The objective of this study was to evaluate the effect of several ophthalmologic prophylactic treatment strategies for the management of ocular side effects (OSEs) in participants with epidermal growth factor receptor (EGFR)-amplified glioblastoma (GBM) who were being treated with depatuxizumab mafodotin (ABT-414).

Start Date30 Jul 2018

Sponsor / Collaborator

AbbVie, Inc.

CTR20170455 / SuspendedPhase 2/3

对初诊为伴有EGFR扩增的GBM受试者在同步放化疗及辅助TMZ化疗中联合使用ABT-414进行的一项随机安慰剂对照2b/3期临床研究

[Translation] A randomized, placebo-controlled, phase 2b/3 study of ABT-414 in combination with concurrent chemoradiotherapy and adjuvant TMZ chemotherapy in subjects with newly diagnosed GBM with EGFR amplification

测定在放疗与TMZ化疗联合+辅助TMZ化疗的治疗方案中加入ABT-414是否可延长初诊的伴EGFR扩增GBM受试者的无进展生存期（PFS）和总生存期（OS）。

[Translation]

To determine whether the addition of ABT-414 to radiation therapy plus TMZ chemotherapy plus adjuvant TMZ chemotherapy can prolong progression-free survival (PFS) and overall survival (OS) in subjects with newly diagnosed GBM with EGFR amplification.

Start Date19 Jan 2018

Sponsor / Collaborator

BSP Pharmaceuticals SpA

[+2]

100 Clinical Results associated with EGFRvIII x Tubulin

100 Translational Medicine associated with EGFRvIII x Tubulin

0 Patents (Medical) associated with EGFRvIII x Tubulin

Literatures (Medical) associated with EGFRvIII x Tubulin

01 Jun 2000·Journal of Biological ChemistryQ2 · BIOLOGY

Expression of Oncogenic Epidermal Growth Factor Receptor Family Kinases Induces Paclitaxel Resistance and Alters β-Tubulin Isotype Expression

Q2 · BIOLOGY

Article

Author: William L. Stahl ; R.Bruce Montgomery ; Junitta Guzman ; Donald M. O'Rourke

Oncogenic transformation confers resistance to chemotherapy through a variety of mechanisms, including suppression of apoptosis, increased drug metabolism, and modification of target proteins. Oncogenic epidermal growth factor receptor family members, including EGFRvIII and HER2, are expressed in a broad spectrum of human malignancies. Cell lines transfected with EGFRvIII and HER2 are more resistant to paclitaxel-mediated cytotoxicity, and tubulin polymerization induced by paclitaxel is suppressed compared with cells expressing wild type epidermal growth factor receptor. Because differential expression of beta-tubulin isotypes has been proposed to modulate paclitaxel resistance, we analyzed beta-tubulin isotypes expressed in cell lines transfected with different oncogenes. EGFRvIII- and HER2-expressing cells demonstrated equivalent total beta-tubulin protein compared with cells transfected with wild type receptor or untransfected controls. EGFRvIII-expressing cells demonstrated increases in class IVa (2.5-fold) and IVb (3.1-fold) mRNA, and HER2-expressing cells showed increases in class IVa (2. 95-fold) mRNA. Expression of oncogenic Ha-Ras did not change class IV RNA levels significantly. Inhibition of EGFRvIII kinase activity using a mutant allele with an inactivating mutation in the kinase domain decreased expression of class IVa by 50% and partially reversed resistance to paclitaxel. Expression of oncogenic epidermal growth factor receptor family members is associated with modulation of both beta-tubulin isotype expression and paclitaxel resistance in cells transformed by expression of the receptor. This effect on tubulin expression may modulate drug resistance in human malignancies that express these oncogenes.

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