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Journal articles on the topic 'Cetuximab'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 March 2023

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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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7

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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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1382 (December 2011): 15. http://dx.doi.org/10.2165/00128415-201113820-00048.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1382 (December 2011): 15. http://dx.doi.org/10.2165/00128415-201113820-00051.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1384 (January 2012): 18. http://dx.doi.org/10.2165/00128415-201213840-00066.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1386 (January 2012): 15. http://dx.doi.org/10.2165/00128415-201213860-00049.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1392 (March 2012): 16. http://dx.doi.org/10.2165/00128415-201213920-00045.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1164 (August 2007): 11. http://dx.doi.org/10.2165/00128415-200711640-00028.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1167 (September 2007): 10. http://dx.doi.org/10.2165/00128415-200711670-00028.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1176 (November 2007): 9–10. http://dx.doi.org/10.2165/00128415-200711760-00026.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1176 (November 2007): 9. http://dx.doi.org/10.2165/00128415-200711760-00028.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1178 (November 2007): 13. http://dx.doi.org/10.2165/00128415-200711780-00036.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1184 (January 2008): 13. http://dx.doi.org/10.2165/00128415-200811840-00038.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1186 (January 2008): 16. http://dx.doi.org/10.2165/00128415-200811860-00050.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1191 (March 2008): 8. http://dx.doi.org/10.2165/00128415-200811910-00021.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1193 (March 2008): 11. http://dx.doi.org/10.2165/00128415-200811930-00031.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1194-1195 (March 2008): 13. http://dx.doi.org/10.2165/00128415-200811940-00040.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1127 (November 2006): 9. http://dx.doi.org/10.2165/00128415-200611270-00029.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1128 (November 2006): 8–9. http://dx.doi.org/10.2165/00128415-200611280-00025.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1131 (December 2006): 12. http://dx.doi.org/10.2165/00128415-200611310-00031.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1134 (January 2007): 10. http://dx.doi.org/10.2165/00128415-200711340-00035.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1135 (January 2007): 12–13. http://dx.doi.org/10.2165/00128415-200711350-00046.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1135 (January 2007): 13. http://dx.doi.org/10.2165/00128415-200711350-00047.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1143 (March 2007): 9. http://dx.doi.org/10.2165/00128415-200711430-00026.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1153 (May 2007): 8–9. http://dx.doi.org/10.2165/00128415-200711530-00027.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1154 (June 2007): 8. http://dx.doi.org/10.2165/00128415-200711540-00026.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1160 (July 2007): 13–14. http://dx.doi.org/10.2165/00128415-200711600-00033.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1160 (July 2007): 14. http://dx.doi.org/10.2165/00128415-200711600-00037.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1358 (July 2011): 12. http://dx.doi.org/10.2165/00128415-201113580-00041.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1359 (July 2011): 13. http://dx.doi.org/10.2165/00128415-201113590-00041.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1363 (August 2011): 14. http://dx.doi.org/10.2165/00128415-201113630-00050.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1368 (September 2011): 12. http://dx.doi.org/10.2165/00128415-201113680-00042.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1369 (September 2011): 13. http://dx.doi.org/10.2165/00128415-201113690-00043.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1371 (October 2011): 12. http://dx.doi.org/10.2165/00128415-201113710-00036.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1372 (October 2011): 12. http://dx.doi.org/10.2165/00128415-201113720-00032.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1373 (October 2011): 10–11. http://dx.doi.org/10.2165/00128415-201113730-00030.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1373 (October 2011): 10. http://dx.doi.org/10.2165/00128415-201113730-00031.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1376 (November 2011): 10–11. http://dx.doi.org/10.2165/00128415-201113760-00032.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1402 (May 2012): 15. http://dx.doi.org/10.2165/00128415-201214020-00050.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1404 (June 2012): 13. http://dx.doi.org/10.2165/00128415-201214040-00036.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1409 (July 2012): 17. http://dx.doi.org/10.2165/00128415-201214090-00051.

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&NA;. "Cetuximab." Reactions Weekly &NA;, no. 1412 (July 2012): 13. http://dx.doi.org/10.2165/00128415-201214120-00045.

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