Relevant bibliographies by topics / EGFR and NF-kB

Academic literature on the topic 'EGFR and NF-kB'

Author: Grafiati
Published: 9 March 2023
Last updated: 11 March 2023

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Journal articles on the topic "EGFR and NF-kB"

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Rahaju, Pudji, Rio Auricknaga Kintono, Ahmad Dian Wahyudiono, Arif Satria, and Ferry Sandra. "Immunohistochemical Expression of EGFR, NF-kB and Cyclin D1 in Sinonasal Inverted Papilloma and Squamous Cell Carcinoma." Indonesian Biomedical Journal 12, no. 3 (September 5, 2020): 239–44. http://dx.doi.org/10.18585/inabj.v12i3.1172.

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BACKGROUND: Sinonasal inverted papilloma (SIP), a benign epithelial growth in the sinonasal region with epidermoid epithelial transformation, has been known for its invasiveness, recurrency, and its link with malignancy. Meanwhile sinonasal squamous cell carcinoma (SSCC) is an epithelial malignancy on squamous cells from the sinonasal region. Epidermal growth factor receptor (EGFR), Nuclear Factor kB (NF-kB), and Cyclin D1 are factors those might play important role in proliferation of SIP and SSCC. This research was conducted to investigate the expressions of EGFR, NF-kB and Cyclin D1 in SIP and SSCC.METHODS: A cross-sectional study by examining the EGFR, NF-kB, and Cyclin D1 immunohistochemical expressions of SIP and SSCC was conducted. Subjects whose blocks were used in this research, were diagnosed as SIP and SSCC at the Otorhinolaryngology-Head and Neck Surgery Clinic, Dr. Saiful Anwar General Hospital. Samples were selected, processed for inmmunohistochemistry, evaluated and statistical analyzed.RESULTS: Twenty-four SIP and 9 SSCC subjects with their paraffin blocks were selected. Clear immunohistochemical expressions of EGFR, NF-kB, and Cyclin D1 were observed for both SIP and SSCC. Significantly higher immunostaining levels of EGFR (45.6%, p=0.001) and NF-kB (42.2%, p=0.013) were observed in SSCC. Immunostaining levels of EGFR vs. NF-kB were moderately correlated (p=0.03, r=0.437), while the immunostaining levels of NF-kB vs. Cyclin D1 were strongly correlated (p=0.002, r=0.602).CONCLUSION: Expression of EGFR and NF-kB in SSCC were higher than the EGFR and NF-kB expression in SIP, suggesting that EGFR and NF-kB play important role in sinonasal malignancy.KEYWORDS: sinonasal, inverted papilloma, SCC, EGFR, NF-kB, Cyclin D1
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Scartozzi, M., I. Bearzi, C. Pierantoni, A. Mandolesi, F. Loupakis, V. Catalano, R. Berardi, R. Silva, A. Falcone, and S. Cascinu. "Nuclear factor kB (NF-kB) may predict efficacy of cetuximab therapy in EGFR-positive colorectal cancer." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 14036. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.14036.

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14036 Background: NF-kB is part of the aberrant activation of the EGFR-downstream signalling pathway in colorectal tumours, which is described to be inhibited by anti-EGFR therapies. Methods: We retrospectively analysed nuclear immunoreactivity for NF-kB with the aim to determine a correlation between NF-kB expression and outcome in terms of response rate and time to progression in EGFR-positive advanced colorectal cancer patients receiving cetuximab and irinotecan. Results: To date 67 patients (40 males and 27 females, median age 62, range 38–78) were analysed. Cetuximab and irinotecan were administered as a second-line in 18 cases (27%) and after = 3 lines of chemotherapy in the remaining 49 patients (63%). Among the 56 patients evaluable for response we observed a partial (PR) or a complete response (CR) in 10 and 1 cases respectively for an overall response rate of 20%. Twenty-seven patients (48%) obtained progressive disease, median time to progression (TTP) was 3,6 months, median overall survival was 16 months. NF-kB was positive in 46 cases (69%). All main clinical characteristics resulted well balanced between NF-kB positive and NF-kB negative patients. Response rate was 6% (2 PR) vs 43% (8 PR and 1 CR) (p= 0.001) in NF-kB positive and NF-kB negative tumours respectively whereas progressive disease was observed in 19 (54%) vs 8 (23%) cases in NF-kB positive and NF-kB negative cases respectively. Median TTP in NF- kB positive patients was 2.9 months versus 6.8 months in the remaining NF-kB negative patients (p= 0.01). Conclusions: Both the difference in median TTP and in response rate seem to confirm that NF-kB may play a crucial role in predicting the efficacy of cetuximab therapy in advanced colorectal tumours. The analysis is ongoing and updated results on an expanded number of cases will be presented. No significant financial relationships to disclose.
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Ashktorab, Hassan, Alfred Johnson, Mohammad Daremipouran, Awana Ferguson, Biniam Kifle, and Duane T. Smoot. "Cross talk between EGFR and NF-kB altered by H. pylori in human gastric epithelial cells." Gastroenterology 124, no. 4 (April 2003): A587—A588. http://dx.doi.org/10.1016/s0016-5085(03)82975-x.

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Shukla, Vinay, Vishal Chandra, Pushplata Sankhwar, Pooja Popli, Jyoti Bala Kaushal, Vijay Kumar Sirohi, and Anila Dwivedi. "Phytoestrogen genistein inhibits EGFR/PI3K/NF-kB activation and induces apoptosis in human endometrial hyperplasial cells." RSC Advances 5, no. 69 (2015): 56075–85. http://dx.doi.org/10.1039/c5ra06167a.

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Hassanein, Sarah Sayed, Sherif Abdelaziz Ibrahim, and Ahmed Lotfy Abdel-Mawgood. "Cell Behavior of Non-Small Cell Lung Cancer Is at EGFR and MicroRNAs Hands." International Journal of Molecular Sciences 22, no. 22 (November 19, 2021): 12496. http://dx.doi.org/10.3390/ijms222212496.

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Lung cancer is a complex disease associated with gene mutations, particularly mutations of Kirsten Rat Sarcoma Viral Oncogene Homolog (KRAS) and epidermal growth factor receptor (EGFR). Non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC) are the two major types of lung cancer. The former includes most lung cancers (85%) and are commonly associated with EGFR mutations. Several EGFR-tyrosine kinase inhibitors (EGFR-TKIs), including erlotinib, gefitinib, and osimertinib, are effective therapeutic agents in EGFR-mutated NSCLC. However, their effectiveness is limited by the development (acquired) or presence of intrinsic drug resistance. MicroRNAs (miRNAs) are key gene regulators that play a profound role in the development and outcomes for NSCLC via their role as oncogenes or oncosuppressors. The regulatory role of miRNA-dependent EGFR crosstalk depends on EGFR signaling pathway, including Rat Sarcoma/Rapidly Accelerated Fibrosarcoma/Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated Kinase 1/2 (Ras/Raf/MEK/ERK1/2), Signal Transducer and Activator of Transcription (STAT), Nuclear Factor Kappa-Light-Chain-Enhancer of Activated B Cells (NF-kB), phosphoinositide 3-kinase/protein kinase B (PI3K/AKT), Janus kinase 1 (JAK1), and growth factor receptor-bound protein 2 (GRB2). Dysregulated expression of miRNAs affects sensitivity to treatment with EGFR-TKIs. Thus, abnormalities in miRNA-dependent EGFR crosstalk can be used as diagnostic and prognostic markers, as well as therapeutic targets in NSCLC. In this review, we present an overview of miRNA-dependent EGFR expression regulation, which modulates the behavior and progression of NSCLC.
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Berardi, Rossana, Anna Campanati, Azzurra Onofri, Chiara Pierantoni, Irene Conte, Katia Giuliodori, E. Molinelli, Fabiana Marcucci, Annamaria Offidani, and Stefano Cascinu. "A novel approach to manage skin toxicity caused by therapeutic agents targeting epidermal growth factor receptor." Journal of Clinical Oncology 30, no. 4_suppl (February 1, 2012): 636. http://dx.doi.org/10.1200/jco.2012.30.4_suppl.636.

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636 Background: Inhibition of EGFR represents an important field in cancer therapy.Skin rash is a common adverse reaction in patients receiving EGFR inhibitors. Nicotinamide has been shown to be an effective treatment for skin inflammation in various conditions, since nicotinamide inhibits IL-8 production through the NF-kB and MAPK pathways in an in vitro keratinocytes/P. acnes model of inflammation. Furthermore green tea polyphenols could be useful in attenuation of solar UVB light-induced oxidative stress-mediated and MAPK-caused skin disorders in humans.In this study we evaluated the effect of nicotinamide and green tea polyphenols on skin toxicity EGFRI related. Methods: Patients with skin toxicity induced by EGFRI were enrolled. They underwent a skin biopsy and skin samples for microbiological analyses at first presentation of skin toxicity (T0). Skin toxicity was assessed with NCI-CTACE,EGFR index and Dermatology Life Quality Index (DLQI) test. Therapy protocol consisted in topical application of moisturizing cream containing green tea polyphenols plus oral administration of nicotinamide 200 mg/die for 12 weeks. Topical application of 1% clindamycin gel and/or systemic administration of minocicline were provided in case of superbacterial infection. All treated patients were monitored for at least 12 weeks (T12), across three time points (T0,T6,T12). Results: 24 colorectal cancer patients receiving anti-EGFR monoclonal antibodies (cetuximab or panitumumab) and developing skin toxicity were treated by a multidisciplinary team including oncologists, dermatologists, a pathologist and a nurse. All the patients experienced a significant reduction of skin toxicity according to the NCI-CTACE and EGFR index (p<0.05). Papulo-pustular eruption and itching significantly improved after 6 weeks of treatment and erythema decreased after 12 weeks. A significative improvement of the global score and of DLQI was evident. No toxicity related to the treatment of skin toxicity was observed. Conclusions: Treatment with nicotinamide and green tea polyphenols represent a novel effective approach to manage skin toxicity caused by EGFRI.
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Foulke-Abel, Jennifer D., Nesrin Hasan, Mark Donowitz, Mary Estes, and Olga Kovbasnjuk. "Su1039 – Human Differentiated Enteroid Monolayers Exhibit Egfr/Mek- and Nf-Kb-Dependent Plasticity in a Model of Intestinal Trauma." Gastroenterology 156, no. 6 (May 2019): S—491—S—492. http://dx.doi.org/10.1016/s0016-5085(19)38093-x.

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Pan, Shaojun, Yuhui Zhang, Mark Huang, Zhoufeng Deng, Amin Zhang, Lijia Pei, Lirui Wang, et al. "Urinary exosomes-based Engineered Nanovectors for Homologously Targeted Chemo-Chemodynamic Prostate Cancer Therapy via abrogating EGFR/AKT/NF-kB/IkB signaling." Biomaterials 275 (August 2021): 120946. http://dx.doi.org/10.1016/j.biomaterials.2021.120946.

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Berardi, R., A. Campanati, A. Onofri, A. Bittoni, C. Pierantoni, K. Giuliodori, G. Ganzetti, M. Scartozzi, A. Offidani, and S. Cascinu. "A novel approach to manage skin toxicity caused by cetuximab and panitumumab." Journal of Clinical Oncology 29, no. 4_suppl (February 1, 2011): 616. http://dx.doi.org/10.1200/jco.2011.29.4_suppl.616.

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616 Background: Inhibition of the EGFR represents one of the most important fields for research and development in cancer therapy. Skin rash has been documented as one of the most common adverse reactions in patients receiving EGFR inhibitors. Several approaches have been attempted to manage skin toxicity. Nicotinamide has been shown to be an effective treatment for skin inflammation in various conditions, since nicotinamide inhibits IL-8 production through the NF-kB and MAPK pathways in an in vitro keratinocytes/P. acnes model of inflammation. Furthermore green tea polyphenols could be useful in attenuation of solar UVB light-induced oxidative stress-mediated and MAPK-caused skin disorders in humans. Methods: Therapy protocol for skin toxicity consisted of: topic applications of green tea and a mostouizer and orally given nicotinamide. Patients were monitored weekly and data regarding skin toxicity (NCI-CTC grade, the Dermatology Life Quality Index (DLQI), a global score evaluating all the parameters) were recorded. Results: Between September 2009 and September 2010, 13 colorectal cancer patients receiving anti-EGFR monoclonal antibodies (cetuximab or panitumumab) and developing skin toxicity, were treated by a multidisciplinary team including oncologists, dermatologists, a pathologist, and a nurse. All the patients experienced a significative eduction of erythema, papulo-pustular rash, paronychia, fissuring, xerosis, and itching. A significative improvement of the global score and of DLQI was evident. No toxicity related to the treatment of skin toxicity was observed. Conclusions: Treatment with nicotinamide, green tea, and moisturizer represents a novel effective approach to manage skin toxicity caused by cetuximab and panitumumab. No significant financial relationships to disclose.
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Cho, Sang Hee, Jo-Heon Kim, Chang-Soo Hong, Eun-Gene Sun, Kyung-Hyun Ryu, Jun Eul Hwang, Woo Kyun Bae, Ik-Joo Chung, and Hyun-Jin Bang. "The role of fibroblast growth factor receptor 4 (FGFR4) signaling in anti-EGFR resistance in colon cancer." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): 4060. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.4060.

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4060 Background: Anti-EGFR therapy has been used as a standard treatment for metastatic colon cancer, but the innate resistance is still issues of increasing significance. Fibroblast growth factor receptor 4 (FGFR4) plays an important role in cell proliferation, invasion and anti-apoptosis, through the pathway of MAPK-ERK and PI3K-AKT. We investigated potential crosstalk between FGFR4 and EGFR signaling to identify new resistant mechanism of anti-EGFR therapy and how to overcome it in colon cancer. Methods: RNA-Seq was used to identify the associated signal pathway and down targets induced by FGFR4. Molecular studies including RTK array, RT-qPCR, western blotting were performed to validate the interaction between FGFR4 and EGFR signaling in vitro and in vivo. Next, the effect of FGFR4 in cetuximab resistance was investigated in vitro and in colon cancer patients. Results: FGFR4 overexpression in colon cancer cells activates downstream signaling, such as, PI3K/Akt and RAS/RAF/Erk pathway. Gene Ontology (GO) analysis from RNA-seq revealed that differentially expressed genes (DEGs) altered by expression of FGFR4 were related to biological functions, including cell proliferation, epidermal growth factor receptor signaling, NIK/NF-kB signaling, interferon-gamma signaling, wound healing. RT–qRCR showed that FGFR4 promotes the EGFR and ErbB3 by inducing the expression of EGFR ligands such as AREG, BTC, EREG, HBEGF. In vivo tumorigenesis, we found that FGFR4 promotes tumor growth and high expression of AREG in xenograft tumors. FGFR4 expression reduced the sensitivity to cetuximab in colon cancer cells and synergistic effect was shown when treated with FGFR4 inhibitor with cetuximab. A positive correlation between FGFR4 and AREG expression was observed in cancer, but not in normal tissues and high FGFR4 or AREG expression showed significantly inferior overall survival than low expression in patients treated with cetuximab for metastatic colon cancer. Conclusions: We demonstrated a pivotal mechanism of FGFR4 in colon cancer progression and cetuximab resistance through inducing AREG. Our data point to FGFR4 as a new biomarker to predict cetuximab response and dual targeting of FGFR4 and EGFR may be a promising treatment modality for colon cancer.
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Dissertations / Theses on the topic "EGFR and NF-kB"

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PATANE', MONICA. "Genetic and molecular signature of glioblastoma stem-like cells." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/43582.

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In the past years it was made a very huge effort to understand the genetic and molecular signatures of glioblastoma in order to improve targeted molecular therapy: but to date several things remain still unclear and new markers or new relationships have to been disclosed. Our aim is, therefore, to better clarify genetic signatures and pathways’ cross-talks in our glioblastoma-stem like cells model: actually we believe that these cells represent a real reservoir for the tumor of cells, which are able alone to maintain tumor growth, to give raise to a relapse and to determine radio- and chemo-resistance. First we presented a paper published in collaboration with our laboratory in 2012: in this study we found that the expression of MET oncogene was associated with a mesenchymal signature in our glioblastoma stem-like cells model and this expression is mutually exclusive with EGFR amplification; these cells also displayed different growth requirements in vitro and generated tumors with distinctive features in vivo; this suggested that MET could be a new target for therapy of a specific subset of GBMs (De Bacco et al 2012). Then we tried to better understand the possible cross-talk between EGFR and NF-kB signalling through a specific genetic signature disclosed in a precedent paper (Bredel et al 2011): a heterozygous deletion of NFKBIA gene, mutually exclusive with EGFR amplification. Surprisingly we found that this signature is a rare event in the primary tumor, but it is very frequent in our glioblastoma stem-like cells model in vitro and has also clear functional consequences. Our results raise the possibility that this deletion may be amplified in vitro, favored by the presence of EGF, mostly in that lines in which EGFR pathway is predominant; furthermore in these cells seems to be favored the constitutive active mutant of EGFR gene, EGFRvIII, probably in order to preserve EGFR-NF-kB axis. All these data suggest that our model is a much better system than serum-dependent cultures to study GBMs biology, bu at the same time various GSCs subgroups can be defined, that require both different factors to grow and also display different behaviours based on their genetic and molecular signatures.
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Granet, Corinne. "Mécanismes d'adaptation de cellules ostéoblastiques Ros17/2. 8 aux variations des contraintes mécaniques dans des modèles de micro-gravité simulée et de déformation du support de culture : implication des facteurs de transcription : AP-1, Egr-1, NF-kB." Saint-Etienne, 2000. http://www.theses.fr/2000STET006T.

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Pahlavan, Payam Samareh. "Transcription factors NF-kB, CREB and Egr-2 and their potential role in memory formation." 2013. http://hdl.handle.net/1993/21705.

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Memory is subdivided into short- and long-term memory. The interaction between transcription factors (TF) and expressed genes are essential steps in memory formation. Some TFs that might be involved in memory formation include CREB, NF-kB and Egr-2. We hypothesized that there would be a difference in the expression levels of these TFs following learning in the Morris Water Maze (MWM). In study one, CD1 mice were categorized into two groups. Group 1 assigned as non-trained control group. Group 2 (experimental group) underwent 9 consecutive days of MWM training. In the second study, male C57BL/6 mice were categorized into four groups. Group 1 was a non-trained control group (allowed to swim randomly). Groups 2, 3, and 4 (experimental groups) had variations in their MWM training. Search strategies, escape latency, time spending in the target quadrant and number of attempts passing the missing platform, were measured. To evaluate the expression levels of TFs pre- versus post-learning, mice were sacrificed at the end of MWM. Hippocampi were separated and Western blot and immunohistochemical procedures were done. In study one, the escape latency decreased progressively toward the end of the acquisition phase in the trained group. The search pattern showed that the mice used primarily spatial strategies. Mice spent more time in the target quadrant during the retention phase. The number of passes over the missing platform peaked on the first day of the retention phase. NF-kB and CREB were expressed significantly higher in the control group versus the MWM trained mice (p = 0.0031 and p < 0.0001 respectively). There was no statistically significant difference in expression of Egr-2 between the two groups (p = 0.3092). In study two, Group 4 showed the highest and Group 1 the lowest levels of CREB expression. CREB and NF-kB were decreased following MWM training in study one. In study two CREB levels were highest in the Group 4 which had interval between the acquisition and retention phases. These differences could be due to multiphasic expression patterns and/or other experimental design issues. Further studies are warranted to examine time dependent differential expression of TFs in memory.
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Conference papers on the topic "EGFR and NF-kB"

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Wang, Wei, Rong Wang, Shunli Peng, Qi Li, Xiaojuan Zhang, and Yueyun Ma. "Abstract 4156: Inhibition of NF-kB improves sensitivity to radiation and EGFR inhibitor and decreases radiation-induced lung toxicity in lung cancer." In 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.am2018-4156.

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Singh, UP, JK Shrivastava, A. Verma, and HR Bhat. "AB0075 Targeting immune and non-immuno synovitis by 1,3,5-TRIAZINE-THIAZOLE via dual inhibition of NF-KB and EGFR-TKS for possible benefit in rheumatoid arthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.5612.

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