Gotowe bibliografie tematyczne / EGFR

Gotowa bibliografia na temat „EGFR”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 6 lipca 2024

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Artykuły w czasopismach na temat "EGFR"

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Chemmalar, S., A. R. Intan Shameha, Che Azurahanim Che Abdullah, Nor Asma Ab Razak, Loqman Mohamad Yusof, Mokrish Ajat, Kim Wei Chan i Md Zuki Abu Bakar Zakaria. "Busting the Breast Cancer with AstraZeneca’s Gefitinib". Advances in Pharmacological and Pharmaceutical Sciences 2023 (4.12.2023): 1–26. http://dx.doi.org/10.1155/2023/8127695.

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Breast cancer is the most common cancer diagnosed in women, and in 2020, there were 684, 996 deaths due to this disease. Epidermal growth factor receptors (EGFRs) and their respective ligands have been blamed for the pathogenesis and resistance to treatment in specific breast cancer cases. With EGFR having four homologues: EGFR1, EGFR2, EGFR3, and EGFR4, in-depth understanding of EGFR biology led to the discovery of small-molecule inhibitors and antibodies against this receptor. Gefitinib (GEF), a tyrosine kinase inhibitor of EGFR1, possesses a vast potential for treatment against breast cancer and is supported by a multiplicity of experiments. Unfortunately, in clinical trials, GEF did not show the outcomes expected with complete response and disease progress. This is due to incomplete understanding of the molecular mechanisms involved in EGFR signaling and endocrine sensitivity. Hence, additional in-depth experiments are needed regarding various molecular pathways and crosstalk pathways to comprehend GEF’s action mechanism thoroughly in breast cancer patients. In this review, the role of EGFR in the development and pathogenesis of breast cancer and the pharmacokinetics and pharmacotherapy of GEF for the treatment of breast cancer have been elaborated. Nanomedicines synthesized with GEF have shown positive experimental response, paving a promising path for GEF against breast cancer.
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Rengifo, Charles E., Rancés Blanco, Damián Blanco, Mercedes Cedeño, Milagros Frómeta i Enrique Rengifo Calzado. "Immunohistochemical Characterization of Three Monoclonal Antibodies Raised against the Epidermal Growth Factor and Its Receptor in Non-Small-Cell Lung Cancer: Their Potential Use in the Selection of Patients for Immunotherapy". Journal of Biomarkers 2013 (11.12.2013): 1–9. http://dx.doi.org/10.1155/2013/627845.

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Adequate methods to identify which lung cancer patients are most likely to benefit from the targeted drugs against both epidermal growth factor receptor/epidermal growth factor (EGFR/EGF) are needed. For this reason, we evaluated both the tissue reactivity of ior egf/r3 monoclonal antibody (Mab) in human lung carcinomas and its biological activity in NCI-H125 cells. Additionally, we assessed the tissue expression of EGF using two Mabs, CB-EGF1 and CB-EGF2. The overexpression of EGFR was detected in 33.33% and 62.71% of small-cell lung carcinoma (SCLC) and non-small-cell lung carcinoma (NSCLC), respectively. The ability of ior egf/r3 Mab to bind the extracellular domain of EGFR inhibiting cell proliferation and inducing apoptosis in NCI-H125 cells was also demonstrated. The EGF expression was observed in about 17% and 70% of SCLC and NSCLC, respectively. However, differences in the reactivity of CB-EGF1 and CB-EGF2 were evidenced. A dual expression of EGFR and EGF was observed in 16.67% and 57.63% of SCLC and NSCLC patients, respectively. But, a correlation between them was only obtained in NSCLC. Our results permit to recommend the development of diagnostic kits using ior egf/r3 and/or CB-EGF1 Mabs in order to achieve a better selection of patients to EGFR/EGF-targeting treatment.
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Jezierska, Michalina, Anna Owczarzak i Joanna Stefanowicz. "Dimethylarginines in Children after Anti-Neoplastic Treatment". Medicina 58, nr 1 (11.01.2022): 108. http://dx.doi.org/10.3390/medicina58010108.

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Background and Objectives: According to a recent Cochrane systematic review, renal impairment can develop in 0–84% of childhood cancer survivors in the future. The renal function impairment in this patient group can be related to nephrectomy, nephrotoxic agents therapy, abdominal radiotherapy, and combinations of these treatment methods. In this study, in a population of patients after anti-neoplastic therapy, with particular emphasis on patients after Wilms’ tumour treatment, we compared new substances which play role in the chronic kidney disease (CKD) pathogenesis (asymmetric dimethylarginine—ADMA, symmetric dimethylarginine—SDMA) with standard renal function markers (e.g., creatinine and cystatin C in serum, creatinine in urine, etc.) to assess the usefulness of the former. Materials and Methods: Eighty-four children, without CKD, bilateral kidney tumours, congenital kidney defects, or urinary tract infections, with a minimum time of 1 year after ending anti-neoplastic treatment, aged between 17 and 215 months, were divided into three groups: group 1—patients after nephroblastoma treatment (n = 21), group 2—after other solid tumours treatment (n = 44), and group 3—after lymphoproliferative neoplasms treatment (n = 19). The patients’ medical histories were taken and physical examinations were performed. Concentrations of blood urea nitrogen (BUN), creatinine, cystatin C, C-reactive protein (CRP), ADMA, and SDMA in blood and albumin in urine were measured, and a general urine analysis was performed. The SDMA/ADMA ratio, albumin–creatine ratio, and estimated glomerular filtration rate (eGFR) were calculated. eGFR was estimated by three equations recommended to the paediatric population by the KDIGO from 2012: the Schwartz equation (eGFR1), equation with creatinine and urea nitrogen (eGFR2), and equation with cystatin C (eGFR3). Results: Both the eGFR1 and eGFR2 values were significantly lower in group 1 than in group 3 (eGFR1: 93.3 (83.1–102.3) vs. 116.5 (96.8–126.9) mL/min/1.73 m2, p = 0.02; eGFR2: 82.7 (±14.4) vs. 94.4 (±11.9) mL/min/1.73 m2, p = 0.02). Additionally, there were weak positive correlations between SDMA and creatinine (p < 0.05, r = 0.24), and cystatin C (p < 0.05, r = 0.32) and weak negative correlations between SDMA and eGFR1 (p < 0.05, r = −0.25), eGFR2 (p < 0.05, r = −0.24), and eGFR3 (p < 0.05, r = −0.32). Conclusions: The usefulness of ADMA and SDMA in the diagnosis of renal functional impairment should be assessed in further studies. eGFR, calculated according to equations recommended for children, should be used in routine paediatric practice.
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Al-Shaibani, Eshrak, Taylor Young, Eshetu Atenafu, Verna Cheung, Safwan Alsibai, Vikas Gupta, Dawn C. Maze, Marta Beata Davidson, Aniket Banker i Hassan Sibai. "Impact of Kidney Dysfunction on Overall Survival in Myeloproliferative Neoplasms: A Single-Center Retrospective Study". Blood 142, Supplement 1 (28.11.2023): 6439. http://dx.doi.org/10.1182/blood-2023-189318.

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Introduction: Myeloproliferative neoplasms (MPN) are clonal hematopoietic stem cell disorders that can lead to the deposition of fibrous tissue, and by a propensity toward extramedullary hematopoiesis. The progression of kidney function and frequency of chronic kidney disease (CKD) in patients with MPN is unknown, although CKD is linked to increased mortality. In our study, we aimed to investigate the relationship between kidney function as measured by glomerular filtration rate (eGFR) and MPN disease and risk of thrombosis. Moreover, we analyzing the risk factors for CKD, impact of different treatment modalities and effect of CKD on survival. Patients & Method: We haveretrospectively screened 762 patients between Jan 1989 to May 2019 with MPN at Princess Margaret Cancer Centre. Diagnosis, of Polycythemia (PV), essential thrombocytosis (ET), and myelofibrosis (MF; comprising PMF, post-ET-PMF, and post-PV-PMF) was required as defined by the WHO classification. Patients with other MPNs (CNL, CEL, HES, MDS/MPN, MPN-U, Mastocytosis accelerating phase MPN and blast phase) or missing serial creatinine measurement or their CKD attributed to other causes (diabetic nephropathy, High blood pressure, polycystic kidney disease obstructive uropathy, Glomerulonephritis before MPN diagnosis and other) were excluded, resulting in study sample of 232 patients. The total cohort was subdivided according to the calculated eGFR, (ml/min/1.73m2) into eGFR1 (≥90, n=154), eGFR2 (60-89, n=12), and eGFR3 (&lt;60, n=66). eGFR was collected retrospectively, because of small number of patients, we combined eGFR2 and eGFR3 in one group. Overall Survival (OS) was calculated using the Kaplan-Meier and log-rank test was used to assess impact variables of interest. Cox proportional hazards model was used to assess for prognostic factors of OS as well as to assess the joint effect of potential prognostic factors. Results: Median age for the total cohort was 58 years (range;18-88.3), 54% were male. Median follow-up duration was 86 months (range:45.5-135). Diagnosis of MPN involved ET; n=21(9%)), PV; n=32 (14%) and MF; n=179 (77%). JAK2V617F status was documented in 219 patients; 67% were positive; of 106 patients analyzed for CARL 40.6% were positive. Cardiovascular risk factors were higher in PV and MF than in ET (59.4%, 57% &38%) respectively. A higher uric acid and LDH levels were found in PV and MF. A total of 19% had a history of thrombosis and rate was higher in ET (28.6%) than PV (21.9%) or MF (16.8%). Further patient's characteristics summarized in Table1. Kidney biopsy performed in 8 patients. The most prominent histological finding included focal segmental glomerulosclerosis (n=3), Ig A nephropathy (n=3), mesangial hypercellularity and sclerosis, extramedullary haematopoiesis (n=1) and lupus nephritis (n=1). The risk factors for CKD based on eGFR group are presented in (Table 2). MPN diagnosis is a significant risk factor for kidney function (p=0.0117). In MF a higher rate of eGFR 88.5% compared with PV and ET. JAK2V617 demonstrates a significant impact on abnormal eGFR (p=0.05);. IPSS and DIPSS score are a significant risk factor for kidney dysfunction (p=0.0014, and 0.0074 respectively). High uric acid levels and neutrophil counts were higher in high eGFR group (p=0.0014, and 0.0074 respectively). No association found between thrombosis and high eGFR. Hydroxyurea treatment does not have an impact on CKD, however, more patients received Ruxolitinb in abnormal eGFR (p=0.001). CKD has significant impact on OS. The 5 years OS for eGFR1 was 75% (95% CI 67%-81%), and for abnormal eGFR was 63.9% (95% CI 52%-73%), p=0004 (Fig 1). Conclusion: Higher incidence of kidney dysfunction associated in MF compared to PV and ET, there was no association between thrombosis and high eGFR as we excluded all other cause of CKD. MF with abnormal eGFR associated with high DIPSS score. MPN patients with kidney dysfunction significantly affects OS, which indicate close monitoring and prospective study is required.
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Maennling, Amaia Eleonora, Mehmet Kemal Tur, Marcus Niebert, Torsten Klockenbring, Felix Zeppernick, Stefan Gattenlöhner, Ivo Meinhold-Heerlein i Ahmad Fawzi Hussain. "Molecular Targeting Therapy against EGFR Family in Breast Cancer: Progress and Future Potentials". Cancers 11, nr 12 (20.11.2019): 1826. http://dx.doi.org/10.3390/cancers11121826.

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The epidermal growth factor receptor (EGFR) family contains four transmembrane tyrosine kinases (EGFR1/ErbB1, Her2/ErbB2, Her3/ErbB3 and Her4/ErbB4) and 13 secreted polypeptide ligands. EGFRs are overexpressed in many solid tumors, including breast, pancreas, head-and-neck, prostate, ovarian, renal, colon, and non-small-cell lung cancer. Such overexpression produces strong stimulation of downstream signaling pathways, which induce cell growth, cell differentiation, cell cycle progression, angiogenesis, cell motility and blocking of apoptosis.The high expression and/or functional activation of EGFRs correlates with the pathogenesis and progression of several cancers, which make them attractive targets for both diagnosis and therapy. Several approaches have been developed to target these receptors and/or the EGFR modulated effects in cancer cells. Most approaches include the development of anti-EGFRs antibodies and/or small-molecule EGFR inhibitors. This review presents the state-of-the-art and future prospects of targeting EGFRs to treat breast cancer.
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Huang, Hsien-Neng, Pin-Feng Hung, Yai-Ping Chen i Chia-Huei Lee. "Leucine Zipper Downregulated in Cancer-1 Interacts with Clathrin Adaptors to Control Epidermal Growth Factor Receptor (EGFR) Internalization and Gefitinib Response in EGFR-Mutated Non-Small Cell Lung Cancer". International Journal of Molecular Sciences 25, nr 3 (23.01.2024): 1374. http://dx.doi.org/10.3390/ijms25031374.

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The epidermal growth factor receptor (EGFR) is a common driver of non-small cell lung cancer (NSCLC). Clathrin-mediated internalization (CMI) sustains EGFR signaling. AXL is associated with resistance to EGFR-tyrosine kinase inhibitors (TKIs) in EGFR-mutated (EGFRM) NSCLC. We investigated the effects of Leucine zipper downregulated in cancer-1 (LDOC1) on EGFR CMI and NSCLC treatment. Coimmunoprecipitation, double immunofluorescence staining, confocal microscopy analysis, cell surface labelling assays, and immunohistochemistry studies were conducted. We revealed that LDOC1 interacts with clathrin adaptors through binding motifs. LDOC1 depletion promotes internalization and plasma membrane recycling of EGFR in EGFRM NSCLC PC9 and HCC827 cells. Membranous and cytoplasmic EGFR decreased and increased, respectively, in LDOC1 (−) NSCLC tumors. LDOC1 depletion enhanced and sustained activation of EGFR, AXL, and HER2 and enhanced activation of HER3 in PC9 and HCC827 cells. Sensitivity to first-generation EGFR-TKIs (gefitinib and erlotinib) was significantly reduced in LDOC1-depleted PC9 and HCC827 cells. Moreover, LDOC1 downregulation was significantly associated (p < 0.001) with poor overall survival in patients with EGFRM NSCLC receiving gefitinib (n = 100). In conclusion, LDOC1 may regulate the efficacy of first-generation EGFR-TKIs by participating in the CMI of EGFR. Accordingly, LDOC1 may function as a prognostic biomarker for EGFRM NSCLC.
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Nicholson, Christopher J., Samuel J. Roth, Arudhir Singh, Caitlin Brown, Simon P. Fricker, Jon Hu i Samantha Dale Strasse. "Abstract C052: Circumventing EGFR inhibitor resistance in NSCLC using transomics". Molecular Cancer Therapeutics 22, nr 12_Supplement (1.12.2023): C052. http://dx.doi.org/10.1158/1535-7163.targ-23-c052.

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Abstract Drug discovery continues to be refined to enhance efficiency, yet &gt;80% of new drugs fail in the clinical trial stage. It is apparent that a novel approach is needed. COMPASS is a transomic analysis platform that integrates data across multiple omics layers; genomics, transcriptomics, proteomics, and phosphoproteomics. This analysis allows us to interpret complex biological relationships and provide a functional map of the biochemical drivers of disease. We have used EGFR inhibitor (EGFRi) resistance as a case study. EGFRi have been successful in treating non-small cell lung cancer (NSCLC) patients with activating EGFR mutations (EGFRm), however, this success is temporary. The emergence of resistance is a problem and limits long-term treatment for many patients, even with osimertinib, a third-generation inhibitor and current standard of care. As resistance to EGFRi occurs through mutations in EGFR we adopted a novel strategy using COMPASS to identify and validate alternative, non-EGFR targets that could potentially recapitulate the pharmacological effects of EGFRi in EGFRm NSCLC. The transomic signatures of EGFRi were generated using a NSCLC cell line containing the activating mutation ex19del. The drug concentration required to inhibit cell growth (IC50) was first determined. For transomic analyses, cells were incubated for 24 h with the drug IC50 concentration and harvested for genomic, transcriptomic, proteomic, and phosphoproteomic analyses. We have previously shown transomics analysis can differentiate between EGFRi that have been designed to treat EGFRm NSCLC with the transomics signature for osimertinib being significantly different from comparator drugs that failed during drug development. We employed our proprietary target prioritization algorithm to further analyze the omics data to identify and rank novel targets. Targets were then filtered to select those with an available pharmacological tool compound (PTC). The PTCs were used to evaluate the targets in a xenograft model of osimertinib resistant NSCLC, PC9-Del19/T790M/C797S; which contains the activating EGFR mutation (ex19del), and two mutations conferring EGFRi resistance, T790M gatekeeper mutation, and C797S which confers resistance to osimertinib. Of the targets tested 82% (9/11) were associated with &gt;25% inhibition of tumor growth. Furthermore, 36% (4/11) targets were associated with &gt;50% inhibition by the PTCs, with inhibition of one target giving &gt;85% inhibition resulting in stasis of tumor growth. Future work will investigate targets using gene silencing, as PTCs were not available for many of the novel high-ranked targets. These data show that using COMPASS transomic analysis, it is possible to identify novel drug targets to treat difficult-to-treat cancers such as EGFRi-resistant NSCLC and provides validation of this discovery platform by disease-relevant in vivo pharmacology. Further validation studies are ongoing against other difficult-to-treat cancers to identify novel clinical targets and drug candidates. Citation Format: Christopher J Nicholson, Samuel J Roth, Arudhir Singh, Caitlin Brown, Simon P Fricker, Jon Hu, Samantha Dale Strasse. Circumventing EGFR inhibitor resistance in NSCLC using transomics [abstract]. In: Proceedings of the AACR-NCI-EORTC Virtual International Conference on Molecular Targets and Cancer Therapeutics; 2023 Oct 11-15; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2023;22(12 Suppl):Abstract nr C052.
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Kumar, Sachin, Jeff Vassallo, Kalpana Nattamai, Jose A. Cancelas i Hartmut Geiger. "EGFR Signaling in Osteoblasts Regulates Circadian Rhythm of HSPC in Circulation". Blood 126, nr 23 (3.12.2015): 665. http://dx.doi.org/10.1182/blood.v126.23.665.665.

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Abstract EGFR signaling regulates growth, differentiation, proliferation and migration in multiple organ systems. We previously demonstrated that inhibition of EGFR signaling on hematopoietic stem and progenitor cells (HSPCs) enhances G-CSF induced stem cell mobilization, while preliminary data suggested that inhibition of EGFR signaling in the stem cell niche actually had the opposite effect of inhibiting mobilization (Ryan et al., Nat Med, 2010). We thus tested the novel hypothesis that there is a role for EGFR signaling in the bone marrow (BM) niche with respect to regulating hematopoiesis. We utilized a set of mouse strains that express the recombinase Cre under distinct promoters to specifically delete EGFR in various types of stroma cells including Col-Cre; EGFRf/f (deletion in osteoprogenitor/osteoblasts (OBs)), Dermo-Cre; EGFRf/f (mesenchymal stem cells (MSCs) including chondrocytes and OB), Tie2-Cre; EGFRf/f (Endothelial cells) and Nestin-Cre; EGFRf/f (Schwann/neural cells) and compared them to no Cre-EGFRf/f mice as control wild type for EGFR. Basic parameters of steady-state hematopoiesis were not altered in mice devoid of EGFR signaling in the various types of stroma cells listed above. We further investigated HSPC mobilization in EGFRf/f mice and interestingly, Col-cre and Dermo-cre EGFRf/f mice exhibited a lower number of circulating HSPC in blood in comparison to wild type mice, as determined by colony forming units (CFUs) or flow cytometry. Deletion of the EGFR in endothelial (Tie2-Cre) and neuronal (Nestin-Cre) compartments did not result in a decline in the number of circulating HSPCs. Upon G-CSF challenge, Col-cre and Dermo-cre EGFRf/f mice mobilized HSPCs similar to controls, suggesting that EGFR signaling in OBs/MSCs is dispensable for G-CSF induced mobilization. HSPCs circulation under steady state follows a circadian rhythm. We next tested whether EGFR signaling in OBs might play a role in circadian rhythm driven HSPC circulation. After 5 hours of light cycle i.e. Zeitgeber time-5 (ZT-5), when the number of circulating HSPCs is high, Col-Cre EGFRf/f and Dermo-Cre EGFRf/f mice presented with low numbers of circulating HSPCs. After 13 hours of light cycle (ZT-13) (low number of circulating HSPCs), the number of HSPCs in blood in Col-Cre EGFRf/f and Dermo-Cre EGFRf/f mice were similar to controls. Together, this suggests that EGFR signaling in OBs is essential for the rhythmic increase in circulating HSPC in blood at ZT5. Currently, we are investigating molecular mechanisms driven by EGFR signaling in OBs that regulate HSPC retention in BM and circadian regulation of EGFR signaling. In summary, our data suggest an important and also very specific (no other phenotype altered) role of EGFR signaling for regulating the circadian rhythm of HSPC circulation in peripheral blood. Disclosures No relevant conflicts of interest to declare.
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Zhou, Caicun, Fumio Imamura, Ying Cheng, Isamu Okamoto, Byoung Chul Cho, Meng Chih Lin, Margarita Majem i in. "Early clearance of plasma EGFR mutations as a predictor of response to osimertinib and comparator EGFR-TKIs in the FLAURA trial." Journal of Clinical Oncology 37, nr 15_suppl (20.05.2019): 9020. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.9020.

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9020 Background: In the Phase III FLAURA trial (NCT02296125), osimertinib, a third generation EGFR-TKI, showed superior efficacy to comparator EGFR-TKIs as first line treatment for EGFR mutation-positive (EGFRm) advanced NSCLC. In an exploratory analysis, we investigated clinical outcomes associated with detection of plasma EGFRm at 3 or 6 weeks (wks) after start of treatment. Methods: Treatment-naïve patients (pts) with EGFRm (ex19del or L858R) locally advanced or metastatic NSCLC were randomized 1:1 to receive osimertinib 80 mg once daily (QD) or comparator EGFR-TKIs (gefitinib 250 mg QD or erlotinib 150 mg QD). Plasma EGFR mutation analysis was conducted at baseline (BL), wks 3 and 6 by droplet digital PCR. Clearance was defined as undetectable levels of EGFRm in ctDNA at wks 3/6, where they were detectable at BL. Progression-free survival (PFS) was investigated based on early clearance of EGFRm. Results: In total 489/556 (88%) pts (osimertinib: 244/279; comparator: 245/277) had evaluable ctDNA at BL and wks 3/6. Of these, 342/489 (70%; osimertinib: 168/244; comparator: 174/245) had detectable BL EGFRm and were included in this analysis. See table. Conclusions: Clearance of plasma EGFRm after 3/6 wks of EGFR-TKI therapy was associated with a numerical improvement in PFS. The efficacy of osimertinib was superior to comparator EGFR-TKIs regardless of clearance status. Clinical trial information: NCT02296125. [Table: see text]
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Lee, Eugine, Padraich Flahardy, Cameron Vergato, Stephen Siecinski, Justin Chen, Charles O’Donnell, Graeme Hodgson, Defne Yarar i Thomas McCauley. "Abstract 1726: Targeted epigenomic control of MYC as a strategy to treat EGFR inhibitor-resistant NSCLC". Cancer Research 84, nr 6_Supplement (22.03.2024): 1726. http://dx.doi.org/10.1158/1538-7445.am2024-1726.

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Abstract EGFR tyrosine kinase inhibitors (EGFRi) have improved outcomes for non-small cell lung cancer (NSCLC) patients harboring activating EGFR mutations. However, patients receiving EGFRi therapy frequently relapse with an EGFR T790M mutation. While osimertinib, a third generation EGFRi, blocks EGFR T790M activity, resistance eventually develops through various EGFR-dependent and EGFR-independent mechanisms, such as acquiring additional mutations in EGFR (e.g. C797S), activating bypass signaling pathways, or undergoing an epithelial to mesenchymal transition (EMT). MYC is a master transcription factor critical for mediating oncogenic signal transduction and has been implicated in EGFRi resistance, suggesting that MYC targeting may overcome multiple EGFRi resistance mechanisms. To evaluate this, we have developed a NSCLC-specific programmable epigenomic mRNA therapy, termed a MYC epigenomic controller (NSCLC MYC-EC), designed to selectively target regulatory elements in MYC’s insulated genomic domain and downregulate MYC expression. We have previously shown that NSCLC MYC-EC effectively decreases MYC expression pre-transcriptionally and have demonstrated that MYC-EC combination with osimertinib synergistically reduces viability of EGFR mutant NSCLC cells. Here, we demonstrate NSCLC MYC-EC activity in models that have developed EGFRi resistance through EGFR-dependent and -independent mechanisms. To test the effect of NSCLC MYC-EC in NSCLC cells with T790M mutant EGFR, we treated H1975 (L858R, T790M) and PC9-T790M cells (del19, engineered T790M) with MYC-EC alone or in combination with osimertinib. MYC-EC combination with osimertinib enhanced MYC protein downregulation and synergistically reduced cell viability in both models. To evaluate the effect of MYC-EC in osimertinib-resistant cells, we engineered H1975 and PC9-T790M cells with an EGFR C797S mutation. While osimertinib treatment did not impact cell viability in these models, MYC-EC maintained activity, downregulating MYC levels and reducing cell viability. To investigate MYC-EC activity in cells with alternative resistance mechanisms, we generated osimertinib-resistant H1975 cells by stepwise dose escalation. Protein analysis showed highly reduced phospho-EGFR levels, suggesting an EGFR-independent mechanism of survival. RNA-sequencing analysis revealed that EMT pathway was highly activated in these resistant cells. Importantly, this model retained sensitivity to NSCLC MYC-EC treatment, demonstrating that selectively targeting MYC can treat osimertinib-resistant NSCLC cells with a mesenchymal phenotype. Together, these data demonstrate that pre-transcriptional downregulation of MYC through NSCLC MYC-EC treatment effectively inhibits viability of EGFRi-resistant NSCLC through both EGFR-dependent and -independent mechanisms and supports the development of NSCLC MYC-EC in EGFRi-resistant NSCLC. Citation Format: Eugine Lee, Padraich Flahardy, Cameron Vergato, Stephen Siecinski, Justin Chen, Charles O’Donnell, Graeme Hodgson, Defne Yarar, Thomas McCauley. Targeted epigenomic control of MYC as a strategy to treat EGFR inhibitor-resistant NSCLC [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 1726.
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Rozprawy doktorskie na temat "EGFR"

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Barbosa, Keila Cardoso. "Estudo de polimorfismos dos genes EGF e EGFR em astrocitomas difusamente infiltrativos". Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5138/tde-24062008-150231/.

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INTRODUÇÃO: Os astrocitomas difusamente infiltrativos são os tumores mais freqüentes de Sistema Nervoso Central (SNC) com uma taxa de 5-7 novos casos por 100.000 pessoas ano. São tumores altamente invasivos e estão associados com alterações de alguns genes como EGF (fator de crescimento epidérmico) e o EGFR (receptor do fator de crescimento epidérmico), que podem criar um aumento da atividade mitogênica, acarretando aumento de proliferação e maturação celular, apoptose, angiogênese e metástase. O nível de expressão destes genes pode ser influenciado por alterações genéticas, como a presença de polimorfismos. Uma mudança única de base (SNP) pode alterar a expressão gênica e, sendo assim, estar associada ao aumento do risco de desenvolver astrocitomas. Nesse trabalho, foram analisados 2 SNPs na região não traduzida (c.-191C>A e c.-216G>T) e um SNP no exon 16 (c.2073A>T) do gene EGFR, e um outro SNP na região não traduzida no gene EGF (c.61A>G). Os SNPs foram associados a expressão gênica do EGFR e a sobrevida dos pacientes. MÈTODOS: Foi realizado um estudo caso-controle com 193 casos de astrocitomas difusamente infiltrativos e 200 controles por amplificação por PCR seguido de digestão enzimática. Os produtos digeridos das amostras foram analisados por eletroforese em gel de agarose e poliacrilamida e corados com brometo de etídeo. A expressão gênica foi realizada após extração de RNA do tecido tumoral seguida de transcrição reversa e PCR em tempo real. Testes de qui-quadrado, odds ratio (OR), intervalo de confiança 95% (IC95%), t de Student e curvas de Kaplan-Meier foram realizados para análises estatística. RESULTADOS: A análise das freqüências dos genótipos dos polimorfismos mostrou uma diferença na distribuição entre casos e controles para o polimorfismo c.2073A>T. Pacientes com o genótipo TT apresentou um menor risco para astrocitoma quando comparados com o genótipo AA (OR=0,51, IC95%=0,29-0,99). Nenhuma correlação foi encontrada para os outros polimorfismos analisados. Também não foi encontrada correlação entre os genótipos dos polimorfismos e os níveis de expressão de EGFR e a sobrevida dos pacientes. CONCLUSÃO: Nosso trabalho mostrou haver um possível fator de proteção quando o paciente é portador do genótipo TT, o que pode levar a uma diminuição do risco de desenvolver o tumor. Pacientes com genótipo TT do polimorfismo c.2073A>T do gene EGFR apresentam um menor risco para astrocitomas difusamente infiltrativos do que os com o genótipo AA.
INTRODUCTION: Diffusely infiltrative astrocytomas are the most frequent tumors of the Central Nervous System (CNS) with a rate of 5-7 new cases in 100,000 individuals per year. They are highly invasive, and they are associated to alterations in some genes as EGF (epidermal growth factor) and EGFR (epidermal growth factor receptor), which may increase mitogenic activity, leading to increase of proliferation, cellular maturation, apoptosis, angiogenesis, and metastasis. Genetic alterations, as presence of polymorphisms of single nucleotide change (SNP) could influence their expression level, and thus could be associated to increased risk in developing astrocytomas. In the present study, two SNP of non-coding region (c.-191C>A and c.-216G>T) and one SNP in exon 16 (c.2073A>T) of EGFR, and another SNP of non-coding region of EGF (c.61A>G) were analyzed. The SNPs were associated to EGFR expression level and to survival time. METHOD: a case-control study of 193 of diffusely infiltrative astrocytomas and 200 controls was carried out, with PCR amplification and enzymatic digestion, which products were analyzed in agarose gel or polyacrylamide gel electrophoresis stained by ethidium bromide. EGFR expression level was studied by real time PCR after RNA extraction followed by reverse transcription of tumor tissues compared to epileptic non-neoplastic brain tissues. Stastistical analysis were performed by chi-square, odds ratio (OR), 95% confidence interval (95% CI), Student-t test and Kaplan Meier. RESULTS: The polymorphic genotype frequency was different between case and controls for the polymorphism c.2073A>T. Patients with TT genotype presented lower risk to develop astrocytoma when compared to genotype AA (OR=0.51, CI95%=0.29- 0.99). No other correlation was observed for the remaining studied polymorphisms. There was neither correlation between the polymorphic genotypes and the EGFR expression levels nor with survival time. CONCLUSION: The present study showed a possible protection factor in developing astrocytomas for the patients harboring the genotype TT of c.2073A>T polymorphism of EFGR, thus the patients presenting TT genotype have lower risk to develop diffusely infiltrative astrocytoma than patients presenting the genotype AA.
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Bauer, Philip [Verfasser]. "Der Einfluss der EGFR Expressionsdichte auf die EGFR Antikörper gerichteten Abwehrmechanismen / Philip Bauer". Kiel : Universitätsbibliothek Kiel, 2017. http://d-nb.info/1127044206/34.

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Hamilton, S. J. "An investigation of EGFR binding and modulation of EGFR signalling pathways using synthetic peptides". Thesis, Queen's University Belfast, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403480.

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Balko, Justin M. "THE PHARMACOGENOMICS OF EGFR-DEPENDENT NSCLC: PREDICTING AND ENHANCING RESPONSE TO TARGETED EGFR THERAPY". Lexington, Ky. : [University of Kentucky Libraries], 2009. http://hdl.handle.net/10225/1062.

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Thesis (Ph. D.)--University of Kentucky, 2009.
Title from document title page (viewed on September 17, 2009). Document formatted into pages; contains: viii, 175 p : ill. (some col.). Includes abstract and vita. Includes bibliographical references (p. 103-123).
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Januário, Mara Elisama da Silva. "Estudo da função de AP1y2 e Alix no direcionamento de proteínas para degradação em lisossomos ou liberação em vesículas extracelulares". Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/17/17136/tde-23042018-164806/.

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A degradação lisossomal de proteínas de membrana endocitadas ocorre por meio do direcionamento destas proteínas para vesículas intralumenais (ILVs), formadas no lúmen dos corpos multivesiculares (MVBs), e subsequente fusão dos MVBs com lisossomos. Apesar de sua importância na degradação de proteínas transmembrana, os MVBs possuem outra importante função, a de produzir e liberar vesículas extracelulares (EVs). Neste processo os MVBs não se fundem com lisossomos, mas sim com a membrana plasmática o que resulta na liberação das vesículas residentes no interior dos MVBs para o meio extracelular. Diversas proteínas participam do direcionamento de cargas para os MVBs. Os estudos que delinearam a via de tráfego mediada por AP1 concentraram-se nos complexos contendo a subunidade ?1 que medeia o transporte de proteínas entre a rede trans-Golgi (TGN) e endossomos. Contudo, o genoma humano codifica uma segunda isoforma desta subunidade, denominada ?2, e evidências presentes na literatura e também observadas por nosso grupo indicam que AP1?2 pode regular uma via de tráfego distinta da via classicamente atribuída a AP1. Utilizando ensaios de uptake de EGF em condições onde foi realizado o KD de ?1 ou ?2, foi observado que o silenciamento de ?2 prejudica a degradação de EGF internalizado por seu receptor. Efeito também observado para o próprio receptor de EGF (EGFR) em ensaios de biotinilação da superfície celular. Demonstrando que a degradação lisossomal do complexo EGF-EGFR pela via canônica dos MVBs requer o complexo AP1?2, mas não AP1?1. Em conjunto com este estudo também foi analisado o mecanismo molecular de direcionamento da proteína Nef do HIV-1 para os MVBs associados a liberação de EVs. A proteína Nef do HIV é determinante na modulação do ambiente intracelular favorecendo a replicação do vírus e progressão à AIDS. Nef é ativamente secretado em EVs e sua liberação pode levar a apoptose de células vizinhas aceptoras dessas vesículas. Nef também medeia a redução dos níveis de CD4 e moléculas de MHC-I em EVs. Ainda não é conhecido o mecanismo molecular utilizado por Nef para ser exportado em EVs, mas sabe-se que Nef interage fisicamente com a proteína II acessória da maquinaria ESCRT, Alix, importante no processo de formação das ILVs e seleção das cargas que serão internalizadas nos MVBs. EVs coletadas de células HeLa e linfócitos T CD4+ silenciados para Alix demostraram reduções significativas na liberação de Nef. Estes resultados indicam que Nef requer Alix para sua eficiente liberação em EVs.
Lysosomal degradation of endocytosed membrane proteins occurs through the targeting of these proteins to intraluminal vesicles (ILVs), formed in the multivesicular bodies (MVBs) lumen, and the subsequent fusion of MVBs with lysosomes. Despite its importance in the degradation of transmembrane proteins, MVBs have another important function, the production and release of extracellular vesicles (EVs). In this process, the MVBs do not fuse with lysosomes, but fuse with the plasma membrane resulting in the release of these vesicles that reside within MVBs to the extracellular environment. Several proteins regulate the targeting of cargo to MVBs. Studies that delineated the functions of AP1 in protein trafficking, focused on complexes containing the ?1 subunit, which mediates transport between trans-Golgi network (TGN) and endosomes. However, the human genome encodes a second isoform of this subunit, named ?2. Evidences from the literature, as well as results from our research group, indicate that AP1?2 regulates transport pathways that are distinct from the pathways classically attributed to AP1. By performing EGF-uptake assays under ?1 or ?2 knockdown (KD) conditions, it was observed that ?2 is required for degradation of internalized EGF, effect also observed for the EGF receptor (EGFR) using cell surface biotinylation assays. These results demonstrate that the lysosomal degradation of the EGFEGFR complexes via the canonical MVBs pathway requires the AP1?2 complex, but not AP1?1. In parallel with this study, we also analyzed the molecular mechanism of HIV-1 Nef targeting to MVBs associated with the EVs release. Nef is an important determinant in the modulation of the intracellular environment for efficient HIV replication and progression to AIDS. Nef is actively secreted via EVs and its release may lead to apoptosis of bystander acceptor cells. Moreover, Nef reduces the levels of CD4 and MHC-I molecules in EVs. Despite the importance of Nef release in EVs, the molecular mechanism used by Nef to be exported via EVs is unknown. Nef physically interacts with the ESCRT machinery accessory protein Alix, an important player in the process of ILVs formation and cargo selection. EVs released from HeLa cells and CD4+ T lymphocytes under Alix KD conditions demonstrated a significant IV reduction in Nef release via EVs. These results indicate that Nef requires Alix for its efficient release in EVs.
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Liccardi, G. "Nuclear EGFR modulation of DNA repair". Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1335897/.

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Overexpression of the epidermal growth factor receptor (EGFR) is associated with resistance to chemotherapy and radiotherapy. EGFR involvement, in repair of radiation-induced DNA damage, is mediated by association with the catalytic subunit of DNA protein kinase (DNAPKcs). This study investigated the role of EGFR nuclear import, and its association with DNAPKcs, on DNA repair following treatment either with cisplatin or ionizing radiation (IR). EGFR- null murine NIH3T3 cells were transfected with wild type or with mutated EGFR (mutations found in human cancers L858R, EGFRvIII and mutations in the EGFR nuclear localization signal (NLS) sequence NLS123, LNLS123). Comet assay analysis, which measures unhooking of cisplatin crosslinks and repair of IR induced strand breaks, demonstrated that wtEGFR and EGFRvIII completely repair cisplatin and IR induced DNA damage. Immunoprecipitation studies show that repair is associated with the binding of both wtEGFR and EGFRvIII to DNAPKcs, which increases by 2- fold 18 hours following cisplatin treatment. Confocal analysis and proximity ligation assay indicated that this association takes place both in the cytoplasm and in the nucleus resulting in a significant increase of DNA-PK kinase activity. Intermediate levels of repair as shown by the L858R construct with impaired nuclear localization demonstrated that EGFR kinase activity is partially involved in repair but is not sufficient to determine EGFR nuclear expression. EGFR-NLS mutants showed impaired nuclear localization and impaired DNAPKcs association resulting in significant inhibition of DNA repair and downregulation of DNA-PK kinase activity. Our data suggest that EGFR nuclear localization is required for the modulation of cisplatin and IR induced DNA damage repair. The EGFR-DNAPKcs binding is triggered by cisplatin or IR and not by EGFR nuclear translocation per se. Understanding mechanisms regulating EGFR subcellular distribution in relation to DNA repair kinetics will be a critical determinant of improved molecular targeting and response to therapy.
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Housden, B. "Notch targets and EGFR pathway regulation". Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604264.

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Previous work in the lab identified potential Notch targets in a muscle related Drosophila cell line using a combination of genome wide expression array, chromatin immunoprecipitation (ChIP) and bioinformatics approaches. My project was focussed on investigating the regulation of EGFR pathway components by Notch signalling and unravelling mechanisms by which this crosstalk is dependent on context. Previous genetic studies have demonstrated extensive crosstalk between the Notch and EGFR pathways. The unexpected result from the genome wide studies was the overrepresentative of EGFR pathway components that were direct targets. This group of nine targets included both positive and negative regulators of the pathway. One of my first goals was to validate these as direct targets, for which I used a combination of luciferase and in-vivo reporter assays. To address the question of how activation and inhibition of the EGFR pathway is resolved into a final effect on EGFR output the temporal profiles of the different components was investigated. Initial results show that there are distinct temporal activation profiles for different EGFR related genes following Notch activation. This is predicted to lead to an initial inhibition of EGFR signalling (due to fast initial inhibitor accumulation) followed by an activation of signalling (due to inhibitor decrease and activator production). Current work on this project is focussed on identifying different classes of temporal response at the genome wide scale and asking whether there is any consistency in the types of genes that adopt specific profiles. One of the challenges in dissecting the response to Notch is understanding why genes respond only in certain contexts. Argos, which encodes an EGFR inhibitor, is one example of a gene whose response to Notch signalling is context dependent. My results show that argos is positively regulated in the muscle progenitors. However, in the wing pouch, argos expression is reduced upon Notch activation. I have mapped these contrasting responses to separable enhancers, one active in the muscle precursors that I have shown to be directly regulated by Notch and the other active in the wing pouch where it integrates both EGFR and Notch signals. The latter is mediated by the Notch target E(spl)mβ and is therefore indirectly affected by Notch. Further studies to distinguish the components acting through the different enhancers revealed that the bHLH protein Twist is required for Notch activation of the muscle precursor enhancer and the wing pouch enhancer activity appears to involve an interplay between general activation and restricted repressors.
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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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Oliveira, Carolina Barbara Nogueira de, Ivan Andrade de Araújo Penna i Antonio Marcos Saraiva. "Avaliação de polimorfismos nos genes EGF e EGFR e a susceptibilidade à pré-eclâmpsia severa". Universidade Federal Fluminense, 2012. https://app.uff.br/riuff/handle/1/4715.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico
Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
Fundação Oswaldo Cruz. Instituto Nacional de Controle de Qualidade em Saúde (INCQS-Fiocruz)
Cerca de 10-15% das causas de mortalidade e morbidade materna em países desenvolvidos e 37% das causas de morte obstétricas diretas no Brasil podem ser associadas à pré-eclâmpsia. A pré-eclâmpsia é uma patologia multissistêmica definida por uma hipertensão associada a uma proteinúria, após a 20ª semana de gestação. As manifestações clínicas desta doença podem se apresentar como uma síndrome materna ou fetal e de acordo com a gravidade podem ser classificadas em leve ou severa e de início precoce ou tardio. Apesar do conhecimento limitado sobre esta patologia, existem fortes evidências de envolvimento do componente genético na etiologia da pré-eclâmpsia. O fator de crescimento epidérmico (EGF) desempenha um papel importante na regulação do crescimento, proliferação e diferenciação celular, através da ligação ao seu receptor, o EGFR. Acredita-se que este fator esteja relacionado com a regulação do crescimento e da função placentária durante a gestação. Variações na sequência do DNA desses genes podem levar a uma alteração nos níveis de transcrição gênica e, como consequência, ser responsável por mudanças nos níveis de produção e/ou atividade desses fatores. O polimorfismo EGF +61 G>A está associado com a produção in vitro da proteína EGF e os polimorfismos EGFR -216 G>T e -191 C>A estão correlacionados a mudanças na atividade do promotor e na expressão de RNAm desse gene. O objetivo geral do nosso estudo foi avaliar uma possível associação entre polimorfismos funcionais nos genes EGF (+61 G>A) e EGFR (-216 G>T e -191 C>A) e a susceptibilidade à pré-eclâmpsia severa na população de gestantes do Estado do Rio de Janeiro, através de um estudo caso-controle. Como objetivos específicos, além de analisarmos uma possível interação entre os polimorfismos no desenvolvimento da pré-eclâmpsia severa, buscamos associar os polimorfismos ao histórico familiar da doença. O estudo foi composto por dois grupos, pareados por etnia: um grupo caso composto por 98 mulheres com pré-eclâmpsia severa e um grupo controle com 98 mulheres saudáveis. Os polimorfismos EGF (+61 G>A) e EGFR (-216 G>T e -191 C>A) foram avaliados pela reação em cadeia da polimerase seguida por análise de polimorfismos por tamanho de fragmentos de restrição (PCR-RFLP). As variáveis categóricas, frequências alélicas e genotípicas foram comparadas através do teste do exato de Fisher, e o teste t de Student foi utilizado para comparação das variáveis contínuas em cada grupo. Os resultados demonstram que o alelo A do polimorfismo -191 do gene EGFR está associado com a susceptibilidade à pré-eclâmpsia severa (p<0,05). Não houve associação significativa entre os outros polimorfismos (EGF +61 G>A e EGFR -216 G>T) e a susceptibilidade à pré-eclâmpsia severa (p>0,05), assim como também não foi encontrada relação entre a interação dos polimorfismos, histórico familiar e o desenvolvimento da pré-eclâmpsia severa. Além desses resultados, também foram encontradas diferenças significativas ao avaliarmos as características demográficas e clínicas entre os grupos. Este é o primeiro estudo a avaliar associações entre pré-eclâmpsia severa e os polimorfismos -216 G>T e -191C>A do gene EGFR e o primeiro estudo na população brasileira a investigar a associação do polimorfismo EGF +61 G>A e a doença. Com esse achado, podemos sugerir que o polimorfismo, o -191C>A do gene EGFR, possa ser o responsável por alguma regulação na produção do EGFR, e que através dessa regulação possa desempenhar algum papel importante na susceptibilidade à pré-eclâmpsia severa em mulheres do Estado do Rio de Janeiro.
About 10-15% of maternal deaths in development countries and approximately 37% of direct obstetrics deaths in Brazil can be assigned to preeclampsia. Preeclampsia is a multisystem disorder that usually occurs after 20 week of pregnancy and it is determined by the presence of hypertension associated with proteinuria. The clinical findings of preeclampsia can manifest as either a maternal syndrome or fetal syndrome. In addition, the preeclampsia can be classified as mild to severe, and in early or late-onset preeclampsia. Despite the limited knowledge of this pathology, there is a strong evidence of involvement of the genetic component in the etiology of preeclampsia. The epidermal growth factor (EGF) plays an important role in regulating cell growth, proliferation and differentiation, through binding its receptor, EGFR. Evidences suggest that this growth factor and its receptor are involved in growth regulation of placental function during the pregnancy. Variations in the DNA sequence in the EGF and EGFR genes can lead to an altered gene transcription and consequently can be responsible for changes in production and/or activity of these factors. The EGF +61 G>A polymorphism is significantly associated with in-vitro EGF protein production and the EGFR -216 G>T and -191 C>A polymorphisms are correlated with changes in promoter activity and expression of EGFR mRNA. The aim of this study was to verify the association between EGF +61 G>A, EGFR -216 G>T and -191 C>A polymorphisms and susceptibility to severe preeclampsia in the population of Rio de Janeiro through a case-control design. The specific objectives were to assess the association between these polymorphisms and the history family of preeclampsia, and also to analyze a possible interaction among these polymorphisms on the development of severe preeclampsia. The study was composed by two groups matched by ethnicity: the case group with 98 women with severe preeclampsia and the control group with 98 healthy women. Polymerase chain reaction restriction fragment length polymorphism analyses (PCR-RFLP) were performed to genotype EGF +61 G>A, EGFR -216 G>T and -191 C>A polymorphisms. Categorical variables, allelic and genotype frequencies were compared in each group applying Fisher´s exact test and a Student t test was used for continuous variables. The results showed that the A allele of the -191 C>A polymorphism of the EGFR gene is associated with susceptibility to severe preeclampsia (P<0,05). There were no significant association between severe preeclampsia and +61 G>A EGF and -216 G>T EGFR polymorphisms (P>0,05), as well as no correlation was found between the interaction of these polymorphisms, history family and the development of severe preeclampsia. We also found differences when we evaluated demographic and clinical characteristics between the two groups. This is the first study to assess the associations between -191 C>A and -216 G>T EGFR genetics polymorphisms and severe preeclampsia and the first study in Brazilian population to investigate the association between +61 G>A EGF polymorphism and severe preeclampsia. These findings suggest that the polymorphism-191C>A of the EGFR gene may be responsible for some regulation in the production of the EGFR, and that through this regulation this polymorphism might play an important role in the susceptibility to severe preeclampsia in women from Rio de Janeiro.
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Vanlandingham, Phillip Allen. "Rab7 regulation of EGFR trafficking and signaling". Oklahoma City : [s.n.], 2009.

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Książki na temat "EGFR"

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Haley, John D., i William John Gullick, red. EGFR Signaling Networks in Cancer Therapy. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-356-1.

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Cappuzzo, Federico. Guide to Targeted Therapies: EGFR mutations in NSCLC. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-03059-3.

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D, Haley John, i Gullick William John, red. EGFR Signaling Networks in Cancer Therapy / edited by John D. Haley, William John Gullick. New York, NY: Humana Press, 2008.

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Rudzik, Nicholas James. A genetic analysis of the role of neuralized in the notch and EGFR pathways of Drosophila melanogaster. Ottawa: National Library of Canada, 1999.

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Saki, Mohammad. Radiolabeling of anti-EGFR antibody, Cetuximab, overcomes the radiotherapy resistance of Cetuximab resistant head and neck cancer cells. [S.l: s.n.], 2014.

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Faber, Anthony. Overcoming Resistance to EGFR Inhibitors in EGFR Mutant NSCLC. Elsevier Science & Technology, 2022.

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Faber, Anthony. Overcoming Resistance to EGFR Inhibitors in EGFR Mutant NSCLC. Elsevier Science & Technology Books, 2021.

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Patel, Harun M., Rahul Pawara i S. J. Surana. Third-Generation EGFR Inhibitors: Overcoming EGFR Resistance and Toxicity Problems. Elsevier, 2018.

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Patel, Harun M., Rahul Pawara i Sanjay J. Surana. Third Generation EGFR Inhibitors: Overcoming EGFR Resistance and Toxicity Problems. Elsevier, 2018.

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Schaeybroeck, Sandra Van. Egfr Activity As a Determinant of Response to Egfr-targeted Therapy. Leuven Univ Pr, 2006.

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Części książek na temat "EGFR"

1

Weiner, Louis M., i Christina Wu. "EGFR, Immunology". W Cancer Therapeutic Targets, 199–208. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4419-0717-2_27.

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Weiner, Louis M., i Christina Wu. "EGFR, Immunology". W Cancer Therapeutic Targets, 1–10. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6613-0_27-2.

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Bourdeanu, Laura, Ellen Liu, Suzanne Brint i David Langdon. "EGFR Resistance". W Resistance to Targeted Anti-Cancer Therapeutics, 103–16. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-70142-4_4.

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Kobayashi, Kunihiko, i Hiroshi Kagamu. "EGFR Mutant". W Molecular Targeted Therapy of Lung Cancer, 167–89. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-2002-5_10.

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Cooley, Laura A., Daniel G. Bausch, Marija Stojkovic, Waldemar Hosch, Thomas Junghanss, Marija Stojkovic, Waldemar Hosch i in. "eGFR, Concept of". W Encyclopedia of Intensive Care Medicine, 811–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_280.

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Noor, Zorawar S., i Jonathan W. Goldman. "EGFR Targeted Therapy". W Targeted Therapies for Lung Cancer, 1–30. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-17832-1_1.

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Bhutani, Manisha, i Helen Gharwan. "EGFR, Growth Factors". W Cancer Therapeutic Targets, 707–17. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4419-0717-2_72.

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Senellart, H., i J. Bennouna. "Anticorps anti-EGFR". W Les thérapies ciblées, 35–44. Paris: Springer Paris, 2008. http://dx.doi.org/10.1007/978-2-287-36008-4_2.

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Bhutani, Manisha, i Helen Gharwan. "EGFR, Growth Factors". W Cancer Therapeutic Targets, 1–11. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6613-0_72-3.

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Distefano, Veronica, Maria Mannone, Irene Poli i Gert Mayer. "Clustering Trajectories to Study Diabetic Kidney Disease". W Communications in Computer and Information Science, 271–83. Cham: Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-57430-6_21.

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AbstractDiabetic kidney disease (DKD) is a serious complication of type-2 diabetes, defined prominently by a reduction in estimated glomerular filtration rate (eGFR), a measure of renal waste excretion capacity. However DKD patients present high heterogeneity in disease trajectory and response to treatment, making the one-model-fits-all protocol for estimating prognosis and expected response to therapy as proposed by guidelines obsolete. As a solution, precision or stratified medicine aims to define subgroups of patients with similar pathophysiology and response to the therapy, allowing to select the best drug combinations for each subgroup. We focus on eGFR when aiming to identify eGFR decline trends by clustering patients according to their eGFR trajectory shape-similarity.The study involved 256 DKD patients observed annually for four years. Using the Fréchet distance, we built clusters of patients according to the similarity of their eGFR trajectories to identify distinct clusters. We formalized the trajectory-clustering approach through category theory. Characteristics of patients within different progression clusters were compared at the baseline and over time.We identified five clusters of eGFR progression over time. We noticed a bifurcation of eGFR mean trajectories and a switch between two other mean trajectories. This particular clustering approach identified different mean eGFR trajectories. Our findings suggest the existence of distinct dynamical behaviors in the disease progression.
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Streszczenia konferencji na temat "EGFR"

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Lee, An-Chun, Chia-Cherng Yu, Yuan-Hung Wang i Yu-Ting Chou. "Abstract 5906: EGFR and SOX2 crosstalk determines EGFR-TKI". W Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5906.

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Allen, Fred D., Clara F. Asnes, Alan Wells, Elliot L. Elson i Douglas A. Lauffenburger. "Alternative Pathways of Epidermal Growth Factor Receptor Mediated Contractile Force in NR6 Fibroblasts". W ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0403.

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Abstract We investigated the contractile force response to epidermal growth factor (EGF) stimulation in 3T3-derived NR6 fibroblast cells in order to determine significant pathways of biochemical signaling that mediate the response. We examined the force generating specificity of the EGF receptor (EGFR) signaling mechanism by using mutant NR6 fibroblasts expressing variations of the EGFR construct. The wild-type (WT) cell presented the complete internalizing EGFR signaling construct while the c’973 cell presented an internalization-defective EGFR construct, and the M721 cell presented a kinase-defective EGFR construct making it signaling inert. Additionally we examined the roles of the phospholipasc C-γ (PLCγ) pathway by using the PLC inhibitor U73122 (1 μM) and the mitogen activated protein kinase (MAPK) pathway using the inhibitor PD98059 (10 μM) in the observed contractile force responses. We found that the WT cells showed a rapid but transient force increase within the first hour post-stimulation and the c’973 showed a more gradual increase in force which it sustained for several hours post-stimulation. Blocking the PLCγ activation in the WT cells reduced the peak force increase by 50% while blocking MAPK did not affect the force development in either WT or c’973 cells.
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Weng, Ting-Wei, Sheng-Yao Huang, Chun-Liang Lu, Chiun-Li Chin, Hao-Hung Tsai i I.-Fang Chung. "Distinguish EGFR+ and EGFR- patients in LA using CT images". W 2016 International Conference on Fuzzy Theory and Its Applications (iFuzzy). IEEE, 2016. http://dx.doi.org/10.1109/ifuzzy.2016.8004960.

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Milewska, Marta, Justin Micah Balko i Esther Penni Black. "Abstract 2896: MEK inhibition controls EGFR level in EGFR-dependent NSCLC cells via deregulated expression of EGF-like ligands". W Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2896.

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Makinoshima, Hideki, Masahiro Takita, Shingo Matsumoto, Atsushi Yagishita, Satoshi Owada, Hiroyasu Esumi i Katsuya Tsuchihara. "Abstract 3361: EGFR signaling regulates aerobic glycolysis in EGFR-mutated lung adenocarcinoma". W 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.am2014-3361.

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Raimbourg, Judith, Mathilde Cabart, Marie-Pierre Joalland, Didier Decaudin, Ludmilla Deplater, Didier Lanoe, Jean-Yves Douillard, Jaafar Bennouna, François Vallette i Lisenn Lalier. "Abstract 2559: Optimisation of EGFR TKI efficiency wild-type EGFR lung cancer". W Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2559.

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

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Hong, Shiao-Ya, Yi-Ping Shih, Tianhong Li, Kermit Carraway i Su Hao Lo. "Abstract A40: CTEN prolongs EGFR signaling by reducing ligand-induced EGFR degradation". W Abstracts: Third AACR International Conference on Frontiers in Basic Cancer Research - September 18-22, 2013; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.fbcr13-a40.

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Makhov, Peter, Alexander Kudinov, Alexander Deneka, Brian L. Egleston, Emmanuelle Nicolas, Kathy Q. Cai, Rohan Brebion i in. "Abstract 4452: Musashi-2 regulates EGFR/HER3 expression in NSCLC, cell proliferation and response to EGFR inhibitors in EGFR-mutant NSCLC". W Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4452.

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Koba, Hayato, Hideharu Kimura, Shingo Nishikawa, Taro Yoneda, Takashi Sone i Kazuo Kasahara. "Abstract 2268: Detection of T790M mutation in EGFR gene, an EGFR-TKI resistant mutation, in tumor samples unexposed to EGFR TKIs". W Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2268.

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Raporty organizacyjne na temat "EGFR"

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Song, Yaowen, Shuiyu Lin, Jun Chen, Silu Ding i Jun Dang. First-line treatment with TKI plus brain radiotherapy vs TKI alone in EGFR-mutated non-small-cell lung cancer with brain metastases: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, styczeń 2023. http://dx.doi.org/10.37766/inplasy2023.1.0013.

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Review question / Objective: It remains uncertain whether first-line treatment with upfront brain radiotherapy (RT) in combination with epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) is superior to EGFR-TKIs alone in EGFR-mutated non-small-cell lung cancer with newly diagnosed brain metastases (BMs). We performed a meta-analysis to address this issue. Condition being studied: Brain radiotherapy (RT) has been shown to damage the blood-brain barrier (BBB) and improve the concentration of EGFR-TKIs in the CSF. Additionally, RT can result in a reduction of EGFR-TKIs resistance. Therefore, EGFR-TKIs in combination with brain RT should be more effective than EGFR-TKIs alone theoretically. However, results from retrospective studies are inconsistent. There is the possibility that patients characteristics or brain RT technique affect the efficacy of treatments. To date, there is still no randomized controlled trials (RCTs) comparing the two treatment strategies.
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Goodrich, Jennifer S. EGFR Activation by Spatially Restricted Ligands. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2004. http://dx.doi.org/10.21236/ada426969.

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Backer, Joseph M. Development of Cu-64 labeled EGF for In Vivo PET Imaging of EGFR Expression. Office of Scientific and Technical Information (OSTI), lipiec 2009. http://dx.doi.org/10.2172/958568.

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Hong, Xiaohua, Guangyao Wang, Chunmei Mo i Zhen Rong. Prognostic value of EGFR/p-EGFR in nasopharyngeal carcinoma: a protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, maj 2021. http://dx.doi.org/10.37766/inplasy2021.5.0010.

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Lin, Chutong, Fengling Hu, Hongling Chu, Peng Ren, Shanwu Ma, Jingdi Wang, Jie Bai, Xuan Han i Shaohua Ma. The Role of EGFR-TKIs as Adjuvant Therapy in EGFR Mutation-Positive Early-Stage NSCLC: a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, październik 2020. http://dx.doi.org/10.37766/inplasy2020.10.0098.

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Wang, Zexian, Yaru Guo, Xiaojin Wu, Xiaohan Qin, Zhiling Wan i Chen Liu. Bevacizumab plus Epidermal Growth Factor Receptor (EGFR)-Tyrosine Kinase Inhibitor versus EGFR-TKI alone for advanced EGFR-mutant non-small cell lung cancer: a meta-analysis of randomized clinical trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, grudzień 2023. http://dx.doi.org/10.37766/inplasy2023.12.0059.

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Qin, Xiaohan, Yaru Guo, Xiaojin Wu, Zexian Wang, Zhiling Wan i Chen Liu. Chemotherapy plus Epidermal Growth Factor Receptor (EGFR)-Tyrosine Kinase Inhibitor versus EGFR-TKI alone for advanced EGFR-mutant non-small cell lung cancer: a meta-analysis of randomized clinical trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, styczeń 2024. http://dx.doi.org/10.37766/inplasy2024.1.0128.

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Marks, James. Structural Basis of EGFR Dimerization for Drug Design. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2000. http://dx.doi.org/10.21236/ada396569.

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Li, Chia-Wei. Role of IKKalpha in the EGFR Signaling Regulation. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2011. http://dx.doi.org/10.21236/ada610026.

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Li, Chia-Wei. Role of IKKalpha in the EGFR Signaling Regulation. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2012. http://dx.doi.org/10.21236/ada610027.

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