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Journal articles on the topic 'Epidermal growth factor pathway'

Author: Grafiati

Published: 7 September 2021

Last updated: 29 July 2025

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1

Bonomi, Philip. "Epidermal Growth Factor Receptor Pathway." Journal of Thoracic Oncology 5, no. 12 (2010): S470—S471. http://dx.doi.org/10.1097/01.jto.0000391370.86753.90.

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2

Baselga, Jose. "Epidermal growth factor receptor pathway inhibitors." Update on Cancer Therapeutics 1, no. 3 (2006): 299–310. http://dx.doi.org/10.1016/j.uct.2006.08.002.

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3

Salcini, Anna Elisabetta, Hong Chen, Gioacchin Iannolo, Pietro De Camilli, and Pier Paolo Di Fiore. "Epidermal growth factor pathway substrate 15, Eps15." International Journal of Biochemistry & Cell Biology 31, no. 8 (1999): 805–9. http://dx.doi.org/10.1016/s1357-2725(99)00042-4.

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4

Zhang, Mingdi, Shizhong Cai, Bin Zuo, et al. "Arctigenin induced gallbladder cancer senescence through modulating epidermal growth factor receptor pathway." Tumor Biology 39, no. 5 (2017): 101042831769835. http://dx.doi.org/10.1177/1010428317698359.

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Gallbladder cancer has poor prognosis and limited therapeutic options. Arctigenin, a representative dibenzylbutyrolactone lignan, occurs in a variety of plants. However, the molecular mechanisms involved in the antitumor effect of arctigenin on gallbladder cancer have not been fully elucidated. The expression levels of epidermal growth factor receptor were examined in 100 matched pairs of gallbladder cancer tissues. A positive correlation between high epidermal growth factor receptor expression levels and poor prognosis was observed in gallbladder cancer tissues. Pharmacological inhibition or

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Goffin, John R., and Kevin Zbuk. "Epidermal Growth Factor Receptor: Pathway, Therapies, and Pipeline." Clinical Therapeutics 35, no. 9 (2013): 1282–303. http://dx.doi.org/10.1016/j.clinthera.2013.08.007.

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6

Dai, Chenyue, Bing Liu, Shaolei Li, et al. "Construction of a circRNA-miRNA-mRNA Regulated Pathway Involved in EGFR-TKI Lung Adenocarcinoma Resistance." Technology in Cancer Research & Treatment 20 (January 2021): 153303382110568. http://dx.doi.org/10.1177/15330338211056809.

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Objectives: Epidermal growth factor receptor-tyrosine kinase inhibitors are widely used for lung epidermal growth factor receptor-positive lung adenocarcinomas, but acquired resistance is inevitable. Although non-coding RNAs, such as circular RNA and microRNA, are known to play vital roles in epidermal growth factor receptor-tyrosine kinase inhibitor resistance, comprehensive analysis is lacking. Thus, this study aimed to explore the circular RNA-microRNA-messenger RNA regulatory network involved in epidermal growth factor receptor-tyrosine kinase inhibitor resistance. Methods: To identify dif

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Zhang, Lingling, Xiaoxue Zhang, and Liang Zhao. "Progress toward resistance mechanism to epidermal growth factor receptor tyrosine kinase inhibitor." Open Life Sciences 11, no. 1 (2016): 427–31. http://dx.doi.org/10.1515/biol-2016-0056.

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AbstractThe EGFR signaling pathway plays an important role in the occurrence and development of many malignant tumors. It has become a hot spot in the treatment of advanced cancer. At present, the small molecule epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI), has been shown to advanced non-small-cell lung cancer (NSCLC), has a marked drug resistance or has developed one. The EGFR signaling pathway regulates a variety of cellular functions, and its drug resistance may be related to a number of signal transduction pathways, including drug resistance mutations, structural a

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Brightman, Frances A., Simon Thomas, and David A. Fell. "Simulation of The Epidermal Growth Factor Signal Transduction Pathway." Biochemical Society Transactions 27, no. 1 (1999): A48. http://dx.doi.org/10.1042/bst027a048a.

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9

Wakui, Shin, Masakuni Furusato, Mitsugu Tanaka, William C. Allsbrook, Yutaka Kano, and Shinichiro Ushigome. "Endothelium and pericyte interdigitation: Pathway for epidermal growth factor?" Microvascular Research 40, no. 2 (1990): 285–91. http://dx.doi.org/10.1016/0026-2862(90)90026-n.

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10

Chang, Jui-Yoa, Patrick Schindler, Ueli Ramseier, and Por-Hsiung Lai. "The Disulfide Folding Pathway of Human Epidermal Growth Factor." Journal of Biological Chemistry 270, no. 16 (1995): 9207–16. http://dx.doi.org/10.1074/jbc.270.16.9207.

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11

Jimeno, A., A. C. Tan, J. Coffa, et al. "Coordinated Epidermal Growth Factor Receptor Pathway Gene Overexpression Predicts Epidermal Growth Factor Receptor Inhibitor Sensitivity in Pancreatic Cancer." Cancer Research 68, no. 8 (2008): 2841–49. http://dx.doi.org/10.1158/0008-5472.can-07-5200.

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12

Xu, Mei, Lynnette Shorts-Cary, Aaron J. Knox, B. Kleinsmidt-DeMasters, Kevin Lillehei, and Margaret E. Wierman. "Epidermal Growth Factor Receptor Pathway Substrate 8 Is Overexpressed in Human Pituitary Tumors: Role in Proliferation and Survival." Endocrinology 150, no. 5 (2008): 2064–71. http://dx.doi.org/10.1210/en.2008-1265.

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Based on prior work showing that human pituitary tumors overexpress epidermal and fibroblast growth factor receptors, we hypothesized that downstream components of growth factor signaling pathways may also be dysregulated. Epidermal growth factor pathway substrate number 8 (Eps8) was identified as a transcript overexpressed (5.9-fold) in human pituitary tumors compared with normal pituitary by DNA microarrays. Eps8 mRNA up-regulation was confirmed by semiquantitative RT-PCR. Immunoblot analysis showed that Eps8 protein levels and its downstream target phosphorylated ERK were also up-regulated

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13

Morgillo, F., W. K. Hong, and H. Lee. "Insulin-like growth factor-1 receptor/epidermal growth factor receptor (EGFR) heterodimerization and resistance to epidermal growth factor receptor tyrosine kinase inhibitors in non-small-cell lung cancer." Journal of Clinical Oncology 24, no. 18_suppl (2006): 13032. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.13032.

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13032 Background: Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) have been used to treat lung cancers, but resistance to these agents has been observed. This study was designed to investigate whether the insulin-like growth factor (IGF)-mediated signaling pathway induces resistance to the EGFR TKIs in lung cancer. Methods: The antitumor activities and action mechanisms of EGFR inhibitors (erlotinib, gefinitib, cetuximab), single or in combination with IGF-IR inhibitors, were assessed in vitro in a subset of non-small-cell lung cancer (NSCLC) cell lines by the MTT ass

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14

Badenes, Marina. "Epidermal growth factor receptor pathway in central nervous system regenerative medicine: a narrative review." Regenerative Medicine Reports 1, no. 2 (2024): 172–86. https://doi.org/10.4103/regenmed.regenmed-d-24-00020.

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The epidermal growth factor receptor (signaling pathway is involved in numerous important mammal cell functions, such as growth, survival, proliferation, and differentiation. Associated with this, it is involved in tissue normal development and growth, tumorigenesis, and in tissue repair. Epidermal growth factor receptor is broadly expressed in the organism, including in the central and peripheral nervous system, where it has important neurotrophic functions. The central nervous system has a limited capacity for regeneration upon lesion, leading to severe disabilities, such as blindness, senso

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15

Sobani, Zain A., Ashwin Sawant, Mikram Jafri, Amit Keith Correa, and Ibrahim Halil Sahin. "Oncogenic fingerprint of epidermal growth factor receptor pathway and emerging epidermal growth factor receptor blockade resistance in colorectal cancer." World Journal of Clinical Oncology 7, no. 5 (2016): 340. http://dx.doi.org/10.5306/wjco.v7.i5.340.

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16

Krane, J. F., A. B. Gottlieb, D. M. Carter, and J. G. Krueger. "The insulin-like growth factor I receptor is overexpressed in psoriatic epidermis, but is differentially regulated from the epidermal growth factor receptor." Journal of Experimental Medicine 175, no. 4 (1992): 1081–90. http://dx.doi.org/10.1084/jem.175.4.1081.

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Insulin-like growth factor I (IGF-I)/somatomedin C is an important mediator of keratinocyte growth in vitro, and the expression of IGF-I receptors in the basal layer of normal epidermis suggests that this growth pathway may function in the regulation of keratinocyte growth in vivo as well. The pattern of IGF-I receptor expression in normal skin is distinct from that of the epidermal growth factor (EGF) receptor, suggesting that these receptors might be differentially regulated. The purpose of this study was to obtain a better understanding of IGF-I receptor function in the skin by examining IG

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17

Lee, Kyoung-Jin, Yuri Kim, Min Seo Kim, et al. "CD99–PTPN12 Axis Suppresses Actin Cytoskeleton-Mediated Dimerization of Epidermal Growth Factor Receptor." Cancers 12, no. 10 (2020): 2895. http://dx.doi.org/10.3390/cancers12102895.

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The epidermal growth factor receptor (EGFR), a member of ErbB receptor tyrosine kinase (RTK) family, is activated through growth factor-induced reorganization of the actin cytoskeleton and subsequent dimerization. We herein explored the molecular mechanism underlying the suppression of ligand-induced EGFR dimerization by CD99 agonists and its relevance to tumor growth in vivo. Epidermal growth factor (EGF) activated the formation of c-Src/focal adhesion kinase (FAK)-mediated intracellular complex and subsequently induced RhoA-and Rac1-mediated actin remodeling, resulting in EGFR dimerization a

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18

Fang, Jingqin, Xiao Chen, Letian Zhang, et al. "P2X7R suppression promotes glioma growth through epidermal growth factor receptor signal pathway." International Journal of Biochemistry & Cell Biology 45, no. 6 (2013): 1109–20. http://dx.doi.org/10.1016/j.biocel.2013.03.005.

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19

C. Quant, Eudocia, Catherine L. Nutt, Daphne Wang, and Tracy T. Batchelor. "Targeting the Epidermal Growth Factor Pathway as Therapy for Glioblastoma." Current Cancer Therapy Reviews 7, no. 1 (2011): 65–77. http://dx.doi.org/10.2174/157339411794474146.

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20

Grossmann, Allie H., and Wade S. Samowitz. "Epidermal Growth Factor Receptor Pathway Mutations and Colorectal Cancer Therapy." Archives of Pathology & Laboratory Medicine 135, no. 10 (2011): 1278–82. http://dx.doi.org/10.5858/arpa.2011-0047-ra.

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Context.—Rational anticancer therapy is beginning to expand the practice of surgical pathology beyond a primarily morphologic and immunophenotypic analysis into the molecular arena. Molecular testing of tumors can have both diagnostic and therapeutic value, which guides treatment decisions. This is true for colorectal cancer in which mutations in signaling mediators predict resistance to anti–epidermal growth factor receptor (anti-EGFR) therapy. Objective.—To review the clinically relevant mutations that currently guide treatment decisions in metastatic colorectal cancer, summarize additional

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21

Harskamp, Laura R., Ron T. Gansevoort, Harry van Goor, and Esther Meijer. "The epidermal growth factor receptor pathway in chronic kidney diseases." Nature Reviews Nephrology 12, no. 8 (2016): 496–506. http://dx.doi.org/10.1038/nrneph.2016.91.

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22

Sah, Jerome F., Sivaprakasam Balasubramanian, Richard L. Eckert, and Ellen A. Rorke. "Epigallocatechin-3-gallate Inhibits Epidermal Growth Factor Receptor Signaling Pathway." Journal of Biological Chemistry 279, no. 13 (2003): 12755–62. http://dx.doi.org/10.1074/jbc.m312333200.

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23

Liu, Kai, Dongdong Lin, Yabo Ouyang, et al. "Amphiregulin impairs apoptosis-stimulating protein 2 of p53 overexpression–induced apoptosis in hepatoma cells." Tumor Biology 39, no. 3 (2017): 101042831769502. http://dx.doi.org/10.1177/1010428317695026.

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Overexpression of apoptosis-stimulating protein 2 of p53 (ASPP2) induces apoptotic cell death in hepatoma cells (e.g. HepG2 cells) by enhancing the transactivation activity of p53, but long-term ASPP2 overexpression fails to induce more apoptosis since activation of the epidermal growth factor/epidermal growth factor receptor/SOS1 pathway impairs the pro-apoptotic role of ASPP2. In this study, in recombinant adenovirus-ASPP2-infected HepG2 cells, ASPP2 overexpression induces amphiregulin expression in a p53-dependent manner. Although amphiregulin initially contributes to ASPP2-induced apoptosi

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24

Carroll, Rona S., Peter M. Black, Jianping Zhang, et al. "Expression and activation of epidermal growth factor receptors in meningiomas." Journal of Neurosurgery 87, no. 2 (1997): 315–23. http://dx.doi.org/10.3171/jns.1997.87.2.0315.

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✓ Previous studies have demonstrated expression of epidermal growth factor receptors (EGFRs) in human cerebral meningiomas. However, the activation status of the EGFRs and whether they activate cytoplasmic mitogenic signaling pathways are not known. In this study, using Northern blot analysis and the polymerase chain reaction, the authors report expression of epidermal growth factor, transforming growth factor—α, and EGFR messenger RNA in 27 meningioma specimens. Using Western blot and immunohistochemical analyses of the meningioma samples, the authors demonstrate that the EGFRs expressed by t

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25

Laurie, Scott A., and Glenwood D. Goss. "Role of Epidermal Growth Factor Receptor Inhibitors in Epidermal Growth Factor Receptor Wild-Type Non–Small-Cell Lung Cancer." Journal of Clinical Oncology 31, no. 8 (2013): 1061–69. http://dx.doi.org/10.1200/jco.2012.43.4522.

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Worldwide, the majority of patients with advanced non–small-cell lung cancer (NSCLC) do not have activating mutations in the tyrosine kinase domain of the epidermal growth factor receptor (EGFR). These wild-type patients comprise a significant proportion of those treated with inhibitors of this pathway, and data from randomized trials suggest that some of these wild-type patients will derive a modest benefit from these agents. Although the detection of an activating mutation predicts for a greater likelihood of response and longer progression-free survival from an EGFR tyrosine kinase inhibito

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26

Goudar, Ranjit K., Qing Shi, Mark D. Hjelmeland, et al. "Combination therapy of inhibitors of epidermal growth factor receptor/vascular endothelial growth factor receptor 2 (AEE788) and the mammalian target of rapamycin (RAD001) offers improved glioblastoma tumor growth inhibition." Molecular Cancer Therapeutics 4, no. 1 (2005): 101–12. http://dx.doi.org/10.1158/1535-7163.101.4.1.

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Abstract Malignant gliomas are highly lethal tumors that display striking genetic heterogeneity. Novel therapies that inhibit a single molecular target may slow tumor progression, but tumors are likely not dependent on a signal transduction pathway. Rather, malignant gliomas exhibit sustained mitogenesis and cell growth mediated in part through the effects of receptor tyrosine kinases and the mammalian target of rapamycin (mTOR). AEE788 is a novel orally active tyrosine kinase inhibitor that decreases the kinase activity associated with the epidermal growth factor receptor and, at higher conce

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27

Donald, Chancellor E., Luis E. Raez, and Edgardo S. Santos. "Epidermal growth factor receptor pathway as therapeutic development in head and neck cancers: present and future." Oncology Reviews 2, no. 2 (2011): 137. http://dx.doi.org/10.4081/oncol.2009.137.

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The understanding of the epidermal growth factor pathway in terms of intracellular signaling and its role in proliferation and cell survival has impacted the therapeutic management of many solid tumor malignancies in which this pathway has been dysregulated. Once the receptor is targeted at its cellular membrane level or tyrosine kinase domain, its blockage induces downregulation of oncogenic and tumorigenesis mechanisms which were in place, and thus inhibits proliferation and induces apoptosis of the malignant cell. Nowadays, we have several monoclonal antibodies as well as small molecules wh

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28

Clarke, Nicole, Natalia Arenzana, Tsonwin Hai, Audrey Minden, and Ron Prywes. "Epidermal Growth Factor Induction of the c-jun Promoter by a Rac Pathway." Molecular and Cellular Biology 18, no. 2 (1998): 1065–73. http://dx.doi.org/10.1128/mcb.18.2.1065.

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ABSTRACT The c-jun proto-oncogene encodes a transcription factor which is activated by mitogens both transcriptionally and by phosphorylation by Jun N-terminal kinase (JNK). We have investigated the cellular signalling pathways involved in epidermal growth factor (EGF) induction of the c-jun promoter. We find that two sequence elements, which bind ATF1 and MEF2D transcription factors, are required in HeLa cells, although they are not sufficient for maximal induction. Activated forms of Ras, RacI, Cdc42Hs, and MEKK increased expression of the c-jun promoter, while dominant negative forms of Ras

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29

Friedman, BethAann, and Marsha Rich Rosner. "Growth factors modify the epidermal growth factor receptor through multiple pathways." Journal of Cellular Biochemistry 34, no. 1 (1987): 1–11. http://dx.doi.org/10.1002/jcb.240340102.

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30

Krzemieniecki, Krzysztof, Elzbieta Szpyt, Iran Rashedi, Katarzyna Gawron, and Marek Los. "Targeting of solid tumors and blood malignancies by antibody-based therapies — EGFR-pathway as an example." Open Life Sciences 1, no. 2 (2006): 167–82. http://dx.doi.org/10.2478/s11535-006-0014-6.

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AbstractA well-coordinated interaction between extracellular signals and intracellular response forms the basis of life within multicellular organisms, with growth factors playing a crucial role in these interactions. Discoveries in recent years have shown that components of the Epidermal Growth Factor (EGF) signaling system have frequently been used by cancer cells to autonomously provide survival and proliferation signals. The main focus of this review is the ErbB epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases including ErbB1/EGFR, ErbB2/HER2/neu, ErbB3/HER3, and

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31

Chou, Chung-Lin, Nipun U. Jayatissa, Elena T. Kichula, Shuo-Ming Ou, Kavee Limbutara, and Mark A. Knepper. "Phosphoproteomic response to epidermal growth factor in native rat inner medullary collecting duct." American Journal of Physiology-Renal Physiology 328, no. 1 (2025): F29—F47. https://doi.org/10.1152/ajprenal.00182.2024.

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EGF negatively regulates transepithelial water and salt transport across the kidney collecting duct. This study identified phosphoproteins affected by EGF stimulation in normal rat collecting ducts, providing insights into global cell signaling mechanisms. Bioinformatic analyses highlighted enhanced canonical ERK signaling alongside a diminished activity in the PI3K-Akt pathway, which is crucial for cell proliferation and survival. This EGF response differs somewhat from prior studies where both pathways were prominently activated.

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32

AUGOFF, K., R. TABOłA, J. KULA, J. GOSK, and R. RUTOWSKI. "Epidermal Growth Factor Receptor (EGF-R) in Dupuytren’s Disease." Journal of Hand Surgery 30, no. 6 (2005): 570–73. http://dx.doi.org/10.1016/j.jhsb.2005.06.008.

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The aim of this paper was to examine participation of the epidermal growth factor receptor (EGF-R) signal pathway in the pathogenesis of Dupuytren’s disease. The study showed changes in the ratio of membrane EGF-R to its intracellular level during the different clinical stages of Dupuytren’s contracture progression. Our observations of a high ratio of surface to intracellular EGF-R in the palmar aponeurosis of patients with second degree of Dupuytren’s disease (Iselin’s classification), which was significantly higher than this ratio in control palmar fascia ( P = 0.022), would suggest that EGF

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Gui, T., Y. Wei, L. Luo, et al. "Targeting cartilage epidermal growth factor receptor signaling pathway for osteoarthritis treatment." Osteoarthritis and Cartilage 29 (April 2021): S67—S68. http://dx.doi.org/10.1016/j.joca.2021.02.096.

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34

Scagliotti, G. V., S. Novello, and M. G. Levra. "Epidermal Growth Factor Receptor Pathway in Non-Small-Cell Lung Cancer." Annals of Oncology 23 (October 2012): xi12. http://dx.doi.org/10.1093/annonc/mds546.

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35

Scaltriti, M., and J. Baselga. "The Epidermal Growth Factor Receptor Pathway: A Model for Targeted Therapy." AACR Education book 2008, no. 1 (2008): 91–98. http://dx.doi.org/10.1158/aacr.edb-ccr-06-1554.

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36

Shilo, B. "Signaling by the Drosophila epidermal growth factor receptor pathway during development." Experimental Cell Research 284, no. 1 (2003): 140–49. http://dx.doi.org/10.1016/s0014-4827(02)00094-0.

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37

Steen, Hanno, Bernhard Kuster, Minerva Fernandez, Akhilesh Pandey, and Matthias Mann. "Tyrosine Phosphorylation Mapping of the Epidermal Growth Factor Receptor Signaling Pathway." Journal of Biological Chemistry 277, no. 2 (2001): 1031–39. http://dx.doi.org/10.1074/jbc.m109992200.

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38

Sagir, Fatma, and Asuman Demiroglu-Zergeroglu. "Targeting epidermal growth factor receptor pathway with irreversible tyrosine kinase inhibitor." Turkish Journal of Biochemistry 44, no. 1 (2019): 62–69. http://dx.doi.org/10.1515/tjb-2017-0276.

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Abstract Background Malignant mesothelioma (MM) is an endemic disease around central Anatolia region in Turkey, where people are exposed to erionite- and asbestos-contaminated soil. Aberrant EGFR signalling has implicated in several cancers including MMs. Tyrosine kinase inhibitors are new treatment options harbouring deregulated signalling network components. In this study, we aimed to investigate anti-proliferative effect of CL-387,785 in MM cells. Materials and methods Alteration of cell proliferation was evaluated with using MTS assay. Profile of EGFR, ERK, AKT, JNK and p38 proteins and EL

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Joyner, David E., Albert J. Aboulafia, Timothy A. Damron, and R. Lor Randall. "Fas Death Pathway in Sarcomas Correlates with Epidermal Growth Factor Transcription." Clinical Orthopaedics and Related Research 466, no. 9 (2008): 2092–98. http://dx.doi.org/10.1007/s11999-008-0313-5.

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40

Mundschau, L. J., and D. V. Faller. "BALB/c-3T3 fibroblasts resistant to growth inhibition by beta interferon exhibit aberrant platelet-derived growth factor, epidermal growth factor, and fibroblast growth factor signal transduction." Molecular and Cellular Biology 11, no. 6 (1991): 3148–54. http://dx.doi.org/10.1128/mcb.11.6.3148-3154.1991.

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Several lines of evidence now exist to suggest an interaction between the platelet-derived growth factor (PDGF) growth-stimulatory signal transduction pathway and the beta interferon (IFN-beta) growth-inhibitory signal transduction pathway. The most direct examples are inhibition of PDGF-mediated gene induction and mitogenesis by IFN-beta and the effects of activators and inhibitors of the IFN-inducible double-stranded RNA-dependent eIF2 kinase on expression of PDGF-inducible genes. To further investigate the nature of this PDGF/IFN-beta interaction, we selected BALB/c-3T3 cells for resistance

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Mundschau, L. J., and D. V. Faller. "BALB/c-3T3 fibroblasts resistant to growth inhibition by beta interferon exhibit aberrant platelet-derived growth factor, epidermal growth factor, and fibroblast growth factor signal transduction." Molecular and Cellular Biology 11, no. 6 (1991): 3148–54. http://dx.doi.org/10.1128/mcb.11.6.3148.

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Several lines of evidence now exist to suggest an interaction between the platelet-derived growth factor (PDGF) growth-stimulatory signal transduction pathway and the beta interferon (IFN-beta) growth-inhibitory signal transduction pathway. The most direct examples are inhibition of PDGF-mediated gene induction and mitogenesis by IFN-beta and the effects of activators and inhibitors of the IFN-inducible double-stranded RNA-dependent eIF2 kinase on expression of PDGF-inducible genes. To further investigate the nature of this PDGF/IFN-beta interaction, we selected BALB/c-3T3 cells for resistance

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Balaram, P., M. John, S. Enose та P. K. Symaladevi. "Demonstration of TGF-α–EGFR and EGF-EGFR autocrine loops and their relation to proliferation in complete hydatidiform moles (CHM)". International Journal of Gynecologic Cancer 11, № 5 (2001): 397–402. http://dx.doi.org/10.1136/ijgc-00009577-200109000-00010.

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Complete hydatidiform moles (CHM) are the most common form of gestational trophoblastic disease. The prevalence rate is much higher in the state of Kerala, India, than in other parts of the world. The biology and role of growth factors are not fully understood in these tumors. In this study, we have immunohistochemically evaluated the expression of epidermal growth factor (EGF) and transforming growth factor alpha (TGF-α) along with their receptor, epidermal growth factor receptor (EGFR), and we have related them to the proliferative activity in normal placenta and CHM using the expression of

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Chen, John D., Jean-Christophe Lapiere, Daniel N. Sauder, Christina Peavey та David T. Woodley. "Interleukin-1α Stimulates Keratinocyte Migration Through an Epidermal Growth Factor/Transforming Growth Factor-α-Independent Pathway". Journal of Investigative Dermatology 104, № 5 (1995): 729–33. http://dx.doi.org/10.1111/1523-1747.ep12606970.

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44

Amorino, George P., Virginia M. Hamilton, Kristoffer Valerie, Paul Dent, Guido Lammering, and Rupert K. Schmidt-Ullrich. "Epidermal Growth Factor Receptor Dependence of Radiation-induced Transcription Factor Activation in Human Breast Carcinoma Cells." Molecular Biology of the Cell 13, no. 7 (2002): 2233–44. http://dx.doi.org/10.1091/mbc.01-12-0572.

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Ionizing radiation (1–5 Gy) activates the epidermal growth factor receptor (EGFR), a major effector of the p42/44 mitogen-activated protein kinase (MAPK) pathway. MAPK and its downstream effector, p90 ribosomal S6 kinase (p90RSK), phosphorylate transcription factors involved in cell proliferation. To establish the role of the EGFR/MAPK pathway in radiation-induced transcription factor activation, MDA-MB-231 human breast carcinoma cells were examined using specific inhibitors of signaling pathways. Gel-shift analysis revealed three different profile groups: 1) transcription factors that respond

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45

Dlugosz, Paula, Magdalena Teufl, Maximilian Schwab, Katharina Eva Kohl, and Johannes Nimpf. "Disabled 1 Is Part of a Signaling Pathway Activated by Epidermal Growth Factor Receptor." International Journal of Molecular Sciences 22, no. 4 (2021): 1745. http://dx.doi.org/10.3390/ijms22041745.

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Disabled 1 (Dab1) is an adapter protein for very low density lipoprotein receptor (VLDLR) and apolipoprotein E receptor 2 (ApoER2) and an integral component of the Reelin pathway which orchestrates neuronal layering during embryonic brain development. Activation of Dab1 is induced by binding of Reelin to ApoER2 and VLDLR and phosphorylation of Dab1 mediated by Src family kinases. Here we show that Dab1 also acts as an adaptor for epidermal growth factor receptor (EGFR) and can be phosphorylated by epidermal growth factor (EGF) binding to EGFR. Phosphorylation of Dab1 depends on the kinase acti

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Duffy, Michael J., and John Crown. "Companion Biomarkers: Paving the Pathway to Personalized Treatment for Cancer." Clinical Chemistry 59, no. 10 (2013): 1447–56. http://dx.doi.org/10.1373/clinchem.2012.200477.

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BACKGROUND Companion biomarkers are biomarkers that are used in combination with specific therapies and that prospectively help predict likely response or severe toxicity. In this article we review the role of companion biomarkers in guiding treatment in patients with cancer. CONTENT In addition to the established companion biomarkers such as estrogen receptors and HER2 (human epidermal growth factor receptor 2) in breast cancer, several new companion biomarkers have become available in recent years. These include v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations for the se

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Lee, Daniel A., Justin Liu, Young Hong, et al. "Evolutionarily conserved regulation of sleep by epidermal growth factor receptor signaling." Science Advances 5, no. 11 (2019): eaax4249. http://dx.doi.org/10.1126/sciadv.aax4249.

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The genetic bases for most human sleep disorders and for variation in human sleep quantity and quality are largely unknown. Using the zebrafish, a diurnal vertebrate, to investigate the genetic regulation of sleep, we found that epidermal growth factor receptor (EGFR) signaling is necessary and sufficient for normal sleep levels and is required for the normal homeostatic response to sleep deprivation. We observed that EGFR signaling promotes sleep via mitogen-activated protein kinase/extracellular signal–regulated kinase and RFamide neuropeptide signaling and that it regulates RFamide neuropep

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YUE, Linlin, Ling LI, Bin WANG, et al. "Molecular Mechanism of EGFR Signaling Pathway Mediating Proliferation and Migration of U251 Glioma Cell Line." International Journal of Sciences Volume 5, no. 2016-11 (2016): 61–66. https://doi.org/10.5281/zenodo.3349299.

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The EGFR, epidermal growth factor recepor, is a 170 kDa transmembrane glycoprotein and belongs to receptor tyrosine kinases family. Actual evidence shows that overexpression of EGFR is involved in 50% –70% of various diseases. However, there is limited evidence regarding the role of EGFR in the tumorigenesis of human gliomas. In the present study, its effects on U251 cell proliferation and migration were examined using CCK and scratch-wound assay. We found that AG1478 inhibit EGF-induced U251 cells proliferation and migration. Moreover, it was demonstrated that the downregulation of p-EGFR in

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Rahman, Muhammad M., Dimalee Herath, John C. Bladen, et al. "Differential expression of phosphorylated MEK and ERK correlates with aggressive BCC subtypes." Carcinogenesis 42, no. 7 (2021): 975–83. http://dx.doi.org/10.1093/carcin/bgab036.

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Abstract Basal cell carcinoma (BCC) is associated with aberrant Hedgehog (HH) signalling through mutational inactivation of PTCH1; however, there is conflicting data regarding MEK/ERK signalling in BCC and the signalling pathway interactions in these carcinomas. To address this, expression of active phospho (p) MEK and ERK was examined in a panel of 15 non-aggressive and 14 aggressive BCCs. Although not uniformly expressed, both phospho-proteins were detected in the nuclei and/or cytoplasm of normal and tumour-associated epidermal cells however, whereas phospho-MEK (pMEK) was present in all no

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Czarnecka, Anna M., Ewa Bartnik, Michał Fiedorowicz, and Piotr Rutkowski. "Targeted Therapy in Melanoma and Mechanisms of Resistance." International Journal of Molecular Sciences 21, no. 13 (2020): 4576. http://dx.doi.org/10.3390/ijms21134576.

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The common mutation BRAFV600 in primary melanomas activates the mitogen-activated protein kinase/extracellular-signal-regulated kinase (MAPK/ERK) pathway and the introduction of proto-oncogene B-Raf (BRAF) and mitogen-activated protein kinase kinase (MEK) inhibitors (BRAFi and MEKi) was a breakthrough in the treatment of these cancers. However, 15–20% of tumors harbor primary resistance to this therapy, and moreover, patients develop acquired resistance to treatment. Understanding the molecular phenomena behind resistance to BRAFi/MEKis is indispensable in order to develop novel targeted thera

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