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Relevant bibliographies by topics / IGF1R target therapy

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Journal articles
Dissertations / Theses
Conference papers

Academic literature on the topic 'IGF1R target therapy'

Author: Grafiati

Published: 4 September 2021

Last updated: 29 July 2025

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Journal articles on the topic "IGF1R target therapy"

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Krieger, Christine C., Susanne Neumann, and Marvin C. Gershengorn. "Is There Evidence for IGF1R-Stimulating Abs in Graves’ Orbitopathy Pathogenesis?" International Journal of Molecular Sciences 21, no. 18 (2020): 6561. http://dx.doi.org/10.3390/ijms21186561.

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In this review, we summarize the evidence against direct stimulation of insulin-like growth factor 1 receptors (IGF1Rs) by autoantibodies in Graves’ orbitopathy (GO) pathogenesis. We describe a model of thyroid-stimulating hormone (TSH) receptor (TSHR)/IGF1R crosstalk and present evidence that observations indicating IGF1R’s role in GO could be explained by this mechanism. We evaluate the evidence for and against IGF1R as a direct target of stimulating IGF1R antibodies (IGF1RAbs) and conclude that GO pathogenesis does not involve directly stimulating IGF1RAbs. We further conclude that the prep

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Noh, MinHye, Jin Muk Kang, Grace Nguyen, et al. "TMIC-58. LEVERAGING VIRO-IMMUNOTHERAPY BY TARGETING IGF2-IGF1R SIGNALING." Neuro-Oncology 26, Supplement_8 (2024): viii311. http://dx.doi.org/10.1093/neuonc/noae165.1236.

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Abstract While an FDA-approved oncolytic herpes simplex-1 virus (oHSV) has shown therapeutic promise with superior safety, accumulating clinical data revealed that its therapeutic efficacy is observed in a small subset of patients. Here, we show that NFκB-mediated Insulin-like Growth Factor 2 (IGF2)/Insulin-like Growth Factor-1 Receptor (IGF1R) signaling pathway as a key modulator for oHSV therapy-mediated tumor resistance. RNA sequencing on the oHSV-infected primary glioblastoma (GBM) and breast cancer (BC) cells identified IGF2 as one of the top 10 upregulated secretomes. Transcriptomic anal

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Ochnik, Aleksandra M., and Robert C. Baxter. "Combination therapy approaches to target insulin-like growth factor receptor signaling in breast cancer." Endocrine-Related Cancer 23, no. 11 (2016): R527—R550. http://dx.doi.org/10.1530/erc-16-0218.

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Insulin-like growth factor receptor (IGF1R) signaling as a therapeutic target has been widely studied and clinically tested. Despite the vast amount of literature supporting the biological role of IGF1R in breast cancer, effective clinical translation in targeting its activity as a cancer therapy has not been successful. The intrinsic complexity of cancer cell signaling mediated by many tyrosine kinase growth factor receptors that work together to modulate each other and intracellular downstream mediators in the cell highlights that studying IGF1R expression and activity as a prognostic factor

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Noh, Min Hye, Alexandra Miller, Grace Nguyen, et al. "Abstract LB262: Reprogramming the tumor microenvironment by targeting IGF2-IGF1R signaling, enhancing viro-immunotherapy." Cancer Research 84, no. 7_Supplement (2024): LB262. http://dx.doi.org/10.1158/1538-7445.am2024-lb262.

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Abstract While an FDA-approved oncolytic herpes simplex-1 virus (oHSV) has shown therapeutic promise with superior safety, accumulating clinical data revealed that its therapeutic efficacy is observed in a small subset of patients. Here, we show that NFκB-mediated Insulin-like Growth Factor 2 (IGF2)/Insulin-like Growth Factor-1 Receptor (IGF1R) signaling pathway as a key modulator for oHSV therapy-mediated tumor resistance. RNA sequencing on the oHSV-infected primary glioblastoma (GBM) and breast cancer (BC) cells identified IGF2 as one of the top 10 upregulated secretomes. Transcriptomic anal

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5

Baar, Courtney, Emily Chiu, Yvette Soignier, et al. "Abstract B040: Trispecific killer engagers against IGF1R and fetal form of insulin receptor induce human natural killer cell mediated killing of hormone receptor positive breast cancer in vitro and in vivo." Cancer Research 84, no. 3_Supplement_1 (2024): B040. http://dx.doi.org/10.1158/1538-7445.advbc23-b040.

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Abstract Patients with hormone receptor-positive (HR+) breast cancers frequently recur with metastatic disease 5-20 years after the initial diagnosis and completion of chemotherapy and prolonged treatment with hormonal therapy. Thus, patients with metastatic HR+ breast cancer need new therapeutic options. A potential mechanism of therapeutic resistance in HR+ patients is the presence of slow-growing, well-differentiated cancer cells that result in clinically detectable metastases after a prolonged latency. One way to eliminate these cancer cells is with immunotherapy (IT). Unfortunately HR+ br

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Yee, Douglas. "40 YEARS OF IGF1: Anti-insulin-like growth factor therapy in breast cancer." Journal of Molecular Endocrinology 61, no. 1 (2018): T61—T68. http://dx.doi.org/10.1530/jme-17-0261.

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Early preclinical and population data suggested a role for the type I insulin-like growth factor receptor (IGF1R) in the regulation of breast cancer growth and survival. To target this pathway, multiple monoclonal antibodies and tyrosine kinase inhibitors were developed and tested in clinical trials. While some of the early clinical trials suggested a benefit for these drugs, none of the attempts showed improved outcomes when compared to conventional therapy. This failure of the IGF1R inhibitors was pronounced in breast cancer; multiple trials testing IGF1R inhibition in estrogen receptor-posi

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Vewinger, Nadine, Sabrina Huprich, Larissa Seidmann, et al. "IGF1R Is a Potential New Therapeutic Target for HGNET-BCOR Brain Tumor Patients." International Journal of Molecular Sciences 20, no. 12 (2019): 3027. http://dx.doi.org/10.3390/ijms20123027.

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(1) Background: The high-grade neuroepithelial tumor of the central nervous system with BCOR alteration (HGNET-BCOR) is a highly malignant tumor. Preclinical models and molecular targets are urgently required for this cancer. Previous data suggest a potential role of insulin-like growth factor (IGF) signaling in HGNET-BCOR. (2) Methods: The primary HGNET-BCOR cells PhKh1 were characterized by western blot, copy number variation, and methylation analysis and by electron microscopy. The expression of IGF2 and IGF1R was assessed by qRT-PCR. The effect of chemotherapeutics and IGF1R inhibitors on

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Baar, Courtney, Emily Chiu, Yvette Soignier, Jeffrey Miller, Martin Felices, and Deepali Sachdev. "Abstract LB231: IGF1R targeted NK cell engager kills proliferating and quiescent hormone receptor positive breast cancers." Cancer Research 85, no. 8_Supplement_2 (2025): LB231. https://doi.org/10.1158/1538-7445.am2025-lb231.

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Abstract Patients with hormone receptor-positive (HR+) breast cancers frequently recur with metastatic disease 5-20 years after initial diagnosis and completion of chemotherapy and prolonged hormonal therapy treatment. A potential mechanism of resistance in HR+ patients is the presence of slow dividing or dormant well-differentiated cancer cells that result in clinically detectable metastases after a prolonged latency. One way to eliminate these is immunotherapy. The objective of this study is to target HR+ breast cancers using a natural killer (NK) cell based approach that targets cell surfac

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Corless, C. L., C. Beadling, E. Justusson, and M. C. Heinrich. "Evaluation of the presence of IGF1R overexpression in wild-type and kinase mutant GI stromal tumors." Journal of Clinical Oncology 27, no. 15_suppl (2009): 10506. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.10506.

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10506 Background: Most adult GI stromal tumors have gain-of-function mutations in KIT (80%) or PDGFRA (5–7%). These pathogenetic mutations are the target for kinase inhibitor therapy. The pathogenesis of the 10–15% of GISTs lacking kinase mutations (WT GIST) is unknown; this includes most pediatric GISTs. Recently, Tarn et al. (PNAS 2008) identified IGF1R over-expression in all WT GIST in their series of cases, including one pediatric case. IGF1R may represent a novel therapeutic target for WT GISTs. Methods: We developed a quantitative RQ-PCR assay for IGF1R and GAPDH transcripts that is line

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Lima, Keli, and João Agostinho Machado-Neto. "NT157 as an Anticancer Drug Candidate That Targets Kinase- and Phosphatase-Mediated Signaling." Kinases and Phosphatases 2, no. 2 (2024): 179–89. http://dx.doi.org/10.3390/kinasesphosphatases2020011.

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Cancer, characterized by uncontrolled cell growth and metastasis, represents a significant challenge to public health. The IGF1/IGF1R axis plays a pivotal role in tumor proliferation and survival, presenting an attractive target for intervention. NT157, a small molecule tyrphostin, has emerged as a promising inhibitor of this axis, displaying potent antineoplastic effects across various cancer types. This review synthesizes the literature on NT157’s mechanism of action and its impact on cellular processes in experimental cancer models. Initially identified for inducing the serine phosphorylati

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Dissertations / Theses on the topic "IGF1R target therapy"

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Bohula, Erin. "The type 1 insulin-like growth factor receptor (IGF1R) as a target for anti-cancer therapy of malignant melanoma." Thesis, University of Oxford, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.275360.

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Ganhoto, Rita de Almeida. "Terapêutica com inibidores do recetor IGFIR no carcinoma adrenocortical." Master's thesis, 2012. http://hdl.handle.net/10316/85244.

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Trabalho final de mestrado integrado em Medicina área científica de Endocrinologia, apresentado á Faculdade de Medicina da Universidade de Coimbra<br>The adrenocortical carcinoma is a rare and aggressive malignancy. Most patients present at diagnosis an advanced stage disease and the therapeutics arsenal is frequently inefficient in controlling the tumour’s progression. The overall 5year survival remains under 50% whereas its therapeutic management has not been updated for the last 20years. Radical surgical resection of the lesion followed by adjuvant mitotane remains the main treatment for th

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Conference papers on the topic "IGF1R target therapy"

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Shackleford, Terry J., Seethalakshmi Hariharan, Hemant K. Bid, and Peter J. Houghton. "Abstract 2472: Mechanisms of resistance to IGFR-targeted therapy in pediatric sarcomas." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2472.

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Isoyama, Sho, Gensei Kajiwara, Naomi Tamaki, et al. "Abstract C96: Development of combination therapy with an IGF1R inhibitor and a PI3K inhibitor ZSTK474 in cancer cells exhibiting the intrinsic resistance to PI3K inhibitors." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-c96.

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Sachdev, D., JE Lin, C. Lunzer, M. Marjanska, M. Garwood, and D. Yee. "P5-13-05: Non-Invasive In Vivo 1H Magnetic Resonance Spectroscopy (MRS) Monitoring of Breast Tumor Response to IGF1R Targeted Therapy." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p5-13-05.

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Donguyen, Huy T., Joseph C. Weber, and Deepali Sachdev. "Abstract 1327: IGF-I and insulin signaling enhances levels of choline kinase in breast cancer cells: Implications for developing noninvasive magnetic resonance spectroscopy of choline containing compounds as a biomarker of response to IGF1R targeted therapy." In 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.am2013-1327.

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