Relevant bibliographies by topics / EGFR-Inhibition

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers
  5. Reports

Academic literature on the topic 'EGFR-Inhibition'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 July 2024

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Journal articles on the topic "EGFR-Inhibition"

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Gursel, Demirkan B., Cody D. Schlaff, and John A. Boockvar. "EGFR Targeted Inhibition Resistance." Neurosurgery 71, no. 4 (October 2012): N17—N18. http://dx.doi.org/10.1227/01.neu.0000419710.25405.7f.

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Gaipl, Udo S. "EGFR-Inhibition bei NSCLC-Tumorzelllinien." Strahlentherapie und Onkologie 192, no. 6 (May 11, 2016): 425–27. http://dx.doi.org/10.1007/s00066-016-0977-9.

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Patel, Rajvi. "EGFR Signaling and its inhibition by EGFR inhibitors in NSCLC." International Journal of Applied Sciences and Biotechnology 2, no. 4 (December 25, 2014): 375–88. http://dx.doi.org/10.3126/ijasbt.v2i4.11263.

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Lung cancer is the third most cancer among the population. The American society’s estimation for lung cancer in the United States for 2014 states that about 2,24,210 people are suffering from the lung cancer and 1,59,260 deaths are occur from lung cancer. Among all the types of lung cancer, NSCLC (Non-Small cell Lung Cancer) represents 85% of the lung cancer. The estimated spread of NSCLC is 2,26,160 and 1,60,340 cases are of death in 2012. One of the risk factor for NSCLC is over expression of epidermal growth factor receptor (EGFR) and its intracellular signaling pathways. EGFR is over expressed in 40-80 % cases of NSCLC. EGFR belongs to the ErbB family of receptor tyrosinekinases (RTK) having molecular weight 170 to 185 kDa. Epidermal Growth Factor (EGF) binds to the EGFR at its extracellular domain and this binding leads to the homo or hetero dimerization and autophosphorylation of EGFR which initiates the several intracellular pathways. Several mutations in EGFR or in any of the proteins of the pathway leads to the growth and survival of the tumor cells. So in order to inhibit the growth of tumor cell, several EGFR inhibitors and targeted therapies are found to target the particular mutations.DOI: http://dx.doi.org/10.3126/ijasbt.v2i4.11263 Int J Appl Sci Biotechnol, Vol. 2(4): 375-388
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Kalyankrishna, Shailaja, and Jennifer R. Grandis. "Epidermal Growth Factor Receptor Biology in Head and Neck Cancer." Journal of Clinical Oncology 24, no. 17 (June 10, 2006): 2666–72. http://dx.doi.org/10.1200/jco.2005.04.8306.

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Epidermal growth factor receptor (EGFR) is overexpressed in several epithelial malignancies, including head and neck squamous cell carcinoma (HNSCC), which exhibits EGFR overexpression in up to 90% of tumors. EGFR ligands such as transforming growth factor alpha are also overexpressed in HNSCC. EGFR plays a critical role in HNSCC growth, invasion, metastasis and angiogenesis. However, EGFR inhibitors as monotherapy have yielded only modest clinical outcomes. Potential mechanisms for lack of response to EGFR inhibition in HNSCC include constitutive activation of signaling pathways independent of EGFR, as well as genetic aberrations causing dysregulation of the cell cycle. EGFR-directed therapy may be optimized by identifying and selecting those HNSCC patients most likely to benefit from EGFR inhibition. Resistance to EGFR inhibition may be circumvented by combination therapy employing EGFR inhibitors together with other treatment modalities.
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Guo, Gao, Ke Gong, Jann Sarkaria, and Amyn Habib. "DRES-01. EFFICACY OF EGFR PLUS TNF INHIBITION IN A PRECLINICAL MODEL OF GLIOBLASTOMA." Neuro-Oncology 21, Supplement_6 (November 2019): vi71. http://dx.doi.org/10.1093/neuonc/noz175.289.

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Abstract EGFR gene amplification and mutation are common in glioblastoma (GBM), but EGFR inhibition is not effective in treating this tumor. EGFR inhibition may fail because EGFR is not a driver of the malignant phenotype in GBM, or because adaptive compensatory mechanisms are triggered by EGFR inhibition that prevent cell death from a loss of EGFR signaling. We have recently identified a TNFα-JNK-Axl-ERK signaling axis that mediates primary resistance to EGFR inhibition in GBM. Temozolomide (TMZ) is the most effective chemotherapy in GBM, although it has only a modest effect on overall survival. The efficacy of TMZ depends on the absence of the DNA repair protein O6-alkylguanine DNA alkyltransferase (MGMT) which reverses the DNA damage induced by TMZ. The MGMT promoter is hypermethylated in about 45% of GBMs, resulting in lack of MGMT expression. TMZ is less effective in MGMT unmethylated GBMs. Moreover, even initially responsive tumors develop a secondary resistance to TMZ. No treatment is effective in recurrent TMZ-resistant GBM. In this study, we compare the efficacy of temozolomide versus EGFR plus TNF inhibition in an orthotopic model of GBM. We find that efficacy of the two treatments is similar in MGMT-methylated GBMs. However, in MGMT-unmethylated GBMs, a combination of EGFR plus TNF inhibition is more effective. We demonstrate that the two treatment approaches target distinct and non-overlapping pathways. Furthermore, and importantly, EGFR plus TNF inhibition remains effective in TMZ-resistant recurrent GBMs and in GBMs rendered experimentally resistant to TMZ. Since the EGFR is expressed in the majority of GBMs, EGFR inhibition combined with a blunting of the accompanying TNF-driven adaptive response could be a broadly applicable and viable therapeutic approach in primary GBMs with MGMT unmethylation and in recurrent GBMs.
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Corkery, B., N. O’Donovan, M. Clynes, and J. Crown. "Epidermal growth factor receptor (EGFR) inhibition in triple-negative breast cancer (BrCa)." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 14071. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.14071.

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14071 Background: Triple-negative BrCa lacks expression of hormone receptors and HER-2 but does express EGFR. It is associated with early relapse and poor survival. There is no targeted therapy for triple-negative BrCa. We are studying the potential role of EGFR inhibition. Methods: EGFR expression was examined in triple-negative BrCa cell lines, (BT20, HCC1937, and MDA-MB-231) by western blot. IC50 assays were determined for three EGFR inhibitors, gefitinib (G) and erlotinib (T), which are small-molecule tyrosine kinase inhibitors, and cetuximab (E) which is a monoclonal antibody against EGFR, and chemotherapy (CRx) drugs docetaxel (D) and carboplatin (P)), using the acid phosphatase assay. The controls were HER2+ BrCa cell lines, BT474 and SKBR3 which express low levels of EGFR. Results: The three triple-negative cell lines over-express EGFR. IC50 values for G and T were significantly higher in the triple-negative than in the HER2+ cell lines. E did not cause significant inhibition in any cell line (max inhibition 20% at 100 μg/ml E). IC50 values for G were lower than for T in the triple-negative cell lines (IC50s for HCC1937: G - 8.4 ± 1.5 μM; T - 26.2 ± 9.3 μM). Combined EGFR inhibition with CRx was tested in HCC1937 cells. G combined with P or with D for 5 days showed an additive effect on inhibition of proliferation ( Table 1 ). Alternate scheduling of the drugs did not significantly influence response. Conclusions: Our results suggest that triple-negative BrCa cells over-express EGFR but are not as sensitive to EGFR inhibition as HER2+ BrCa cells. However, EGFR inhibition may enhance response to CRx in triple-negative BrCa. [Table: see text] No significant financial relationships to disclose.
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Guo, Gao, Ke Gong, Vineshkumar Thidil Puliyappadamba, Nishah Panchani, Edward Pan, Bipasha Mukherjee, Ziba Damanwalla, et al. "Efficacy of EGFR plus TNF inhibition in a preclinical model of temozolomide-resistant glioblastoma." Neuro-Oncology 21, no. 12 (July 31, 2019): 1529–39. http://dx.doi.org/10.1093/neuonc/noz127.

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Abstract Background Glioblastoma (GBM) is the most common primary malignant adult brain tumor. Temozolomide (TMZ) is the standard of care and is most effective in GBMs that lack the DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT). Moreover, even initially responsive tumors develop a secondary resistance to TMZ and become untreatable. Since aberrant epidermal growth factor receptor (EGFR) signaling is widespread in GBM, EGFR inhibition has been tried in multiple clinical trials without success. We recently reported that inhibiting EGFR leads to increased secretion of tumor necrosis factor (TNF) and activation of a survival pathway in GBM. Here, we compare the efficacy of TMZ versus EGFR plus TNF inhibition in an orthotopic mouse model of GBM. Methods We use an orthotopic model to examine the efficacy of TMZ versus EGFR plus TNF inhibition in multiple subsets of GBMs, including MGMT methylated and unmethylated primary GBMs, recurrent GBMs, and GBMs rendered experimentally resistant to TMZ. Results The efficacy of the 2 treatments was similar in MGMT methylated GBMs. However, in MGMT unmethylated GBMs, a combination of EGFR plus TNF inhibition was more effective. We demonstrate that the 2 treatment approaches target distinct and non-overlapping pathways. Thus, importantly, EGFR plus TNF inhibition remains effective in TMZ-resistant recurrent GBMs and in GBMs rendered experimentally resistant to TMZ. Conclusion EGFR inhibition combined with a blunting of the accompanying TNF-driven adaptive response could be a viable therapeutic approach in MGMT unmethylated and recurrent EGFR-expressing GBMs.
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Harris, Zachary M., Ying Sun, John Joerns, Brian Clark, Buqu Hu, Asawari Korde, Lokesh Sharma, et al. "Epidermal Growth Factor Receptor Inhibition Is Protective in Hyperoxia-Induced Lung Injury." Oxidative Medicine and Cellular Longevity 2022 (September 20, 2022): 1–18. http://dx.doi.org/10.1155/2022/9518592.

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Aims. Studies have linked severe hyperoxia, or prolonged exposure to very high oxygen levels, with worse clinical outcomes. This study investigated the role of epidermal growth factor receptor (EGFR) in hyperoxia-induced lung injury at very high oxygen levels (>95%). Results. Effects of severe hyperoxia (100% oxygen) were studied in mice with genetically inhibited EGFR and wild-type littermates. Despite the established role of EGFR in lung repair, EGFR inhibition led to improved survival and reduced acute lung injury, which prompted an investigation into this protective mechanism. Endothelial EGFR genetic knockout did not confer protection. EGFR inhibition led to decreased levels of cleaved caspase-3 and poly (ADP-ribosyl) polymerase (PARP) and decreased terminal dUTP nick end labeling- (TUNEL-) positive staining in alveolar epithelial cells and reduced ERK activation, which suggested reduced apoptosis in vivo. EGFR inhibition decreased hyperoxia (95%)-induced apoptosis and ERK in murine alveolar epithelial cells in vitro, and CRISPR-mediated EGFR deletion reduced hyperoxia-induced apoptosis and ERK in human alveolar epithelial cells in vitro. Innovation. This work defines a protective role of EGFR inhibition to decrease apoptosis in lung injury induced by 100% oxygen. This further characterizes the complex role of EGFR in acute lung injury and outlines a novel hyperoxia-induced cell death pathway that warrants further study. Conclusion. In conditions of severe hyperoxia (>95% for >24 h), EGFR inhibition led to improved survival, decreased lung injury, and reduced cell death. These findings further elucidate the complex role of EGFR in acute lung injury.
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Warta, Rolf, and Christel Herold-Mende. "Helping EGFR inhibition to block cancer." Nature Neuroscience 20, no. 8 (July 26, 2017): 1035–37. http://dx.doi.org/10.1038/nn.4605.

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Martz, Lauren. "EGFR inhibition boosts stem cell mobilization." Science-Business eXchange 3, no. 40 (October 2010): 1197. http://dx.doi.org/10.1038/scibx.2010.1197.

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Dissertations / Theses on the topic "EGFR-Inhibition"

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Lee, Richard William. "MET-EGFR dimerisation in lung adenocarcinoma is dependent on EGFR mutations and altered by MET kinase inhibition." Thesis, King's College London (University of London), 2017. https://kclpure.kcl.ac.uk/portal/en/theses/metegfr-dimerisation-in-lung-adenocarcinoma-is-dependent-on-egfr-mutations-and-altered-by-met-kinase-inhibition(3a738a35-f82d-4eb6-83a3-150160d12045).html.

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Prognosis in advanced stage lung cancer is extremely poor with few effective therapies. EGFR tyrosine kinase inhibitors (TKIs) have high response rates in patients with activating EGFR mutations and are now an established part of therapy in selected patients. Such advances herald a previously unprecedented enthusiasm for the possibilities of targeted therapy. Acquired resistance however is widespread - the EGFR T790M mutation in particular represents approximately 50% of these. MET amplification is also an important route of resistance and preclinical data suggests synergy between therapies targeting these two receptors. We hypothesized that EGFR mutation status determines the EGFR-MET interaction and response to MET inhibition. We tested this hypothesis by using cells derived from NCI-H1975, which possess L858R and T790M EGFR mutations. This cell model and a derived murine xenograft experiment provided a platform with which to test these ideas by using assays of tumorigenicity in vitro; tumour growth/stroma formation in vivo and a selective MET kinase inhibitor, SGX523. EGFR-MET interaction was assessed by a Förster Resonance Energy Transfer (FRET) Fluorescence Lifetime Imaging Microscopy (FLIM) assay developed as part of this thesis that quantified EGFR-MET dimer formation. SGX523 significantly reduced cell proliferation, xenograft tumour growth and ERK phosphorylation in the presence of the EGFR L858R-T790M mutations but not with EGFR L858R alone where SGX523 reduced stroma formation but not growth. SGX523 reduced EGFR-MET dimerisation in the EGFR L858R-T790M mutant but increased EGFR-MET interaction in the presence of EGFR L858R alone. Little effect was seen with EGFR WT in response to SGX523 for any of these indices. This thesis provides novel data for the mechanistic understanding of EGFR-MET heterodimerisation and the accompanying discussion explores how this is relevant for EGFR and MET targeted therapies.
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Starok, Marcelina Anna. "EGFR inhibition by curcumin in cancer cells : a dual mode of action." Thesis, Compiègne, 2014. http://www.theses.fr/2014COMP2093.

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Le récepteur de facteur de croissance épidermique (EGFR) est une cible commune de thérapie anticancéreuse. Aujourd'hui, la recherche de nouvelles molécules inhibitrices de ce récepteur se tourne vers des substances naturelles. Un des composés naturels les plus prometteurs qui ont montré une activité anti-EGFR est la curcumine, un polyphénol présent dans les rhizomes de Curcuma longa. Il y a de nombreux rapports décrivant son effet sur l'activité kinase du récepteur, le rendement d'autophosphorylation, le niveau d'expression et les processus liés à la fonction EGFR comme la prolifération cellulaire. Néanmoins, l'ensemble des mécanismes d’intercation de la curcumine avec l'de l'EGFR n’est pas entièrement élucidée. Nous avons démontré que le mode d'action de la curcumine est double. La curcumine est capable d'inhiber partiellement, mais directement l'activité enzymatique du domaine intracellulaire de l'EGFR. Mais le travail présenté attire l'attention sur le rôle de l'environnement de la membrane de l'EGFR au niveau d'action de la curcumine. Nous avons montré que l'insertion de curcumine dans la membrane plasmique aboutit à sa rigidification et par conséquent la limitation de la diffusion du récepteur. Le suivi de particules à l'unité analyses a confirmé que le coefficient de diffusion de l'EGFR dans la membrane des cellules cancéreuses diminué de manière significative en présence de la curcumine, susceptibles d'influencer la dimérisation du récepteur et l'activation tour à tour
Epidermal Growth Factor Receptor (EGFR) is a common target of anticancer therapy. Nowadays the search for new molecules inhibiting this receptor is turning towards natural substances. One of the most promising natural compounds that have shown an anti-EGFR activity is curcumin, the polyphenol found in the rhizomes of Curcuma longa. There are numerous reports describing its effect on the receptor kinase activity, the autophosphorylation yield, the expression level and the processes related to EGFR function like cell proliferation. Nevertheless, the entire mechanism of how curcumin interact with the EGFR is not fully elucidated. We demonstrated that the mode of action of curcumin is dual. Curcumin is able to inhibit directly but partially the enzymatic activity of the EGFR intracellular domain. But the presented work brings attention to the role of the EGFR membrane environment at the curcumin action level. We showed that the curcumin insertion in plasma membrane leads to its rigidification and as a consequence to limitation of the receptor diffusion. Single particle tracking analyses confirmed that the diffusion coefficient of EGFR in the cancer cell membrane significantly decreased in the presence of the curcumin, which might influence the receptor dimerization and in turns its activation
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Gebel, Lena [Verfasser], Anja C. [Akademischer Betreuer] [Gutachter] Pickhard, and Stephanie E. [Gutachter] Combs. "EGFR-Inhibition bei simultaner Strahlentherapie in Abhängigkeit der EGFR vIII-Variante bei HNSCC / Lena Gebel ; Gutachter: Stephanie E. Combs, Anja C. Pickhard ; Betreuer: Anja C. Pickhard." München : Universitätsbibliothek der TU München, 2017. http://d-nb.info/1143826280/34.

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McGarry, Sarah. "Inhibition of Hypoxia and EGFR Sensitizes TNBC to Cisplatin and Suppresses Bulk and Cancer Stem Cells." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/41506.

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Despite progress being made in our understanding of triple negative breast cancer (TNBC), the overall survival and disease-free survival for TNBC patients continues to be considerably poorer than their ER/PR/HER2+ counterparts. Metastasis and chemoresistance are the pivotal issues holding back the long-term success of TNBC treatments. In addition to the bulk tumor cells, cancer stem cells (CSCs) have emerged as important targets for alleviating TNBC progression and relapse. Cisplatin, a platinum based chemotherapeutic agent, has shown promising potential for the treatment of TNBC in clinical trials; however, cisplatin treatment is associated with tumor hypoxia that in turn promotes CSC enrichment and drug resistance. My work is to develop a combinational treatment to improve the long-term therapeutic potential of cisplatin that not only targeted the bulk TNBC population but also ALDHhigh and CD44+/CD24- CSC populations. Through clinical dataset analysis, I found that patient TNBC tumors expressed high levels of epidermal growth factor receptor (EGFR) and hypoxia genes. A similar expression pattern was demonstrated in cisplatin-resistant ovarian cancer. I therefore developed a combinational therapeutic to co-inhibit EGFR and hypoxia using metformin (an AMPK activator) and gefitinib (an EGFR inhibitor), which sensitized bulk TNBC cells to cisplatin and also led to the effective inhibition of both CD44+/CD24- and ALDHhigh CSCs. I obtained similar results by using clinically relevant TNBC patient samples ex vivo. Since these drugs are already frequently used in the clinic, this study illustrates a novel, clinically translatable therapeutic approach to improve the long-term therapeutic outcome of cisplatin for TNBC treatment.
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Lopez, Corcino Yalitza Z. "Inhibition of Epidermal Growth Factor Receptor (EGFR) Leads to Autophagy-mediated Killing of Toxoplasma gondii and Control of Disease." Case Western Reserve University School of Graduate Studies / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1560350001767936.

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Fehrmann, Astrid. "Interaktion einer Blockade des Rezeptors für den Epidermalen Wachstumsfaktor (EGFR) mit der Gabe von Keratinozyten-Wachstumsfaktor (KGF) bei der Strahlenreaktion der Mundschleimhaut – tierexperimentelle Untersuchungen an Mäusen." Doctoral thesis, Universitätsbibliothek Leipzig, 2010. http://nbn-resolving.de/urn:nbn:de:bsz:15-20100526-071222-8.

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Bei der Strahlentherapie fortgeschrittener Tumoren im Kopf-Hals-Bereich gilt die radiogene Mucositis enoralis als schwerwiegende und dosislimitierende frühe Nebenwirkung. Sehr häufig führt sie zu einer Unterbrechung der Behandlung, mit der Folge einer Reduktion der Tumorheilungschancen. Während einer fraktionierten Strahlenexposition kommt es in der Mundschleimhaut zu einer erhöhten Expression des Epidermalen Wachstumsfaktors (Epidermal Growth Factor, EGF) und dessen Rezeptors (EGFR). Durch eine Blockade des EGFR, als anerkannte Strategie zur Verbesserung der Tumorheilung, besteht deshalb die Gefahr, dass es zu einer Verschlimmerung der Schleimhaut-Nebenwirkungen kommt. Der Einsatz von Keratinozyten-Wachstumsfaktor (KGF) zeigt positive Ergebnisse bezüglich einer Reduktion der Schleimhautveränderungen. In dieser Arbeit wird deshalb im Tiermodell einerseits die Auswirkung einer Blockade des EGFR auf die Schleimhautreaktion, und andererseits eine mögliche Interaktion der Blockade mit der schleimhautschützenden Wirkung von KGF untersucht. Insgesamt kann keine signifikante Veränderung der Schleimhauttoleranz durch die EGFR-Inhibition mittels BIBX1382BF innerhalb der ersten beiden Wochen einer fraktionierten Bestrahlung festgestellt werden; lediglich das Auftreten ulzerativer Läsionen nach der zweiten Woche ist vorverlagert
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Wong, Matthew Ho Fai. "Overcoming primary and acquired erlotinib resistance with epidermal growth factor receptor (EGFR) and phosphoinositide 3-kinase (PI3K) co-inhibition in pancreatic cancer." Thesis, The University of Sydney, 2014. http://hdl.handle.net/2123/13868.

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PI3K/Akt is over-expressed in 50-70% of pancreatic ductal adenocarcinoma (PDAC). The hypothesis of this study is that PI3K and EGFR co-inhibition may be effective in PDAC with upregulated PI3K/Akt/mTOR (PAM) signaling. Five primary PDAC and two erlotinib acquired resistant (ER) cell lines with significantly over-expressed AKT2 gene, total Akt and pAkt, were used. Multiple inhibitors of the MAPK and PAM were tested alone or in combination by western blotting, cell proliferation, cell cycle, clonogenic, apoptosis, and migration assays. Erlotinib acted synergistically with PI3Kα inhibitor BYL in both ER cell lines (synergy index, SI=1.71 and 1.44 respectively). Treatment of ER cell lines by this dual blockade caused significant G1 cell cycle arrest (71%, P<0.001; 58%, P=0.003), inhibition of colony formation (69% and 72%, both P<0.001), and necrosis and apoptosis (75% and 53%, both P<0.001), more so compared to parent cell lines. In primary patient-derived tumor subrenal capsule (n=90) and subcutaneous (n=22) xenografts, Erlotinib plus BYL significantly reduced tumor volume (P=0.005). Strong pEGFR and pAkt immunostaining (2+/3+) was correlated with high response to erlotinib and low response to erlotinib plus BYL respectively. In conclusion, PDAC with increased expression of the PAM signaling were susceptible to PI3K/ EGFR co-inhibition suggesting oncogenic dependence. Erlotinib plus BYL should be considered for a clinical study in PDAC; further evaluation of pEGFR and pAkt expression as potential predictive biomarkers is warranted.
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Spiegelberg, Diana. "Towards Personalized Cancer Therapy : New Diagnostic Biomarkers and Radiosensitization Strategies." Doctoral thesis, Uppsala universitet, Medicinsk strålningsvetenskap, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-247539.

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This thesis focuses on the evaluation of biomarkers for radio-immunodiagnostics and radio-immunotherapy and on radiosensitization strategies after HSP90 inhibition, as a step towards more personalized cancer medicine. There is a need to develop new tracers that target cancer-specific biomarkers to improve diagnostic imaging, as well as to combine treatment strategies to potentiate synergistic effects. Special focus has been on the cell surface molecule CD44 and its oncogenic variants, which were found to exhibit unique expression patterns in head and neck squamous cell carcinoma (HNSCC). The variant CD44v6 seems to be a promising target, because it is overexpressed in this cancer type and is associated with radioresistance. Two new radioconjugates that target CD44v6, namely, the Fab fragment AbD15179 and the bivalent fragment AbD19384, were investigated with regard to specificity, biodistribution and imaging performance. Both conjugates were able to efficiently target CD44v6-positive tumors in vitro and in vivo. PET imaging of CD44v6 with 124I-AbD19384 revealed many advantages compared with the clinical standard 18F-FDG. Furthermore, the efficacy of the novel HSP90 inhibitor AT13387 and its potential use in combination with radiation treatment were evaluated. AT13387 proved to be a potent new cancer drug with favorable pharmacokinetics. Synergistic combination effects at clinically relevant drug and radiation doses are promising for both radiation dose reduction and minimization of side effects, or for an improved therapeutic response. The AT13387 investigation indicated that CD44v6 is not dependent on the molecular chaperone HSP90, and therefore, radio-immunotargeting of CD44v6 in combination with the HSP90 inhibitor AT13387 might potentiate treatment outcomes. However, EGFR expression levels did correlate with HSP90 inhibition, and therefore, molecular imaging of EGFR-positive tumors may be used to assess the treatment response to HSP90 inhibitors. In conclusion, these results demonstrate how tumor targeting with radiolabeled vectors and chemotherapeutic compounds can provide more specific and sensitive diagnostic tools and treatment options, which can lead to customized treatment decisions and a functional diagnosis that provides more precise and safer drug prescribing, as well as a more effective treatment for each patient.
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Lobe, Cindy. "Rôle du facteur de transcription ZEB1 dans la progression et chimiorésistance du cholangiocarcinome The IGF2/IR/IGF1R pathway in tumor cells and myofibroblasts mediates resistance to EGFR inhibition in cholangiocarcinoma Unveiling resistance mechanisms to EGFR inhibitors in cholangiocarcinoma." Thesis, Sorbonne université, 2019. http://www.theses.fr/2019SORUS618.

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ZEB1 (Zinc finger E-box binding homeobox 1) est un facteur de transcription qui favorise l'invasion et les métastases tumorales en induisant une transition épithélio-mésenchymateuse (TEM) dans les cellules de carcinome. La TEM joue un rôle majeur dans l’embryogenèse et la progression maligne, mais aussi dans l'acquisition de propriétés des cellules souches cancéreuses (CSC) et la résistance aux traitements. L’objectif de ce travail était d’étudier le rôle de ZEB1 dans la progression et la chimiorésistance du CCA. Nos précédents travaux, ont montré une surexpression de ZEB1 dans les cellules résistantes au traitement anti-EGFR dans le CCA. Les données cliniques, ont révélé une expression de ZEB1 dans les échantillons humains de CCA et ont associé son expression à un mauvais pronostic. Pour les études in vitro, des modèles d’études cellulaires ont été réalisés dans lesquels l’expression de ZEB1 a été soit invalidée soit forcée. Les résultats ont montré l’implication de ZEB1 dans la plasticité cellulaire, par la mise en place d’un phénotype de TEM et de CSC dans les cellules exprimant ZEB1 comparées aux cellules contrôles. Les modèles d’invalidation de ZEB1 ont montré une inhibition de ces processus. Par ailleurs, les expériences ont permis d’identifier ZEB1 comme un facteur de résistance au traitement anti-EGFR dans les modèles de CCA. Les modèles d’invalidation de ZEB1 ont montré une sensibilisation des cellules à ce traitement. En conclusion, nous avons démontré dans cette étude que ZEB1 contribuerait à la plasticité cellulaire et à la chimiorésistance des cellules de CCA, faisant de lui une cible de choix dans le développement de nouvelles stratégies thérapeutiques
ZEB1 (Zinc Finger E-box Binding Homeobox 1) is a transcription factor that promotes tumor invasion and metastasis by inducing epithelial-mesenchymal transition (EMT) in carcinoma cells. EMT not only plays an important role in embryonic development and malignant progression, but is also implicated in acquisition of cancer stem cell properties and cancer therapy resistance. The aim of the study was to evaluate ZEB1 role in cholangiocarcinoma progression and chemoresistance. Our previous study in the first article showed ZEB1 overexpression in resistant cells to anti-EGFR treatment in CCA. Clinical data revealed ZEB1 expression in human tumor CCA samples and correlated its expression with a poor prognosis. To perform in vitro studies, different CCA cellular models were established, in which ZEB1 expression has been either invalidated or forced. We showed that ZEB1 regulates cellular plasticity characterized by an acquisition of TEM and CSC phenotypes in overexpressing ZEB1 cells. ZEB1 invalidation models showed a downregulation of these processes. In addition, cell viability analyzes identified ZEB1 as a resistance factor to anti-EGFR treatment in CCA models. ZEB1 inhibition models showed a cell re-sensitization to anti-EGFR treatment. In conclusion, we propose in this study that ZEB1 regulates CCA cells plasticity and chemoresistance, that could be a prime target in the development of new therapeutic strategies in CCA
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Holzinger, Barbara [Verfasser], and Philipp [Akademischer Betreuer] Baumeister. "Vergleich der Stimulation und therapeutischen Inhibition des Epidermal Growth Faktor-Rezeptors (EGFR) im 2D- und 3D-Kulturmodell bei Karzinomen im Kopf-Hals-Bereich / Barbara Holzinger ; Betreuer: Philipp Baumeister." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2021. http://d-nb.info/1232645389/34.

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Book chapters on the topic "EGFR-Inhibition"

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De Pauw, Ines, Carolien Boeckx, and An Wouters. "Mechanisms of Cetuximab Resistance and How to Overcome It." In Critical Issues in Head and Neck Oncology, 21–51. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_3.

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AbstractDeregulated or increased signalling of the epidermal growth factor receptor (EGFR) plays an integral role in the development of various cancer types, including head and neck squamous cell carcinoma (HNSCC), making it a compelling drug target. However, after initially promising results of EGFR-targeted therapies, such as the monoclonal antibody cetuximab, it became clear that both intrinsic and acquired therapeutic resistance are major roadblocks in the field of personalised cancer treatments.In order to unravel and overcome resistance to cetuximab, at least two strategies can be adopted.Firstly, therapeutic resistance to anti-EGFR therapy may arise from mechanisms that can compensate for reduced EGFR signalling and/or mechanisms that can modulate EGFR-dependent signalling. In this chapter, we discuss which mechanisms of cetuximab resistance are already known and which ones deserve further investigation. This enhanced knowledge will guide us to rationally design and test novel combination therapies that overcome resistance to EGFR-targeting agents in cancer treatment.Secondly, an urgent need remains to develop novel targeted treatments for single-agent or combined therapy use. In this view, due to the particular mode of activation of the EGFR receptor, involving ligand-induced homo- and heterodimerization of the four HER receptors, an increased inhibition scope of HER receptors most likely results in a more potent blockade of the HER network, preventing premature emergence of resistance and leading to a more pronounced therapeutic benefit. We discuss two multitargeted compounds, being MEHD7945A (duligotuzumab) and afatinib, in this chapter.Despite the huge efforts to unravel the molecular landscape of HNSCC, the main clinically validated target remains EGFR. However, immune checkpoints, like programmed cell death protein 1 (PD-1), are gaining clinical approvals as well. We underscore the importance of adopting rational drug combinations to enhance the therapeutic effect of the EGFR-inhibitor cetuximab and highlight the ongoing search for predictive biomarkers, with the ultimate goal of delivering individualized cancer therapy to HNSCC patients.
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Roden, Dylan F., Jennifer M. Johnson, Petr Szturz, Paolo Bossi, and Athanassios Argiris. "New and Promising Targeted Therapies in First and Second-Line Settings." In Critical Issues in Head and Neck Oncology, 277–96. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_18.

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AbstractDeeper understanding of the molecular pathogenesis of malignancies, including head and neck squamous cell carcinoma (HNSCC), has led to the investigation of several novel targeted therapies. These therapeutic approaches may eventually replace or complement existing treatment modalities, such as surgery, radiation therapy, and traditional cytotoxic chemotherapy. Epidermal growth factor receptor (EGFR) inhibitors, and specifically cetuximab, are as of now the only class of targeted agents, excluding immune checkpoint inhibitors, with approval in the treatment of HNSCC. Beyond EGFR inhibition, novel therapies under evaluation are directed against vascular endothelial growth factor (VEGF) and VEGF receptor (VEGFR), PI3K/AKT/mTOR pathway, cell cycle regulation (for example, cyclin dependent kinases 4 and 6), HRAS, DNA repair mechanisms, and others. Development of new therapies has to take into consideration the complexity of solid tumors and their heterogeneity. Multitargeted combination therapy approaches may be required in certain cases in order to maximize antitumor effect. Ways to individualize treatment using validated biomarkers are likely to improve outcomes. We review the most relevant molecular targets in HNSCC and provide updates on clinical trial data with promising new targeted agents.
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Zucali, Paolo. "Signal Transduction Inhibitors, HER Family, EGFR Inhibition and Clinical Achievements." In Targeted Therapies in Oncology, 19–44. CRC Press, 2007. http://dx.doi.org/10.3109/9781420020588-3.

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Qian, Kewen, Changhai Lei, and Shi Hu. "Novel Toll-like receptor 9 agonist induces epidermal growth factor receptor (EGFR) inhibition and synergistic antitumor activity with EGFR inhibitors." In Novel Sensitizing Agents for Therapeutic Anti-EGFR Antibodies, 185–88. Elsevier, 2023. http://dx.doi.org/10.1016/b978-0-12-821584-5.00030-4.

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Panda, Pravati, Subhendu Chakroborty, and M. V. B. Unnamatla. "Structure-Activity-Relationship (SAR) Studies of Novel Hybrid Quinoline and Quinolone Derivatives as Anticancer Agents." In Key Heterocyclic Cores for Smart Anticancer Drug–Design Part I, 167–204. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815040074122010007.

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Cancer, caused by uncontrolled cell growth in any part of the body, is a significant life-threatening burden for the growing civilization. Though cancer research has reached a high level, considering the high cost of the available therapies to treat various cancers, the morbidity and mortality rates are still high. Organ toxicity, lack of cell specificity, drug resistance, and short half-life with adverse side effects are the major hurdles associated with currently used therapeutics. Therefore, there is a high need to search for new anticancer agents with minimal side effects and toxicity. In this connection, nature always acts as a treasury for scientists by offering its natural sources to fight the war against various life-harvesting diseases. Nowadays, hybrid molecule drug designs attract much attention among organic and medicinal chemists. What is more interesting about the hybrid molecule is that, depending upon the target disease creating protein, scientists are designing and optimising the target molecule by considering their structure-activity relationship studies (SARs). Among the different natural sources, quinoline, quinolone, and their hybrid derivatives are the most privileged ones. They are found as the central core of many bioactive natural products as well as drug molecules (camptothecin, bosutinib, cabozantinib, pelitinib, lenvatinib, levofloxacin, voreloxin, ciprofloxacin, garenofloxacin, etc.) acting as anticancer agents. Literature is enriched with the excellent achievements of hybrid quinoline and quinolone derivatives which function as anticancer agents through various mechanisms such as Bcl-2 inhibition, ALDH inhibition, kinase inhibition, topo-II, and EGFR-TK inhibition, etc. Given the excellent performance of quinoline and quinolone hybrid derivatives, it will be worthwhile to continue researching them.&nbsp;
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Li, Tian, and Shi Hu. "Primary and acquired resistance of colorectal cancer cells to anti-EGFR antibodies converge on MEK/ERK pathway activation and can be overcome by combined MEK/EGFR inhibition." In Novel Sensitizing Agents for Therapeutic Anti-EGFR Antibodies, 137–44. Elsevier, 2023. http://dx.doi.org/10.1016/b978-0-12-821584-5.00014-6.

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Qian, Kewen, Wenyan Fu, Changhai Lei, and Shi Hu. "Dual inhibition of EGFR and c-Src by cetuximab and dasatinib combined with FOLFOX chemotherapy in patients with metastatic colorectal cancer." In Novel Sensitizing Agents for Therapeutic Anti-EGFR Antibodies, 99–103. Elsevier, 2023. http://dx.doi.org/10.1016/b978-0-12-821584-5.00028-6.

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Karpel-Massler, Georg, and Marc-Eric Halatsch. "The Molecular Basis of Resistance to the Antiproliferative Effect of EGFR Inhibition in Human Glioblastoma Multiforme Cell Lines." In Brain Tumors - Current and Emerging Therapeutic Strategies. InTech, 2011. http://dx.doi.org/10.5772/24053.

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Fukuoka, H., A. Ben-Shlomo, A. Mamelak, C. Zhou, J. Mizutani, S. Ren, D. Bruyette, and S. Melmed. "Inhibition of EGF Receptor (EGFR) Signaling in Cushing's Disease: A Novel Pathway for Abrogating STAT3 Regulation of ACTH." In The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego, P1–613—P1–613. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part1.p13.p1-613.

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Ma, Zetong, Tian Li, Wenyan Fu, Changhai Lei, and Shi Hu. "Inhibition of SLC1A5 sensitizes colorectal cancer to cetuximab." In Novel Sensitizing Agents for Therapeutic Anti-EGFR Antibodies, 161–66. Elsevier, 2023. http://dx.doi.org/10.1016/b978-0-12-821584-5.00023-7.

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Conference papers on the topic "EGFR-Inhibition"

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Lee, Richard, Elena Ortiz-Zapater, Gregory Weitsman, Gilbert Fruhwirth, Will Owen, Tony Ng, and George Santis. "EGFR mutations determine EGFR-MET crosstalk and MET inhibition in lung cancer." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa539.

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Ortiz-Cuarán, Sandra, Jakob Schöttle, Ilona Dahmen, Martin Peifer, Caroline Wieczoreck, Mirjam Koker, Michaela A. Ihle, et al. "Abstract 1690: Attacking EGFR mutant lung cancer by combined EGFR and c-Met inhibition." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1690.

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Momcilovic, Milica, Sean T. Bailey, Jason T. Lee, Daniel Braas, Thomas G. Graeber, Melissa Works, Francesco Parlati, et al. "Abstract 1830: Targeted inhibition of EGFR and glutaminase induces metabolic crisis in EGFR mutant lung cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1830.

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Momcilovic, Milica, Sean T. Bailey, Jason T. Lee, Clara Magyar, Daniel Braas, Thomas Graeber, Francesco Parlati, et al. "Abstract B28: Targeted inhibition of EGFR and glutaminase induces metabolic crisis in EGFR-mutant lung cancer." In Abstracts: Fifth AACR-IASLC International Joint Conference: Lung Cancer Translational Science from the Bench to the Clinic; January 8-11, 2018; San Diego, CA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.aacriaslc18-b28.

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Whitley, Alexander, Somaira Nowsheen, Tiffiny Cooper, Albert LoBuglio, James Bonner, and Eddy S. Yang. "Abstract 4684: Synthetic lethal interaction between EGFR and PARP inhibition." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4684.

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Quesnelle, Kelly M., Sonali C. Joyce, and Jennifer R. Grandis. "Abstract C47: Dual kinase inhibition of EGFR and HER2 can overcome resistance to an EGFR‐targeting agent." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-c47.

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Madden, Julie, Kelly Mueller, Aliccia Bollig-Fischer, Paul Stemmer, and Julie Boerner. "Abstract 1068: Inhibition of the phosphorylation of eIF4 molecules sensitizes EGFR expressing breast cancers to EGFR inhibitors." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1068.

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Koh, King Xin, Bhaskar Bhattacharya, Joanne Loh, Hong Kiat Ng, Ross Soo, Barry Iacopetta, and Richie Soong. "Abstract 5650: Determinants of acquired resistance to PI3K/mTOR inhibition in cells refractory to EGFR inhibition." 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.am2013-5650.

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Scharadin, Tiffany M., Matthew Saldana, Michael Schlein, Steven Hoang-Phou, Denise Trans, Dennis Chang, Wei He, et al. "Abstract 3321: Using NLPs to study EGFR structure, activation, and inhibition." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3321.

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Zhao, Tianna, Riccardo Serra, Michelle Guo, Peter C. Burger, Lisa M. Rooper, Betty Tyler, Christine L. Hann, and Gary L. Gallia. "CDKS Blockade Enhances In Vivo Efficacy of EGFR Inhibition in Chordomas." In Special Virtual Symposium of the North American Skull Base Society. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1725264.

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Reports on the topic "EGFR-Inhibition"

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Lee, Michael J. Systems-Level Analysis of EGFR Inhibition-DNA Damage Combination Treatment in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada568739.

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Lee, Michael J. Systems-Level Analysis of EGFR Inhibition-DNA Damage Combination Treatment in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2011. http://dx.doi.org/10.21236/ada555032.

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Afaq, Farrukh. Delphinidin: A Novel Agent for Inhibition of Breast Tumor Kinase Signaling by Targeting EGFR. Fort Belvoir, VA: Defense Technical Information Center, August 2006. http://dx.doi.org/10.21236/ada462406.

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