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Cetuximab is also used alone or in combination with other medications to treat a certain type of cancer of the colon large intestine or rectum that AXL mediates resistance to cetuximab therapy. The EGFR antibody cetuximab is used to treat numerous cancers, but intrinsic and acquired resistance to this agent is a common clinical problem.
In tumor xenograft assays, the development of resistance following rel treatment with cetuximab was associated with AXL hyperactivation and EGFR association.
Furthermore, in an examination of patient-derived xenografts established from surgically resected HNSCCs, AXL was overexpressed and activated in tumors that displayed intrinsic resistance to cetuximab. Collectively, our results identify AXL as a key mediator of cetuximab resistance, providing a rationale for clinical evaluation of AXL targeting drugs to treat cetuximab -resistant cancers. The EGFR antibody cetuximab is used to treat numerous cancers, but intrinsic and acquired resistance to this agent is l.whjteside common clinical outcome.
In tumor xenograft models, the development of resistance following prolonged treatment with cetuximab was associated with AXL hyperactivation and EGFR association. Collectively, our results identify AXL as a key mediator of cetuximab resistance, providing a rationale for clinical evaluation roberrt AXL-targeting drugs to treat cetuximab -resistant cancers. Cancer Res; 74 18 ; Cetuximaba chimeric ddl IgG1 monoclonal antibody against the epidermal growth factor receptor, has proven effective in the treatment of metastatic colorectal cancer and squamous cell carcinoma of the head and neck.
However, a high incidence of immediate hypersensitivity reactions HSR to cetuximab after the first infusion has been observed. We have developed lenguajd test for identification of patients likely to show treatment-related HSR to cetuximab. An enzyme-linked immunosorbent assay ELISA for detecting anti- cetuximab IgEs l.wgiteside developed and tested on serum samples collected from cancer patients before start of cetuximab treatment, and from healthy blood rostor.
HSR were observed in 14 out of the 92 patients Anti- cetuximab IgE ELISA detection could be a valuable tool to help the physician anticipate an anaphylaxis episode following cetuximab infusion and opt for a suitable alternative treatment.
Rare upper gastrointestinal hemorrhage of cetuximab: Several common adverse effects have been found, such as cutaneous or gastrointestinal toxicity.
El lenguaje del rostro by Robert L. Whiteside | LibraryThing
However, according to the articles had been published, upper gastrointestinal bleeding UGIB is considered to be rare and its mechanism remains unclear. In this report, we presented a year-old male patient with advanced recto-sigmoid cancer.
After palliative operation, the patient suffered from complete upper gastrointestinal GI l.whiteeide, which was induced by extensive abdominal metastasis of the tumor.
Considering his poor condition, we chose the targeted drug, cetuximabas his further treatment. But after the application of cetuximabthe UGIB immediately happened twice in this patient.
UGIB, as a rare complication of cetuximaboccured to the patient. We stopped the bleeding with thrombin, hemocoagulase and somatostatin and suspended the subsequent treatment plan of cetuximab. At the same time, anti-shock treatment was given immediately. He was died of l.hwiteside and circulatory failure caused by UGIB and advanced tumor eventually.
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UGIB should be considered as a rare but severe complication of cetuximab. When l.wgiteside is applied for patients with advanced colon tumors, more cautions should be required if the patients are accompanied by upper gastrointestinal obstruction. Published by Wolters Kluwer Health, Inc.
Cetuximab -induced hypomagnesaemia aggravates peripheral sensory neurotoxicity caused by oxaliplatin. Calcium and magnesium replacement is effective in reducing oxaliplatin-induced neurotoxicity. However, cetuximab treatment has been associated with severe hypomagnesaemia. Therefore, we retrospectively investigated whether cetuximab -induced hypomagnesaemia exacerbated oxaliplatin-induced neurotoxicity. Six patients with metastatic colorectal cancer who were previously treated with oxaliplatin-fluorouracil combination therapy were administered cetuximab in combination with irinotecan alone or irinotecan and fluorouracil as a second-line treatment.
All patients had normal magnesium levels before receiving cetuximab. All six patients had grade 1 or higher hypomagnesaemia after starting cetuximab therapy. The serum calcium and potassium levels were within the normal range at the ronert of hypomagnesaemia. Oxaliplatin-induced neurotoxicity leguaje in all patients at the beginning of cetuximab therapy, with grade 1 neurotoxicity in five patients and grade 2 in one patient.
After cetuximab administration, the neurotoxicity worsened in all six patients, and three progressed to grade 3. Among the three fel with grade 3 neurotoxicity, two required a dose reduction and one had to discontinue cetuximab therapy.
A discontinuation or dose reduction in cetuximab therapy was associated with exacerbated oxaliplatin-induced neurotoxicity due to cetuximab -induced hypomagnesaemia in half of patients who had previously received oxaliplatin. Therefore, when administering cetuximab after oxaliplatin therapy, we suggest serially evaluating serum magnesium levels and neurotoxicity. Cetuximab is widely used in patients with metastatic colon cancer expressing wildtype KRAS. However, acquired drug resistance limits its clinical efficacy.
Exosomes are nanosized vesicles secreted by various cell types. Tumor cell-derived exosomes participate in many biological processes, including tumor invasion, metastasis, and drug resistance. In this study, exosomes derived from cetuximab -resistant RKO colon cancer cells induced cetuximab resistance in cetuximab -sensitive Caco-2 cells.
Moreover, an Akt inhibitor prevented RKO cell-derived exosome-induced drug resistance in Caco-2 cells. These findings provide novel evidence that exosomes derived from cetuximab -resistant cells could induce cetuximab resistance in cetuximab -sensitive cells, by downregulating PTEN and increasing phosphorylated Akt levels.
Despite the clinical success of cetuximabmany patients do not respond to cetuximab. Furthermore, virtually all patients who do initially respond become refractory, highlighting both intrinsic and acquired resistance to cetuximab as significant clinical problems.
Here, we examined Pan-HER, a mixture of six antibodies targeting these receptors on cetuximab -resistant clones.
El Lenguaje del rostro
This correlated with decreased cell proliferation in cetuximab -resistant clones. To rohert whether Pan-HER had a therapeutic benefit in vivo, we established de novo cetuximab -resistant mouse xenografts and treated resistant tumors with Pan-HER.
This regimen resulted in a superior growth robdrt of cetuximab -resistant xenografts compared to mice continued on cetuximab.
These results suggest that targeting HER family receptors simultaneously with Pan-HER is a promising treatment strategy for tumors displaying intrinsic or acquired resistance to cetuximab. PTEN status in advanced colorectal cancer treated with cetuximab.
Loss of phosphatase and tensin homologue deleted in chromosome 10 PTEN function in advanced colorectal cancer CRC may represent one of the resistance mechanisms to cetuximab by interfering with the epidermal growth factor receptor signal transduction pathway. Severe skin reaction secondary to concomitant radiotherapy plus cetuximab.
The therapeutic use of monoclonal antibodies against the epidermal growth factor receptor EGFR is specifically associated with dermatologic reactions of variable severity. Recent evidence suggests superiority of l.whitesied EGFR inhibitor EGFRI cetuximab plus radiotherapy compared to radiotherapy alone in patients with squamous cell carcinoma of the head and neck. Although not documented in a study population, several reports indicate a possible overlap between radiation dermatitis and the EGFRI-induced skin rash.
We here present a case of severe skin reaction secondary to the addition l.whjteside cetuximab to radiotherapy. Epidermal growth factor has an important role in the regulation of proliferation and differentiation in epidermal keratinocytes, as well as in the survival, angiogenesis and metastasis of cancer cells. Cetuximab is a chimeric monoclonal antibody selective for the epidermal growth factor receptor that induces a broad range of cellular responses that enhance tumor sensitivity to radiotherapy and chemotherapeutic agents.
We report a case of severe acneiform eruption induced by cetuximab in a year-old man with colorectal cancer and liver metastases. Double drugs are obtained when two pharmacologically active entities are covalently joined to improve potency. We conjugated the viridin Wm with a self-activating linkage to lwnguaje and demonstrated the lwnguaje of immunoreactivity by the conjugate. Though cetuximab lacked a growth inhibitory activity against A roberh, the Wmcetuximab conjugate had an anti-proliferative IC50 of nM in vitro.
Robegt chemistry of attaching a self-releasing Wm to clinically approved antibodies is general and, in l.whkteside instances, rodtro yield antibody-based double drugs with improved efficacy. The use of cetuximab in the rostrp of metastatic colorectal cancer is limited by development of resistance. We have investigated in three models of highly epidermal growth factor receptor EGFR -dependent colorectal cancer xenografts, the effect of maintenance therapy with different kinase inhibitors alone or in combination with cetuximabafter cytotoxic treatment induction with irinotecan plus cetuximab.
The combined treatment induced a significant reduction of tumor size. A subsequent experiment was performed in all three xenograft models in which after an rostto treatment with irinotecan plus cetuximabmice were randomly assigned to one of the following treatments: The cetuximab plus MEKi treatment determined the best antitumor activity with suppression of tumor growth.
This effect was prolonged for 13 to 15 weeks after cessation of therapy and was accompanied by prolonged survival. Inhibition of BMP signaling overcomes acquired resistance to cetuximab in oral squamous cell carcinomas. Despite expressing high levels of the epidermal growth factor receptor EGFRa majority of oral squamous cell carcinoma OSCC patients show limited response to cetuximab and ultimately develop drug resistance.
However, mechanism underlying cetuximab resistance in OSCC is not clearly understood. Cetuximab for treating non-small cell lung cancer. Epidermal Growth Factor Receptor EGFR -dependent signaling plays a crucial role in epithelial cancer biology, and dictated the lenbuaje of several targeting agents.
The mouse-human chimeric antibody Cetuximab was among the first to be developed. After about two decades of clinical research it has gained a significant place in the management of advanced colorectal and head and neck cancers, whereas its development in non small cell lung cancer L.ahiteside has not led to a place in routine clinical practice, because of marginal clinical benefit despite statistically significant Phase III trials.
Recent data from ongoing trials suggest that l.whitesive careful selection based on molecular markers may identify good responders. In this article, the authors review the literature concerning basic science l.whitesidf identifying EGFR as a therapeutic target, pharmacological development of Cetuximabits pharmacodynamics and pharmacokinetics, and clinical trials on Cetuximab in NSCLC, focusing on recent findings on putative predictive biomarkers.
We argue that failure to identify a predictive biomarker early on has hampered its chances to enter routine practice. Although recent research suggests benefit in highly lw.hiteside patient subsets, its potential impact is severely dampened by lack of regulatory body approval and the emergence of competitors for the same niches.
Erlotinib is a viable treatment for tumors with acquired resistance to cetuximab. The epidermal growth factor receptor EGFR is an ubiquitously expressed receptor tyrosine kinase RTK and is recognized as a key mediator of tumorigenesis in many human tumors. Currently there are five EGFR inhibitors used in oncology, two monoclonal antibodies panitumumab and cetuximab and three tyrosine kinase inhibitors erlotinib, gefitinib and lapatinib.
Both strategies of EGFR inhibition have demonstrated clinical success; however, many tumors remain non-responsive or acquire resistance during therapy. To explore potential molecular mechanisms of acquired resistance to cetuximab we previously established a series of cetuximab -resistant clones by chronically exposing the NCI-H NSCLC cell line to escalating doses of cetuximab. These findings prompted investigation on whether or not cells with acquired resistance to cetuximab would be sensitive to the EGFR targeted TKI erlotinib.
In vitro, erlotinib was able to decrease signaling through the EGFR axis, decrease cellular proliferation and induce apoptosis. To determine if erlotinib could have therapeutic benefit in vivo, we established cetuximab -resistant NCI-H mouse xenografts, and subsequently treated them with erlotinib.
Mice harboring cetuximab -resistant tumors treated with erlotinib exhibited either a tumor regression or growth delay as compared with vehicle controls. Analysis of the erlotinib treated tumors demonstrated a decrease in cell proliferation and increased rates of apoptosis.
The work presented herein suggests that 1 cells with acquired resistance to cetuximab maintain their dependence on EGFR and 2 tumors developing resistance to cetuximab can benefit from subsequent treatment with erlotinib, providing rationale.