Relevant bibliographies by topics / Cetuximab

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

Academic literature on the topic 'Cetuximab'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 March 2023

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Journal articles on the topic "Cetuximab"

1

Chang, Wenju, Wenbai Huang, Yijiao Chen, Li Ren, Ye Wei, and Jianmin Xu. "Comparison of HER2 overexpression with total Her2 mutation on resistance of EGFR-targeted therapy in Ras wild-type mCRC patients." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): 3594. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.3594.

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3594 Background: Cetuximab has shown clinical benefit in patients with metastatic colorectal cancer (mCRC) harboring wild-type Ras, however, only partial patients respond to cetuximab treatment. The effect of human epidermal growth factor receptor 2 (HER2) protein overexpression and Her2 gene mutant on the efficacy of cetuximab treatment was not well elucidated in patients with Ras wild-type unresectable mCRC. Methods: From June 2008 to December 2014, we identified 216 patients with Ras wild-type unresectable liver-limited mCRC base on our previous study (ClinicalTrials: NCT01564810.), whose Her2 gene mutation was analyzed by next-generation sequencing for single nucleotide polymorphism (SNP) of Her2 gene and HER2 protein overexpression was determined by immunohistochemistry and fluorescence in situ hybridization (FISH). Results: Of these 216 patients, 103 were received cetuximab plus chemotherapy (cetuxima group) and 113 were received chemotherapy alone (chemotherapy group). The total rate of HER2 overexpression was 8.8%, including 9.7% in cetuximab group and 7.9% in chemotherapy group. HER2 overexpression caused impaired survival compared with HER2 non-overexpression patients in cetuxima group, with a median progression-free survival (PFS) of 4 months (95% CI 2.482-5.518) versus 10 months (95% CI 8.963-11.037; P< 0.0001), and a median overall survival (OS) of 15 months (95% CI 7.5-22.2) versus 36 months (95% CI 31.4-40.5) ( P< 0.0001). While, HER2 overexpression had no effect on treatment efficacy in chemotherapy group, when compared with HER2 non-overexpression paitents, with a median PFS of 5 months (95% CI 2.228-7.772) versus 5 months (95% CI 4.004-5.996; P= 0.615), and a median OS of 21 months (95% CI 6.975-35.025) versus 21 months (95% CI 17.772-24.228; P= 0.629). Meanwhile, we observed 25.5% of total Her2 mutant (24.2% in cetuximab group and 26.5% in cetuximab group), among of them 5 patients are HER2 overexpression. Total Her2 mutation has no impact on survival compared with Her2 wild-type ones in neither cetuximab group nor chemotherapy group. In further bioinformatics analysis is underdoing, and which subgroup or type of Her2 mutant potential affect cetuximab treatment need confirm. Conclusions: We show HER2 overexpression rather than total Her2 mutant contribute to resistance of cetuximab treatment in patients with mCRC harboring wild-type Ras. Next, the subgroup mutant in total Her2 mutant needs further analysis to confirm their roles in survival after cetuximab treatment.
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Timoney, J., K. Y. Chung, V. Park, R. Trocola, C. Peake, and L. B. Saltz. "Cetuximab use without chronic antihistamine premedication." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 13521. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.13521.

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13521 Background: Cetuximab is a human-murine chimeric monoclonal antibody against EGFR with approximately a 3% reported incidence of severe (≥ grade 3) anaphylactoid reactions. The overwhelming majority of such reactions have been reported with the initial dose of cetuximab. Diphenhydramine (Benedryl)or a related antihistamine is often given as a premedication for cetuximab, however this may cause fatigue or other side effects. Most early clinical trials of cetuximab permitted investigator discretion in use of premedication beyond the initial cetuximab dose. Methods: We obtained an IRB waiver of authorization to review the records of patients treated with cetuximab at Memorial Sloan Kettering Cancer Center for the first year of commercial availability of cetuximb (Feb, 2004 through Feb, 2005). Computerized pharmacy records were reviewed to identify all patients who were treated with cetuximab (outside of a clinical trial) and use of premedication was then evaluated. Records of institutional adverse event reports regarding chemotherapy administration were reviewed, and, any moderate or severe/life-threatening reactions were evaluated for presence or absence of concurrent premedication. Results: As per our institutional guidelines, all patients received 50 mg of diphenhydramine prior to the initial loading dose of cetuximab, and 25 mg of diphenhydramine prior to the second dose. While there was inconsistency in terms of cessation of diphenhydramine, overall a total of 115 patients received one or more doses of cetuximab without premedication. A total of 746 doses of cetuxmab without diphenhydramine premedication were given over this time period. No severe/life-threatening reactions to cetuximab occurred during these doses given without premedication. Conclusions: Omission of diphenhydramine premedication after the initial two doses of cetuximab is our current institutional practice, and appears not to alter the safety profile of cetuximab. Considering the side effects of diphenhydramine, routine long tern use of antihistamine premedication with cetuximab administration does not appear to be warranted. [Table: see text]
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Landi, Nicola, Vincenza Ciaramella, Sara Ragucci, Angela Chambery, Fortunato Ciardiello, Paolo V. Pedone, Teresa Troiani, and Antimo Di Maro. "A Novel EGFR Targeted Immunotoxin Based on Cetuximab and Type 1 RIP Quinoin Overcomes the Cetuximab Resistance in Colorectal Cancer Cells." Toxins 15, no. 1 (January 9, 2023): 57. http://dx.doi.org/10.3390/toxins15010057.

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Cetuximab is a monoclonal antibody blocking the epidermal growth factor receptor (EGFR) in metastatic colorectal cancer (mCRC). However, cetuximab treatment has no clinical benefits in patients affected by mCRC with KRAS mutation or in the presence of constitutive activation of signalling pathways acting downstream of the EGFR. The aim of this study was to improve cetuximab’s therapeutic action by conjugating cetuximab with the type 1 ribosome inactivating protein (RIP) quinoin isolated from quinoa seeds. A chemical conjugation strategy based on the use of heterobifunctional reagent succinimidyl 3-(2-pyridyldithio)propionate (SPDP) was applied to obtain the antibody-type 1 RIP chimeric immunoconjugate. The immunotoxin was then purified by chromatographic technique, and its enzymatic action was evaluated compared to quinoin alone. Functional assays were performed to test the cytotoxic action of the quinoin cetuximab immunoconjugate against the cetuximab-resistant GEO-CR cells. The novel quinoin cetuximab immunoconjugate showed a significant dose-dependent cytotoxicity towards GEO-CR cells, achieving IC50 values of 27.7 nM (⁓5.0 μg/mL) at 72 h compared to cetuximab (IC50 = 176.7 nM) or quinoin (IC50 = 149.3 nM) alone assayed in equimolar amounts. These results support the therapeutic potential of quinoin cetuximab immunoconjugate for the EGFR targeted therapy, providing a promising candidate for further development towards clinical use in the treatment of cetuximab-resistant metastatic colorectal cancer.
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Ikezawa, Nobuaki, Satoru Iwasa, Hirokazu Shoji, Yoshitaka Honma, Atsuo Takashima, Natsuko T. Okita, Ken Kato, and Yasuhiro Shimada. "Panitumumab or cetuximab combined with irinotecan in patients with KRAS wild-type metastatic colorectal cancer previously treated with fluoropyrimidine-, oxaliplatin-, and irinotecan-based regimens." Journal of Clinical Oncology 32, no. 3_suppl (January 20, 2014): 642. http://dx.doi.org/10.1200/jco.2014.32.3_suppl.642.

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642 Background: Panitumumab and cetuximab are known to be effective in KRAS wild-type metastatic colorectal cancer (mCRC). However, it is not clear whether panitumumab and irinotecan confers benefit that are comparable to those of cetuximab and irinotecan in patients with KRAS wild-type mCRC previously treated with fluoropyrimidine-, oxaliplatin-, and irinotecan-based regimes. Methods: We analyzed 139 patients who had received panitumumab or cetuximabu combined with irinotecan for KRAS wild-type mCRC previously treated with fluor opyrimidine-, oxaliplatin-, and irinotecan-based regimes.We evaluated and compared efficacy and safety of panitumumab plus irinotecan and cetuximab plus irinotecan. Results: Baseline characteristics were similar for the two groups receving cetuximab pulus irinotecan (n = 97) and panitumumab plus irinotecan (n = 42),respectively.In patients with measurable lesions,the response rate (unconfirmed complete or partial response) were 20% (18/92) in the group receving cetuximab plus irintecan and 34% (14/41) in that receving panitumumab plus irinotecan. Median progression-free survival was 5.7 months in the cetuximab plus irinotecan group versus 4.3 months in the panitumumab plus irinotecan group. Median overall survival was 11.2 months in the cetuximab plus irinotecan group versus 13.6 months in the panitumumab plus irinotecan group. The most common adverse events in the cetuximab plus irinotecan versus panitumumab plus irinotecan groups were all-grade rash acneiform (82% versus 90%), paronychia (61% versus 52%), and grade 3-4 neutropenia (26% versus 19%). Conclusions: Panitumumab or cetuximab plus irinotecan were well tolerated and produced similar response rate and survivals compared to those previous clinical traials.These combinations are cosidered as standard treatment in patients with KRAS wild-type mCRC previously treated with fluoropyrimidine-, oxaliplatin-, and irinotecan-based regimes.
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Chung, Ki Young, Jinru Shia, Nancy E. Kemeny, Manish Shah, Gary K. Schwartz, Archie Tse, Audrey Hamilton, et al. "Cetuximab Shows Activity in Colorectal Cancer Patients With Tumors That Do Not Express the Epidermal Growth Factor Receptor by Immunohistochemistry." Journal of Clinical Oncology 23, no. 9 (March 20, 2005): 1803–10. http://dx.doi.org/10.1200/jco.2005.08.037.

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Purpose To establish evidence of activity, or lack thereof, of cetuximab-based therapy in patients with refractory colorectal cancer with tumors that do not demonstrate epidermal growth factor receptor (EGFR) expression by immunohistochemistry (IHC). Patients and Methods Pharmacy computer records were reviewed to identify all patients who received cetuximab at Memorial Sloan-Kettering Cancer Center in a nonstudy setting during the first 3 months of cetuximab's commercial availability. Medical records of these patients were then reviewed to identify colorectal cancer patients who had experienced failure with a prior irinotecan-based regimen and who had a pathology report indicating an EGFR-negative tumor by IHC. Pathology slides from these patients were reviewed by a reference pathologist to confirm EGFR negativity, and computed tomography scans during cetuximab-based therapy were reviewed by a reference radiologist. Response rates were reported using WHO criteria. Results Sixteen chemotherapy-refractory, EGFR-negative colorectal cancer patients who received cetuximab in a nonstudy setting were identified. Fourteen of these patients received cetuximab plus irinotecan, and two received cetuximab monotherapy. In the 16 patients, four major objective responses were seen (response rate, 25%; 95% CI, 4% to 46%). Conclusion Colorectal cancer patients with EGFR-negative tumors have the potential to respond to cetuximab-based therapies. EGFR analysis by current IHC techniques does not seem to have predictive value, and selection or exclusion of patients for cetuximab therapy on the basis of currently available EGFR IHC does not seem warranted.
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Kohrt, Holbrook Edwin, Roch Houot, Kipp Weiskopf, Matthew Goldstein, Peder Lund, Ruth R. Lira, Emily Troutner, et al. "Targeting CD137 to enhance the antitumor efficacy of cetuximab by stimulation of innate and adaptive immunity." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 3015. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.3015.

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3015 Background: Cetuximab therapy results in beneficial, yet limited, clinical improvement for patients with KRAS wildtype (WT) colorectal (CRC) and head and neck (HN) cancer. The efficacy of cetuximab, an IgG1 monoclonal antibody against EGFR, is due in part to antibody-dependent cell-mediated cytotoxicity (ADCC) by natural killer (NK) cells. CD137 is a costimulatory molecule expressed following activation on NK and memory, antigen-specific, CD8 T cells. Methods: We investigated the hypothesis that the combination of cetuximab with anti-CD137 mAb will enhance innate and adaptive immunity, thereby improving cetuximab’s anti-tumor efficacy in preclinical models and a prospective trial, NCT01114256. Results: NK cells increased their expression of CD137 by a factor of 30-40 when exposed to cetuximab-coated, EGFR-expressing HN and CRC cell lines. An agonistic anti-CD137 mAb enhanced NK cell degranulation and cytotoxicity 2-fold (~45 to 90% tumor lysis assayed by chromium release). The combination of cetuximab and anti-CD137 mAbs was synergistic in a syngeneic, human-EGFR-transfected murine tumor leading to complete tumor resolution and prolonged survival. NK cell depletion, significantly, and CD8 T cell depletion, partly, abrogated the anti-tumor efficacy of this combination. A series of HN and both KRAS WT and mutant CRC xenotransplant models demonstrated synergy with cetuximab and anti-CD137 mAbs. In our clinical trial, 54 patients with HN cancer receiving cetuximab therapy, circulating and intratumoral NK cells upregulated CD137 with amplitude influenced by duration post-cetuximab and host FcyRIIIa polymorphism. Interestingly, in 10 HLA-A2+ patients, following cetuximab, an increase in EGFR-specific, CD137-expressing, CD8 T cells directly correlated with the percent increase in CD137-expressing NK cells. Conclusions: Our results demonstrate the synergy of combining an agonistic mAb, anti-CD137, augmenting ADCC and T cell memory following a tumor-targeting mAb, cetuximab, in HN and KRAS mutant and WT CRC cancer. These results support a novel, sequential antibody approach by targeting first the tumor and then the host innate and adaptive immune system. Clinical trial information: NCT01114256.
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Thanikachalam, Kannan, Jayasree Krishnan, Farzan Siddiqui, Haythem Y. Ali, and Jawad Sheqwara. "Carboplatin versus cetuximab chemoradiation in cisplatin ineligible locally advanced head and neck squamous cell carcinoma." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e18555-e18555. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e18555.

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e18555 Background: Squamous cell carcinomas (SCC) of Head and neck are associated with tobacco, alcohol use and HPV infection. About 60% of patients with head and neck cancers(HNC) are locally advanced on diagnosis. Concurrent chemoradiation (CCRT) is standard of care in inoperable locally advanced HNC(LA-HNC), high risk adjuvant setting and organ function preservation. While cisplatin (CDDP) is the standard of care for CCRT, alternatives are carboplatin alone or cetuximab alone or carboplatin in combination with 5-FU or paclitaxel CCRT in CDDP ineligible setting. Methods: Patients with LA-HNC (SCC), from 01/01/2013-12/31/2018, who were ineligibile for CDDP CCRT and who received either carboplatin or cetuximab CCRT were included. Patients who received induction chemotherapy and had nasopharynx primary were excluded. 68 patients were analyzed to evaluate outcomes in patients who received carboplatin CCRT and cetuximab CCRT. Progression free survival (PFS) and Overall survival (OS) were calculated by Kaplan Meier analysis with SPSS v26. Results: There was a trend toward improved PFS in CarboRT group among oropharynx HNC patients who were P16 Negative(-ve) (59.5 months(m) vs 37.7 m, p value – 0.069). Among oropharynx HNC patients who were p16 positive, there was no statistically significant difference in PFS among CarboRT vs CetuximabRT (45.8 m vs. 39.77 m, p value – 0.51). OS was favorable towards carboRT in oropharynx SCC p16-ve group (59.5 m vs. 40.97 m, p value – 0.41). There was no difference in OS in p16+ve Oropharynx SCC group, who received CarboRT and CetuximabRT (45.74 vs. 45.94 m, p value – 0.77). When patients were analyzed regardless of their p16 status, site or stage, patients who received CarboRT had a higher OS at 56.30 m (95% CI 45.10-67.50%) vs. 38.11 m (95% CI 28.84-47.38%) among patients who received CetuximabRT (p value-0.048). Though PFS clinically favored carboRT group, when compared to CetuximabRT (55.43 m vs. 36.75 m), it was not statistically significant (p value – 0.10). Conclusions: In our analysis, patients who received single agent carboplatin CCRT had higher OS when compared to cetuximab CCRT. Though other outcomes favored carboplatinRT including PFS among entire group and p16-ve group, OS in p16-ve patients, it was not statistically significant, which is likely due to low power. Based on our analysis, for LA-HNC, carboplatin CCRT should be favored over cetuximab CCRT for patients ineligible for CDDP, particularly in P-16 -ve disease. Further randomized clinical trials can shed more data in this reduced intensity regimen.
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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1377 (November 2011): 13. http://dx.doi.org/10.2165/00128415-201113770-00038.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1379 (November 2011): 12. http://dx.doi.org/10.2165/00128415-201113790-00041.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1381 (December 2011): 9. http://dx.doi.org/10.2165/00128415-201113810-00029.

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Dissertations / Theses on the topic "Cetuximab"

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Angles, M., and John B. Bossaer. "Cetuximab-related Hypersensitivity Reactions in Northeast Tennessee." Digital Commons @ East Tennessee State University, 2012. https://dc.etsu.edu/etsu-works/2357.

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Primary Objective: To confirm the findings of several small studies conducted in the southeastern United States showing hypersensitivity infusion reaction (HIR) rates as high as 22% with the monoclonal antibody, cetuximab. Although well known for a risk of HIRs, early clinical studies showed much lower reaction rates of 3%.
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De, Angelis Maria Laura. "Cetuximab effect on human colon cancer stem cells." Doctoral thesis, Università di Catania, 2014. http://hdl.handle.net/10761/1488.

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Cancer Stem cells (CSCs), recently identified in the majority of solid tumors, are thought to drive tumor growth, giving rise to a cascade of differentiated cells composing the bulk of the tumor. Tumor relapse that most often follows treatment with anti-proliferative and cytotoxic drugs would be explained by selective resistance of CSC to these agents. Colon cancer stem cells (cCSCs), first isolated in the host laboratory from surgical specimens, can be grown in vitro as clusters called tumor spheres that maintain an undifferentiated state and are able, upon injection in immunodeficient mice, to generate a xenograft identical to the parental tumor, in terms of both antigen expression and histological tissue organization. Because of all these features cCSCs may represent predictive tools for patient s therapeutic response. Cetuximab (Erbitux), currently in use for metastatic colorectal cancer, is a recombinant chimeric human:murine immunoglobulin IgG1 that binds to EGFR displacing its natural ligands. Cetuximab also induces receptor internalization and degradation. Mutations in signaling pathway mediators acting downstream of EGFR, including KRAS, BRAF, NRAS, or PIK3CA are believed to determine resistance to the drug. In particular, KRAS-mutated patients are currently excluded from treatment. In order to verify whether Cetuximab treatment affects the stem cell compartment within tumors, in this study I analyzed its effect in a panel of cCSCs generated by individual patients, both in vitro and in xenografts. The data show that the effect of Cetuximab on individual cCSCs reflects the known clinical data on individual tumor mutations in the EGFR signaling pathway molecules. The study therefore confirms that panels of cCSCs generated by individual patients represent good predictive tools for the preclinical screening of pathway-oriented, cancer stem cell-directed therapeutics. Most importantly, the analysis of stem cell content in Cetuximab-treated xenografts by cytofluorimetry, agarose assay, and serial re-transplantation into secondary hosts clearly demonstrate that Cetuximab, differently than the classical chemotherapeutics currently in use for colon cancer, is able to effectively hit cCSC populations included in the tumors.
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Adams, C. B., D. S. Street, and John B. Bossaer. "Incidence of Cetuximab-related Infusion Reactions in Northeastern Tennessee." Digital Commons @ East Tennessee State University, 2015. https://dc.etsu.edu/etsu-works/2351.

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Adams, C. B., D. S. Street, and John B. Bossaer. "Incidence of Cetuximab-related Infusion Reactions in Northeastern Tennessee." Digital Commons @ East Tennessee State University, 2014. https://dc.etsu.edu/etsu-works/2352.

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Cyran, Carolin Anna Maria. "Immunologische Veränderungen bei Patienten mit akneiformem Exanthem unter Cetuximab-Therapie." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-124322.

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Santoro, V. "The interaction of cetuximab with chemotherapeutic agents in colon cancer." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1454999/.

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Cetuximab is a monoclonal antibody targeting the epidermal growth factor receptor (EGFR) and is used for the treatment of metastatic colorectal cancer (mCRC) as monotherapy or in combination with chemotherapy. Recent clinical trials have shown little benefit in combining cetuximab with oxaliplatin in contrast to the positive interactions observed with irinotecan. This thesis aims to understand why a subset of colorectal cancers do not benefit from cetuximab and oxaliplatin combined treatment. In vitro drug combination assays showed that the addition of cetuximab to oxaliplatin resulted in antagonistic effects on cell proliferation as opposed to the synergism observed with 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan. Although both oxaliplatin and SN-38 increased the levels of reactive oxygen species (ROS), only oxaliplatin was able to induce ROS-mediated apoptosis via the activation of p38 Mitogen-Activated Protein Kinase (MAPK). RT-PCR oxidative stress array analysis revealed that oxaliplatin can produce ROS through the upregulation of the NADPH oxidase ROS generating enzyme Dual Oxidase 2 (DUOX2) and that cetuximab, by preventing DUOX2 induction, can inhibit ROS generation by oxaliplatin. Chromatin Immunoprecipitation (ChIP) of Signal Transducer and Activator of Transcription 1 (STAT1) following oxaliplatin treatment, indicated a role for this protein in the transcriptional upregulation of DUOX2 by direct promoter-binding. Cetuximab, by impairing STAT1 activation and DUOX2 upregulation, can antagonise ROS-mediated apoptosis by oxaliplatin through the activation of the p38 pathway. Microarray analysis was employed to identify deregulated genes in the p38 pathway following cetuximab and oxaliplatin treatment in order to better clarify the role that p38-regulated genes play in the negative interactions of these drugs. The results presented in this thesis highlight the importance of ROS generation for the cytotoxic effects of oxaliplatin and indicate that combination with ROS-reducing agents such as cetuximab can result in negative cellular effects. Understanding how these drug interactions lead to antagonistic effects will be useful for the optimisation of future therapeutic combinations in the clinical setting.
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SAXENA, GUNJAN. "SYNTHESIS AND CHARACTERIZATION OF DOXORUBICIN CARRYING CETUXIMAB-PAMAM DENDRIMER BIOCONJUGATES." VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/2788.

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A tumor targeted dendrimer based drug delivery system was designed and synthesized to carry chemotherapy drug doxorubicin. Polyamidoamine (PAMAM) dendrimer G4.5 was chosen as the underlying carrier. Anionic G4.5 is a good option for drug delivery as it consists of 128 surface groups, is less cytotoxic and favorably biodistributed. The delivery system was synthesized using a layer-by layer arrangement of three functional entities: chemotherapy drug doxorubicin, monoclonal antibody Cetuximab against EGF receptor, and polyethylene glycol (PEG). Doxorubicin was attached via an acid-sensitive hydrazon linkage to the dendrimer. Macromolecules are taken in by cells through endocytosis. pH inside the early endosomes to lysosomes ranges from pH 6 to 4.5. These acidic conditions are favorable for release of drug bound to the dendrimer vehicle through acid-sensitive linkage. 35% of all solid tumors of brain express exceptionally high EGF receptors whereas normal brain tumors express less EGFR. This makes the EGFR a potent targeting moiety for targeted drug delivery. Cetuximab will serve as a targeting ligand to help the delivery system target tumor cells. PEG was incorporated as a linker between Cetuximab and dendrimer to avoid reticuloendothelial system (RES) uptake of the system, increase biocompatibility, increase drug half-life and other shortcomings associated with nanomaterials. Nuclear magnetic resonance spectroscopy (NMR), fluorescence anisotropy, and western blotting were used to confirm the conjugation of PEG, doxorubicin and cetuximab to the dendrimer. The synthesized delivery system was characterized using ultraviolet-visible spectroscopy (UV-Vis) to approximate the number of doxorubicin attached. Dynamic light scattering (DLS) and zeta potential were used to analyze the change in size and surface properties of dendrimer during the synthesis. Doxorubicin release studies were conducted at different pHs. Maximum doxorubicin was released at pH 4.5 indicating the successful acid-sensitive linkage between the drug and dendrimer. Cytotoxicity studies indicated that the addition of PEG increased the biocompatibility as compared to free doxorubicin whereas; combination of doxorubicin and cetuximab exerted a significant toxic effect over a period of 72 hours. The cellular uptake of the delivery system was higher than that of free doxorubicin. Free DOX localized mainly in the nucleus whereas, CTX-G4.5-PEG-DOX conjugate localized within both cytoplasm and nucleus after 6 hour incubation. The synthesized delivery system represents a potential targeted drug delivery system.
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Espinosa-Cotton, Madelyn. "Interleukin-1 signaling contributes to the anti-tumor efficacy of Cetuximab in head and neck squamous cell carcinoma." Diss., University of Iowa, 2018. https://ir.uiowa.edu/etd/6570.

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Despite the incorporation of the epidermal growth factor receptor (EGFR) inhibitor cetuximab into the clinical management of recurrent and metastatic (R/M) head and neck squamous cell carcinoma (HNSCC), only a small subset of patients responds to cetuximab, despite EGFR overexpression in virtually all of their tumors. At this time, there is a lack of validated predictive biomarkers to predict which patients will respond to cetuximab. Our previous work suggests that cetuximab activates the interleukin-1 (IL-1) pathway via tumor release of IL-1 alpha (IL-1α), although the implications of activating this pathway are unclear. The IL-1 pathway plays a central role in immune response and displays both pro-tumor and anti-tumor activities. IL-1 may promote tumor growth by upregulating the secretion of pro-inflammatory mediators involved in angiogenesis and metastasis. On the other hand, IL-1 signaling may promote antitumor immunity via enhancement of natural killer (NK)-cell mediated antibody-dependent cell-mediated cytotoxicity (ADCC) and T cell activity, which are important mechanisms of action of cetuximab. The goal of this work is to determine how modulation of the IL-1 pathway affects HNSCC tumor response to cetuximab and if IL-1 may serve as a predictive biomarker for patient response to cetuximab. Blockade of IL-1 signaling did not enhance the anti-tumor efficacy of cetuximab, while IL-1α overexpression and treatment with recombinant IL-1α and IL-1α nanoparticles increased HNSCC tumor response to cetuximab in immunodeficient and immunocompetent HNSCC mouse models. Mechanistically, these results appear to be due to activation of an anti-tumor NK and T cell-mediated immune response. Additionally, we found that both nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) and inducible nitric oxide synthase (iNOS) activity may be involved in the efficacy of IL-1-induced ADCC against cetuximab-coated HNSCC cells. Altogether, these results suggest that IL-1 signaling is necessary for HNSCC tumor response to cetuximab. Furthermore, we have shown that pre-treatment serum and tumor IL-1 ligands can predict progression-free survival of HNSCC patients treated with standard-of-care cetuximab and chemotherapy, cetuximab combined with other targeted therapies, and cetuximab monotherapy. Overall, we propose that IL-1α warrants further study as a novel therapeutic to enhance response to cetuximab and as a predictive biomarker for HNSCC response to cetuximab.
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Ziegler, Katharina Melanie. "Untersuchungen zur Stabilisierung und Interaktion von Cetuximab mit nicht-ionischen Tensiden." Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-164761.

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Gomes, Ana Catarina Domingues. "O papel do cetuximab no tratamento do carcinoma colo-rectal matastizado." Master's thesis, Faculdade de Medicina da Universidade do Porto, 2010. http://hdl.handle.net/10216/61075.

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Books on the topic "Cetuximab"

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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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An inquiry into the ImClone cancer-drug story: Hearings before the Subcommittee on Oversight and Investigations of the Committee on Energy and Commerce, House of Representatives, One Hundred Seventh Congress, second session, June 13 and October 10, 2002. Washington: U.S. G.P.O., 2002.

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Book chapters on the topic "Cetuximab"

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Knowlton, Christin A., Michelle Kolton Mackay, Tod W. Speer, Robyn B. Vera, Douglas W. Arthur, David E. Wazer, Rachelle Lanciano, et al. "Cetuximab." In Encyclopedia of Radiation Oncology, 99. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_628.

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Schwab, Manfred. "Cetuximab." In Encyclopedia of Cancer, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_1038-2.

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Tridente, Giuseppe. "Cetuximab." In Adverse Events with Biomedicines, 159–72. Milano: Springer Milan, 2013. http://dx.doi.org/10.1007/978-88-470-5313-7_15.

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Wilke, Sonja, and Michael Hust. "Cetuximab (Erbitux)." In Handbook of Therapeutic Antibodies, 1501–20. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2014. http://dx.doi.org/10.1002/9783527682423.ch52.

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

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AbstractDeregulated or increased signalling of the epidermal growth factor receptor (EGFR) plays an integral role in the development of various cancer types, including head and neck squamous cell carcinoma (HNSCC), making it a compelling drug target. However, after initially promising results of EGFR-targeted therapies, such as the monoclonal antibody cetuximab, it became clear that both intrinsic and acquired therapeutic resistance are major roadblocks in the field of personalised cancer treatments.In order to unravel and overcome resistance to cetuximab, at least two strategies can be adopted.Firstly, therapeutic resistance to anti-EGFR therapy may arise from mechanisms that can compensate for reduced EGFR signalling and/or mechanisms that can modulate EGFR-dependent signalling. In this chapter, we discuss which mechanisms of cetuximab resistance are already known and which ones deserve further investigation. This enhanced knowledge will guide us to rationally design and test novel combination therapies that overcome resistance to EGFR-targeting agents in cancer treatment.Secondly, an urgent need remains to develop novel targeted treatments for single-agent or combined therapy use. In this view, due to the particular mode of activation of the EGFR receptor, involving ligand-induced homo- and heterodimerization of the four HER receptors, an increased inhibition scope of HER receptors most likely results in a more potent blockade of the HER network, preventing premature emergence of resistance and leading to a more pronounced therapeutic benefit. We discuss two multitargeted compounds, being MEHD7945A (duligotuzumab) and afatinib, in this chapter.Despite the huge efforts to unravel the molecular landscape of HNSCC, the main clinically validated target remains EGFR. However, immune checkpoints, like programmed cell death protein 1 (PD-1), are gaining clinical approvals as well. We underscore the importance of adopting rational drug combinations to enhance the therapeutic effect of the EGFR-inhibitor cetuximab and highlight the ongoing search for predictive biomarkers, with the ultimate goal of delivering individualized cancer therapy to HNSCC patients.
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Nolting, Arno, Floyd E. Fox, and Andreas Kovar. "Clinical Drug Development of Cetuximab, a Monoclonal Antibody." In Pharmacokinetics and Pharmacodynamics of Biotech Drugs, 353–71. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2006. http://dx.doi.org/10.1002/9783527609628.ch14.

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Hildebrandt, Bert, Philipp le Coutre, Annett Nicolaou, Konrad Kölble, Hanno Riess, and Bernd Dörken. "Cetuximab: Appraisal of a Novel Drug Against Colorectal Cancer." In Targeted Therapies in Cancer, 135–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-46091-6_11.

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Beyaert, Simon, and Jean-Pascal Machiels. "Is there a Role for Neoadjuvant Targeted Therapy and Immunotherapy?" In Critical Issues in Head and Neck Oncology, 193–203. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_13.

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AbstractNeoadjuvant chemotherapy in head and neck cancer is the subject of much debate. Multiple trials have shown that the concomitant addition of targeted therapies, such as cetuximab to neoadjuvant chemotherapy (docetaxel, cisplatin, 5-fluorouracil), results in increased toxicity. Furthermore, no apparent significant benefit has been demonstrated in small randomized studies. Additional trials are currently being conducted to investigate the role of neoadjuvant immunotherapy, such as anti-PD-(L)1 inhibitors.On the other hand, window of opportunity studies are trials in which patients receive one investigational compound in the period between their cancer diagnosis and the start of standard therapy. The evaluation of new compounds using this approach enables translational research and provides information on molecular and clinical activity as well as predictive biomarkers.
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Boutayeb, Saber, and Mohammed Anass Majbar. "General Oncology Care in Morocco." In Cancer in the Arab World, 163–74. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-7945-2_11.

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AbstractThe current population of Morocco is estimated to be 37 million based on the projection of the United Nations data. The median age in the Moroccan population is young. Around 25% of the population is aged under 14 years. Morocco is currently in an epidemiological transition called “double burden,” with the coexistence of infectious and chronic diseases. The most frequent cancers in men are lung, prostate, bladder, colorectum, and lymphoma. Whereas, for women, the most frequent are breast, cervix, colorectum, thyroid, and ovary. The first Moroccan cancer plan (2010–2019) has given the priority to breast and cervix cancers. Concerning treatments, the classical chemotherapies, hormonal therapies, and the first generation of monoclonal antibodies (Trastuzumab, Rituximab, Bevacizumab, Cetuximab, etc.,) are widely available for the entire population. Two immunotherapies are available in Morocco: Pembrolizumab and Atezolizumab. However, their reimbursement is still conflictual. 3D and new irradiation techniques are available in the major cities. Advanced minimally invasive techniques are now routinely performed for colorectal, liver, gynecologic, thoracic, and urologic cancers. The first surgical robot was acquired by the university hospital in Fez in 2019.
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Roden, Dylan F., Jennifer M. Johnson, Petr Szturz, Paolo Bossi, and Athanassios Argiris. "New and Promising Targeted Therapies in First and Second-Line Settings." In Critical Issues in Head and Neck Oncology, 277–96. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_18.

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

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Levi, Mattan, Aaron Popovtzer, Moran Tzabari, Salomon M. Stemmer, Ruth Shalgi, and Irit Ben-Aharon. "Abstract 3840: Cetuximab-induced testicular toxicity." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3840.

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Marzi, Laetitia, Eve Combès, Nadia Vezzio-Vié, Gaelle Thomas, Christel Larbouret, Laetitia Linares, Clara Montagut, et al. "Abstract A62: p38MAPK implication in cetuximab response." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-a62.

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Brand, Toni M., Emily F. Dunn, Mari Iida, Rebecca Myers, Chunrong Li, and Deric L. Wheeler. "Abstract 726: Erlotinib overcomes acquired resistance to cetuximab." In 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.am2011-726.

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Herrmann, Delia, Guido Seitz, Steven W. Warmann, Michael Bonin, Jörg Fuchs, and Sorin Armeanu-Ebinger. "Abstract 3416: Cetuximab promotes immunotoxicity against rhabdomyosarcoma in vitro." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3416.

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Brand, Toni, Yan Zeng, Brandon Leonard, Rachel O' Keefe, Hua Li, Daniel Johnson, Jennifer Grandis, and Neil E. Bhola. "Abstract 95: Targeting BRD4 overcomes cetuximab resistance in HNSCC." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-95.

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Yonesaka, Kimio, Isamu Okamoto, Taroh Satoh, Kohji Takeda, Minoru Takada, Kazuto Nishio, Masahiro Fukuoka, Pasi A. Janne, and Kazuhiko Nakagawa. "Abstract 3733: Heregulin as a novel resistant factor for cetuximab." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3733.

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Dunn, Emily F., Mari Iida, Eric Armstrong, and Deric L. Wheeler. "Abstract C43: Dasatinib resensitizes Kras mutant colorectal tumors to cetuximab." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-c43.

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Santoro, Valeria, John A. Hartley, and Daniel Hochhauser. "Abstract 5468: Interaction between cetuximab and chemotherapy in colon cancer." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5468.

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Li, Xinqun, Yang Lu, Ke Liang, and Zhen Fan. "Abstract 1259: Cetuximab induces autophagy that is mediated through downregulation of HIF1α/Bcl-2 and protects cancer cells escape from cetuximab-mediated therapeutic effects." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1259.

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Bonizzi, Arianna, Miriam Colombo, Maria Antonietta Rizzuto, Chiara Pacini, Laura Pandolfi, Marta Truffi, Matteo Monieri, et al. "Cetuximab-Conjugates Nanoparticles for the Treatment of Triple Negative Breast Cancer." In The 4th World Congress on Recent Advances in Nanotechnology. Avestia Publishing, 2019. http://dx.doi.org/10.11159/nddte19.104.

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Reports on the topic "Cetuximab"

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Wheeler, Deric L., Toni M. Brand, and Mari Iida. Targeting Nuclear EGFR: Strategies for Improving Cetuximab Therapy in Lung Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada599892.

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