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Cancer: HER2
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Total 260 results found since Jan 2013.
Abstract A65: A novel regulatory mechanism involving Ras-mediated activation of the zinc-finger transcription factor, SAF-1/MAZ induces EGFR/HER1 expression in breast cancer cells
Tumor microenvironment (TME) plays a critical role in tumor growth, invasion and metastasis. In TME, epidermal growth factor receptor (EGFR) family members, including HER1, HER2, HER3 and HER4, are involved in determining aggressive growth of breast cancer due to their ability to transduce the growth promoting functions of growth factors. This activity is potentiated by the over-expression of these receptor molecules in cancer cells. To reduce the activity of EGFR molecules, various inhibitors have been developed. EGFR/HER1 tyrosine kinase inhibitors (TKIs), gefitinib and erlotinib, show antitumor activity but these drugs ...
Source: Molecular Cancer Therapeutics - January 7, 2016 Category: Cancer & Oncology Authors: Ray, A., Havis, B., Ray, B. Tags: EGFR / Her2: Poster Presentations - Proffered Abstracts Source Type: research
Black Rice Anthocyanins Suppress Metastasis of Breast Cancer Cells by Targeting RAS/RAF/MAPK Pathway.
In this study, we examined the molecular mechanisms underlying the chemopreventive effects of black rice anthocyanins (BRACs) extract and identified their molecular targets in HER2(+) breast cancer cells. Treatment of MDA-MB-453 cells (HER2(+)) with BRACs inhibited cell migration and invasion, suppressed the activation of mitogen-activated protein kinase kinase kinase (RAF), mitogen-activated protein kinase kinase (MEK), and c-Jun N-terminal kinase (JNK), and downregulated the secretion of matrix metalloproteinase 2 (MMP2) and MMP9. BRACs also weakened the interactions of HER2 with RAF, MEK, and JNK proteins, respectively,...
Source: Biomed Res - December 12, 2015 Category: Research Authors: Chen XY, Zhou J, Luo LP, Han B, Li F, Chen JY, Zhu YF, Chen W, Yu XP Tags: Biomed Res Int Source Type: research
Dual inhibition of Type I and Type III PI3 kinases increases tumor cell apoptosis in HER2+ breast cancers
Conclusions:
These studies highlight the important role of Vps34-mediated autophagy in limiting the anti-tumor response to inhibitors of HER2 or type I PI3K in HER2+ breast cancers. The type III PI3K Vps34 represents a potential therapeutic target to block treatment-induced autophagy and enhance tumor cell killing.
Source: Breast Cancer Research - December 4, 2015 Category: Cancer & Oncology Authors: Christian YoungCarlos ArteagaRebecca Cook Source Type: research
CCNE1 amplification is associated with aggressive potential in endometrioid endometrial carcinomas.
Abstract
The clinicopathological significance of amplification was investigated of the gene encoding cyclin E (CCNE1) and we assessed whether CCNE1 was a potential target in endometrioid endometrial carcinomas. CCNE1 amplification and CCNE1 or F-box and WD repeat domain-containing 7 (FBXW7) expression in endometrial endometrioid carcinoma was assessed by immunohistochemistry and fluorescence in situ hybridization. CCNE1 knockdown by small interfering RNA (siRNA) was used to assess the CCNE1 function. The results showed that CCNE1 amplification was present in 9 (8.3%) of 108 endometrial carcinomas. CCNE1 amplifica...
Source: International Journal of Oncology - November 26, 2015 Category: Cancer & Oncology Authors: Nakayama K, Rahman MT, Rahman M, Nakamura K, Ishikawa M, Katagiri H, Sato E, Ishibashi T, Iida K, Ishikawa N, Kyo S Tags: Int J Oncol Source Type: research
Anti-cancer effect of metformin by suppressing signaling pathway of HER2 and HER3 in tamoxifen-resistant breast cancer cells
Abstract
Development of new therapeutic strategies is becoming increasingly important to overcome tamoxifen resistance. Recently, much interest has been focused on anti-tumor effects of metformin commonly used to treat type II diabetes. Increased protein expression and signaling of epidermal growth factor receptor (EGFR) family is a possible mechanism involved in tamoxifen resistance. Since HER2/HER3 heterodimers are able to induce strong downstream signaling and activate various biological responses such as cellular proliferation and growth, we investigated the anti-cancer effect of metformin by inhibition of sig...
Source: Tumor Biology - November 18, 2015 Category: Cancer & Oncology Source Type: research
EpCAM Aptamer-siRNAs for Targeted Breast Cancer Treatment
Effective therapeutic strategies for in vivo siRNA delivery to knockdown genes in cells outside the liver are needed to harness RNA interference for treating cancer. EpCAM is a tumor-associated antigen highly expressed on common epithelial cancers and their tumor-initiating cells (TIC, also known as cancer stem cells). Here, we show that aptamer–siRNA chimeras (AsiC, an EpCAM aptamer linked to an siRNA sense strand and annealed to the siRNA antisense strand) are selectively taken up and knock down gene expression in EpCAM+ cancer cells in vitro and in human cancer biopsy tissues. PLK1 EpCAM-AsiCs inhibit colony and m...
Source: Molecular Cancer Therapeutics - October 5, 2015 Category: Cancer & Oncology Authors: Gilboa-Geffen, A., Hamar, P., Le, M. T. N., Wheeler, L. A., Trifonova, R., Petrocca, F., Wittrup, A., Lieberman, J. Tags: Large Molecule Therapeutics Source Type: research
Abstract PR03: Targeting multiple cell cycle regulatory points for the prevention of triple-negative breast cancer
Conclusions: These studies demonstrate that dinaciclib alone or the combination therapy of LG100268 and dinaciclib causes inhibition of premalignant cell growth and delayed ER-negative mammary tumorigenesis in SV40 Tag mice. While an additive effect of dinaciclib and LG100268 was observed in vitro, the in vivo combination therapy was not significantly more effective than dinaciclib treatment alone. Future studies should investigate different combinations of dosages of dinaciclib and LG100268 in vivo. These studies were supported by an NCI/NIH R25T grant (R25CA057730, BL) and Susan G. Komen for the Cure Promise grant (KG081...
Source: Cancer Prevention Research - October 2, 2015 Category: Cancer & Oncology Authors: Litzenburger, B. C., Uray, I. P., Hill, J., Zhang, J., Mazumdar, A., Brown, P. H. Tags: Combinatorial Approaches to Chemoprevention: Oral Presentations - Proffered Abstracts Source Type: research
Cadmium promotes the proliferation of triple-negative breast cancer cells through EGFR-mediated cell cycle regulation.
Abstract
Cadmium (Cd) is a carcinogenic metal which is implicated in breast cancer by epidemiological studies. It is reported to promote breast cancer cell growth in vitro through membrane receptors. The study described here examined Cd-mediated growth of non-metastatic human breast cancer derived cells that lack receptors for estrogen, progesterone, and HER2. Treatment of triple-negative HCC 1937 cells with 0.1-0.5μM Cd increased cell growth by activation of AKT and ERK. Accelerated cell cycle progression was achieved by increasing the levels of cyclins A, B, and E, as well as those of CDKs 1 and 2. Although tri...
Source: Toxicology and Applied Pharmacology - September 15, 2015 Category: Toxicology Authors: Wei Z, Song X, Shaikh ZA Tags: Toxicol Appl Pharmacol Source Type: research
ErbB-2 signaling plays a critical role in regulating androgen-sensitive and castration-resistant androgen receptor-positive prostate cancer cells.
Abstract
While androgen deprivation therapy (ADT) reduces tumor burden, autocrine growth factor loops such as human epidermal growth factor receptor 2 (HER2/ErbB-2/neu) have been proposed to contribute to prostate cancer (PCa) survival and relapse. However, the role of ErbB-2 in regulating androgen-sensitive (AS) and castration-resistant (CR) cell proliferation remains unclear. Here, we determined the role of ErbB-2 in PCa progression and survival under steroid-reduced conditions using two independent PCa cell progression models. In AR-positive androgen-independent (AI) PCa cells that exhibit the CR phenotype, Erb...
Source: Cellular Signalling - August 6, 2015 Category: Cytology Authors: Muniyan S, Chen SJ, Lin FF, Wang Z, Mehta PP, Batra SK, Lin MF Tags: Cell Signal Source Type: research
Abstract 1966: Role of Wnt-Beta-Catenin signals in the control of vascular mimicry in TNBC
Background: TNBC or basal-like subtype of breast cancer confers poor clinical outcome mostly due to its inherent aggressive nature and its high frequency of metastasis. Malignancy in TNBC is associatedwith micro-vascular proliferations. Vascular Mimicry (VM) of solid tumor is an endothelium-independent matrix-embedded, blood-perfused non-angiogenic micro-circulatory phenomenon. VM of tumor cells refer to the characteristic plasticity of aggressive cancer cells forming de novo vascular networks which perfuse rapidly growing tumors, transporting fluid from leaky vessels and/or connect with the constitutional endothelial-line...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Leyland-Jones, B., Carlson, J. H., De, P., Dey, N. Tags: Molecular and Cellular Biology Source Type: research
Abstract 1980: Identification of the transcription factor ZNF217 in ER+ subset of BC: A functional relationship with the PI3K-AKT-mTOR pathway
ZNF217 gene encodes for a Krüppel-like finger protein transcription factor. Here we report an amplification of ZNF217 gene in breast cancer (BC) patients. Retrospective study of 72 BC patients showed that ZNF217 gene was amplified in 12.5% of patients enrolled in our center over last ten months from February 2014 through November 2014. We found a similar level of amplification of ZNF217 gene at 20q13 in different epithelial cancers including lung, uterus, ovary, stomach, bladder and breast using data from c-Bioportal. The observed percentage of the amplification of ZNF217 gene in our patients (12.5%) was comparable to the...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Dey, N., Williams, C., Krie, A., Solomon, B., Starks, D., Rojas, L., Carlson, J. H., Sun, Y., Lin, X., Abramovitz, M., Metzger-Nelson, T., Williams, K., Klein, J., De, P., Leyland-Jones, B. Tags: Molecular and Cellular Biology Source Type: research
Abstract 1992: Evidence for modulation of FoxM1 by p21 in ovarian cancer
The oncogenic transcription factor forkhead box M1 (FoxM1) is overexpressed in many cancers, including 84% of ovarian cancer and plays a role in DNA repair, mitotic checkpoint, cell proliferation, and cancer drug resistance. Similar to Her2 in breast cancer, the constitutive expression of FoxM1 makes it a plausible gene target for novel anti-cancer therapies, but the regulation of FoxM1 has yet to be elucidated. Evidence suggests FoxM1 up-regulation is a result of TP53 mutations, however, no TP53 response element has been found within the FoxM1 promoter, thus there is likely another molecule mediating p53-induced FoxM1 ove...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Madden, J., Chien, J. Tags: Molecular and Cellular Biology Source Type: research
Abstract 737: Clonal evolution of the HER2 L755S mutation as a mechanism of acquired HER-targeted therapy resistance
Conclusion: Acquired L/LT resistance in the two BT474 R lines is due to selection of HER2 L755S subclones present in parental cells. The higher HER2 L755S levels in BT474 parentals compared with other parentals, and detection of its subclonal presence in a pre-treatment HER2+ BC patient, suggest that sensitive mutation detection methods will be needed to identify patients with potentially actionable HER family mutations in primary tumor. Treating this patient group with an irreversible TKI like Afa may prevent resistance and improve clinical outcome of this subset of HER2+ BC.Citation Format: Xiaowei Xu, Agostina Nardone, ...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Xu, X., Nardone, A., Hu, H., Qin, L., Nanda, S., Heiser, L., Wang, N., Covington, K., Chen, E., Renwick, A., Mitchell, T., Shea, M., Wang, T., De Angelis, C., Contreras, A., Gutierrez, C., Fuqua, S., Chamness, G., Shaw, C., Li, M., Wheeler, D., Hilsenbeck Tags: Experimental and Molecular Therapeutics Source Type: research
Abstract LB-299: Gene knockdown by EpCAM aptamer-siRNA chimeras suppresses epithelial breast cancers and their tumor-initiating cells
Effective therapeutic strategies for in vivo siRNA delivery to knockdown genes in cells outside the liver are needed to harness RNA interference for treating cancer. EpCAM is a tumor-associated antigen highly expressed on common epithelial cancers and their tumor-initiating cells (T-IC, also known as cancer stem cells). Here we show that aptamer-siRNA chimeras (AsiC, an EpCAM aptamer linked to an siRNA sense strand and annealed to the siRNA antisense strand) are selectively taken up and knockdown gene expression in EpCAM+ cancer cells in vitro and in human cancer biopsy tissues. PLK1 EpCAM-AsiCs inhibit colony and mammosph...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Gilboa-Geffen, A., Hamar, P., Wheeler, L. A., Trifonova, R., Petrocca, F., Wittrup, A., Lieberman, J. Tags: Molecular and Cellular Biology Source Type: research
Abstract LB-200: Loss of the scaffold protein Kibra in a mouse model of triple-negative breast cancer
Introduction: Targeted therapies in breast cancer rely on tumor cell expression of Estrogen and/or HER2 receptors. Triple negative breast cancers (TNBCs), lacking these receptors, have no targeted therapies. We have developed a preclinical murine model expressing a naturally occurring oncogenic variant of the Met receptor in the mammary gland combined with loss of function of the tumour suppressor p53 (MMTV-Met;Trp53fl/+;Cre). This model recapitulates many features of TNBC at the level of gene expression, pathological markers and genomic alterations. Notably, this model spontaneously undergoes loss of a genomic region synt...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Knight, J. F., Gruosso, T., de Verteuil, D. A., Saleh, S., Lesurf, R., Zhao, H., Davis, R., Zuo, D., Cardiff, R., Gregg, J., Hallett, M., Park, M. Tags: Tumor Biology Source Type: research
