Prognostic implications of epidermal growth factor receptor variant III expression and nuclear translocation in Chinese human gliomas

Yang, Kaiyuan; Ren, Xiaohui; Tao, Liyuan; Wang, Peipei; Jiang, Haihui; Shen, Li; Zhao, Yiming; Cui, Yong; Li, Mingxiao; Lin, Song

doi:10.21147/j.issn.1000-9604.2019.01.14

Cited by 12 publications

(7 citation statements)

References 46 publications

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“…CE-MRI was meticulously followed within 4 weeks after CCRT and regularly surveilled with an interval of 8-12 weeks or if necessary. PFS (progression-free survival) was defined as the duration from the initial surgery to the time of true tumor progression, which meant the time span between initial surgery and reemerged constantly enlarging lesions in the PsP group, and overall survival (OS) was termed as the duration between the initial surgery and the death, or date of the last followup (15,17). Perfusion MRI by dynamic susceptibility contrast (DSC) was available to some, but not all, patients during the follow-up to provide valuable information in distinguishing PsP from TeP.…”

Section: Treatment and Follow-upmentioning

confidence: 99%

Distinguishing Pseudoprogression From True Early Progression in Isocitrate Dehydrogenase Wild-Type Glioblastoma by Interrogating Clinical, Radiological, and Molecular Features

Ren

Dong

et al. 2021

Front. Oncol.

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Background: Pseudoprogression (PsP) mimics true early progression (TeP) in conventional imaging, which poses a diagnostic challenge in glioblastoma (GBM) patients who undergo standard concurrent chemoradiation (CCRT). This study aimed to investigate whether perioperative markers could distinguish and predict PsP from TeP in de novo isocitrate dehydrogenase (IDH) wild-type GBM patients.Methods: New or progressive gadolinium-enhancing lesions that emerged within 12 weeks after CCRT were defined as early progression. Lesions that remained stable or spontaneously regressed were classified as PsP, otherwise persistently enlarged as TeP. Clinical, radiological, and molecular information were collected for further analysis. Patients in the early progression subgroup were divided into derivation and validation sets (7:3, according to operation date).Results: Among 234 consecutive cases enrolled in this retrospective study, the incidences of PsP, TeP, and neither patterns of progression (nP) were 26.1% (61/234), 37.6% (88/234), and 36.3% (85/234), respectively. In the early progression subgroup, univariate analysis demonstrated female (OR: 2.161, P = 0.026), gross total removal (GTR) of the tumor (OR: 6.571, P < 001), located in the frontal lobe (OR: 2.561, P = 0.008), non-subventricular zone (SVZ) infringement (OR: 10.937, P < 0.001), and methylated O-6-methylguanine-DNA methyltransferase (MGMT) promoter (mMGMTp) (OR: 9.737, P < 0.001) were correlated with PsP, while GTR, non-SVZ infringement, and mMGMTp were further validated in multivariate analysis. Integrating quantitative MGMTp methylation levels from pyrosequencing, GTR, and non-SVZ infringement showed the best discriminative ability in the random forest model for derivation and validation set (AUC: 0.937, 0.911, respectively). Furthermore, a nomogram could effectively evaluate the importance of those markers in developing PsP (C-index: 0.916) and had a well-fitted calibration curve.Conclusion: Integrating those clinical, radiological, and molecular features provided a novel and robust method to distinguish PsP from TeP, which was crucial for subsequent clinical decision making, clinical trial enrollment, and prognostic assessment. By in-depth interrogation of perioperative markers, clinicians could distinguish PsP from TeP independent from advanced imaging.

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Section: Treatment and Follow-upmentioning

confidence: 99%

Distinguishing Pseudoprogression From True Early Progression in Isocitrate Dehydrogenase Wild-Type Glioblastoma by Interrogating Clinical, Radiological, and Molecular Features

Ren

Dong

et al. 2021

Front. Oncol.

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“…The cellular proliferation features of EGFR render it heavily implicated in malignant tumors; this has been confirmed by a large amount of pre-clinical and clinical evidence. 2 , 7 , 42 , 43 , 44 The majority of aberrant forms of EGFR in malignant tumors emerge as mutations and/or gene amplification, which has been reported to occur in lung cancer, 45 , 46 , 47 colorectal cancer, 48 , 49 squamous cell carcinoma of the head and neck (SCCHN), 50 , 51 pancreatic cancer, 52 , 53 , 54 renal cell cancer, 55 hepatocellular carcinoma, 56 breast cancer, 57 , 58 , 59 prostate cancer, 60 , 61 , 62 gastric cancer, 63 , 64 glioma, 65 , 66 , 67 and ovarian cancer, 68 , 69 and others ( Table 2 ). Among these malignancies, the involvement of EGFR in lung cancer, especially NSCLC, has received the most research attention.…”

Section: Egfr-targeted Therapy In the Clinicmentioning

confidence: 99%

Acquired resistance to third-generation EGFR-TKIs and emerging next-generation EGFR inhibitors

Yang

et al. 2021

The Innovation

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Summary The discovery that mutations in the EGFR gene are detected in up to 50% of lung adenocarcinoma patients, along with the development of highly efficacious epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), has revolutionized the treatment of this frequently occurring lung malignancy. Indeed, the clinical success of these TKIs constitutes a critical milestone in targeted cancer therapy. Three generations of EGFR-TKIs are currently approved for the treatment of EGFR mutation-positive non-small cell lung cancer (NSCLC). The first-generation TKIs include erlotinib, gefitinib, lapatinib, and icotinib; the second-generation ErbB family blockers include afatinib, neratinib, and dacomitinib; whereas osimertinib, approved by the FDA on 2015, is a third-generation TKI targeting EGFR harboring specific mutations. Compared with the first- and second-generation TKIs, third-generation EGFR inhibitors display a significant advantage in terms of patient survival. For example, the median overall survival in NSCLC patients receiving osimertinib reached 38.6 months. Unfortunately, however, like other targeted therapies, new EGFR mutations, as well as additional drug-resistance mechanisms emerge rapidly after treatment, posing formidable obstacles to cancer therapeutics aimed at surmounting this chemoresistance. In this review, we summarize the molecular mechanisms underlying resistance to third-generation EGFR inhibitors and the ongoing efforts to address and overcome this chemoresistance. We also discuss the current status of fourth-generation EGFR inhibitors, which are of great value in overcoming resistance to EGFR inhibitors that appear to have greater therapeutic benefits in the clinic.

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“…Time to progression (TTP) was defined as the duration from the initial surgery to the time of true tumor progression, and overall survival (OS) was termed as the duration between the initial surgery and the death, or date of the last follow-up (19,22). Post-progression survival (the time span between tumor progression and death) was also calculated and documented for further analysis.…”

Section: Treatment and Follow-upmentioning

confidence: 99%

T2/FLAIR Abnormity Could be the Sign of Glioblastoma Dissemination

Huang

Chen

et al. 2022

Front. Neurol.

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PurposeNewly emerged or constantly enlarged contrast-enhancing (CE) lesions were the necessary signs for the diagnosis of glioblastoma (GBM) progression. This study aimed to investigate whether the T2-weighted-Fluid-Attenuated Inversion Recovery (T2/FLAIR) abnormal transformation could predict and assess progression for GBMs, especially for tumor dissemination.MethodsA consecutive cohort of 246 GBM patients with regular follow-up and sufficient radiological data was included in this study. The series of T2/FLAIR and T1CE images were retrospectively reviewed. The patients were separated into T2/FLAIR and T1CE discordant and accordant subgroups based on the initial progression images.ResultsA total of 170 qualified patients were finally analyzed. The incidence of discordant T2/FLAIR and T1CE images was 25.9% (44/170). The median time-span of T2/FLAIR indicated tumor progression was 119.5 days (ranging from 57 days-unreached) prior to T1CE. Nearly half of patients (20/44, 45.5%) in the discordant subgroup suffered from tumor dissemination, substantially higher than accordant patients (23/126, 20.6%, p < 0.001). The median time to progression (TTP), post-progression survival (PPS), and overall survival (OS) were not statistically different (all p > 0.05) between discordant and accordant patients.ConclusionsT2/FLAIR abnormity could be the sign of GBM progression, especially for newly emerged lesions disseminating from the primary cavity. Physicians should cast more attention on the dynamic change of T2/FLAIR images, which might be of great significance for progression assessment and subsequent clinical decision-making.

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Prognostic implications of epidermal growth factor receptor variant III expression and nuclear translocation in Chinese human gliomas

Cited by 12 publications

References 46 publications

Distinguishing Pseudoprogression From True Early Progression in Isocitrate Dehydrogenase Wild-Type Glioblastoma by Interrogating Clinical, Radiological, and Molecular Features

Distinguishing Pseudoprogression From True Early Progression in Isocitrate Dehydrogenase Wild-Type Glioblastoma by Interrogating Clinical, Radiological, and Molecular Features

Acquired resistance to third-generation EGFR-TKIs and emerging next-generation EGFR inhibitors

T2/FLAIR Abnormity Could be the Sign of Glioblastoma Dissemination

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