Filtered By:
Source: Cancer Research
This page shows you your search results in order of date. This is page number 11.
Order by Relevance | Date
Total 807 results found since Jan 2013.
Abstract 905: Influence of high fat diet and APC status on epigenetic regulation of FXR in colon cells
We examined the effects on CpG pmethylation of Fxr, and expression of FXR, peroxisome-proliferator activated receptor-gamma (PPARγ), and cyclooxygenase-2 (COX-2) mRNA. Also, we studied the influence of APC status on CpG methylation of the Fxr gene, and expression of FXR, ileal bile acid-binding protein (IBABP), small heterodimer partner (SHP), and COX-2 mRNA in normal colonic mucosa and colon tumors from APCMin/+ mice. Mice fed the HFD had reduced (60%) Fxr promoter methylation and increased (2∼3-fold) FXR, COX-2, and PPARγ mRNA levels. Conversely, APC-deficiency was associated with constitutive hypermethylation of the...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Selmin, O. I., Lyon, A. M., Fang, C., Doetschman, T. C., Thompson, P. A., Martinez, J. D., Smith, J., Lance, P. M., Romagnolo, D. F. Tags: Prevention Research Source Type: research
Abstract 916: The molecular landscape of colorectal cancer cell lines unveils clinically actionable targets
In conclusion our data suggest that overexpression of TK outliers drives primary resistance to EGFR blockade, and could be used to identify patients unlikely to respond to cetuximab or panitumumab. Moreover, the approach described here can be used to pinpoint colorectal cancers with exquisite dependencies to individual kinases for which clinically approved drugs are already available.Citation Format: Mariangela Russo, Gabriele Picco, Carlotta Cancelliere, Giorgio Corti, Emanuele Valtorta, Silvio Veronese, Marco Beccuti, Francesca Cordero, Federica Di Nicolantonio, Enzo Medico, Alberto Bardelli. The molecular landscape of c...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Russo, M., Picco, G., Cancelliere, C., Corti, G., Valtorta, E., Veronese, S., Beccuti, M., Cordero, F., Di Nicolantonio, F., Medico, E., Bardelli, A. Tags: Prevention Research Source Type: research
Abstract 924: GM-CSF induces CREB signaling pathways and modulates tobacco carcinogen-induced pancreatic tumorigenesis
Introduction: Nicotine and nitrosamine exposure from smoking causes pancreatic cell injury and contributes to a cascade of oncogenic events that may be contributing to the rising rate of pancreatic cancer (PDAC). Cytokines activate kinases and transcription factors including cyclic AMP response element binding (CREB) protein. CREB activation through phosphorylation regulates diverse cellular responses. We studied whether granulocyte-macrophage colony stimulating factor (GM-CSF)-dependent phosphorylated CREB plays a role in smoking-induced pathogenesis of PDAC.Experimental procedure: Human tissue microarray analysis was per...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Castellanos, J., Honnenahally, K., Shi, C., Merchant, N., Nagathihalli, N. Tags: Carcinogenesis Source Type: research
Abstract 945: Synthetic lethal screen identifies Aurora A as a selective target in HPV driven cervical cancer
HPV has been identified as the definitive agent in cancers of the cervix, penis, vulva, vagina, anus, skin, eye, and head and neck, and is responsible for 5% of the total cancer burden worldwide. HPV oncogenes disable a number of tumour suppressor pathways, including p53 and Rb, contributing to the transformed phenotype. We have performed an siRNA screen using the kinome (779 genes) library to identify genes that when depleted are synthetically lethal with HPV transformation. The primary and validations screens have confirmed Aurora A kinase (AURKA) as a potential synthetic lethal target selective for HPV transformed cells...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Gabrielli, B. G., Bokhari, F., Ranall, M., Oo, Z. Y., Stevenson, A., Wang, W., McKee, S., Leggatt, G., Leo, P., Gonda, T. J., McMillan, N. A. Tags: Experimental and Molecular Therapeutics Source Type: research
Abstract 990: Saxifragifolin D induces autophagy via activating IRE1{alpha}/ JNK pathway in breast cancer cells
Conclusion: SD induces autophagy associated with IRE1α/ JNK pathway in breast cancer cells and these findings will provide molecular bases for molecular mechanistic studies of SD-treated breast cancer cells.Key words: Saxifragifolin D, autophagy, breast cancer.Citation Format: Liang-Liang Bai, Jun-Min Shi, Min-Feng Chen, Dong-Mei Zhang, Ying Wang, Wen-Cai Ye. Saxifragifolin D induces autophagy via activating IRE1α/ JNK pathway in breast cancer cells. [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 Re...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Bai, L.-L., Shi, J.-M., Chen, M.-F., Zhang, D.-M., Wang, Y., Ye, W.-C. Tags: Molecular and Cellular Biology Source Type: research
Abstract 744: Transactivation of HER3 via heterodimerization with epidermal growth factor receptor (EGFR) or insulin-like growth factor 1 receptor (IGF-1R) contributes to adaptive resistance to NVP-BKM120 in non-small cell lung cancer (NSCLC) and squamous cell carcinom
Conclusions: Transactivation of HER3 via EGFR or IGF-1R attenuates the effectiveness of NVP-BKM120 in multiple NSCLC and SCCHN cells. Our results suggest that either targeting HER3 directly or indirectly by inhibiting transactivation partners, such as EGFR or IGF-1R, may be potential therapeutic options to overcome adaptive resistance to NVP-BKM120.Note: This abstract was not presented at the meeting.Citation Format: Miran Yun, Jinyoung Sohn, Byoung Chul Cho. Transactivation of HER3 via heterodimerization with epidermal growth factor receptor (EGFR) or insulin-like growth factor 1 receptor (IGF-1R) contributes to adaptive ...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Yun, M., Sohn, J., Cho, B. C. Tags: Experimental and Molecular Therapeutics Source Type: research
Abstract 746: Activation of EGFR bypass signaling through TGF{alpha} overexpression induces acquired resistance to alectinib in ALK-translocated lung cancer cells
Conclusion: Activation of EGFR signaling pathway through TGFα overexpression induces acquired resistance to alectinib in ALK-translocated lung cancer cells.Citation Format: Tetsuo Tani, Hiroyuki Yasuda, Junko Hamamoto, Aoi Kuroda, Daisuke Arai, Kota Ishioka, Keiko Ohgino, Ichiro Kawada, Katsuhiko Naoki, Hayashi Yuichiro, Tomoko Betsuyaku, Kenzo Soejima. Activation of EGFR bypass signaling through TGFα overexpression induces acquired resistance to alectinib in ALK-translocated lung cancer cells. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philade...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Tani, T., Yasuda, H., Hamamoto, J., Kuroda, A., Arai, D., Ishioka, K., Ohgino, K., Kawada, I., Naoki, K., Yuichiro, H., Betsuyaku, T., Soejima, K. Tags: Experimental and Molecular Therapeutics Source Type: research
Abstract 1005: Dual targeting of MEK/MAPK1/2 and pro-survival autophagy to optimize antiestrogen treatment toward the eradication of antiestrogen resistant breast cancer
In this study, we tested the hypothesis that the MEK1/MAPK1/2/BimEL signaling node simultaneously regulates antiestrogen- induced pro-survival autophagy and apoptosis in ER+ breast cancer cells. In our approach, we utilized T47-D and MCF-7 breast cancer cells and modulated the activity of MEK1/MAPK1/2/ BimEL expression with U0126, a small molecule inhibitor of MEK1, BimEL cDNA over-expression, or siRNA targeting under a variety of endocrine treatments. We also conducted studies in the presence or absence of the pan-caspase inhibitor ZVAD-fmk so that autophagy levels/function could be analyzed independent of effects mediate...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Manning, M., Takhar, S., Periyasamy-Thandavan, S., Cheng, M., Barrett, T., Hill, W., Browning, D., Thangaraju, M., McGee-Lawrence, M., Schoenlein, P. V. Tags: Molecular and Cellular Biology Source Type: research
Abstract 757: Activation of receptor-interacting serine/threonine protein kinase-2 (RIP2K) via EGFR-mediated CRAF transactivation induces the acquired resistance to Dabrafenib in BRAF V600E mutant non-small cell lung cancer
Discussion: Taken together, these findings suggest that the acquired resistance to Dabrafenib in BRAF V600E mutant NSCLC is uniquely mediated by EGFR-RAS-RIPK2-ERK signaling, bypassing MEK1/2, which may necessitate therapeutic strategies different from those of melanoma.Citation Format: Kangwon Jang, Jinyoung Sohn, Sung-Moo Kim, Kyoung Jin Kim, Byoung Chul Cho. Activation of receptor-interacting serine/threonine protein kinase-2 (RIP2K) via EGFR-mediated CRAF transactivation induces the acquired resistance to Dabrafenib in BRAF V600E mutant non-small cell lung cancer. [abstract]. In: Proceedings of the 106th Annual Meeting...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Jang, K., Sohn, J., Kim, S.-M., Kim, K. J., Cho, B. C. Tags: Experimental and Molecular Therapeutics Source Type: research
Abstract 758: Loss of USP1 translational control as a targetable cisplatin resistance mechanism in non-small cell lung cancer (NSCLC)
Conclusion:Our original approach led to the identification of USP1 as a potential determinant of cisplatin resistance of a lung cancer cell line. USP1 protein levels in tumor samples could potentially serve as a predictive marker of the response to cisplatin. We suggest that small molecule inhibitors of USP1 should be tested as cisplatin-sensitizers. The analysis of the ‘nascent proteome’ by polysome profiling could enable the identification of additional candidates mediating cisplatin-resistance.Citation Format: Carole Helissey, Tony Sourisseau, Hélène Mahieu, Céline Lefebvre, Stephan Vagner, Jean-Charles Soria, Ke...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Helissey, C., Sourisseau, T., Mahieu, H., Lefebvre, C., Vagner, S., Soria, J.-C., Olaussen, K. Tags: Experimental and Molecular Therapeutics Source Type: research
Abstract 1016: Caveolin-1-dependent and -independent uPAR signaling pathways contribute to ganglioside GT1b-induced early apoptosis in A549 lung cancer cells
In this study, we show that the ganglioside GT1b induces proapoptotic signaling through two uPAR-ERK signaling pathways in A549 lung cancer cells. GT1b downregulated the expression of α5β1 integrin, caveolin-1, fibronectin, FAK, and ERK, whereas GT1b upregulated the expression of p53 and uPAR, suggesting GT1b mediated depletion of caveolin-1 in uPAR-expressing A549 cells also disrupts uPAR/integrin complexes, resulting in downregulation of fibronectin-α5β1-integrin-ERK signaling. Following p53 siRNA treatment, FAK and ERK expression was recovered, meaning the presence of reentry uPAR-FAK-ERK signaling pathway. These fi...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Jang, H.-J., Chung, Y.-H., Park, J., Jang, I.-S. Tags: Molecular and Cellular Biology Source Type: research
Abstract 767: Oncogenic mutant KRAS modulates EZH2 expression through MEK-ERK and PI3K/AKT signaling in NSCLC: differential effects of different KRAS mutations and increased efficacy of inhibition combined with EZH2 targeted therapy
Conclusions. Our findings suggest that: 1. oncogenic KRAS G12C and G12D mutations differentially modulate EZH2 expression through MEK-ERK and PI3K/AKT signaling respectively - indicating the need for specific KRAS mutation guided therapy; 2. Inhibition of MEK-ERK and PI3K/AKT in combination with an EZH2 inhibitor should result in a significant increased sensitivity to MEK-ERK and PI3K/AKT targeted therapy in KRAS mutant lung cancers. (Grant support: 5 R01 CA155196 and P50CA70907)Citation Format: Erick M. Riquelme, Li Shen, Jing Wang, Carmen Behrens, George Simon, Vassiliki Papadimitrakopoulou, John D. Minna, Ignacio I. Wis...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Riquelme, E. M., Shen, L., Wang, J., Behrens, C., Simon, G., Papadimitrakopoulou, V., Minna, J. D., Wistuba, I. I. Tags: Experimental and Molecular Therapeutics Source Type: research
Abstract 768: A kinome-wide siRNA screen identifies modifiers of sensitivity to the EGFR T790M-targeted tyrosine kinase inhibitor (TKI), AZD9291, in EGFR mutant lung adenocarcinoma
In conclusion, through a kinome wide siRNA screen, we identified that gene products in the MAP kinase signaling pathway modify sensitivity to AZD9291. Such sensitivity may be associated with ERK re-phosphorylation within 96h of drug treatment. Collectively, these data suggest rational drug combinations that could be used to forestall resistance to AZD9291. Additional hits from the screen are currently under investigation.This study is supported by AstraZeneca Oncology Innovative Medicines, National Institutes of Health (NIH) NCI grants R01-CA121210, P01-CA129243, U54-CA143798, and the Uehara Memorial Foundation.Citation Fo...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Ichihara, E., Bauer, J. A., Lu, P., Ye, F., Cross, D., Pao, W., Lovly, C. M. Tags: Experimental and Molecular Therapeutics Source Type: research
Abstract 813: Human papillomavirus 16 oncoprotein E6 upregulates c-Met partially through p53 in squamous cell carcinoma of the head and neck
Conclusion: Our results show that c-Met expression is upregulated by HPV E6, which is partially mediated by p53. The data suggest that targeting c-Met may serve as a novel approach for treating HPV-associated OPSCC.(This study was supported by grants from Small Business Innovation Research (SBIR) Program (HHSN261201200097C), National Institutes of Health (R33 CA161873), and National Cancer Institute (NCI P50 CA 128613, Head and Neck SPORE).Citation Format: Guoqing Qian, Dongsheng Wang, Kelly R. Magliocca, Praveen Duggal, Sreenivas Nannapaneni, Sungjin Kim, Zhengjia Chen, Dong M. Shin, Nabil F. Saba, Zhuo G. Chen. Human pap...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Qian, G., Wang, D., Magliocca, K. R., Duggal, P., Nannapaneni, S., Kim, S., Chen, Z., Shin, D. M., Saba, N. F., Chen, Z. G. Tags: Carcinogenesis Source Type: research
Abstract 814: Truncated HBx-dependent silencing of growth arrest-specific 2 promotes hepatocarcinogenesis through inhibition of p53-mediated apoptosis
In conclusion, our integrated study uncovered a novel viral mechanism in hepatocarcinogenesis, wherein HBxΔ35 ablates p53-driven apoptosis via direct silencing of GAS2, and thereby provides survival advantage for pre-neoplastic hepatocytes to facilitate cancer development.Citation Format: Alfred S. L. Cheng, Ranxu Zhu, Myth T.S. Mok, Wai Kang, Ka-Fai To, Joseph J.Y. Sung, Henry L.Y. Chan. Truncated HBx-dependent silencing of growth arrest-specific 2 promotes hepatocarcinogenesis through inhibition of p53-mediated apoptosis. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Rese...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Cheng, A. S. L., Zhu, R., Mok, M. T. S., Kang, W., To, K.-F., Sung, J. J. Y., Chan, H. L. Y. Tags: Carcinogenesis Source Type: research
