PFS), time to tumor progression (TTP), duration of overall response and adverse events. Eligible patients were randomly assigned to receive either Genexol-PM or standard paclitaxel. Genexol-PM or standard paclitaxel was administered on the first day of every 3 weeks. Measurable disease was assessed by imaging using the RECIST 1.0 criteria. Results: The objective response rate (ORR) was higher by the administration of the study drug (39.05% v 24.30% in ITT, 56.92% v 39.29% in PP). One-sided 95% upper confidence limit was -4.36%, which is lower than the non-inferiority threshold (7%), indicating that the study group is not inferior to the control group. OS, PFS, TTP and duration of overall response were analyzed in the ITT population. The analysis of OS showed no significant difference (p=0.5878) (859 days, 95% CI : 732.00∼1,025.00 v 726 days, 95% CI : 553.00∼ -). Median PFS periods were 232 days (95% CI: 164.00∼274.00) vs. 191 days (95% CI: 159.00∼237.00). Median TTPs were 233 days (95% CI: 165.00∼286.00) vs. 191 days (95% CI: 159.00∼241.00) between the groups. Difference in PFSs and TTPs between the groups were not statistically significant. (p=0.2407, 0.2076, respectively) Genexol-PM was not significantly different from the comparator in terms of safety. Conclusion: Genexol-PM demonstrated non-inferior efficacy and comparable safety profile compared with standard paclitaxel in this patient population. Of note, Genexol-PM permits the delivery of a higher paclitaxel dose without additional toxicity achieved with CrEL-based formulation. In the absence of CrEL, no filter or special tubing is required that conventional PVC infusion sets can be used. Citation Format: Jung Sil Ro, Joo Hyuk Sohn, Sung Bae Kim, Keun Seok Lee, Joo Seop Chung, Jae Hoo Park, Soo Hyeon Lee, Tae You Kim, Kyung Hae Jung, Eun Kyung Cho, Yang Soo Kim, Hong Suk Song, Jae Hong Seo, Hun Mo Ryoo, Sun Ah Lee, So Young Yoon, Chul Soo Kim, Yong Tai Kim, Hwa Jung Sung, Si Young Kim, Yong Jin Lee. A open-label, randomized, parallel, phase III trial to evaluate the efficacy and safety of Genexol®-PM compared to Genexol®(conventional paclitaxel with cremorphor EL) in recurrent or metastatic breast cancer patients [abstract] . In: Proceedings of the Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2014 Dec 9-13; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2015;75(9 Suppl):Abstract nr P3-10-04.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.SABCS14-P3-10-04
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
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  • 5
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    Targeting FGFR Pathway in Human Hepatocellular Carcinoma: Expressing pFGFR and pMET for Antitumor Activity
    American Association for Cancer Research (AACR) ; 2015
    In:  Molecular Cancer Therapeutics Vol. 14, No. 11 ( 2015-11-01), p. 2613-2622
    Details
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 14, No. 11 ( 2015-11-01), p. 2613-2622
    Abstract: The MET receptor tyrosine kinase, the receptor for hepatocyte growth factor (HGF), has been implicated in cancer growth, invasion, migration, angiogenesis, and metastasis in a broad variety of human cancers, including human hepatocellular carcinoma (HCC). Recently, MET was suggested to be a potential target for the personalized treatment of HCC with an active HGF–MET signaling pathway. However, the mechanisms of resistance to MET inhibitors need to be elucidated to provide effective treatment. Here, we show that HCC cells exhibit different sensitivities to the MET inhibitor PHA665752, depending on the phosphorylation status of FGFR. Treatment of cells expressing both phospho-FGFR and phospho-MET with the inhibitor PHA665752 did not cause growth inhibition and cell death, whereas treatment with AZD4547, a pan-FGFR inhibitor, resulted in decreased colony formation and cleavage of caspase-3. Moreover, silencing of endogenous FGFR1 and FGFR2 by RNAi of HCC cells expressing phospho-FGFR, phospho-FGFR2, and phospho-MET overcame the resistance to PHA665752 treatment. Treatment of primary cancer cells from patients with HCC expressing both phospho-FGFR and phospho-MET with PHA665752 did not induce cell death, whereas AZD4547 treatment induced cell death through the cleavage of caspase-3. In addition, treatment of cells resistant to PHA665752 with AZD4547 abrogated the activation of downstream effectors of cell growth, proliferation, and survival. On the basis of these results, we conclude that the FGFR pathway is critical for HCC survival, and that targeting this pathway with AZD4547 may be beneficial for the treatment of patients with HCC-expressing phospho-FGFR and phospho-MET. Mol Cancer Ther; 14(11); 2613–22. ©2015 AACR.
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    URL: Article
    DOI: 10.1158/1535-7163.MCT-14-0780
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
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  • 6
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    Abstract 525: ADAM-9 expression in gastric cancer and its association with invasiveness
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 525-525
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 525-525
    Abstract: The ADAMs (a disintegrin and metalloproteinase) comprise a family of multidomain transmembrane and secreted proteins. Accumulating evidence associates an increased expression of individual ADAM family members with various types of cancer including prostate, breast, skin and lung cancers. However, little is known about its role in gastric cancer. Herein, we investigated the expression of ADAM-9 in gastric cancer, and its implication as a potential therapeutic target for anti-metastaasis therapy. First, we evaluated the expression of ADAM-9 on protein by immunoblotting and transcript level in 24 gastric cancer cell lines by RT-PCR. ADAM-9 protease activity was also measured using ADAM-9 fluorogenic substrate (R & D systems, Minneapolis, MN, USA). We then conducted invasion assay using transwell coated with matrigel in the presence or absence of ADAM-9-specific inhibiting antibody (kindly supplied from Raven Biotechnologies, Inc., South San Francisco, CA). The mRNA expression of ADAM-9 was observed in all the gastric cancer cell lines while the protein expressions of pro- and active-form and protease activities were variable. We selected the cell lines of high baseline ADAM-9 expression (SNU-638, MKN-28 and AGS) and of low baseline expression (SNU-216, MKN-1 and HS-746T) to continue further experiment. Baseline level of ADAM-9 is little correlated with invasion activity though matrigel. Treatment of anti-ADAM-9 antibody does not influence the cytotoxicity. However, it reduced its protease activity and invasiveness, which was dependent on baseline ADAM-9 activity. Actually, protease activity reduced 64.5±0.3% when the specific antibody to ADAM-9 was treated to high expressed cell lines, but 9.6±0.4% were decreased in low expressed cell lines at the 20ug/ml of the antibody. Anti-ADAM-9 antibody inhibited the invasion activity dose dependently, and its effect was more prominent in high ADAM-9-expressing cell lines (67.7±1.9% vs 5.9±4.3% at the 20 ug/ml antibody). Anti-ADAM-9 treatment did not influence on the cell-matrix adhesion, which implies this anti-invasive effect is through its inhibition of protease function. In the hypoxic condition (1% oxygen), invasion was increased along with elevation of both active form of ADAM-9 and its protease activity, suggesting that increased ADAM-9 could have a role of enhancing invasiveness of gastric cancer. To conclude, we presented that ADAM-9 has a role in invasiveness of gastric cancer and would be one of the putative targets for anti-metastasis therapy. This work was supported by the Brain Korea 21 Project for Medical Science, Yonsei University. 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 525.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM10-525
    RVK:
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    RVK:
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 7
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    Abstract C276: Ruxolitinib induces apoptotic cell death through the suppression of pJAK1 in human colon cancer cells.
    American Association for Cancer Research (AACR) ; 2013
    In:  Molecular Cancer Therapeutics Vol. 12, No. 11_Supplement ( 2013-11-01), p. C276-C276
    Details
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 12, No. 11_Supplement ( 2013-11-01), p. C276-C276
    Abstract: Janus kinase (JAK) is one of the main upstream activators of signal transducers and activators of transcription (STAT) that are constitutively activated in various malignancies and are associated with cell growth, survival, and carcinogenesis. Here, we investigated to role of JAKs in colorectal cancer in order to develop effective therapeutic targets for ruxolitinib, which is the first JAK1/2 inhibitor to be approved by FDA. After examining the basal expression levels of phospho-JAK1 and phospho-JAK2, we measured the effects of ruxolitinib on the phosphorylation of JAK1/2 using western blot analysis. Cell viability was determined using the trypan blue exclusion assay. The cell death mechanism was identified by the activation of caspase 3 using western blot and annexin V staining. The basal levels of phospho-JAK1 and phospho-JAK2 were cancer cell type dependent. Colorectal cancer cell lines that phosphorylate both JAK1 and JAK2 include DLD-1 and RKO. Ruxolitinib inactivates both JAK1 and JAK2 in DLD-1 cells but inactivates only JAK1 in RKO cells. Cell death was proportional to the inactivation of JAK1 but not JAK2. Ruxolitinib causes caspase-dependent cell death, which is prevented by treatment with z-VAD. The inhibition of JAK1 phosphorylation seemed sufficient to allow ruxolitinib-mediated apoptosis. JAK1 is a key molecule that is involved in colon cancer cell survival and the inhibition of JAK1 by ruxolitinib results in caspase-dependent apoptosis in colorectal cancer cells. The use of selective JAK1 inhibitors could be an attractive therapy against colorectal cancer, but further clinical investigations are needed to test this possibility. Citation Information: Mol Cancer Ther 2013;12(11 Suppl):C276. Citation Format: Ho Jung An, Eun Kyoung Choi, Jin-Sun Kim, Seung-Woo Hong, Jai-Hee Moon, Jae-Sik Shin, Seung-Hee Ha, Kyu-Pyo Kim, Yong Sang Hong, Jae-Lyun Lee, Eun Kyung Choi, Jung Shin Lee, Dong-Hoon Jin, Tae Won Kim. Ruxolitinib induces apoptotic cell death through the suppression of pJAK1 in human colon cancer cells. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2013 Oct 19-23; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2013;12(11 Suppl):Abstract nr C276.
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    URL: Article
    DOI: 10.1158/1535-7163.TARG-13-C276
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
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  • 8
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    Abstract C277: INCB018424 induces apoptotic cell death through the suppression of pJAK1 in human colon cancer cells.
    American Association for Cancer Research (AACR) ; 2013
    In:  Molecular Cancer Therapeutics Vol. 12, No. 11_Supplement ( 2013-11-01), p. C277-C277
    Details
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 12, No. 11_Supplement ( 2013-11-01), p. C277-C277
    Abstract: Janus kinase (JAK) is one of the main upstream activators of signal transducers and activators of transcription (STAT) that are constitutively activated in various malignancies and are associated with cell growth, survival, and carcinogenesis. Here, we investigated to role of JAKs in colorectal cancer in order to develop effective therapeutic targets for INCB018424, which is the first JAK1/2 inhibitor to be approved by FDA. After examining the basal expression levels of phospho-JAK1 and phospho-JAK2, we measured the effects of INCB018424 on the phosphorylation of JAK1/2 using western blot analysis. Cell viability was determined using the trypan blue exclusion assay. The cell death mechanism was identified by the activation of caspase 3 using western blot and annexin V staining. The basal levels of phospho-JAK1 and phospho-JAK2 were cancer cell type dependent. Colorectal cancer cell lines that phosphorylate both JAK1 and JAK2 include DLD-1 and RKO. INCB018424 inactivates both JAK1 and JAK2 in DLD-1 cells but inactivates only JAK1 in RKO cells. Cell death was proportional to the inactivation of JAK1 but not JAK2. INCB018424 causes caspase-dependent cell death, which is prevented by treatment with z-VAD. The inhibition of JAK1 phosphorylation seemed sufficient to allow INCB018424-mediated apoptosis. JAK1 is a key molecule that is involved in colon cancer cell survival and the inhibition of JAK1 by INCB01424 results in caspase-dependent apoptosis in colorectal cancer cells. The use of selective JAK1 inhibitors could be an attractive therapy against colorectal cancer, but further clinical investigations are needed to test this possibility. Citation Information: Mol Cancer Ther 2013;12(11 Suppl):C277. Citation Format: Eun Kyoung Choi, Seung Hee Ha, Ho Jung An, Jin-Sun Kim, Seung-Woo Hong, Jai-Hee Moon, Jae-Sik Shin, Kyu-Pyo Kim, Yong Sang Hong, Jae-Lyun Lee, Eun Kyung Choi, Jung Shin Lee, Dong-Hoon Jin, Tae Won Kim. INCB018424 induces apoptotic cell death through the suppression of pJAK1 in human colon cancer cells. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2013 Oct 19-23; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2013;12(11 Suppl):Abstract nr C277.
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    URL: Article
    DOI: 10.1158/1535-7163.TARG-13-C277
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
    detail.hit.zdb_id: 2062135-8
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  • 9
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    Abstract LB-092: Programmed death-ligand 1 is overexpressed in bronchial preneoplastic lesions: can it be a risk indicator
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 15_Supplement ( 2015-08-01), p. LB-092-LB-092
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15_Supplement ( 2015-08-01), p. LB-092-LB-092
    Abstract: Compared to the vigorous development of targeted drugs and some of them are already become one of the best treatment of choices in lung adenocarcinoma, squamous lung carcinoma has no definite targets and treatment outcome is not yet superior to lung adenocarcinoma. Demonstration of initial carcinogenesis is benefitial in two aspects: cancer prevention and development of its targets. Studying preneoplastic lesions of bronchus can answer those questions. Preneoplastic lesion, which is considered to have malignant potential, may develop into invasive cancer by escaping from host immune response. CD274 (programmed death-ligand 1, PD-L1) interacts with PD-1, is known to inhibit CD8+ cytotoxic T lymphocyte and induce apoptosis and, also to promote the differentiation of CD4+ T cells into regulatory T cells, so finally evade immune surveillance. We hypothesized that PD-L1 may work as an immune evader in preneoplastic lesion during its carcinogenesis. We performed white light and/or autofluorescence bronchoscopy in patients who have risk factor(s) of lung cancer or are suspected to have a lung cancer. Interestingly, PD-L1 was also overexpressed in preneoplastic lesions especially in severe dysplasia of the bronchus. This finding implies overexpression of PD-L1 can involve at early step of carcinogenesis. Further studies are needed to demonstrate the role of PD-L1 in preneoplastic bronchial lesion potential to develop invasive cancer. Citation Format: Hee Sun Park, Bo Mi Park, Dong Il Park, Chung Jae Uk, Jae Young Moon, Jung Sung Soo, Choong Sik Lee, Ju Ock Kim, Sun Young Kim, Jaseok Peter Koo. Programmed death-ligand 1 is overexpressed in bronchial preneoplastic lesions: can it be a risk indicator. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr LB-092. doi:10.1158/1538-7445.AM2015-LB-092
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2015-LB-092
    RVK:
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    RVK:
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
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  • 10
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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
    detail.hit.zdb_id: 2036787-9
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