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Journal articles on the topic 'IGF1R target therapy'

Author: Grafiati

Published: 4 September 2021

Last updated: 29 July 2025

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1

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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Jen, Hsin-Wei, De-Leung Gu, Yaw-Dong Lang, and Yuh-Shan Jou. "PSPC1 Potentiates IGF1R Expression to Augment Cell Adhesion and Motility." Cells 9, no. 6 (2020): 1490. http://dx.doi.org/10.3390/cells9061490.

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Paraspeckle protein 1 (PSPC1) overexpression in cancers is known to be the pro-metastatic switch of tumor progression associated with poor prognosis of cancer patients. However, the detail molecular mechanisms to facilitate cancer cell migration remain elusive. Here, we conducted integrated analysis of human phospho-kinase antibody array, transcriptome analysis with RNA-seq, and proteomic analysis of protein pulldown to study the molecular detail of PSPC1-potentiated phenotypical transformation, adhesion, and motility in human hepatocellular carcinoma (HCC) cells. We found that PSPC1 overexpre

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Scheffold, Annika, Billy Michael Chelliah Jebaraj, Eugen Tausch та ін. "IGF1R as druggable target mediating PI3K-δ inhibitor resistance in a murine model of chronic lymphocytic leukemia". Blood 134, № 6 (2019): 534–47. http://dx.doi.org/10.1182/blood.2018881029.

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Abstract Targeted therapy is revolutionizing the treatment of cancers, but resistance evolves against these therapies and derogates their success. The phosphatidylinositol 3-kinase delta (PI3K-δ) inhibitor idelalisib has been approved for treatment of chronic lymphocytic leukemia (CLL) and non-Hodgkin lymphoma, but the mechanisms conferring resistance in a subset of patients are unknown. Here, we modeled resistance to PI3K-δ inhibitor in vivo using a serial tumor transfer and treatment scheme in mice. Whole-exome sequencing did not identify any recurrent mutation explaining resistance to PI3K-

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Medyouf, Hind, Samuel Gusscott, Hongfang Wang, et al. "High-level IGF1R expression is required for leukemia-initiating cell activity in T-ALL and is supported by Notch signaling." Journal of Experimental Medicine 208, no. 9 (2011): 1809–22. http://dx.doi.org/10.1084/jem.20110121.

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T cell acute lymphoblastic leukemia (T-ALL) is an aggressive cancer of immature T cells that often shows aberrant activation of Notch1 and PI3K–Akt pathways. Although mutations that activate PI3K–Akt signaling have previously been identified, the relative contribution of growth factor-dependent activation is unclear. We show here that pharmacologic inhibition or genetic deletion of insulin-like growth factor 1 receptor (IGF1R) blocks the growth and viability of T-ALL cells, whereas moderate diminution of IGF1R signaling compromises leukemia-initiating cell (LIC) activity as defined by transpla

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Subbiah, Vivek, and Pete Anderson. "Targeted Therapy of Ewing's Sarcoma." Sarcoma 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/686985.

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Refractory and/or recurrent Ewing's sarcoma (EWS) remains a clinical challenge because the disease's resistance to therapy makes it difficult to achieve durable results with standard treatments that include chemotherapy, radiation, and surgery. Recently, insulin-like-growth-factor-1-receptor (IGF1R) antibodies have been shown to have a modest single-agent activity in EWS. Patient selection using biomarkers and understanding response and resistance mechanisms in relation to IGF1R and mammalian target of rapamycin pathways are areas of active research. Since EWS has a unique tumor-specific EWS-F

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Chakraborty, Sukanya, Bhopal C. Mohapatra, Sameer Mirza, et al. "Abstract 87: EHD1 is required for IGF1R-mediated oncogenic signaling in Ewing Sarcoma." Cancer Research 82, no. 12_Supplement (2022): 87. http://dx.doi.org/10.1158/1538-7445.am2022-87.

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Abstract Background: Ewing Sarcoma (EWS) is the second most common malignant bone tumor of children and adolescents. Patients with metastatic or recurrent disease have very poor outcomes. The receptor tyrosine kinase (RTK) insulin-like growth factor 1 receptor (IGF1R) has been implicated in EWS tumorigenesis and development of metastatic disease, with anti-IGF1R antibodies and kinase inhibitors in clinical studies. However, with only ~10% of patients achieving objective responses, delineation of novel pathways that facilitate IGF1R-driven oncogenesis in EWS could provide avenues for more effec

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Yaktapour, Niuscha, Rudolf Uebelhart, Christine Dierks, et al. "IGF1R Inhibition Induces Apoptosis in Chronic Lymphocytic Leukemia." Blood 120, no. 21 (2012): 3864. http://dx.doi.org/10.1182/blood.v120.21.3864.3864.

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Abstract Abstract 3864 Chronic lymphocytic leukemia (CLL) is characterized by the accumulation of monoclonal B lymphocytes. For decades, nucleoside analogs, alkylating agents, and immunotherapeutics have remained the mainstay in treating this disease. Despite major advances in this field, CLL remains incurable with standard therapy. In recent years, preclinical and early clinical data on the use of kinase inhibitors have sparked new hope in the treatment of CLL. The multikinase inhibitor sorafenib, targeting RAF, platelet-derived growth factor receptor (PDGFR), KIT, FMS-like tyrosine kinase 3

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Gilbert, Judith A., Laura J. Adhikari, Ricardo V. Lloyd, et al. "Molecular markers for novel therapies in neuroendocrine (carcinoid) tumors." Endocrine-Related Cancer 17, no. 3 (2010): 623–36. http://dx.doi.org/10.1677/erc-09-0318.

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Neuroendocrine (carcinoid) tumors (NETs) are endocrine neoplasms occurring most frequently in gastrointestinal and bronchopulmonary (BP) systems. The majority of patients present with advanced disease for which few treatment options exist. We assessed 104 NETs (74 cases) for biomarkers targeted by anticancer drugs under development for other forms of cancer. Activating mutations were assessed in epidermal growth factor receptor (EGFR), stem cell factor receptor (KIT), and platelet-derived growth factor receptor alpha (PDGFRA), as well as non-response mutations in KRAS. Copy number of EGFR and

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Dziadziuszko, R., D. T. Merrick, S. E. Witta, et al. "Insulin-like growth factor receptor 1 (IGF1R) protein expression, mRNA expression and gene copy number in operable non-small cell lung cancer (NSCLC)." Journal of Clinical Oncology 27, no. 15_suppl (2009): 7524. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.7524.

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7524 Background: IGF1R is a promising target for NSCLC therapy. We have evaluated IGF1R protein expression, mRNA expression and gene copy number in primary tumors from surgically treated NSCLC patients (pts) as a reference for correlative biomarker studies in trials using IGF1R inhibitors. Methods: The study included 189 consecutive NSCLC pts who underwent curative pulmonary resection. There were 24% females, 54% squamous cell carcinomas (SCC), 29% adenocarcinomas (AC), 3% large cell carcinomas, 14% other histologies; p stage I: 41%, pII: 22%, pIII: 32% and pIV: 4%. IGF1R expression was evalua

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de Groot, Stefanie, Bas Röttgering, Hans Gelderblom, Hanno Pijl, Karoly Szuhai, and Judith R. Kroep. "Unraveling the Resistance of IGF-Pathway Inhibition in Ewing Sarcoma." Cancers 12, no. 12 (2020): 3568. http://dx.doi.org/10.3390/cancers12123568.

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Insulin-like growth factor-1 receptor (IGF1R) inhibitors are effective in preclinical studies, but so far, no convincing benefit in clinical studies has been observed, except in some rare cases of sustained response in Ewing sarcoma patients. The mechanism of resistance is unknown, but several hypotheses are proposed. In this review, multiple possible mechanisms of resistance to IGF-targeted therapies are discussed, including activated insulin signaling, pituitary-driven feedback loops through growth hormone (GH) secretion and autocrine loops. Additionally, the outcomes of clinical trials of I

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Vella, Veronica, Marika Giuliano, Maria Luisa Nicolosi, et al. "DDR1 Affects Metabolic Reprogramming in Breast Cancer Cells by Cross-Talking to the Insulin/IGF System." Biomolecules 11, no. 7 (2021): 926. http://dx.doi.org/10.3390/biom11070926.

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The insulin receptor isoform A (IR-A), a dual receptor for insulin and IGF2, plays a role in breast cancer (BC) progression and metabolic reprogramming. Notably, discoidin domain receptor 1 (DDR1), a collagen receptor often dysregulated in cancer, is involved in a functional crosstalk and feed forward loop with both the IR-A and the insulin like growth factor receptor 1 (IGF1R). Here, we aimed at investigating whether DDR1 might affect BC cell metabolism by modulating the IGF1R and/or the IR. To this aim, we generated MCF7 BC cells engineered to stably overexpress either IGF2 (MCF7/IGF2) or th

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Bäumer, Nicole, Jessica Tiemann, Annika Scheller, et al. "Targeted siRNA nanocarrier: a platform technology for cancer treatment." Oncogene 41, no. 15 (2022): 2210–24. http://dx.doi.org/10.1038/s41388-022-02241-w.

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AbstractThe small arginine-rich protein protamine condenses complete genomic DNA into the sperm head. Here, we applied its high RNA binding capacity for spontaneous electrostatic assembly of therapeutic nanoparticles decorated with tumour-cell-specific antibodies for efficiently targeting siRNA. Fluorescence microscopy and DLS measurements of these nanocarriers revealed the formation of a vesicular architecture that requires presence of antibody-protamine, defined excess of free SMCC-protamine, and anionic siRNA to form. Only these complex nanoparticles were efficient in the treatment of non-s

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Wang, Daojuan, Xun Tang, Jianguo Ruan, et al. "HSP90AB1 as the Druggable Target of Maggot Extract Reverses Cisplatin Resistance in Ovarian Cancer." Oxidative Medicine and Cellular Longevity 2023 (May 2, 2023): 1–24. http://dx.doi.org/10.1155/2023/9335440.

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Cisplatin resistance is a crucial factor affecting ovarian cancer patient’s survival rate, but the primary mechanism underlying cisplatin resistance in ovarian cancer remains unclear, and this prevents the optimal use of cisplatin therapy. Maggot extract (ME) is used in traditional Chinese medicine for patients with comas and patients with gastric cancer when combined with other drug treatments. In this study, we investigated whether ME enhances the sensitivity of ovarian cancer cells to cisplatin. Two ovarian cancer cells—A2780/CDDP and SKOV3/CDDP—were treated with cisplatin and ME in vitro.

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Besse, Andrej, Tiberiu Totu, Marianne Kraus, et al. "Abstract 4430: Combination of IGF1R/InsR and proteasome inhibition shows strong antitumor activity in proteasome inhibitor resistant multiple myeloma." Cancer Research 85, no. 8_Supplement_1 (2025): 4430. https://doi.org/10.1158/1538-7445.am2025-4430.

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Background: Overcoming proteasome inhibitor (PI) resistance remains an unmet medical need in multiple myeloma (MM) therapy. Anaplastic Lymphoma Kinase (ALK) inhibitors co-target related tyrosine-kinases, such as InsR and IGF1R. Ceritinib, a second-generation ALK inhibitor, has anti-MM activity in monotherapy or in combination with PI carfilzomib (CFZ). MM cells do not express ALK, but are dependent on InsR/IGF1R to sustain their high metabolic demand. Here, we aimed to identify the mechanism of action of ceritinib and the mechanism of synergy between ceritinib and CFZ in MM cells in vitro, in

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Schmidt-Salzmann, Charlotte, Niuscha Yaktapour, Tilman Brummer, Katja Zirlik, and Rainer Claus. "Combined Inhibition of BCR and IGF1R Signaling Leads to Synergistic Apoptosis Induction in Primary CLL Cells in Vitro." Blood 126, no. 23 (2015): 4168. http://dx.doi.org/10.1182/blood.v126.23.4168.4168.

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Abstract Introduction: Chemoimmunotherapy has been the standard of care for chronic lymphocytic leukemia (CLL). However, novel therapeutic strategies targeting the B cell receptor (BCR) pathway like the BTK inhibitor ibrutinib and the PI3K delta inhibitor idelalisib have demonstrated superior results in clinical trials. Consequently, both substances have become standard in relapsed and refractory patients and have replaced conventional chemoimmunotherapy as treatment of choice in high-risk patients with deletion 17p or TP53 mutation. Despite their high clinical effectiveness, these drugs canno

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Kurimchak, Alison M., Vikas Kumar, Carlos Herrera-Montávez, et al. "Kinome Profiling of Primary Endometrial Tumors Using Multiplexed Inhibitor Beads and Mass Spectrometry Identifies SRPK1 as Candidate Therapeutic Target." Molecular & Cellular Proteomics 19, no. 12 (2020): 2068–89. http://dx.doi.org/10.1074/mcp.ra120.002012.

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Endometrial carcinoma (EC) is the most common gynecologic malignancy in the United States, with limited effective targeted therapies. Endometrial tumors exhibit frequent alterations in protein kinases, yet only a small fraction of the kinome has been therapeutically explored. To identify kinase therapeutic avenues for EC, we profiled the kinome of endometrial tumors and normal endometrial tissues using Multiplexed Inhibitor Beads and Mass Spectrometry (MIB-MS). Our proteomics analysis identified a network of kinases overexpressed in tumors, including Serine/Arginine-Rich Splicing Factor Kinase

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Takagi, Satoshi, and Ryohei Katayama. "Abstract 562: Frequent copy number gain of MCL1 is a therapeutic target for osteosarcoma." Cancer Research 84, no. 6_Supplement (2024): 562. http://dx.doi.org/10.1158/1538-7445.am2024-562.

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Abstract Osteosarcoma (OS) is the most common primary malignant bone tumor that predominantly occurs in children, adolescents, and young adults. The treatment for OS that combines surgery with chemotherapy, which consists of a four-drug combination of adriamycin (DOX), cisplatin (CDDP), high-dose methotrexate (MTX), and ifosfamide, was established in 1970s, and it is still used as a standard therapy. Oncogenic driver mutations and fusion genes common to OS have not been identified, which is one of the reasons for the lack of success in drug development for OS. Herein, to explore the characteri

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Hembrough, Todd A., Wei-Li Liao, Sheeno Thyparambil, Marlene Darfler, David Krizman, and Jon Burrows. "Multiplexed mass spectometic quantitation of HER1-3, cMET, and IGF1R in FFPE tumor samples: Implications for targeted therapy and resistance." Journal of Clinical Oncology 30, no. 15_suppl (2012): e21068-e21068. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e21068.

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e21068 Background: The human EGF receptor family (HER’s) consists of two clinically validated drug targets (EGFR and HER2), and two receptors (HER3 and HER4) which are the subject of intensive preclinical and early clinical investigation. Although drugs inhibiting both EGFR and HER2 show significant antitumor activity in the clinic, the acquisition of resistance is a hallmark of these and other targeted therapies. In the case of both targets, one of the emerging resistance mechanisms is the co-expression of other receptor tyrosine kinases, including members of the EGFR superfamily, cMet and IG

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Medyouf, Hind, Samuel Gusscott, Carol Wai, et al. "IGF Signaling Is Critical for Growth and Survival of T-Cell Acute Lymphoblastic Leukemia Cells and Is Potentiated by Notch Upregulation of IGF1R." Blood 112, no. 11 (2008): 3811. http://dx.doi.org/10.1182/blood.v112.11.3811.3811.

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Abstract T-cell acute lymphoblastic leukemia (T-ALL) is a malignancy of immature T cell progenitors in which we described activating mutations of Notch1 to occur in over 50% of cases. As well, others have identified loss-of-function mutations in Sel10/Fbw7 to occur in 8–16% of cases, which also enhance Notch signaling. Notably, inhibition of Notch signaling in these cells induces growth arrest and in some cases apoptosis as well. Subsequent studies have characterized c-myc as a critical downstream target of Notch signaling in this context. More recently, mutations in PTEN (occurring in 17% of

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K, Aswin, and Shabna Roupal Morais. "Unlocking the therapeutic potential of nolatrexed in glioblastoma multiforme through quantum mechanics, network pharmacology, molecular docking and ADMET analysis." Turkish Computational and Theoretical Chemistry 9, no. 2 (2024): 96–110. https://doi.org/10.33435/tcandtc.1518215.

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Introduction: Glioblastoma multiforme (GBM) is a highly aggressive brain tumor that remains challenging to treat due to its resistance to conventional therapies. Despite advances in cancer research, GBM patients face low survival rates often surviving only a few months to a year after diagnosis. Nolatrexed shows notable pharmacological effects and promising therapeutic potential. We explore its interactions, pharmacokinetics and toxicity using computational tools Methods: In-silico investigations were conducted to analyse nolatrexed interactions with GBM targets using network pharmacology whic

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Wu, Jie, and Vivek Subbiah. "RETooling the RET Inhibitor Pralsetinib for ESR1 Fusion–Positive Breast Cancer and Beyond." Cancer Research 83, no. 19 (2023): 3159–61. http://dx.doi.org/10.1158/0008-5472.can-23-1021.

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Abstract Transcriptionally active fusions of ESR1 (ESR1-TAF) and somatic mutations in the estrogen receptor alpha (ERα) ligand-binding domain (LBD) cause endocrine therapy resistance in breast cancer. In searching for therapeutic target kinase(s) in these breast cancers, Gou and colleagues identified FLT4, RET, JAK1, and IGF1R as the top upregulated kinases induced by ESR1-TAFs and ERα LBD mutants in breast cancer cells. Among them, inhibition of RET by pralsetinib suppressed ESR1-TAF–driven and ERα LBD mutant–driven cell proliferation and patient-derived xenograft growth. Pralsetinib is an in

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Gelsomino, Luca, Amanda Caruso, Rocco Malivindi, et al. "Abstract PO3-24-09: May ESR1 mutant breast cancer cells influence fibroblast phenotype?" Cancer Research 84, no. 9_Supplement (2024): PO3–24–09—PO3–24–09. http://dx.doi.org/10.1158/1538-7445.sabcs23-po3-24-09.

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Abstract For almost 50 years, it has been postulated that carcinogenesis relies on the intrinsic genetic abnormalities of tumor cells, but in the last decades, it has been reported that their functional interactions with the tumor microenvironment (TME) might affect therapy response and contribute to the disease progression. Based on these observations, the aim of the present study was to investigate the functional interactions between one of the essential components of TME, the fibroblasts, and breast cancer (BC) cells, expressing mutations in the hormone-binding domain (HBD) of the gene enco

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Yu, Christina, Brian Walker, G. David Roodman, Kun Huang, Michel Sadelain, and Fabiana Perna. "137 Genomics of multiple myeloma influences the expression of CAR T-cell targets." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (2020): A150. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0137.

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BackgroundMultiple Myeloma (MM) is an incurable disease, with a particularly poor prognosis for patients with refractory/relapsed MM or high-risk cytogenetics. Chimeric Antigen Receptor (CAR) T-cell therapy targeting BCMA can induce deep responses in highly pretreated RRMM; however, remissions are not sustained, and the majority of patients eventually relapse. We hypothesized that genomic determinants of MM play a role in dictating the expression of surface targets that can be of use for immune targeting.MethodsWe analyzed the gene expression of 24 immunotherapeutic targets in a combined datas

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Duan, Lei, Sarah J. Calhoun, Ricardo E. Perez, et al. "Prolylcarboxypeptidase promotes IGF1R/HER3 signaling and is a potential target to improve endocrine therapy response in estrogen receptor positive breast cancer." Cancer Biology & Therapy 23, no. 1 (2022): 1–10. http://dx.doi.org/10.1080/15384047.2022.2142008.

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Akoonjee, Ayesha, Athika Rampadarath, Christiana Eleojo Aruwa, Taibat Arinola Ajiboye, Abdulwakeel Ayokun-nun Ajao, and Saheed Sabiu. "Network Pharmacology- and Molecular Dynamics Simulation-Based Bioprospection of Aspalathus linearis for Type-2 Diabetes Care." Metabolites 12, no. 11 (2022): 1013. http://dx.doi.org/10.3390/metabo12111013.

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The medicinal herb Aspalathus linearis (rooibos) is globally recognized in type-2 diabetes mellitus (T2DM) treatment due to its known and distinctive compounds. This work utilized network pharmacology (NP) coupled with molecular dynamics simulation in gaining new insight into the anti-diabetic molecular mechanism of action of rooibos teas. It looked at the interactions between rooibos constituents with various relevant protein receptors and signaling routes associated with T2DM progression. The initial analysis revealed 197 intersecting gene targets and 13 bioactive rooibos constituents linked

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Meher, Abinash, Shailly Varma Shrivastav, Anouska Agarwal, Sheen Dube, Stephanie Portet, and Anuraag Shrivastav. "Abstract 7381: Mathematical modeling and validation of mechanistic target of rapamycin and N-myristoyltransferase signaling pathways in breast cancer." Cancer Research 84, no. 6_Supplement (2024): 7381. http://dx.doi.org/10.1158/1538-7445.am2024-7381.

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Abstract Hormone receptor-positive (HR+) breast cancer (BC) makes up approximately 65% of all breast cancers diagnosed. The prognosis for early-stage disease is excellent with mainstay endocrine therapy (ET). Despite the effectiveness of standard ET, as many as 41% of HR+ early-stage BC diagnosed women will experience distant recurrence. The resistance to endocrine therapy and recurrence is partly attributed to the activation of the insulin pathway and the independence of HR+ BC cells on the ER pathway for their growth. Earlier, we demonstrated the crosstalk between insulin/mTOR and ER pathway

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Marrocco, Ilaria, Yuya Haga, and Yosef Yarden. "Abstract 1097: First-line therapy based on kinase inhibitors and antibodies prevents resistance in EGFR-mutated lung cancer." Cancer Research 82, no. 12_Supplement (2022): 1097. http://dx.doi.org/10.1158/1538-7445.am2022-1097.

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Abstract Introduction: Epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) are commonly used to treat patients with EGFR+ non-small cell lung cancer (NSCLC). Unfortunately, despite the initial response, the long-term efficacy of the five clinically approved TKIs (i.e., gefitinib, erlotinib, afatinib, dacomitinib, osimertinib) is limited by the onset of resistance. Several mechanisms of resistance have been described, including the appearance of new EGFR mutations (e.g., T790M, C797S), activation of bypass pathways (e.g., AXL, HER2, MET and IGF1R) and phenotypic alteration

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Javle, Milind M., Rachna T. Shroff, Gauri R. Varadhachary, et al. "Tumor IGF-1 expression as a predictive biomarker for IGF1R-directed therapy in advanced pancreatic cancer (APC)." Journal of Clinical Oncology 30, no. 15_suppl (2012): 4054. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.4054.

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4054 Background: IGF-1 up-regulates PC proliferation and invasiveness through activation of PI3K/Akt signaling pathway and down-regulates PTEN. We investigated IGF-1 expression in tissue and blood as potential predictive markers in phase II study of IGF1R-directed monoclonal antibody, MK-0646 in APC. Prior phase I established the MTD of MK0646 at 5 mg/kg with gemcitabine (G) and erlotinib (E) and 10 mg/kg with G alone. Methods: Patients (pts) with stage IV, previously untreated APC, ECOG PS 0-1, adequate hematologic and organ function were enrolled. Arm A: G 1,000 mg/m2 over 100 min, weekly x

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Gatalica, Zoran, Kathleen D. Danenberg, Matthew Jerome McGinniss, et al. "Molecular profiling of uveal melanoma patients." Journal of Clinical Oncology 30, no. 15_suppl (2012): 10630. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.10630.

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10630 Background: Although uveal melanoma represents only 5% of all melanomas, it is the most common primary intraocular malignancy of the adult eye. Approximately 50% of patients will develop metastases which are resistant to medical interventions. There is a great need for improved therapy as the prognosis is poor for advanced stages. Our study was undertaken to investigate the presence of novel therapeutic targets. Methods: We analyzed 49 uveal melanoma patients with immunohistochemistry for 16 markers including cKIT, PDGFR, cMET, PTEN and IGF1R. Further, microarray analysis was performed o

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Bresciani, Giulia, Angeliki Ditsiou, Chiara Cilibrasi, et al. "EGF and IGF1 affect sunitinib activity in BP-NEN: new putative targets beyond VEGFR?" Endocrine Connections 8, no. 6 (2019): 680–90. http://dx.doi.org/10.1530/ec-19-0192.

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Broncho-pulmonary neuroendocrine neoplasms (BP-NENs) are neoplasms orphan of an efficient therapy. Available medical treatments derived from clinical trials are not specific for the management of this malignancy. Sunitinib is a multi-receptor tyrosine-kinases (RTKs) inhibitor that has already shown its efficacy in NENs, but there are no available data about its action in BP-NENs. Therefore, our aim was to understand the effects of RTKs inhibition promoted by sunitinib in order to evaluate new putative targets useful in malignancy treatment. Since our results underlined a role for EGFR and IGF1

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Bruckner, Katharina, Daniela Lötsch-Gojo, Lisa Gabler, et al. "ETMR-19.BCOR/L1-ALTERATIONS REWIRE HISTONE REGULATION TO INDUCE ONCOGENIC PATHWAYS IN PEDIATRIC CENTRAL NERVOUS SYSTEM TUMORS." Neuro-Oncology 26, Supplement_4 (2024): 0. http://dx.doi.org/10.1093/neuonc/noae064.189.

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Abstract BACKGROUND Central nervous system (CNS) tumors with BCOR internal tandem duplication (ITD) or BCOR/L1 fusions are recently described tumor types with distinct molecular characteristics and poor clinical outcome. BCOR and its homologue BCORL1 are essential components of the non-canonical polycomb repressor complex (PRC) 1.1 thereby acting as epigenetic regulators exerting a profound impact on central cellular mechanisms. However, the influence of BCOR/L1-alterations on the functionality of PRC1.1 in pediatric CNS tumors remains understudied. METHODS We performed bulk as well as single-

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Sarfstein, Rive, Karthik Nagaraj, Derek LeRoith, and Haim Werner. "Differential Effects of Insulin and IGF1 Receptors on ERK and AKT Subcellular Distribution in Breast Cancer Cells." Cells 8, no. 12 (2019): 1499. http://dx.doi.org/10.3390/cells8121499.

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Insulin and insulin-like growth factor-1 (IGF1) have important roles in breast cancer development. The recent identification of nuclear insulin (INSR) and IGF1 (IGF1R) receptors provides a novel paradigm in the area of signal transduction. The fact that INSR and IGF1R can function as transcription factors, capable of binding DNA and controlling transcription, adds a new layer of biological complexity by conferring upon cell-surface receptors the ability to regulate genomic events. The present study was designed to assess the hypothesis that insulin and IGF1 pathways elicit differential effects

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Guzmán-Flores, Juan Manuel, Fernando Martínez-Esquivias, Antistio Alviz-Amador, Guadalupe Thonanzyn Avilés-Rodríguez, and Michel Fabricio García-Azuela. "Exploring Cannabidiol’s Therapeutic Role in Colorectal Cancer: Network Pharmacology and Molecular Docking Insights." Scientia Pharmaceutica 93, no. 1 (2025): 12. https://doi.org/10.3390/scipharm93010012.

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Background: Colorectal cancer (CRC) is one of the most prevalent cancers worldwide, and current treatments have significant side effects. Cannabidiol (CBD), a compound derived from Cannabis sativa, has demonstrated promising anticancer properties. However, further investigation is required to elucidate its underlying molecular mechanisms. Methods: Network pharmacology and molecular docking analysis approaches were utilized. Molecular targets of CBD and CRC-associated genes were identified using the Swiss Target Prediction, Malacards, and DisGeNet databases. Protein–protein interactions were an

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Petrelli, Annalisa, Sara Erika Bellomo, Ivana Sarotto, et al. "MiR-100 is a predictor of endocrine responsiveness and prognosis in patients with operable luminal breast cancer." ESMO Open 5, no. 5 (2020): e000937. http://dx.doi.org/10.1136/esmoopen-2020-000937.

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PurposeOverexpression of miR-100 in stem cells derived from basal-like breast cancers causes loss of stemness, induction of luminal breast cancer markers and response to endocrine therapy. We, therefore, explored miR-100 as a novel biomarker in patients with luminal breast cancer.MethodsmiR-100 expression was studied in 90 patients with oestrogen-receptor-positive/human-epidermal growth factor receptor 2-negative breast cancer enrolled in a prospective study of endocrine therapy given either preoperatively, or for the treatment of de novo metastatic disease. Response was defined as a Ki67 ≤2.7

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Venkataramanan, Sridhanya, Rajeshwari V Kamat, and Sanjay Ugare. "Molecular Mechanism of Nishamalaki as Rasayana in Diabetes Mellitus." International Journal of Ayurvedic Medicine 15, no. 2 (2024): 375–82. http://dx.doi.org/10.47552/ijam.v15i2.4552.

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Diabetes mellitus, a chronic non-communicable disorder, is on the rise in developing countries. In Ayurveda, a similar condition called Madhumeha is attributed to Dhatu kshaya (Emaciation) and Dosha avarana (occlusion of humoral factors). Rasayana therapy, involving herbal formulations like Nishamalaki, is recommended to strengthen the body's major structural components (dhatus), boost immunity, and promote longevity. Nishamalaki, a combination of Haridra (Curcuma longa Linn.) and Amalaki (Phyllantus emblica Linn.), exhibits antioxidant, anti-inflammatory, and lipid-reducing properties. It hol

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Huizer, Karin, Andrea Sacchetti, Sigrid Swagemakers, Peter van der Spek, Dana Mustafa, and Johan M. Kros. "TAMI-10. CIRCULATING ANGIOGENIC CELLS (CACS) IN GLIOBLASTOMA: TOWARDS DEFINING CRUCIAL FUNCTIONAL DIFFERENCES IN CAC-INDUCED NEOPLASTIC VERSUS REACTIVE NEOVASCULARIZATION." Neuro-Oncology 22, Supplement_2 (2020): ii215. http://dx.doi.org/10.1093/neuonc/noaa215.899.

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Abstract In order to identify suitable therapeutic targets for glioma anti-angiogenic therapy, the process of neovascularization mediated by circulating angiogenic cells (CACs) needs to be scrutinized. In the present study we compared the expression of neovascularization-related genes by three circulating CAC subsets (HPCs, CD34+ and KDR+ cells; internal controls: PBMCs and circulating endothelial cells) of treatment-naïve patients with glioblastoma (GBM) to those of patients undergoing reactive neovascularization (myocardial infarction (MI). CACs from umbilical cord (representing developmenta

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Thyparambil, Sheeno P., Wei-Li Liao, Amanda Strasbaugh, et al. "Personalized therapy for head and neck squamous carcinoma (HNSCC) utilizing tissue proteomics profiling." Journal of Clinical Oncology 41, no. 16_suppl (2023): 6045. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.6045.

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6045 Background: Chemotherapy is widely used in the treatment of HNSCC, yet no biomarkers for chemotherapy is used for selection of the chemo agent in the treatment of HNSCC. We examined 143 HNSCC cancer using targeted proteomics for the protein expression levels of several chemo agents. These include markers of resistance to platinum agents (ERCC1), anti-tubulin inhibitors (TUBB3) and sensitivity markers for topoisomerase inhibitors (Topo1 – irinotecan, topotecan; Topo2A – doxorubicin, etoposide). We also measured markers for several antibody-drug conjugates (EGFR, Her2, Trop2, FR-alpha, Meso

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De Velasco, Marco A., Yurie Kura, Naomi Ando, et al. "Abstract 5211: Therapeutic resistance to anti-AR signal pathway therapies is related to compensatory pathway activation and immune suppression in mouse Pten/Trp53-deficient CRPC." Cancer Research 82, no. 12_Supplement (2022): 5211. http://dx.doi.org/10.1158/1538-7445.am2022-5211.

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Abstract Prostate cancers depend on androgens and the androgen receptor (AR) to drive androgen signaling pathways. Androgen-deprivation therapy (ADT) and second-generation antiandrogens have become the new standard of care for men with prostate cancer. However, resistance to these therapies remains a problem. TP53 mutations and PTEN loss have been associated with patients who fail to respond to anti-androgen therapies and complex interactions between AR signaling and the immune system means that these therapies have the potential to affect antitumor immune responses. Here, we characterize trea

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Scheffold, Annika, Billy Michael Chelliah Jebaraj, Eugen Tausch та ін. "In Vivo modeling of Resistance to PI3Kδ Inhibitor Treatment Using EµTCL1-Tg Tumor Transfer Model". Blood 128, № 22 (2016): 190. http://dx.doi.org/10.1182/blood.v128.22.190.190.

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Abstract Inhibitors of B-cell receptor (BCR) signaling have proven effective in the treatment of chronic lymphocytic leukemia (CLL). An important downstream mediator of BCR signaling is phosphoinositide 3-kinase delta (PI3Kd), which through activation of AKT, controls cell survival, growth and proliferation. Since it is expressed predominantly in cells of hematopoietic origin, PI3Kd is a promising target in CLL, and the novel PI3Kd inhibitor idelalisib is effective in treating relapsed/refractory CLL. However, a subset of patients relapse under therapy, and the mechanisms leading to resistance

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Thyparambil, Sheeno P., Wei-Li Liao, Eunkyung An, et al. "Proteomic profiling to identify therapeutics targets in glioblastoma (GBM)." Journal of Clinical Oncology 38, no. 15_suppl (2020): 2555. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.2555.

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2555 Background: Glioblastoma (GBM) is an aggressive primary brain tumor with poor prognosis. Treatment at diagnosis is largely confined to surgery, radiation and temozolomide (TMZ) with median progression-free survival (PFS) of 7 months and median overall survival (mOS) of 15 months. GBM tumors recur in most cases and in patients with recurrent GBM, the mOS is 6.2 months. The lack of effective therapies underscores the importance of exploring other agents. We propose that quantitating therapy-associated protein biomarkers can improve treatment personalization for GBM. Methods: 97 FFPE GBM tis

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Osuka, Satoru, Dan Zhu, Zhaobin Zhang, et al. "Abstract 1430: N-cadherin is a driver of adaptive radioresistance in malignant brain tumors." Cancer Research 82, no. 12_Supplement (2022): 1430. http://dx.doi.org/10.1158/1538-7445.am2022-1430.

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Abstract Many subtypes of brain tumors are highly malignant and resistant to chemo- and radio- therapy. Tumor cells can shift their phenotype in response to treatments, the so-called adaptive resistance. Adaptive resistance mechanisms in malignant brain tumors are still poorly understood, and effective treatments have not yet been developed. To unveil such mechanisms, we have developed unique new experimental models to identify the adaptive resistance mechanisms to fractionated radiation in malignant brain tumors. We performed repeated irradiation (2-5Gy every 3-4 days, 3-6 weeks) on 6 human G

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