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Source: Cancer Research
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Total 807 results found since Jan 2013.
Abstract P5-03-06: MEDI3039, a novel highly potent tumor necrosis factor (TNF)-related apoptosis inducing ligand (TRAIL) receptor agonist, induces apoptotic cell death in breast cancer cells
In conclusion, MEDI3039 is a potent TRAIL receptor agonist in breast cancer cells and has potential as a cancer drug in breast cancer patients, especially those with TNBC basal B.Citation Format: Greer YE, Tice D, Lipkowitz S. MEDI3039, a novel highly potent tumor necrosis factor (TNF)-related apoptosis inducing ligand (TRAIL) receptor agonist, induces apoptotic cell death in breast cancer cells. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P5-03-06.
Source: Cancer Research - February 18, 2016 Category: Cancer & Oncology Authors: Greer, Y., Tice, D., Lipkowitz, S. Tags: Poster Session Abstracts Source Type: research
Abstract P5-03-13: The anticancer effects of Supinoxin(R) (RX-5902) in triple-negative breast cancer MDA-MB-231 through phosphorylated p68 on Tyr593
In this study, we sought to determine whether phosphorylated p68 on Tyr593 plays a key role in RX-5902's ability to inhibit cancer cell growth by knocking down p68. p68-siRNA efficiently down-regulated the expression of phosphorylated p68 on Tyr593 as well as p68 in the triple-negative (TN) breast cancer cell line, MDA-MB-231. Exposure of p68-siRNA-transfected cells to the IC50 concentration of RX-5902 protected MDA-MB-231 cells from the cytotoxic effects of RX-5902, indicating the phosphorylated p68 on Tyr593 is a key molecule for RX-5902 cytotoxic effects. We also examined the tumor growth inhibition (TGI) of RX-5902 in ...
Source: Cancer Research - February 18, 2016 Category: Cancer & Oncology Authors: Kim, D., Yang, M., Lee, Y., Remenyi, J., Fuller-Pace, F. Tags: Poster Session Abstracts Source Type: research
Abstract P5-04-02: The histone deacetylase inhibitor entinostat enhances the efficacy of the MEK inhibitor pimasertib against aggressive types of breast cancer through Noxa-mediated myeloid cell leukemia 1 degradation
Purpose: Inflammatory breast cancer (IBC) and triple-negative breast cancer (TNBC) are the two most aggressive types of breast cancer whose molecular mechanisms remain unclear, representing a challenge for the development of effective targeted therapies. Single agent targeted therapies are of limited effectiveness in these types of breast cancer. Therefore, we aim to identify new combination therapeutic candidates for these aggressive diseases by comprehensive genomic screening.Experimental Design: We screened kinome siRNA libraries with the mitogen/extracellular signal-regulated kinase (MEK) inhibitor [pimasertib], and ge...
Source: Cancer Research - February 18, 2016 Category: Cancer & Oncology Authors: Torres-Adorno, A., Lee, J., Kogawa, T., Bartholomeusz, C., Pitner, M., Ordentlich, P., Lim, B., Tripathy, D., Ueno, N. Tags: Poster Session Abstracts Source Type: research
Abstract P5-04-13: Pin1 negatively impacts Smad3 tumor suppression in triple negative breast cancer cell lines
Conclusions: Inhibiting the Smad3-Pin1 interaction by knock-down of Pin1 expression in TNBC cells restored Smad3 transcriptional activity, which correlated to an increase in expression of the Smad3 associated protein cdki p15, decrease in c-myc, and a decrease in cellular proliferation. Additionally, Pin1 KD enhanced Smad3 protein levels, suggesting a role of Pin1 in mediating Smad3 stability. Inhibiting the Smad3-Pin1 interaction with Pin1 KD or CDK2 inhibitor treatment also reduced TNBC cell migration. Collectively, these data suggest that the Smad3-Pin1 interaction, facilitated by noncanonical CDK-mediated Smad3 phospho...
Source: Cancer Research - February 18, 2016 Category: Cancer & Oncology Authors: Thomas, A., Hamdan, R., Hong, A., Rosenthal, E., , Jeruss, J. Tags: Poster Session Abstracts Source Type: research
Abstract P5-04-17: From transcriptome meta-analysis to targeted therapies in triple negative breast cancer
Triple-Negative Breast Cancer (TNBC) is a subtype of breast cancer that urgently requires the identification and approval of novel targeted therapies. Even for breast cancer subtypes that have approved targeted therapies such as tamoxifen in ER+ and herceptin in HER2+ patients, there are a proportion of patients that do not respond to these therapies or develop resistance and succumb to metastatic recurrence. Thus, there is a clinical need to identify patients who do not benefit from current standard therapies and developing new strategies for therapy for non-responsive patients across all breast cancer subtypes.We hypothe...
Source: Cancer Research - February 18, 2016 Category: Cancer & Oncology Authors: Rozali, E., Al-Ejeh, F. Tags: Poster Session Abstracts Source Type: research
Abstract P6-13-05: Androgen receptor (AR): A novel target and mechanism for radiosensitization and treatment in triple-negative breast cancers (TNBC)
Background: Increased rates of locoregional recurrence have been observed in TNBC despite chemotherapy and radiation (RT). Thus, approaches that result in radiosensitizaton in TNBC are critically needed. We characterized the RT response of 21 breast cancer cell (BCC) lines using clonogenic survival assays. We paired this with high-throughput drug screen data to identify AR as a top target for radiosensitization and assess AR inhibition as a radiosensitization strategy for TNBC.Methods: Clonogenic survival assays were used to determine the intrinsic RT sensitivity of 21 BCC lines. IC50 values were determined for 130 clinica...
Source: Cancer Research - February 18, 2016 Category: Cancer & Oncology Authors: Speers, C., Zhao, S., Liu, M., Rae, J., Hayes, D., Feng, F., Pierce, L. Tags: Poster Session Abstracts Source Type: research
Abstract P5-08-22: DUSP4 is associated with increased resistance against anti-HER2 therapy in breast cancer
Conclusions. Our findings suggest that DUSP4 is involved in the development of trastuzumab resistance in HER2 positive BC.Citation Format: Györffy B, Munkacsy G, Esteva FJ, Miquel TP, Menyhart O. DUSP4 is associated with increased resistance against anti-HER2 therapy in breast cancer. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P5-08-22.
Source: Cancer Research - February 18, 2016 Category: Cancer & Oncology Authors: Gyorffy, B., Munkacsy, G., Esteva, F., Miquel, T., Menyhart, O. Tags: Poster Session Abstracts Source Type: research
Abstract P3-06-14: DSS1 depletion is a promising strategy increasing chemosensitivity possibly independent of BRCA2 expression
ConclusionConsistent with the cohort study of sporadic breast cancers, we demonstrated that high expression of DSS1 increased resistance of breast cancer cells to cytotoxic chemotherapy in vitro. Conversely, DSS1 knockdown increased the susceptibility to these drugs in spite that BRCA2 depletion did not affect chemosensitivity. These results indicate that DSS1 could be a molecular target to increase chemosensitivity, which is independent of BRCA2 expression.Citation Format: Gondo N, Rezano A, Kuzushima K, Iwata H, Kuwahara K. DSS1 depletion is a promising strategy increasing chemosensitivity possibly independent of BRCA2 e...
Source: Cancer Research - February 18, 2016 Category: Cancer & Oncology Authors: Gondo, N., Rezano, A., Kuzushima, K., Iwata, H., Kuwahara, K. Tags: Poster Session Abstracts Source Type: research
Abstract P3-06-15: Notch3 as a predictor of GSI sensitivity in distinct subtypes of triple negative breast cancer
Conclusions: GSI acts through Notch3 in two TNBC subtypes and combination of chemotherapy with Notch inhibition results in a better outcome as compared to either drug alone. Future experiments would elucidate the role of Notch3 inhibition in targeting cancer stem cells post chemotherapy treatment in different subtypes of TNBC.Citation Format: Shah D, Osipo C. Notch3 as a predictor of GSI sensitivity in distinct subtypes of triple negative breast cancer. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2...
Source: Cancer Research - February 18, 2016 Category: Cancer & Oncology Authors: Shah, D., Osipo, C. Tags: Poster Session Abstracts Source Type: research
Abstract B05: WHSC1L1 and estrogen-independent activation of estrogen receptor-alpha (ER{alpha}) in 8p11 amplicon-bearing cell lines
The 8p11-p12 genomic region is amplified in 15% of breast cancers and 21% of lung squamous cell carcinomas (LSCC) and is associated with poorer prognosis. This genomic region harbors several oncogenes, three of which are epigenetic modifiers of chromatin (WHSC1L1, KAT6A, ASH2L). WHSC1L1 is a histone methyltransferase (HMT) that is expressed in 2 isoforms. The long isoform (WH-long) encompasses the entire coding region and is associated with dimethylation of lysine 36 on histone 3 (H3K36me2) to facilitate transcriptional elongation. The short isoform (WH-short) is produced by alternative splicing at exon 10, resulting in a ...
Source: Cancer Research - January 14, 2016 Category: Cancer & Oncology Authors: Mills, J. N., Irish, J., Turner-Ivey, B., Ethier, S. P. Tags: Cancer Genomics and Epigenomics Source Type: research
Abstract PR06: Analysis of enhancer transcription reveals novel gene regulatory networks in breast cancer
Enhancer transcription is a defining feature of active enhancers. We and others have shown that enhancers that produce transcripts (so called “eRNAs”) are more likely to (1) be associated with active chromatin marks, such as H3K4me1 and K3K27ac, (2) loop to target gene promoters, and (3) be associated with target gene activation. Thus, enhancer transcription is a good predictor of active enhancers. In this regard, we have shown that enhancer transcription can be used in the absence of any other genomic information to predict enhancers. We have used Global Run-On coupled deep sequencing (GRO-seq) in 14 different breast ...
Source: Cancer Research - January 14, 2016 Category: Cancer & Oncology Authors: Franco, H. L., Nagari, A., Xi, Y., Li, W., Richardson, D., Tanaka, K., Li, J., The CPRIT LONESTAR Consortium, Barton, M. C., Shi, X., Keyomarsi, K., Bedford, M. T., , Dent, S. Y. R., Kraus, W. L. Tags: Enhancers Source Type: research
Abstract A16: Different epigenetic mechanisms involved in the regulation of SFRP1 gene in prostate cancer
Among men, prostate cancer (PCa)[1] is the second most common cancer and the fifth cause of death worldwide [2]. Androgens play an important role in the development of the disease. For advanced PCa the standard therapy is androgen depletion. However, after 2 or 3 years a high percentage of patients become resistant to this therapy and castration resistant prostate cancer (CRPC) is developed. There is no successful treatment for CRPC, leading into death [3, 4]. Wingless pathway (WNT) is aberrantly activated in several cancer types and in PCa it is involved in AR activity modulation, promoting cancer development [5]. Secrete...
Source: Cancer Research - January 14, 2016 Category: Cancer & Oncology Authors: Garcia–Tobilla, P., Uribe, O., Rodriguez–Dorantes, M. Tags: Epigenetic Control of Transcription/ Elongation Source Type: research
Abstract B17: Epigenetic regulation of NOTCH oncogenic signaling in breast cancer
Alterations in DNA methylation occur at different stages of cancer, including initiation, and may underlie up-regulation of genes with oncogenic functions. The NOTCH pathway is often overactive in breast cancer and plays roles in cancer development and progression. It is therefore a possible target for anti-cancer strategies. However, the mechanisms of NOTCH regulation in mammary carcinogenesis remain unclear which hinders the development of effective approaches to target this oncogenic pathway. Interestingly, certain dietary compounds such as polyphenols with a stilbenoid structure suppress the NOTCH signals in cancer and...
Source: Cancer Research - January 14, 2016 Category: Cancer & Oncology Authors: Lubecka, K., Kurzava, L., Flower, K., Buvala, H., Teegarden, D., Camarillo, I., Flanagan, J. M., Stefanska, B. Tags: Cancer Genomics and Epigenomics Source Type: research
Abstract A24: PBRM1 alteration in clear cell renal cell carcinoma increases tumorigenicity through ALDH1A1 upregulation
In this study, we investigated the mechanisms by which PBRM1 functions as a tumor suppressor in clear cell renal cell carcinoma (ccRCC). PBRM1, also known as BAF180 or Polybromo, is a member of the PBAF SWI/SNF chromatin remodeling complex. Cancer sequencing studies have revealed that SWI/SNF components are widely mutated in cancer. PBRM1 mutations in particular are found in ~40% of ccRCC tumors, making it the second most highly mutated gene in ccRCC (behind VHL). Although many recent studies have looked at how other SWI/SNF components function in cancer control, relatively little is known about the tumor suppressive mecha...
Source: Cancer Research - January 14, 2016 Category: Cancer & Oncology Authors: Schoenfeld, D., Su, W., Zairis, S., Mathur, D., Rabadan, R., Parsons, R. Tags: Chromatin Organization Source Type: research
Abstract B37: The histone deacetylase inhibitor panobinostat sensitizes cyclin E-amplified ovarian cancer cells to poly ADP ribose polymerase inhibitors via E2F1 downregulation.
Conclusions: The development of a new PARPi combination therapy with panobinostat has immediate prospects for rapid translation to the clinic and great potential for improving clinical outcomes for non-BRCAness, chemoresistant ovarian cancer.Citation Format: Andrew J. Wilson, Jeanette Saskowski, Dineo Khabele. The histone deacetylase inhibitor panobinostat sensitizes cyclin E-amplified ovarian cancer cells to poly ADP ribose polymerase inhibitors via E2F1 downregulation.. [abstract]. In: Proceedings of the AACR Special Conference on Chromatin and Epigenetics in Cancer; Sep 24-27, 2015; Atlanta, GA. Philadelphia (PA): AACR;...
Source: Cancer Research - January 14, 2016 Category: Cancer & Oncology Authors: Wilson, A. J., Saskowski, J., Khabele, D. Tags: Epigenetic Cancer Therapies Source Type: research
