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  • American Association for Cancer Research (AACR)  (11)
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  • American Association for Cancer Research (AACR)  (11)
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  • 1
    Online Resource
    Online Resource
    Verteporfin Inhibits PD-L1 through Autophagy and the STAT1–IRF1–TRIM28 Signaling Axis, Exerting Antitumor Efficacy
    American Association for Cancer Research (AACR) ; 2020
    In:  Cancer Immunology Research Vol. 8, No. 7 ( 2020-07-01), p. 952-965
    Details
    In: Cancer Immunology Research, American Association for Cancer Research (AACR), Vol. 8, No. 7 ( 2020-07-01), p. 952-965
    Abstract: Programmed cell death 1 ligand 1 (PD-L1) is a key driver of tumor-mediated immune suppression, and targeting it with antibodies can induce therapeutic responses. Given the costs and associated toxicity of PD-L1 blockade, alternative therapeutic strategies are needed. Using reverse-phase protein arrays to assess drugs in use or likely to enter trials, we performed a candidate drug screen for inhibitors of PD-L1 expression and identified verteporfin as a possible small-molecule inhibitor. Verteporfin suppressed basal and IFN-induced PD-L1 expression in vitro and in vivo through Golgi-related autophagy and disruption of the STAT1–IRF1–TRIM28 signaling cascade, but did not affect the proinflammatory CIITA-MHC II cascade. Within the tumor microenvironment, verteporfin inhibited PD-L1 expression, which associated with enhanced T-lymphocyte infiltration. Inhibition of chromatin-associated enzyme PARP1 induced PD-L1 expression in high endothelial venules (HEV) in tumors and, when combined with verteporfin, enhanced therapeutic efficacy. Thus, verteporfin effectively targets PD-L1 through transcriptional and posttranslational mechanisms, representing an alternative therapeutic strategy for targeting PD-L1.
    Type of Medium: Online Resource
    ISSN: 2326-6066 , 2326-6074
    URL: Article
    DOI: 10.1158/2326-6066.CIR-19-0159
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
    detail.hit.zdb_id: 2732517-9
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  • 2
    Online Resource
    Online Resource
    Validation of the 12-gene Predictive Signature for Adjuvant Chemotherapy Response in Lung Cancer
    American Association for Cancer Research (AACR) ; 2019
    In:  Clinical Cancer Research Vol. 25, No. 1 ( 2019-01-01), p. 150-157
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 25, No. 1 ( 2019-01-01), p. 150-157
    Abstract: Response to adjuvant chemotherapy after tumor resection varies widely among patients with non–small cell lung cancer (NSCLC); therefore, it is of clinical importance to prospectively predict who will benefit from adjuvant chemotherapy before starting the treatment. The goal of this study is to validate a 12-gene adjuvant chemotherapy predictive signature developed from a previous study using a clinical-grade assay. Experimental Design: We developed a clinical-grade assay for formalin-fixed, paraffin-embedded (FFPE) samples using the NanoString nCounter platform to measure the mRNA expression of the previously published 12-gene set. The predictive performance was validated in a cohort of 207 patients with early-stage resected NSCLC with matched propensity score of adjuvant chemotherapy. Results: The effects of adjuvant chemotherapy were significantly different in patients from the predicted adjuvant chemotherapy benefit group and those in the predicted adjuvant chemotherapy nonbenefit group (P = 0.0056 for interaction between predicted risk group and adjuvant chemotherapy). Specifically, in the predicted adjuvant chemotherapy benefit group, the patients receiving adjuvant chemotherapy had significant recurrence-free survival (RFS) benefit (HR = 0.34; P = 0.016; adjuvant chemotherapy vs. nonadjuvant chemotherapy), while in the predicted adjuvant chemotherapy nonbenefit group, the patients receiving adjuvant chemotherapy actually had worse RFS (HR = 1.86; P = 0.14; adjuvant chemotherapy vs. nonadjuvant chemotherapy) than those who did not receive adjuvant chemotherapy. Conclusions: This study validated that the 12-gene signature and the FFPE-based clinical assay predict that patients whose resected lung adenocarcinomas exhibit an adjuvant chemotherapy benefit gene expression pattern and who then receive adjuvant chemotherapy have significant survival advantage compared with patients whose tumors exhibit the benefit pattern but do not receive adjuvant chemotherapy.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-17-2543
    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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  • 3
    Online Resource
    Online Resource
    Building Practical Risk Prediction Models for Nasopharyngeal Carcinoma Screening with Patient Graph Analysis and Machine Learning
    American Association for Cancer Research (AACR) ; 2023
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 32, No. 2 ( 2023-02-06), p. 274-280
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 32, No. 2 ( 2023-02-06), p. 274-280
    Abstract: To expand nasopharyngeal carcinoma (NPC) screening to larger populations, more practical NPC risk prediction models independent of Epstein–Barr virus (EBV) and other lab tests are necessary. Methods: Patient data before diagnosis of NPC were collected from hospital electronic medical records (EMR) and used to develop machine learning (ML) models for NPC risk prediction using XGBoost. NPC risk factor distributions were generated through connection delta ratio (CDR) analysis of patient graphs. By combining EMR-wide ML with patient graph analysis, the number of variables in these risk models was reduced, allowing for more practical NPC risk prediction ML models. Results: Using data collected from 1,357 patients with NPC and 1,448 patients with control, an optimal set of 100 variables (ov100) was determined for building NPC risk prediction ML models that had, the following performance metrics: 0.93–0.96 recall, 0.80–0.92 precision, and 0.83–0.94 AUC. Aided by the analysis of top CDR-ranked risk factors, the models were further refined to contain only 20 practical variables (pv20), excluding EBV. The pv20 NPC risk XGBoost model achieved 0.79 recall, 0.94 precision, 0.96 specificity, and 0.87 AUC. Conclusions: This study demonstrated the feasibility of developing practical NPC risk prediction models using EMR-wide ML and patient graph CDR analysis, without requiring EBV data. These models could enable broader implementation of NPC risk evaluation and screening recommendations for larger populations in urban community health centers and rural clinics. Impact: These more practical NPC risk models could help increase NPC screening rate and identify more patients with early-stage NPC.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1055-9965.EPI-22-0792
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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  • 4
    Online Resource
    Online Resource
    Abstract 5382: Epigenetic targeting of survivin enhances paclitaxel-mediated antitumor activity against non-small-cell lung cancer
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 15_Supplement ( 2015-08-01), p. 5382-5382
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15_Supplement ( 2015-08-01), p. 5382-5382
    Abstract: Lung cancer is the leading cause of cancer-related deaths worldwide and has a low 5-year survival rate. The current treatment for lung cancer patients is surgical resection followed by chemotherapy. However, the majority of patients will eventually experience disease progression and require further treatment. Increased evidence indicates that overexpression of survivin, the smallest member of IAP (inhibitor of apoptosis) family, results in poor prognosis, tumor recurrence, and drug resistance in various cancers, including non-small-cell lung cancer (NSCLC), which accounts for approximately 85% of all lung cancer cases. Although the precise mechanism leading to survivin overexpression in cancer cells is not fully understood, approach to effectively downregulate survivin is thought to be required to enhance chemotherapy, reduce relapse, and improve the survival of NSCLC patients. In the present study, we have explored the therapeutic potential of the class I HDAC inhibitor (HDACi) entinostat (or MS-275, SNDX-275, LC Laboratories, Woburn, MA) in combination with paclitaxel in the treatment of NSCLC. We show that entinostat significantly enhances paclitaxel-induced anti-proliferative/anti-survival effects and apoptosis in NSCLC cells. It appears that this HDACi selectively reduces the expression levels of survivin, but not the functionally-related molecules Mcl-1 and Bcl-xL. Further studies reveal that entinostat induces expression of two survivin-targeting miRNAs, miR-203 and miR-542-3p; and that both survivin-specific shRNAs and the mimics of miR-203 and/or miR-542-3p effectively downregulate survivin and dramatically promote NSCLC cells undergoing apoptosis upon paclitaxel treatment. Moreover, in a tumor xenografts model-established from NSCLC cells, entinostat maintains its capability to upregulate miR-203 and downregulate survivin in vivo. Importantly, the combinations of entinostat and paclitaxel exhibit a striking activity, as compared to either agent alone, to inhibit tumor growth. These data indicate that entinostat is efficacious to enhance paclitaxel-mediated anti-NSCLC activity. Our findings suggest that epigenetic targeting of survivin with entinostat or miRNA-replacement therapy may be a novel strategy to re-sensitize NSCLC to chemotherapy. Numerous studies demonstrate that entinostat exerts potent antitumor activity in various human cancers. Its clinic activity in NSCLC is currently being tested in combination with the DNA methyltransferase inhibitor Azacitidine or EGFR inhibitor erlotinib, but not conventional chemotherapy (http://www.clinicaltrial.gov/ct2/results?term = entinostat & Search = Search). Our studies provide a strong rationale to initiate clinical evaluation of the combinatorial effects of entinostat and paclitaxel on NSCLC patients. Citation Format: Shuiliang Wang, Ling Zhu, Zhiyong Zeng, Lianghu Huang, Fengjin Lin, Rong Lin, Jin Wang, Jun Lu, Qinghua Wang, Lingjing Lin, Huiyue Dong, Weizhen Wu, Kai Zheng, Jinquan Cai, Shunliang Yang, Yujie Ma, Shixin Ye, Wei Liu, Yinghao Yu, Bolin Liu, Jianming Tan. Epigenetic targeting of survivin enhances paclitaxel-mediated antitumor activity against non-small-cell lung cancer. [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 5382. doi:10.1158/1538-7445.AM2015-5382
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2015-5382
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 5
    Online Resource
    Online Resource
    The Open Chromatin Landscape of Non–Small Cell Lung Carcinoma
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Research Vol. 79, No. 19 ( 2019-10-01), p. 4840-4854
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 79, No. 19 ( 2019-10-01), p. 4840-4854
    Abstract: Non–small cell lung carcinoma (NSCLC) is a major cancer type whose epigenetic alteration remains unclear. We analyzed open chromatin data with matched whole-genome sequencing and RNA-seq data of 50 primary NSCLC cases. We observed high interpatient heterogeneity of open chromatin profiles and the degree of heterogeneity correlated to several clinical parameters. Lung adenocarcinoma and lung squamous cell carcinoma (LUSC) exhibited distinct open chromatin patterns. Beyond this, we uncovered that the broadest open chromatin peaks indicated key NSCLC genes and led to less stable expression. Furthermore, we found that the open chromatin peaks were gained or lost together with somatic copy number alterations and affected the expression of important NSCLC genes. In addition, we identified 21 joint-quantitative trait loci (joint-QTL) that correlated to both assay for transposase accessible chromatin sequencing peak intensity and gene expression levels. Finally, we identified 87 regulatory risk loci associated with lung cancer–related phenotypes by intersecting the QTLs with genome-wide association study significant loci. In summary, this compendium of multiomics data provides valuable insights and a resource to understand the landscape of open chromatin features and regulatory networks in NSCLC. Significance: This study utilizes state of the art genomic methods to differentiate lung cancer subtypes. See related commentary by Bowcock, p. 4808
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-18-3663
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 6
    Online Resource
    Online Resource
    Shikonin circumvents cancer drug resistance by induction of a necroptotic death
    American Association for Cancer Research (AACR) ; 2007
    In:  Molecular Cancer Therapeutics Vol. 6, No. 5 ( 2007-05-01), p. 1641-1649
    Details
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 6, No. 5 ( 2007-05-01), p. 1641-1649
    Abstract: Defect in apoptotic signaling and up-regulation of drug transporters in cancer cells significantly limits the effectiveness of cancer chemotherapy. We propose that an agent inducing non-apoptotic cell death may overcome cancer drug resistance and showed that shikonin, a naturally occurring naphthoquinone, induced a cell death in MCF-7 and HEK293 distinct from apoptosis and characterized with (a) a morphology of necrotic cell death; (b) loss of plasma membrane integrity; (c) loss of mitochondrial membrane potentials; (d) activation of autophagy as a downstream consequence of cell death, but not a contributing factor; (e) elevation of reactive oxygen species with no critical roles contributing to cell death; and (f) that the cell death was prevented by a small molecule, necrostatin-1, that specifically prevents cells from necroptosis. The characteristics fully comply with those of necroptosis, a basic cell-death pathway recently identified by Degterev et al. with potential relevance to human pathology. Furthermore, we proved that shikonin showed a similar potency toward drug-sensitive cancer cell lines (MCF-7 and HEK293) and their drug-resistant lines overexpressing P-glycoprotein, Bcl-2, or Bcl-xL, which account for most of the clinical cancer drug resistance. To our best knowledge, this is the first report to document the induction of necroptosis by a small molecular compound to circumvent cancer drug resistance. [Mol Cancer Ther 2007;6(5):1641–9]
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    URL: Article
    DOI: 10.1158/1535-7163.MCT-06-0511
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2007
    detail.hit.zdb_id: 2062135-8
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Abstract 4091: Mesenchymal stem cells drive paclitaxel-resistance in erbB2-overexpressing breast cancer cells via paracrine of NRG-1
    American Association for Cancer Research (AACR) ; 2016
    In:  Cancer Research Vol. 76, No. 14_Supplement ( 2016-07-15), p. 4091-4091
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 76, No. 14_Supplement ( 2016-07-15), p. 4091-4091
    Abstract: Breast cancer remains the most frequently diagnosed cancer and the leading cause of cancer death in women, both worldwide and in less developed countries. Surgery in conjunction with adjuvant chemotherapy is the main treatment of choice for patients with locally advanced breast cancer, leading to reduce cancer-related symptoms and prolong survival. Paclitaxel as a critical drug in the treatment of breast cancer patients, intrinsic and acquired resistance to paclitaxel represents a significant clinical problem. We had previously demonstrated that increased expression of erbB3 is required for erbB2-mediated paclitaxel resistance in breast cancer cells via PI-3K/Akt/mTOR signaling pathway-dependent upregulation of Survivin. Mesenchymal stem cells (MSCs) are emerging as an important component of tumor microenvironment, which may play an essential role in regulating cancer cell growth, motility, invasion and therapeutic resistance. In the present study, we have explored the possible role of MSCs in regulating the chemo-sensitivity of erbB2-overexpressing breast cancer cells. We show that both human umbilical cord and bone marrow-derived MSCs express significantly higher level of Neuregulin-1 (NRG-1, also Heregulin-β1) as compared with erbB2-overexpressing breast cancer cells themselves. Coculture or treatment with conditioned medium of MSCs not only decreases the anti-proliferation effect of paclitaxel on erbB2-overexpressing breast cancer cells, but also significantly inhibits paclitaxel-induced apoptosis. We further demonstrate that this MSCs-drived paclitaxel-resistance in erbB2-overexpressing breast cancer cells could be attributed to paracrine effect of NRG-1/erbB3 signaling, as specific nutralizaion of NRG-1 or blocking of erbB3 resensitizes erbB2-overexpressing breast cancer cells to paclitaxel treatment. Moreover, overexpression of erbB3 enhances, while knockdown expression of erbB3 abrogates MSCs-drived paclitaxel-resistance. Taken together, our current data indicate that paracrine of NRG-1 by MSCs induce resistance of paclitaxel in erbB2-overexpressing breast cancer cells through activation of erbB3 signaling. Our findings suggest that simultaneously targeting mesenchymal stem cells in tumor microenviroment may be a novel strategy to overcome chemotherapeutic resistance. Citation Format: Ling Zhu, Jin Wang, Weimin Zuo, Rong Lin, Tingting Lin, Yan Lei, Bingshuang Ren, Jun Lu, Huiyue Dong, Lingjing Lin, Lianghu Huang, Qinghua Wang, Yujie Ma, Hui Lyu, Bolin Liu, Jianming Tan, Shuiliang Wang. Mesenchymal stem cells drive paclitaxel-resistance in erbB2-overexpressing breast cancer cells via paracrine of NRG-1. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 4091.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2016-4091
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 8
    Online Resource
    Online Resource
    Abstract LB289: Longitudinal ctDNA levels and clinical outcomes of first-line (1L) tislelizumab (TIS) + chemotherapy (chemo) treatment for advanced non-small cell lung cancer (NSCLC) in the RATIONALE-304 and 307 studies
    American Association for Cancer Research (AACR) ; 2023
    In:  Cancer Research Vol. 83, No. 8_Supplement ( 2023-04-14), p. LB289-LB289
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 83, No. 8_Supplement ( 2023-04-14), p. LB289-LB289
    Abstract: Background: The role of circulating tumor DNA (ctDNA) in monitoring response to immunotherapy in NSCLC is unconfirmed. This is a retrospective analysis of association between longitudinal ctDNA levels and clinical outcomes in 1L TIS (anti-PD-1) + chemo-treated patients (pts) with nonsquamous or squamous NSCLC from RATIONALE-304 (NCT03663205) and 307 (NCT03594747), respectively. Methods: Blood samples were collected at baseline (BL), first response (FR, complete or partial response assessed by investigators), and progressive disease (PD). ctDNA level was tested by OncoScreen Plus520 (Burning Rock) and the variant allele fraction categorized as undetectable (UD)/detectable (D). Paired ctDNA analysis of BL and post-BL (FR or PD) values was by Wilcoxon sign-rank test. Median PFS and OS was calculated by Kaplan-Meier methodology. PD-L1 expression stratified Cox model was used to evaluate the effect of ctDNA on PFS and OS for BL and FR (adjusted with BL ctDNA) in each study. Impact of other BL characteristics was also assessed. Results: Of 217 pts treated with TIS + chemo in RATIONALE-304, 76 (35%) at BL, 40 (18%) at FR, and 30 (14%) at PD had ctDNA results. Of 238 pts treated with TIS + chemo in RATIONALE-307, 80 (34%) at BL, 65 (27%) at FR, and 33 (14%) at PD had ctDNA results. Paired ctDNA analysis showed significantly decreased ctDNA levels from BL to FR (P & lt;0.0001 in 304 and 307); no obvious change was detected from BL to PD in both studies. Pts with UD ctDNA status at FR had notably longer median PFS and OS compared with pts with D ctDNA; no such association was observed using BL ctDNA status in either study (Table). Conclusions: FR ctDNA level is decreased from BL, and seems to correlate with clinical outcomes of 1L TIS in combination with chemotherapy in NSCLC; ctDNA has potential to be a surrogate biomarker for efficacy. This requires further prospective validation. Acknowledgments: This study was sponsored by BeiGene, Ltd. Medical writing support, under the direction of the authors, was provided by Simon Lancaster, BSc, of Ashfield MedComms, an Inizio company, and was funded by BeiGene, Ltd. Table. Analysis summary of ctDNA and PFS/OS by visit Baseline (BL) First response (FR) Study RATIONALE-304 RATIONALE-307 RATIONALE-304 RATIONALE-307 ctDNA UD D UD D UD D UD D n 19 57 8 72 32 8 43 22 mPFS, mo (95% CI)a 9.23(5.75, 9.89) 9.69(7.33, 14.52) NR(4.93, NR) 9.76(7.52, 14.55) 17.31(9.89, NR) 9.20(3.71, 11.99) 20.01(9.82, NR) 9.56(7.39, 13.9) PFS HR (95% CI), UD/D 1.14 (0.61, 2.21) 0.40 (0.09, 1.73) 0.16 (0.05, 0.5) 0.54 (0.24, 1.21) PFS P-valueb 0.6421 0.2205 0.0019 0.1322 mOS, mo (95% CI) NR(9.72, NR) NR(14,23, NR) NR(NR, NR) NR(16.89, NR) NR(NR, NR) 18.78(9.92, NR) NR(NR, NR) NR(12.85, NR) OS HR (95% CI), UD/D 1.04 (0.48, 2.25) NE 0.16 (0.04, 0.69) 0.48 (0.15, 1.51) OS P-valueb 0.9254 NE 0.0147 0.2079 aPrimary endpoint assessed by IRC; bP-values are reported for descriptive purposes only in this exploratory study. Abbreviations: CI, confidence interval; D, detectable ctDNA status; HR, hazard ratio; IRC, independent review committee; mo, months; mOS, median overall survival; mPFS, median progression-free survival; NE, not evaluable; NR, not reached; OS, overall survival; PFS, progression-free survival; UD, undetectable ctDNA status Citation Format: Shun Lu, Jie Wang, Meili Sun, Jun Zhao, Chunhong Hu, Mengzhao Wang, Jianying Zhou, Yong Song, Qinghua Zhou, Jiayuan Zhang, Yang Shi, Ruiqi Huang, Xikun Wu, Wanyu He, Xiaofei Qu, Yun Zhang, Zhirong Shen, Yan Yu. Longitudinal ctDNA levels and clinical outcomes of first-line (1L) tislelizumab (TIS) + chemotherapy (chemo) treatment for advanced non-small cell lung cancer (NSCLC) in the RATIONALE-304 and 307 studies [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 2 (Clinical Trials and Late-Breaking Research); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(8_Suppl):Abstract nr LB289.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2023-LB289
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 9
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    Online Resource
    DNA Methylation in Tumor and Matched Normal Tissues from Non-Small Cell Lung Cancer Patients
    American Association for Cancer Research (AACR) ; 2008
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 17, No. 3 ( 2008-03-01), p. 645-654
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 17, No. 3 ( 2008-03-01), p. 645-654
    Abstract: We used MethyLight assays to analyze DNA methylation status of 27 genes on 49 paired cancerous and noncancerous tissue samples from non-small cell lung cancer (NSCLC) patients who underwent surgical resection. Seven genes (RARB, BVES, CDKN2A, KCNH5, RASSF1, CDH13, and RUNX) were found to be methylated significantly more frequently in tumor tissues than in noncancerous tissues. Only methylation of CCND2 and APC was frequently detected in both cancerous and noncancerous tissues, supporting the hypothesis that the methylation of these two genes is a preneoplastic change and may be associated with tobacco smoking exposure. Methylation of any one of eight genes (RASSF1, DAPK1, BVES, CDH13, MGMT, KCNH5, RARB, or CDH1) was present in 80% of NSCLC tissues but only in 14% of noncancerous tissues. Detection of methylation of these genes in blood might have utility in monitoring and detecting tumor recurrence in early-stage NSCLC after curative surgical resection. (Cancer Epidemiol Biomarkers Prev 2008;17(3):645–54)
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1055-9965.EPI-07-2518
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2008
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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  • 10
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    Online Resource
    Honokiol Induces a Necrotic Cell Death through the Mitochondrial Permeability Transition Pore
    American Association for Cancer Research (AACR) ; 2007
    In:  Cancer Research Vol. 67, No. 10 ( 2007-05-15), p. 4894-4903
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 67, No. 10 ( 2007-05-15), p. 4894-4903
    Abstract: Previous reports have shown that honokiol induces apoptosis in numerous cancer cell lines and showed preclinical efficacies against apoptosis-resistant B-cell chronic lymphocytic leukemia and multiple myeloma cells from relapse-refractory patients. Here, we show that honokiol can induce a cell death distinct from apoptosis in HL60, MCF-7, and HEK293 cell lines. The death was characterized by a rapid loss of integrity of plasma membrane without externalization of phosphatidyl serine. The broad caspase inhibitor z-VAD-fmk failed to prevent this cell death. Consistently, caspase activation and DNA laddering were not observed. The death was paralleled by a rapid loss of mitochondrial membrane potential, which was mechanistically associated with the mitochondrial permeability transition pore regulated by cyclophilin D (CypD) based on the following evidence: (a) cyclosporin A, an inhibitor of CypD (an essential component of the mitochondrial permeability transition pore), effectively prevented honokiol-induced cell death and loss of mitochondrial membrane potential; (b) inhibition of CypD by RNA interference blocked honokiol-induced cell death; (c) CypD up-regulated by honokiol was correlated with the death rates in HL60, but not in K562 cells, which underwent apoptosis after being exposed to honokiol. We further showed that honokiol induced a CypD-regulated death in primary human acute myelogenous leukemia cells, overcame Bcl-2 and Bcl-XL–mediated apoptotic resistance, and was effective against HL60 cells in a pilot in vivo study. To the best of our knowledge, this is the first report to document an induction of mitochondrial permeability transition pore–associated cell death by honokiol. [Cancer Res 2007;67(10):4894–903]
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-06-3818
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2007
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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