Tarceva

Manufactured by Roche

Sourced in Switzerland

Tarceva is a laboratory equipment product offered by Roche. It is used for laboratory analysis and testing. The core function of Tarceva is to assist in the research and development of new medical treatments.

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11 protocols using tarceva

Establishing Tarceva-resistant TNBC Cell Lines

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All cell lines used in this study were obtained from the American Type Culture Collection. The human TNBC (MDA-MB-231 and MDA-MB-468) cell lines were maintained in DMEM/F12 (1:1) with 10% (v/v) fetal bovine serum (GIBCO). The human TNBC lines BT-549 and BT-20 were maintained in RPMI-1640 supplemented with 10% (v/v) fetal bovine serum and 1% (w/v) penicillin/streptomycin. The non-tumorigenic mammary epithelial line MCF-10A was maintained in DMEM/F12 supplemented with 1.05 mM CaCl₂, 100 ng/mL cholera toxin, 5% (v/v) horse serum (Gibco), 10 μg/mL insulin, 100 U/mL penicillin, 100 μg/mL streptomycin, 20 ng/mL EGF (Sigma), and 500 ng/mL hydrocortisone. All cells were maintained in a humidified incubator at 37°C under a 5% CO₂ atmosphere. Capsanthin was dissolved in DMSO at a stock concentration of 60 mM and was stored at –20°C.
In order to establish the MDA-MB-231-Tarceva resistant cells, first, we cultured the cells in increasing doses of Tarceva (Roche) from 5 to 100 μM, which were increased stepwise over 6 months. We cloned the Tarceva-resistant cells after 8 months and keep the capsanthin concentration of 2 μM.

Wu J.Y., Chien Y.C., Tsai I.C., Hung C.C., Huang W.C., Liu L.C, & Yu Y.L. (2021). Capsanthin induces G1/S phase arrest, erlotinib-sensitivity and inhibits tumor progression by suppressing EZH2-mediated epigenetically silencing of p21 in triple-negative breast cancer cells. Aging (Albany NY), 13(9), 12514-12525.

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SRS and TKIs for Brain Metastases

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All metastatic tumors in the brain were treated with SRS using Leksell Gamma Knife model C (Elekta, Stockholm, Sweden). We obtained T1-weighted, high-dose gadolinium enhanced images, with an injected gadolinium volume of 0.4 mmol/kg. We used multiple isocenters to insure a highly conformal dose distribution and defined a prescription dose as a dose covering at least 93% of the target volume. To irradiate the tumor margins, the median peripheral dose of 23 Gy (range, 15-25 Gy) was prescribed at the median 50% isodose line (range, 34-65%). After SRS, the patients were observed to detect any acute adverse effects.
Patients treated with SRS and TKIs for brain metastases received the TKIs within 2 weeks of commencing SRS. These patients received oral gefitinib (Iressa; AstraZeneca, London, UK) 250 mg or erlotinib (Tarceva; Roche, Basel, Switzerland) 150 mg once daily. The other patients were treated with systemic chemotherapy. The guideline recommendations about application of EGFR-TKI treatment for lung cancer patients harboring activating EGFR mutation were changed from the second line treatment to the first line treatment in Korea in 2010. Among various systemic therapy, regimen was chosen for each patient regarding patients' preference, side effect and previous treatment history.

Kim H.J., Kim W.S., Kwon D.H., Cho Y.H, & Choi C.M. (2015). Effects of an Epithelial Growth Factor Receptor-Tyrosine Kinase Inhibitor Add-on in Stereotactic Radiosurgery for Brain Metastases Originating from Non-Small-Cell Lung Cancer. Journal of Korean Neurosurgical Society, 58(3), 205-210.

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Recurrent NSCLC: EGFR-TKI Retreatment Outcomes

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The current research is a retrospective study, 335 consecutive patients with histologically confirmed recurrent or metastatic NSCLC in Sun Yat-Sen University Cancer Center from May 2003 to September 2011 were reviewed. Patients were categorized as never-smoker (less than 100 cigarettes in a life-time), ex-smoker (quit more than 1 year ago) or current smoker(currently smoking or quit less than 1 year ago).
The entry criteria are as follows: (1). Patients that with drug sensitivity associated mutation site(e.g.: G719X, exon 19 deletion, L858R, L861Q); (2). Patients had treated with a EGFR-TKI: gefitinib 250 mg/qd (Iressa™, Astra Zeneca, London, Britain) or erlotinib 150 mg/qd (Tarceva™, Roche Pharma, Basel, Switzerland) with a disease control that more than 3 months; (3). Patients received re-administrated EGFR-TKI after progression to 1^st EGFR-TKIs; (4). Cessation of the 2^nd EGFR-TKIs therapy was permitted only when the patients incurred unbearable toxicity or disease progression according to the guidelines set out by Response Evaluation Criteria in Solid Tumors (RECIST) Committee17 18 (link).

Zhao Z.R., li W, & Long H. (2014). Readministration of EGFR Tyrosine Kinase Inhibitor in Non-small Cell Lung Cancer Patients after Initial Failure, What Affects its Efficacy?. Scientific Reports, 4, 5996.

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Formulation and Evaluation of Erlotinib Eye Drops

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To prepare the eye drops, erlotinib (Tarceva^®; Roche Diagnostics, Indianapolis, IN, USA) was diluted in sterile PBS to a concentration of 20 μM and homogenized by ultrasound vortex (37°C, 100 W, 10 min). The preservative benzyl bromide (Sigma-Aldrich; Merck KGaA, Darmstadt, Germany) was added to the two groups (with a concentration controlled at 0.005%); one group was a control group using PBS eye drops, and the second group was the experimental group that received erlotinib eye drops. Eye drops were stored at 4°C prior to their use.

Yang Q.C., Bao J., Li C., Tan G., Wu A.H., Ye L., Ye L.H., Zhou Q, & Shao Y. (2017). A murine model of dry eye induced by topical administration of erlotinib eye drops. International Journal of Molecular Medicine, 41(3), 1427-1436.

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Erlotinib Dosing and Toxicity Monitoring

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Continuous oral erlotinib (Tarceva, Roche, Switzerland) was given on an outpatient basis at a fixed dose of 150 mg taken at least one hour before or two hours after the ingestion of food or any other medication. In the event of toxicity (e.g. diarrhea, rash), regardless of its severity, that was not controlled by optimal supportive care or not tolerated due to any reason, the daily dose of erlotinib was decreased to 100 mg/day. Patients who could not tolerate the reduced erlotinib dose were permanently discontinued from the study.
Evaluation of response was performed according to the RECIST criteria. Target lesions were assessed by clinical examination and computed tomography (CT). The initial examinations had to be performed within 28 days prior to registration. Evaluation of target lesions was planned every four weeks for the first six cycles and then every eight weeks. Response had to be confirmed by second evaluation performed at least four weeks apart. Study visits for toxicity evaluation were scheduled every four weeks. Toxicity was assessed by Common Toxicity Criteria 3.0 of the National Cancer Institute. Quality of life or lung cancer symptom assessment was not performed in this trial.

Szutowicz-Zielinska E., Konopa K., Kowalczyk A., Suszko-Kazarnowicz M., Duchnowska R., Szczesna A., Ratajska M., Sowa A., Limon J., Biernat W., Burzykowski T., Jassem J, & Dziadziuszko R. (2016). An open label phase II study evaluating first-line EGFR tyrosine kinase inhibitor erlotinib in non-small cell lung cancer patients with tumors showing high EGFR gene copy number. Oncotarget, 8(10), 17270-17278.

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EGFR-Targeted TKI Therapy Response

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A monocentric retrospective cohort study has been conducted on patients with a biopsy-proven non-small-cell lung carcinoma -presenting an identified or suspected EGFR (epidermal growth factor receptor) mutation, (established by a TKI clinical benefit of more than 6 months) -which are non-accessible to local treatment (stage IIIB or IV). Patients were included in the study if 3 CT-scans were available: one at baseline before the first introduction of TKI treatment and two after. The study was approved by Institut Bergonié and IRB approval was obtained for use of the CT images. Informed consents of data collection were waived for research from each patient, in accordance with the related policy of Institut Bergonié.
All patients were exposed to an EGFR-targeting TKI. Two molecules were used: gefitinib (IRESSA, Astra-Zeneca) and erlotinib (TARCEVA, Roche). These two therapies were given until progression, unacceptable toxicity, patient refusal to continue treatment or death.

Collin A., Groza V., Missenard L., Chomy F., Colin T., Palussière J, & Saut O. (2021). A Model-Strengthened Imaging Biomarker for Survival Prediction in EGFR-Mutated Non-small-cell Lung Carcinoma Patients Treated with Tyrosine Kinase Inhibitors. Bulletin of mathematical biology, 83(6).

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Capecitabine and Erlotinib for Cancer Treatment

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All patients received capecitabine (Xeloda; Hoffmann-La Roche, Nutley, NJ) combined with erlotinib (Tarceva; Hoffmann-La Roche). Both drugs in this study were provided free of charge by Shanghai Roche Pharmaceuticals Ltd., Shanghai, P.R.China (ML22206 study). Drug regimens were based on 3-week treatment cycles. Capecitabine (1000 mg/m²) was administered orally twice daily for 14 days followed by 7 days off. Erlotinib (150 mg/day) was administered orally, starting on the same day as capecitabine and continuing for the full 3 weeks of every cycle. The maximum number of cycles was until progression of disease (PD), defined as the emergence of new lesions, an increase in primary lesion > 25%, or the minimum treatment period until the primary lesion increased > 50%.
Patients received both medications until disease progression, unacceptable toxicity, patient refusal, alternate treatment, or the investigator's decision to remove the patient from the study.

Zhao H.Y., Chen G.Y., Huang Y., Li X.L., Feng J.F., Shi M.Q., Cheng Y., Ma L.X., Zhang Y.P., Gu C.P., Song X.Q., Zhou D, & Zhang L. (2015). Erlotinib Plus Capecitabine as First-Line Treatment for Older Chinese Patients With Advanced Adenocarcinoma of the Lung (C-TONG0807): An Open-Label, Single Arm, Multicenter Phase II Study. Medicine, 94(2), e249.

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Molecular Classification of Adenosquamous Carcinoma

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Each surgically resected tumor was systematically sampled according to standard procedures. Paraffin-embedded tumor specimens, which included the widest cross-sections, were reassessed by two senior clinical pathologists. The classification of adenomatous and squamous components within ASCs was performed by immunohistochemical staining of surgically resected tumors. Patients with ASC were subdivided into two groups according to post-surgical EGFR-TKI treatment as follows: the EGFR-TKI group, which included patients who received the TKI treatment in either an adjuvant or a recurrent setting, and the non-TKI group, which included patients who received only chemotherapy (CTx) or chemoradiotherapy (CRTx) over the entire treatment course. Specifically, in the EGFR-TKIs group, most patients received gefitinib (Iressa^®, AstraZeneca; 250 mg once daily; n=27), whereas two patients received erlotinib (Tarceva^®, Roche; 150 mg once daily; n=3). In the non-TKI group, CTx (cisplatin-based doublet) or CRTx (cisplatin-based doublet plus 45–70 Gy radiotherapy) was given.

Zhang C., Yang H., Lang B., Yu X., Xiao P., Zhang D., Fan L, & Zhang X. (2018). Surgical significance and efficacy of epidermal growth factor receptor tyrosine kinase inhibitors in patients with primary lung adenosquamous carcinoma. Cancer Management and Research, 10, 2401-2407.

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Anticancer Tyrosine Kinase Inhibitors

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Erlotinib (150 mg tablets; Tarceva^®; Roche, Basel, Switzerland), gefitinib (250 mg tablets; Iressa^®; AstraZeneca, London, UK), and imatinib (400 mg tablets; Glivec^®; Novartis, Basel, Switzerland) were sourced from our oncology department.

Pitsiou G., Zarogoulidis P., Petridis D., Kioumis I., Lampaki S., Organtzis J., Porpodis K., Papaiwannou A., Tsiouda T., Hohenforst-Schmidt W., Kakolyris S., Syrigos K., Huang H., Li Q., Turner J.F, & Zarogoulidis K. (2014). Inhaled tyrosine kinase inhibitors for pulmonary hypertension: a possible future treatment. Drug Design, Development and Therapy, 8, 1753-1763.

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Erlotinib, Cetuximab, and Staurosporine Assay

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Erlotinib (Tarceva^®; Roche), cetuximab (Erbitux^®; Merck), staurosporine (Sigma-Aldrich) DMSO (vehicle; Roche), propidium iodide (Merck), RNase A (Serva).

Kriegs M., Kasten-Pisula U., Riepen B., Hoffer K., Struve N., Myllynen L., Braig F., Binder M., Rieckmann T., Grénman R., Petersen C., Dikomey E, & Rothkamm K. (2016). Radiosensitization of HNSCC cells by EGFR inhibition depends on the induction of cell cycle arrests. Oncotarget, 7(29), 45122-45133.

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