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Literatura académica sobre el tema "He53"

Autor: Grafiati

Publicado: 25 de julio de 2024

Última modificación: 1 de agosto de 2024

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Artículos de revistas sobre el tema "He53"

Kent, Matthew R., Delia Calderon, Katherine M. Silvius, Jack P. Kucinski, Collette A. LaVigne, Matthew V. Cannon y Genevieve C. Kendall. "Abstract 3533: Zebrafish her3 knockout impacts developmental and rhabdomyosarcoma-related gene signatures". Cancer Research 83, n.º 7_Supplement (4 de abril de 2023): 3533. http://dx.doi.org/10.1158/1538-7445.am2023-3533.

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Abstract HES3 is a basic helix-loop-helix transcription factor that regulates neural stem cell renewal during development. HES3 overexpression is predictive of reduced overall survival in patients with fusion-positive rhabdomyosarcoma, a pediatric cancer that resembles immature and undifferentiated skeletal muscle and is most commonly driven by the fusion-oncogene PAX3-FOXO1. However, the mechanisms of HES3 cooperation in PAX3-FOXO1 driven rhabdomyosarcoma are unclear and are likely related to her3/HES3’s role in neurogenesis. To investigate HES3’s function during development, we generated a zebrafish CRISPR/Cas9 null mutation of her3, the zebrafish ortholog of HES3. Phenotypic characterization revealed that her3 null mutation is not embryonic lethal as they are present at expected Mendelian ratios. We observed a temporary growth delay her3 zebrafish null mutants and, rarely, eye defects in adults. Transcriptomic analysis of her3 null mutant embryos showed early dysregulation of a known downstream target, neurog1 and downregulation of genes involved in organ development, such as pctp and grinab, while genes pointing toward a terminal differentiation state, such as tmod, are upregulated. Differentially expressed genes in her3 null mutant embryos are enriched for HOX and SOX10 motifs, suggesting these may be key genes involved during HES3 dysregulation. Several cancer-related gene pathways are impacted, including the inhibition of matrix metalloproteinases and the tumor microenvironment pathway. To complement our zebrafish model, we are developing a double-inducible cell line model consisting of a tetracycline-inducible HES3 and a cumate-inducible PAX3-FOXO1 to further investigate the hypothesized cooperation between her3/HES3 and PAX3-FOXO1 in fusion-positive rhabdomyosarcoma. These two systems will allow us to elucidate conserved mechanisms of cooperation between HES3 and PAX3-FOXO1, and identify new therapeutic opportunities for children with fusion-driven rhabdomyosarcoma. Citation Format: Matthew R. Kent, Delia Calderon, Katherine M. Silvius, Jack P. Kucinski, Collette A. LaVigne, Matthew V. Cannon, Genevieve C. Kendall. Zebrafish her3 knockout impacts developmental and rhabdomyosarcoma-related gene signatures. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 3533.

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Beckford Vera, Denis, Jason Li, Le-Cun Xu, Debbie Lewis, Amanda Chin, Patrik Brodin, Mary Chen, Monideepa Roy y Helen Kotanides. "Preclinical evaluation of novel HER3-targeting radioconjugates for the imaging and treatment of HER3-expressing cancers." Journal of Clinical Oncology 41, n.º 16_suppl (1 de junio de 2023): e15114-e15114. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.e15114.

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e15114 Background: HER3 overexpression in tumors is associated with poor survival and is implicated in drug resistance mechanisms of HER1 (EGFR) and HER2 targeted therapies. Although antibodies against HER3 have been developed and evaluated in clinical trials, no HER3 targeted therapy has been approved, underscoring the unmet need for novel HER3 therapeutic approaches. We hypothesized that HER3 radioligand targeted therapies could provide enhanced therapeutic efficacy against HER3-positive cancers through the energy deposited by alpha or beta emitting radionuclides in tumor cells. Here we describe the development and preclinical evaluation of novel anti-HER3 antibody radioconjugates (ARCs), 225Ac-HER3 and 177Lu-HER3, using the alpha-emitting Actinium-225 (225Ac) and beta-emitting Lutetium-177 (177Lu) radioisotopes, respectively. Methods: ARCs were prepared by radiolabeling HER3 antibody with 225Ac or 177Lu using S-2-(4-Isothiocyanatobenzyl)-1,4,7,10-tetraazacyclododecane tetraacetic acid (p-SCN-Bn-DOTA) to yield 225Ac or 177Lu-HER3-ARCs. DOTA modified antibodies were characterized by HPLC and MALDI-TOF and HER3-ARCs were fully characterized by instant thin-layer chromatography (iTLC) and HPLC. The in vitro binding properties of the HER3-ARCs were evaluated using HER3 recombinant proteins and cells expressing HER3 in ELISA and flow cytometry. The in vivo pharmacological properties of the HER3-ARCs were evaluated by molecular imaging using Zirconium-89 (89Zr) Positron Emission Tomography (PET), biodistribution and antitumor efficacy studies. Results: HER3 antibody was successfully modified with p-SCN-Bn-DOTA to yield a conjugate with approximately 8 DOTAs per antibody molecule. Results from the in vitro binding assays of ARCs to either HER3 human recombinant protein or cells expressing HER3 demonstrated similar binding properties of 225Ac-HER3 and 177Lu-HER3 to unmodified HER3 antibody. The biodistribution study in NCI-H1975 tumor bearing mice showed that both 225Ac-HER3 and 177Lu-HER3-ARCs specifically accumulate in HER3-expressing tumors relative to other tissues. In agreement with the biodistribution studies, PET images revealed specific uptake of 89Zr-HER3 in NCI-H1975 tumors. Furthermore, 225Ac and 177Lu-HER3-ARCs showed significantly more potent NCI-H1975 tumor growth inhibition compared to controls. Conclusions: Our findings suggest that a HER3 targeted radiotherapy approach can enhance therapeutic response and overcome the limitations of previously explored HER3 targeted drug modalities. Thus, further preclinical evaluation of 225Ac-HER3 and 177Lu-HER3 is warranted, including in settings of tumor drug resistance, which can provide the basis for investigating HER3-ARCs as an effective treatment approach in future clinical trials.

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Koyama, Kumiko, Hirokazu Ishikawa, Manabu Abe, Yoshinobu Shiose, Suguru Ueno, Yang Qiu, Kenji Nakamaru y Masato Murakami. "Patritumab deruxtecan (HER3-DXd), a novel HER3 directed antibody drug conjugate, exhibits in vitro activity against breast cancer cells expressing HER3 mutations with and without HER2 overexpression". PLOS ONE 17, n.º 5 (3 de mayo de 2022): e0267027. http://dx.doi.org/10.1371/journal.pone.0267027.

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ErbB3 (HER3), a member of the HER family, is overexpressed in various cancers and plays an important role in cell proliferation and survival. Certain HER3 mutations have also been identified as oncogenic drivers, making them potential therapeutic targets. In the current study, antitumor activity of patritumab deruxtecan (HER3-DXd), a HER3 directed antibody drug conjugate, was evaluated in tumor models with clinically reported HER3 mutations. MDA-MB-231, a HER3-negative human triple-negative breast cancer cell line, was transduced with lentiviral vectors encoding HER3 wild type (HER3WT), one of 11 HER3 mutations, or HER3 empty vector (HER3EV), in the presence/absence of HER2 overexpression. Targeted delivery of HER3-DXd was assessed using cell-surface binding, lysosomal trafficking, and cell-growth inhibition assays. HER3-DXd bound to the surface of HER3WT and mutant cells in a similar, concentration-dependent manner but not to HER3EV. HER3-DXd was translocated to the lysosome, where time- and concentration-dependent signals were observed in the HER3 mutant and HER3WT cells. HER3-DXd inhibited the growth of HER3WT and HER3 mutant cells. HER3-DXd activity was observed in the presence and absence of HER2 overexpression. These data suggest that HER3-DXd may have activity against tumors expressing wild type HER3 or clinically observed HER3 mutations, supporting further clinical evaluation.

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Komatsu, Nagiho, Saori Sato, Sumie Muramatsu, Ryuichi Nakamura y Kumiko Koyama. "Abstract 3996: The impact of HER3 dynamics on the efficacy of HER3-DXd, a novel HER3 directed antibody-drug conjugate". Cancer Research 83, n.º 7_Supplement (4 de abril de 2023): 3996. http://dx.doi.org/10.1158/1538-7445.am2023-3996.

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Abstract Background: HER3 is broadly expressed in various solid tumor types, and its expression can be upregulated by treatment with receptor tyrosine kinase inhibitors (RTKi) such as EGFR TKIs used to treat EGFR-mutated NSCLC. HER3-DXd, a novel antibody-drug conjugate (ADC) composed of a human anti-HER3 IgG1 monoclonal antibody (patritumab) covalently linked to a topoisomerase I inhibitor payload (DXd), is currently being studied in clinical trials for breast cancer and NSCLC. As previously reported, HER3-DXd treatment transiently decreases HER3 expression levels in tumors and EGFR TKIs increase HER3 membrane expression. However, the impact of HER3 dynamics on payload delivery has not been clarified yet. In this study, we investigated HER3 dynamics including HER3 receptor turnover and payload delivery in cancer cells using HER3-DXd both as a single agent and in combination with RTKi including osimertinib, which is in clinical trials in combination with HER3-DXd. Methods: HER3/ADC internalization was evaluated by using confocal imaging in MDA-MB-453 cells treated with HER3-DXd. Internalization and payload release were quantitatively measured in 3 cancer cell lines treated with HER3-DXd. HER3 turnover on the cell surface was also evaluated upon wash-out of HER3-DXd. In xenograft models, mice were administered two doses of HER3-DXd at different doses and dosing intervals, and membrane HER3 expression and tumor payload concentration were examined over time. NSCLC cell lines harboring EGFR activating mutations, ROS1 fusions, or ALK fusions were used to evaluate the effect of osimertinib, lorlatinib, or ceritinib on cell surface HER3 expression and payload release (osimertinib only). Results: HER3-DXd was rapidly transferred to early endosomes after binding to HER3. HER3 dynamics varied among the cell lines tested in vitro, and payload release reflected cell surface HER3 expression levels, HER3 internalization speed and turnover rates. In xenograft models, a higher dosage of HER3-DXd resulted in a larger decrease in membrane HER3 expression. Dosing interval also affected membrane HER3 expression levels; the degree of tumor payload concentration increase after the second dose was dependent on the recovery of HER3 expression after the first dose. Furthermore, we confirmed that RTKi increased the cell surface HER3 expression in NSCLC cell lines with targetable driver genomic alterations and that osimertinib increased payload delivery in PC-9 cells through the upregulation of cell surface HER3 expression. Conclusion: HER3 expression was dynamically changed by HER3-DXd dosing regimen and by RTKi treatment, resulting in a substantial impact on payload release. These findings support our strategy of clinical studies using HER3-DXd after drugs that increase HER3 expression including EGFR TKI and indicate that HER3 dynamics may play a key role in achieving optimal efficacy of HER3-DXd. Citation Format: Nagiho Komatsu, Saori Sato, Sumie Muramatsu, Ryuichi Nakamura, Kumiko Koyama. The impact of HER3 dynamics on the efficacy of HER3-DXd, a novel HER3 directed antibody-drug conjugate. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 3996.

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O'Hare, Thomas, Jaclyn Cleveland, Valerie M. Jansen y David Dornan. "Abstract 3121: Therapeutic potential of a HER3 antibody-drug conjugate for the treatment of HER3-expressing cancers". Cancer Research 84, n.º 6_Supplement (22 de marzo de 2024): 3121. http://dx.doi.org/10.1158/1538-7445.am2024-3121.

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Abstract To address the need for targeted therapy in the treatment of HER3-positive solid tumors, the human HER3 mAb, seribantumab, was evaluated in the context of an antibody-drug conjugate (ADC). As a proof-of-concept, seribantumab was conjugated with a cleavable valine-citrulline linker and monomethyl auristatin E (MMAE) payload via the stochastic cysteine conjugation method to yield HER3-ADC1. A drug-antibody ratio of 4 was selected for preclinical assessment in HER3-expressing models. Methods: HER3-ADC1 was evaluated in vitro and in vivo, with patritumab deruxtecan (patri-DXd) as a comparator. Binding to BT474 breast carcinoma cells (HER3 high; immunohistochemical (IHC) staining intensity 3+) was measured by flow cytometry. Internalization properties were established using seribantumab and patritumab coupled to Fab-AF488 following 4 hours incubation in SK-BR-3 breast adenocarcinoma (HER3 high; IHC 3+) and HCC1569 breast carcinoma (HER3 low; IHC 0-1+) cell lines. In vitro cytotoxicity was evaluated for HER3-ADC1, isotype-MMAE and free MMAE payload as well as patri-DXd, isotype-DXd and free deruxtecan payload in BT474 cells, SK-BR-3 cells and NCI-H446 lung carcinoma (HER3 low; IHC 0-1+) cells. In vivo anti-tumor activity was assessed for HER3-ADC1, isotype-MMAE, patri-DXd and isotype-DXd in patient derived xenograft (PDX) models of pancreatic (HER3 high; IHC 3+) and breast cancer (HER3 low; IHC 0-1+). Results: HER3-ADC1 binding to cancer cells, endocytosis, MMAE release, and inhibition of proliferation were dependent on HER3 expression. In assays investigating antibody internalization, seribantumab displayed similar internalization capacity as patritumab. For both HER3 mAbs, internalization was greater in a HER3 high than a HER3 low cell line. In cytotoxicity assays, HER3-ADC1 and patri-DXd displayed HER3 expression level-dependent cell killing. HER3-ADC1 outperformed patri-DXd in HER3 high cell lines based on in vitro cytotoxicity. HER3-ADC1 and patri-DXd were ineffective against NCI-H466 cells with low HER3 expression. In a PDX model of pancreatic cancer (HER3 high), HER3-ADC1 induced tumor regression, while isotype-MMAE had only a moderate anti-tumor effect. Both patri-DXd and isotype-DXd had moderate anti-tumor effects, indicating a lack of HER3 target dependence. In a PDX model of breast cancer (HER3 low), HER3-ADC1 and isotype-MMAE lacked anti-tumor activity; isotype-DXd had a moderate anti-tumor effect and patri-DXd had a substantial anti-tumor effect. Conclusions: HER3-ADC1 demonstrated target-dependent in vitro cytotoxicity and in vivo anti-tumor activity in a HER3-expressing pancreatic cancer PDX model. Results from in vitro and in vivo studies highlight the promising therapeutic potential of a seribantumab-based ADC for patients with HER3-expressing cancers. Additional results on the optimization and characterization of HER3-ADC1 will be presented. Citation Format: Thomas O'Hare, Jaclyn Cleveland, Valerie M. Jansen, David Dornan. Therapeutic potential of a HER3 antibody-drug conjugate for the treatment of HER3-expressing cancers [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 3121.

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Beckford-Vera, Denis, Megan McCloskey, Jason Li, Caroline Jennings, Le-Cun Xu, Debbie Lewis, Patrik Brodin et al. "Abstract 5040: Novel HER3 targeting antibody radioconjugates, 225Ac-HER3 ARC and 177Lu-HER3 ARC, exhibit potent antitumor efficacy in HER3-positive solid tumors". Cancer Research 83, n.º 7_Supplement (4 de abril de 2023): 5040. http://dx.doi.org/10.1158/1538-7445.am2023-5040.

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Abstract Background: HER3 is a unique member of the EGFR family that collaborates with other EGFR receptors to induce tumorigenesis and drug resistance. Moreover, HER3 expression is linked to poor survival for patients with solid tumors. Despite HER3 being a rational cancer therapeutic target, no HER3-directed therapies have been approved for clinical use. However, new therapeutic strategies such as antibody drug conjugates (ADCs) are being investigated. Targeted radiotherapy, including radiolabeled antibodies (ARCs), is unique mechanistically by inducing cell death independent of biologic pathway inhibition, and can be efficacious with less toxicity relative to other therapeutic modalities. Therefore, we hypothesized that the cytotoxic effects of alpha (225Ac) or beta (177Lu) emitting radionuclides combined with the specificity of anti-HER3 antibody targeting is a compelling therapeutic approach for HER3-expressing tumors. Here we evaluated the antitumor effects of 225Ac or 177Lu armed HER3 ARCs across multiple HER3-expressing cancer models such as ovarian, colorectal, prostate, and renal cancer. Methods: ARCs were prepared by radiolabeling AT-02, an anti-HER3 antibody, with 225Ac or 177Lu using p-SCN-Bn-DOTA to yield 225Ac or 177Lu-HER3 ARC. The binding activity and tumor cell cytotoxicity of HER3 ARCs were assessed by ELISA using human recombinant HER3, flow cytometry on HER3-expressing cells, and colony forming assays. To evaluate the antitumor growth effects of 225Ac-HER3 and 177Lu-HER3 ARCs in vivo, preclinical human tumor xenograft models were developed. Mice bearing HER3-positive tumors were dosed with 225Ac-HER3 ARC (0.2 or 0.4 µCi), or 177Lu-HER3 ARC (200 or 400 µCi) and tumor growth and body weight was monitored. Results: The pharmacological binding properties of HER3 antibody radiolabeled with 225Ac or 177Lu were similar to that of unmodified antibody as demonstrated by HER3 binding ELISA and flow cytometry. HER3 ARCs induced cytotoxicity and inhibited colony formation of HER3-positive tumor cell lines. Significant in vivo human tumor xenograft growth inhibition was observed in response to 225Ac or 177Lu HER3 ARCs compared to control groups (unmodified AT02 or IgG ARCs) in the models studied. No significant loss of body weight was observed in mice treated with HER3 ARCs suggesting that all treatments were well tolerated. Conclusions: In this study, both 225Ac-HER3 ARC and 177Lu-HER3 ARC demonstrated significant antitumor activity against HER3-expressing tumors in a dose-dependent manner. The HER3 targeted radiotherapy approach that we have undertaken could potentially overcome the limitations of current solid tumor therapies in resistance settings and warrants further evaluation in patients with HER3-expressing tumors. Citation Format: Denis Beckford-Vera, Megan McCloskey, Jason Li, Caroline Jennings, Le-Cun Xu, Debbie Lewis, Patrik Brodin, Amanda Chin, Monideepa Roy, Mary Chen, Helen Kotanides. Novel HER3 targeting antibody radioconjugates, 225Ac-HER3 ARC and 177Lu-HER3 ARC, exhibit potent antitumor efficacy in HER3-positive solid tumors. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 5040.

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Toy, Weiyi, Dipti Thakkar, Roberto Magallanes, Sharon Wu, Ming Poi, Alejandro Mas, Konrad Paszkiewicz, Piers Ingram y Jerome Boyd-Kirkup. "Abstract 5796: A HER3 antibody that uniquely blocks the HER3 heterodimerization interface effectively inhibits tumor growth in pre-clinical models with potentially oncogenic HER3 mutations". Cancer Research 84, n.º 6_Supplement (22 de marzo de 2024): 5796. http://dx.doi.org/10.1158/1538-7445.am2024-5796.

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Abstract HER3 activation, via NRG1 ligand-dependent and -independent heterodimerization with HER2 or EGFR, has been associated with tumor progression and acquired resistance to therapies in multiple indications. HER3 mutations, detected in around 3% of cancer cases, may drive oncogenic signaling, leading to rapid tumor growth. Currently, there are no approved targeted therapies for HER3 mutations. Through analysis of real-world data and structural modelling of HER3 heterodimers, we identified four common HER3 mutations located within or close to the dimerization interface of HER3, suggesting a potential impact on HER3 heterodimerization. Immunoprecipitation assays confirmed that all four mutations increased the heterodimerization of HER3 with both HER2 and EGFR. Further, conversion of an endogenous HER3 mutation to wild type via CRISPR editing significantly reduced the growth of KYSE-150, a HER3 mutant cell line. HMBD-001 is a clinical-stage anti-HER3 antibody rationally developed to uniquely block the HER3 dimerization interface to potently inhibit HER3 heterodimerization. Through structural analysis and FACS binding on HER3 mutation cell lines, we confirmed that the binding epitope of HMBD-001 does not overlap with the selected HER3 mutations and therefore may be a good therapeutic option for patients with HER3 mutations. In vitro, HMBD-001 suppressed HER3 mutation-driven PI3K/AKT signaling, as demonstrated by the reduction of phosphorylated HER3 and AKT levels. In multiple cell- and patient-derived xenograft models with HER3 mutations HMBD-001 response achieved >80% tumor growth inhibition. Based on this encouraging preclinical data, a Phase Ib clinical trial (NCT05919537) has been initiated, evaluating HMBD-001 in patients with aberrant HER3 signaling, including HER3 mutations. Citation Format: Weiyi Toy, Dipti Thakkar, Roberto Magallanes, Sharon Wu, Ming Poi, Alejandro Mas, Konrad Paszkiewicz, Piers Ingram, Jerome Boyd-Kirkup. A HER3 antibody that uniquely blocks the HER3 heterodimerization interface effectively inhibits tumor growth in pre-clinical models with potentially oncogenic HER3 mutations [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 5796.

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Beckford-Vera, Denis, Jason Li, Megan McCloskey, Caroline Jennings, Amanda Chin, Qing Liang, Jesse Hwang, Monideepa Roy, Mary Chen y Helen Kotanides. "Abstract 3306: Targeting HER3 receptor positive cancers with a novel anti-HER3 antibody radioconjugate (ARC)". Cancer Research 82, n.º 12_Supplement (15 de junio de 2022): 3306. http://dx.doi.org/10.1158/1538-7445.am2022-3306.

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Abstract Background: HER3 overexpression is reported to be associated with poor survival in breast, ovarian, lung, gastric and prostate cancer. In addition, upregulation of HER3 in response to HER1 or HER2 targeted therapies, is implicated in the acquired resistance against these therapies. Therefore, effective targeting of HER3 can potentially overcome resistance and enhance therapeutic efficacy. Although a number of anti-HER3 antibodies have failed clinical testing with the development focus being shifted to other approaches such as antibody drug conjugates and bispecific antibodies, there are currently no approved HER3-targeted therapies. Here we describe a novel approach that can enhance therapeutic efficacy in HER3+ cancer patients by conjugating an anti-HER3 antibody with the alpha-emitting cytotoxic radioisotope Actinium-225 (225Ac) to create an anti-HER3 antibody radiation conjugate (225Ac-HER3-ARC). Alpha emitting radioisotopes like 225Ac can cause double-strand DNA breaks for which there is no known resistance mechanism. Due to the cytotoxic properties of the radioisotope, lower levels of antibody may be needed, resulting in reduced incidence or less severe toxicities. We hypothesize that targeting HER3 in solid tumors with an ARC will result in tumor specific cell killing especially in a setting where HER-targeting agents are not a viable option. We developed a novel 225Ac-HER3-ARC and evaluated its efficacy in HER3+ in vitro and in vivo tumor models. Methods: AT-02, an anti-HER3 antibody, was conjugated with p-SCN-Bn-DOTA and radiolabeled with 225Ac. 225Ac-HER3-ARC specific binding to HER3 was assessed by ELISA using human recombinant HER3 and by flow cytometry on HER3+ cells. The cytotoxic effect of HER3 ARC was evaluated in a panel of HER3 expressing cells. We further evaluated the maximum tolerated dose and therapeutic efficacy of the ARC in nude mice bearing human HER3+ xenograft tumors. Results: In this study we successfully radiolabeled anti-HER3 with 225Ac. 225Ac-HER3-ARC showed similar binding properties to those of the native antibody by ELISA (HER3-ARC: EC50 = 0.0017 µg/ml, HER3 EC50 = 0.0022 µg/ml) and flow cytometry. Treatment with ARC was cytotoxic to HER3+ cells in a dose-dependent manner (EC50 = 54 kBq/ml). 225Ac-HER3-ARC showed potent in vivo efficacy in preclinical solid tumor xenograft models that was correlated with the in vitro cytotoxicity findings. Treatment with 225Ac-HER3-ARC (7.4 - 22.2 kBq, 200 - 600 nCi) led to complete responses and significantly prolonged survival compared to control groups (p < 0.0001). Conclusions: Our findings demonstrate that targeting HER3 with a novel 225Ac-HER3-ARC results in potent tumor cell cytotoxicity and complete anti-tumor response in HER3 tumor xenograft model. This approach provides a promising therapeutic strategy for HER3 positive tumors and warrants further assessment. Citation Format: Denis Beckford-Vera, Jason Li, Megan McCloskey, Caroline Jennings, Amanda Chin, Qing Liang, Jesse Hwang, Monideepa Roy, Mary Chen, Helen Kotanides. Targeting HER3 receptor positive cancers with a novel anti-HER3 antibody radioconjugate (ARC) [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 3306.

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Scartozzi, M., A. Mandolesi, R. Giampieri, A. Zaniboni, E. Galizia, L. Giustini, R. R. Silva, R. Berardi, I. Bearzi y S. Cascinu. "The role of HER-3 expression in the prediction of clinical outcome for advanced colorectal cancer patients receiving irinotecan/cetuximab." Journal of Clinical Oncology 29, n.º 4_suppl (1 de febrero de 2011): 404. http://dx.doi.org/10.1200/jco.2011.29.4_suppl.404.

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404 Background: Preclinical data suggested that in presence of HER3 altered activation colorectal cancer cells may escape anti-EGFR mediated cell death. HER3 overexpression may then represent a key factor for resistance to anti-EGFR antibodies in colorectal cancer. The aim of our analysis was to investigate a possible correlation between HER3 expression and clinical outcome in KRAS wild-type advanced colorectal cancer receiving cetuximab and irinotecan. Methods: We retrospectively analyzed immunoreactivity for HER3 in KRAS wild-type advanced colorectal cancer patients receiving irinotecan-cetuximab. Results: Eighty-four advanced KRAS wild- type colorectal cancer patients were available for HER3 analysis. Forty patients (48%) showed HER3 negative colorectal tumor, whereas the remaining 44 cases (52%) were deemed HER3 positive. In HER3 negative and HER3 positive tumors we observed a partial response in 17 (42%) and 8 (18%) patients respectively (p = 0.04). Progressive disease was obtained in 11 (35%) and 26 (53%) patients with respectively HER3 negative and positive tumor (p = 0.007). No differences were observed for stable disease. Median PFS was 6.3 months in patients showing HER3 negative tumors and 2.8 months for those who had HER3 overexpressing tumors (p < 0.0001). Median overall survival was 13.6 months in patients showing HER3 negative tumors and 10.5 months for those who had HER3-expressing tumors (p = 0.01). Conclusions: HER3 proved to be a predictive factor for clinical outcome in KRAS wild-type colorectal cancer patients treated with cetuximab. Combined HER3 and KRAS analysis may represent an effective strategy for a better selection of responding colorectal tumors. Furthermore besides identifying colorectal cancer patients refractory to EGFR directed treatment, HER3 overexpression may also represent a potential biological indicator for the development of a new class of antineoplastic agents in this setting. No significant financial relationships to disclose.

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Martinez Lago, Nieves, Ihab Abdulkader, Dora Insua Santamaria, Patricia Viaño Nuñez, Juan Jose Carrera, Jose Ramón Antunez Lopez, Maria Elena Padin Iruegas y Rafael López López. "Assessment and prognostic impact of a new classification using HER2 and HER3 status in resected gastric cancer in a european cohort." Journal of Clinical Oncology 36, n.º 4_suppl (1 de febrero de 2018): 65. http://dx.doi.org/10.1200/jco.2018.36.4_suppl.65.

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65 Background: HER2 status is a predictive biomarker to response to trastuzumab in metastatic gastric adenocarcinomas. However, relatively little is known about the role of HER2 and HER3 in the non-metastatic disease in European population. Methods: Immunohistochemical expression of HER2 was analyzed using DAKO-HercepTest™ and gene amplification using DAKO-DuoCISH kit; both was scored according to published reports. HER3 expressión was analyzed using HER3 clon DAK-H3-ICHER3 and scored as follows: 0 = no staining, 1+ = light staining, 2+ = moderate staining, and 3+ = strong staining. Slides with score 0 or 1+ were classified as low expression or negative and slides with score 2-3+, as high expression or positive. According HER2 and HER3 status patients were classified into six subtypes: HER2-HER3 negative, HER2 equivocal expression HER3 negative, HER2 positive – HER3 negative, HER2 negative – HER3 positive, HER2 equivocal expression – HER3 positive and HER2-HER3 positive. The relationship between this classification and the clinicopathological characteristics and survival was analyzed retrospectively. Results: We included 106 patients between January 2007 and June 2014. The HER2 positivity was 13.2% and HER3 high expression was identified in 27.4% of patients. HER2 status was significantly associated with HER3 status (p = 0.018). HER2 equivocal or positive subtypes were associated with intestinal subtype (0.020) and HER2 or HER3 positive subtypes were associated with low histological grade (0.050). Our classification have demonstrated prognostic impact (p = 0.032) with a specific mortality rate due to gastric cancer of 45-50% for patients with equivocal or positive HER2 subtypes with HER3 low expression, 30% for patients with HER3 high expression independently of HER2 status, and 18% for patients HER2-HER3 negative. Conclusions: Our classification, using HER2 and HER3 status, stratifies patients into 6 subtypes with differentiated clinical and pathological characteristics and prognostic impact.

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Tesis sobre el tema "He53"

BON, GIULIA. "Dual targeting of HER3 and MEK may overcome HER3-dependent chemoresistance of colon cancers". Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2013. http://hdl.handle.net/2108/202145.

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The medical treatment of colorectal cancer (CRC) has evolved greatly in the last years, involving combined chemotherapy protocols and, more recently, new biologic agents. Nevertheless, prognosis remains adverse for patients with metastatic disease and a significant portion of early-stage patients develop recurrence after chemotherapy. Clinical trials are now directed to evaluate new drug combinations and treatment schedules in order to overcome the mechanisms of chemoresistance. By the use of two patient-derived colon cancer cell lines, CC09 (BRAFV600E) and R511 (wt BRAF), and the established colon cancer cell line HT29 (BRAFV600E ; PIK3CAP449T), we found that the tyrosine kinase receptor HER3 is strongly involved in the mechanisms of resistance to 5FluoroUracil (5-FU) and Oxaliplatin drugs. By the use of a monoclonal antibody targeting HER3, named U3-1287, we found down-regulation of HER3 phosphorylation, HER3 internalization and degradation in all cell lines. Functionally, U3-1287 inhibits tumor cell proliferation inducing growth arrest in the G1 phase of the cell cycle, and reduces tumor mass in a CC09-derived xenograft model. Even though U3-1287 administration is higly efficient in abrogating the HER3-dependent activation of PI3K pathway in colon cancer cells, we also found that it induces a compensatory mechanism, involving the increase of HER2 receptor expression that in turn activates MAPK pathway. To overcome U3-1287-induced activation of MAPK, we used a combination therapy with U3-1287 antibody and the MEK-inhibitor Trametinib. We show that Trametinib alone induces the phosphorylation of HER3 receptor that in turn activates PI3K pathway; the combination therapy results in the complete abrogation of both PI3K and MAPK pathways, and in a significant reduction of cell survival in vitro in all three cancers cell lines. These data identify a new combination strategy that, independently of the genetic background of the cells, may overcome the mechanisms of resistance to chemotherapy in HER3-overexpressing colon cancers.

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Aldana, Hidalgo Julio Xavier, Parodi Augusto José Amador, Palacios Jorge Martin Arredondo, Aguilar Carla Barrionuevo, Ortiz Carol Elizabeth Beltrán, Fuentes Carlos Arturo Capellino, Alcazar Martin Roberto Cervetto et al. "Estrategias de redacción - HE59 201801". Universidad Peruana de Ciencias Aplicadas (UPC), 2018. http://hdl.handle.net/10757/624389.

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Descripción: Estrategias de Redacción es un curso de Humanidades, que brinda al participante un conjunto de herramientas lingüísticas para la redacción en el entorno laboral, tales como el uso apropiado de la normativa del español y la aplicación de estrategias de redacción como la enumerativa y la causal. Estas últimas se emplean en la elaboración de un tipo de documento: el informe de recomendación. Propósito: El curso desarrolla la competencia de comunicación escrita en el primer nivel de logro. La asignatura se orienta a la redacción de textos administrativos que ayuden a optimizar el desempeño profesional del participante, ya sea en el entorno universitario o en el ámbito laboral.

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(UPC), Universidad Peruana de Ciencias Aplicadas y Celis Ingunza Sandy Cecilia. "Creatividad Y Liderazgo-HE50-201601". Universidad Peruana de Ciencias Aplicadas (UPC), 2016. http://hdl.handle.net/10757/639326.

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Creatividad y Liderazgo es un curso de formación general de carácter teórico y práctico que está dirigido a estudiantes de quinto ciclo a más de las Facultades de negocios e Ingeniería y que desarrolla una de las competencias generales de nuestro modelo educativo: Pensamiento Innovador.El curso Creatividad y Liderazgo surge como una respuesta a los vertiginosos cambios tecnológicos y sociales que ocurren en nuestros días los que a su vez producen profundas transformaciones en la cultura corporativa de empresas e instituciones. Esto enfrenta a los ejecutivos a cada vez mayores exigencias profesionales requeridas por las organizaciones que necesitan personas capaces de ejercer un liderazgo en equipos gestores de cambio e innovación. La formación por competencias que se brinda permite al estudiante ejecutivo un aprender haciendo. Las experiencias de aprendizaje se desarrollan en espacios de experimentación y simulación que facilitan al estudiante transferir lo aprendido de manera autónoma a los diferentes ámbitos de su vida y en particular al laboral. Así la formación que llevamos a cabo centra su atención en estrategias de indagación crítica y creativa de problemas reales influencia en los procesos de deliberación así como los modos de interacción. El objetivo central es preparar al ejecutivo para enfrentar de manera exitosa dos problemas: la resolución creativa de problemas y capacitarlos en el ejercicio de un liderazgo proactivo dentro de equipos de trabajo marcados cada vez más por una naturaleza interdisciplinaria.

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(UPC), Universidad Peruana de Ciencias Aplicadas y Garcia Soria Juddy Grethel Nora. "Creatividad Y Liderazgo-HE50-201602". Universidad Peruana de Ciencias Aplicadas (UPC), 2016. http://hdl.handle.net/10757/639327.

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(UPC), Universidad Peruana de Ciencias Aplicadas y Ilizarbe Jurado Anndy Antonio. "Creatividad Y Liderazgo-HE50-201701". Universidad Peruana de Ciencias Aplicadas (UPC), 2017. http://hdl.handle.net/10757/639328.

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Creatividad y Liderazgo es un curso de formación general de carácter teórico y práctico que está dirigido a estudiantes de quinto ciclo a más de las Facultades de Negocios e Ingeniería y busca desarrollar una de las competencias generales de nuestro modelo educativo: Pensamiento Innovador.El curso Creatividad y Liderazgo surge como una respuesta a la necesidad de profesionales que cuenten con estrategias y metodologías para afrontar los vertiginosos cambios que ocurren en nuestros días los que a su vez producen profundas transformaciones en la cultura corporativa de empresas e instituciones. Esto enfrenta a los ejecutivos a cada vez mayores exigencias por parte de las organizaciones las cuales requieren personas capaces de involucrar en su práctica y ejercer cotidianamente un liderazgo en equipos gestores de cambio e innovación.La formación por competencias que se brinda permite al estudiante ejecutivo un aprender haciendo. Las experiencias de aprendizaje se desarrollan en espacios de experimentación y simulación que facilitan al estudiante transferir lo aprendido de manera autónoma a los diferentes ámbitos de su vida y en particular al laboral. Así la formación que llevamos a cabo centra su atención en estrategias de indagación crítica y creativa de problemas reales influencia en los procesos de deliberación así como los modos de interacción. El objetivo central es preparar al ejecutivo para enfrentar de manera exitosa dos situaciones: la resolución creativa de problemas y capacitarlos en el ejercicio de un liderazgo proactivo dentro de equipos de trabajo marcados cada vez más por una naturaleza interdisciplinaria.

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Bass, Tarek. "Affibody molecules targeting HER3 for cancer therapy". Doctoral thesis, KTH, Proteinteknologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-204593.

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The development of targeted therapy has contributed tremendously to the treatment of patients with cancer. The use of highly specific affinity proteins to target cancer cells has become a standard in treatment strategies for several different cancers. In light of this, many cancer cell markers are investigated for their potential use in diagnostics and therapy. One such marker is the human epidermal growth factor receptor 3, HER3. It has been established as an important contributor to many cancer types. The function of HER3 is to relay cell growth signals from outside of the cell to the inside. Interfering with- and inhibit- ing the function of HER3 has emerged as an interesting strategy for cancer therapeutics. The studies presented in this thesis aim to target HER3 with small, engineered affinity domain proteins for therapeutic purposes. Monomeric affibody molecules have previously been engineered to bind and inhibit HER3 in vitro. Due to the relatively low expression of HER3, an increase in valency appears promising to strengthen the therapeutic potential. Affibody molecules targeting the receptor were thus linked to form bivalent and bispecific constructs and evaluated both in vitro and in vivo. In the first study of this thesis affibody molecules specific for HER3 and HER2 were fused to an albumin binding domain to form bivalent and bispecific construct. The constructs inhibited ligand-induced receptor phos- phorylation of both HER2 and HER3 more efficiently than monomeric affibody molecules. A second approach to enhance the potential of affibody molecules in tumor targeting is described in the second study, where monomeric HER3-binding affibody molecules were engineered to increase their affinity for HER3. The resulting variants showed a 20-fold in- creased affinity and higher capacity to inhibit cancer cell growth. Combining the findings of the first two studies, the third study describes the evaluation of a HER3-targeting bivalent affibody construct for potential application as a therapeutic. Here, the bivalent construct inhibited cancer cell growth in vitro and was found to slow down tumor growth in mice, while being well tolerated and showing no visible toxicity. The fourth study built upon these findings and compares a very similar bivalent construct to the clinically-investigated HER3-specific monoclonal antibody seribantumab. The affibody construct showed very comparable efficacy with the antibody in terms of decreasing tumor growth rate and ex- tending mouse survival. Collectively, these works describe for the first time the use of alternative affinity protein constructs with therapeutic potential targeting HER3.

QC 20170330

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Htun, van der Horst Edward. "The role of ErbB3/HER3 in gliomas and breast cancer". Diss., lmu, 2002. http://nbn-resolving.de/urn:nbn:de:bvb:19-5804.

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Claus, J. "The pseudokinase HER3 : structure/function relationships and inhibitor-induced signalling". Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1457524/.

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The receptor tyrosine kinase HER3, a pseudokinase in the epidermal growth factor receptor (EGFR) family, is involved in responses to ligands and in the acquired resistance against HER2-directed targeted therapy in breast cancer. In this thesis I aim to further investigate the structure/function relationships at the basis of HER2- HER3 heterodimerisation, particularly in response to inhibitor treatment. The data presented here shows that in HER2+ breast cancer cells treated with the HER2 inhibitor lapatinib, stimulation with the HER3 ligand NRG is able to not only rescue cytotoxicity, but even promote proliferation in a drug-growth factor cooperative manner. We show that in response to lapatinib treatment, inactive heterodimers of HER2-HER3 can form, and that these heterodimers adopt a different conformation to the canonical, asymmetric active heterodimer. Instead, lapatinib promotes a head-to-head, symmetrical heterodimer, in which the α-C helices of both receptors form the interface. For the formation of the inactive heterodimer, as well as for promoting ligandinduced signalling, we show that HER3 requires ATP-binding capability. Although there are implications that HER3 retains a measure of catalytic activity, I show that the ATP-binding requirement for dimerisation and signalling is independent of activity. To highlight this, I have identified a Src/Abl kinase inhibitor, bosutinib, which has high affinity to HER3. SKBR3 cells treated with bosutinib in the absence of exogenously added ligand show an increase in proliferation in 2D and 3D culture models. This indicates an importance for conformational stabilisation of the HER3 kinase domain in the formation of active signalling heterodimers. As a pseudokinase, the role of HER3 may be conceived as being of lesser importance than that of its heterodimerisation partners such as HER2. The structure/function studies presented here show that HER3 remains of great importance in providing an allosteric platform for HER2, together forming the HER2-HER3 oncogenic heterodimer.

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Franks, P. W. "A He3 magnetometer for the EDM experiment". Thesis, University of Sussex, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.304321.

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Xie, Ting. "Targeting `Undruggable' Cancer Proteins with Irreversible Small Molecule Inhibitors: Her3 and KRas". Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11384.

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With the lighting speed revolution of technologies in chemistry and biology, increasing number of proteins which eluded scientists' efforts to block them before and were labeled as `undruggable', were successfully targeted with small molecule inhibitors. During the past five years, I have been working on figuring out the path to inhibit two elusive cancer targets: Her3 and KRas.
Chemistry and Chemical Biology

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Libros sobre el tema "He53"

cai, Jin sheng. Ping di ke ^wei guan jing ji xue~ (di4 he5 ban) bi ji he ke hou xi ti xiang jie. Bei jing: Zhong guo shi hua chu ban she, 2006.

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Kay, Bartholomew L., ed. Planning health promotion programs: An intervention mapping approach. San Francisco: Jossey-Bass, 2006.

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Sole, Kathy. Making Connections: Understanding Interpersonal Communications. Zovio Inc., 2011.

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Making Meaning, Making Sense: Children's Early Language Learning. Zovio Inc., 2012.

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Financial Management of Health Care Organizations: An Introduction to Fundamental Tools, Concepts and Applications. Wiley & Sons, Incorporated, John, 2020.

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Financial Management of Health Care Organizations: An Introduction to Fundamental Tools, Concepts and Applications. Wiley & Sons, Limited, John, 2020.

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Kaya, Gökalp. He3. Independently Published, 2020.

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Fischer, Benjamin. He3 the Novel. Independently Published, 2017.

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He3: The Novel. Independent Publisher, 2010.

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Popkin, Michael H. Preparation for Active Parenting/He23. South-Western Pub, 1988.

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Capítulos de libros sobre el tema "He53"

Lugovskoy, Alexey, Michael Curley, Johanna Lahdenranta, Ashish Kalra, Akos Czibere, Gavin MacBeath y Birgit Schoeberl. "HER3". En Cancer Therapeutic Targets, 719–37. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4419-0717-2_95.

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Lugovskoy, Alexey, Michael Curley, Johanna Lahdenranta, Ashish Kalra, Akos Czibere, Gavin MacBeath y Birgit Schoeberl. "HER3". En Cancer Therapeutic Targets, 1–19. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6613-0_95-1.

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MacLeod, Sheena H., Kyle G. Potts, Shyambabu Chaurasiya y Mary M. Hitt. "Assessment of Specificity of an Adenovirus Targeted to HER3/4". En Methods in Molecular Biology, 275–93. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7219-7_18.

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Heindler, Manfred. "Feasibility, Safety and Environmental Aspects of D-He3 Fusion". En Safety, Environmental Impact, and Economic Prospects of Nuclear Fusion, 173–79. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-0619-1_11.

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Kartavtsev, O. I. "Universal description of the He3 system at low energy". En Few-Body Problems in Physics ’98, 199–202. Vienna: Springer Vienna, 1999. http://dx.doi.org/10.1007/978-3-7091-6798-4_33.

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Rostoker, Norman y Michl Binderbauer. "Self-Colliding Beams as an Alternative Fusion System for D-He3 Reactors". En Current Trends in International Fusion Research, 33–41. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5867-5_4.

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Moldover, M. R. y W. A. Little. "Specific Heat of He3 and He4 in the Neighborhood of their Critical Points". En From High-Temperature Superconductivity to Microminiature Refrigeration, 53–55. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0411-1_7.

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Sarkar, Mitul y John G. Koland. "Fluorescence Recovery After Photobleaching Analysis of the Diffusional Mobility of Plasma Membrane Proteins: HER3 Mobility in Breast Cancer Cell Membranes". En Methods in Molecular Biology, 97–105. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3170-5_9.

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"HER3". En Encyclopedia of Cancer, 1680. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2678.

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Hesketh, Robin. "HER3/ERbB-3". En The Oncogene & Tumour Suppressor Gene Factsbook, 212–15. Elsevier, 1997. http://dx.doi.org/10.1016/b978-012344548-3/50043-1.

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Actas de conferencias sobre el tema "He53"

Chen, Min. "Influence of Helium Cluster Structure on Diffusion Behavior". En 2013 21st International Conference on Nuclear Engineering. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/icone21-15478.

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The migration processes of He cluster in Ti have been simulated in detail using molecular dynamics. It is observed that He2 has no preferred molecular orientation in the migration process. He2 is observed to migrate quickly across the Ti atom layer when its molecular orientation is in the direction of perpendicularity to [001] axis. And it is difficult for He2 to migrate across the Ti atom layer when its orientation is along the [001] axis. He2 only induce a slight rearrangement of its nearby Ti atoms as it migration. As He3 significantly deviates from the orientation of (001) plane, it migrates quickly in the direction along [001] axis. As the deviation of the orientation of He3 from the (001) plane is small, He3 tends to embed in a (001) monolayer and dislocation will be induced at this condition. The molecular orientation of He3 tends to lay in the (001) plane for most of the time. He trimer consequently diffuses slower than He atom and dimer do. Results demonstrate that the details of the migration process of Hen are obviously different for different n.

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Kol, Arjan, Martin Pool, Steven de Jong, Elisabeth GE de Vries, Marjolijn N. Lub-de Hooge y Anton GT Terwisscha van Scheltinga. "Abstract LB-B11: Assessment of HER3 status during lapatinib treatment in HER3-positive breast cancer using 89Zr-anti-HER3 mAb". En Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-lb-b11.

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Hettmann, Thore, Matthias Schneider, Selam Ogbagabriel, Jiansong Xie, Gloria Juan, Susanne Hartmann, Robert Radinsky y Daniel J. Freeman. "Abstract LB-306: U3-1287 (AMG 888), a fully human anti-HER3 mAb, inhibits HER3 activation and induces HER3 internalization and degradation". En Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-306.

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Ghoranneviss, Mahmoud, Babak Malekynia, Nader Azizi, Henrich Hora y George H. Miley. "Alternative Laser Driven Fusion Reactions for Nuclear Energy Without Radioactivity". En 18th International Conference on Nuclear Engineering. ASMEDC, 2010. http://dx.doi.org/10.1115/icone18-29945.

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Following the first result of generating nuclear fusion energy without dangerous radioactive radiation by laser ignition of the proton-11Boron reaction (HB11), we applied this method to evaluate other fusion reactions with no primary neutron production as the proton-7Lithium reaction (HLi7) and of the burning of solid density helium isotope 3He (He3-He3). The new method is a combination of now available laser pulses of 10 petawatt (PW) power and duration in the range of picoseconds (ps) or less. The new mechanism follows the initial theory of Chu and of Bobin for side-on ignition of solid state density fusion fuel developed in about 1972 where some later known physics phenomena had to be added. The essential innovation is the use of the discovery of a predicted anomaly when the mentioned laser pulses are sufficiently clean, i.e. free from prepulses by at least a contrast ratio 108 where acceleration by the nonlinear (ponderomotive) force is dominating.

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"HE3: power measurements". En Proceedings of the 21st IEEE Instrumentation and Measurement Technology Conference. IEEE, 2004. http://dx.doi.org/10.1109/imtc.2004.1351506.

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"HE5: temperature measurement". En Proceedings of the 21st IEEE Instrumentation and Measurement Technology Conference. IEEE, 2004. http://dx.doi.org/10.1109/imtc.2004.1351517.

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Pinzon-Ortiz, Maria C., Xianhui Rong, Richard Versace, Qing Sheng y Z. Alexander Cao. "Abstract 5320: Targeting HER3 and EGFR in NRG1 positive and HER3 mutated lung squamous cell carcinoma". En Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5320.

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Mukherjee, A., Y. Badal, X. Nguyen, J. Miller, S. Pidaparthi, L. Chen, A. Newton, J. Cheung, G. Parry y S. Williams. "Proximity-based assays for the detection of activated HER3, HER2/HER3 heterodimers and HER3/PI3K complexes in formalin-fixed, paraffin-embedded cell line controls and tumors." En CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-4040.

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Zhang, Weixing, Way Kuo y Victor M. Tamashunas. "Simulating the (HE3/HE3/S):(PRP/ ∞ / ∞) queuing model for a maintenance problem". En the 17th conference. New York, New York, USA: ACM Press, 1985. http://dx.doi.org/10.1145/21850.253317.

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Garrett, Joan T., Cammie R. Sutton, Carl Uli Bialucha, Seth A. Ettenberg, Jerry Wallweber, Lisa DeFazio-Eli y Carlos L. Arteaga. "Abstract 5461: A HER3 antibody that blocks ligand-independent HER2-HER3 dimerization sensitizes to HER2 and PI3K inhibitors ." En Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5461.

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Informes sobre el tema "He53"

Lyerly, H. K. Developing a HER3 Vaccine to Prevent Resistance to Endocrine Therapy. Fort Belvoir, VA: Defense Technical Information Center, octubre de 2014. http://dx.doi.org/10.21236/ada612924.

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Lyerly, H. K. Developing a HER3 Vaccine to Prevent Resistance to Endocrine Therapy. Fort Belvoir, VA: Defense Technical Information Center, octubre de 2013. http://dx.doi.org/10.21236/ada597890.

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Dittrich, T. R., B. A. Hammel y C. J. Keane. Diagnosis of pusher-fuel mix in indirectly driven Nova implosions (HEP3). Office of Scientific and Technical Information (OSTI), junio de 1996. http://dx.doi.org/10.2172/376961.

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Ong, Nai P. Acquisition of He3 Cryostat Insert for Experiments on Topological Insulators. Fort Belvoir, VA: Defense Technical Information Center, enero de 2016. http://dx.doi.org/10.21236/ad1007436.

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Trichtchenko, L., L. Nikitina y M. Harrison. Statistical analysis of space environment on highly elliptical orbits. HEO1 and HEO3 missions data. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2013. http://dx.doi.org/10.4095/292717.

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