No abstract available.
Genes, erbB-1

No abstract available.
Alopecia Areata ; Alopecia ; Epidermal Growth Factor ; Genes, erbB-1

Animals ; Genes, BRCA2 ; Genes, erbB-1 ; Genes, erbB-2 ; Genes, p16 ; Genes, p53 ; Genes, ras ; Genetic Predisposition to Disease ; genetics ; Humans ; Pancreatic Neoplasms ; classification ; genetics ; pathology

The EGFR Tyrosine kinase inhibitors (TKIs) show significant clinical benefit in selected population with no smoking history, adenocarcinoma or mutations in EGFR gene. Mutations of K-ras gene are associated with resistance to EGFR TKIs. Three published studies of gefitinib experience from Korea are reviewed. Mutations of EGFR gene published up to now and correlation with response to EGFR-TKIs is summarized. This review also discusses the suggested mechanisms of acquired resistance to EGFR TKIs
Adenocarcinoma ; Genes, erbB-1 ; Genes, ras ; Korea ; Protein-Tyrosine Kinases* ; Smoke ; Smoking ; Tyrosine*

Sarcomatoid carcinoma of the lung is defined as a group of poorly differentiated non-small cell carcinomas that contain a component of sarcoma or a sarcoma-like element. Most sarcomatoid carcinomas are known to have a poor prognosis. We describe a 45-year-old female never smoker and 49-year-old female never smoker with sarcomatoid carcinomas of the lung that expressed a specific EGFR mutation: microdeletion of exon 19. Their cancers progressed rapidly, despite appropriate conventional chemotherapy. After they took the EGFR-targeted agent gefitinib, there was a dramatic reduction in tumor size. Sarcomatoid carcinoma of the lung is a rare cancer whose pathogenesis is not well understood. According to these cases, the EGFR mutation could be a driver mutation and the potential therapeutic target of EGFR-targeted agents for sarcomatoid carcinoma in lung cancer patients, especially never smokers.
Exons ; Female ; Genes, erbB-1 ; Humans ; Lung ; Lung Neoplasms ; Prognosis ; Quinazolines ; Sarcoma

DNA ; isolation & purification ; Formaldehyde ; Genes, erbB-1 ; genetics ; Genetic Techniques ; Humans ; Mutation ; Paraffin ; Tissue Fixation

Carcinoma, Non-Small-Cell Lung ; genetics ; Exons ; genetics ; Genes, erbB-1 ; genetics ; Humans ; Lung Neoplasms ; pathology

PURPOSE: Amplification and mutation of the epidermal growth factor receptor(EGFR) and HER-2 genes were analyzed in the tissues of hormone refractory prostate cancer(HRPC) patients. MATERIALS AND METHODS: Gene amplifications of the EGFR and HER-2 gene were analyzed by fluorescence in situ hybridization(FISH) with direct sequencing. Studies were performed on 10 patients; tissues were sampled at the time of initial diagnosis and after the conversion to HRPC(a total of 20 tissue samples). Direct sequencing was performed on exons 18-24 of the EGFR gene and exons 19 and 20 of the HER-2 gene. The amplifications and mutations were compared with the clinicopathologic features. RESULTS: Gene amplification of the EGFR gene was observed in 6(30%) out of 20 samples. A total of six EGFR mutations in exons 18 and 19 were detected in three pairs of tissues(three patients). One patient with a hormone refractory status had a novel deletion mutation in EGFR exon 19. EGFR mutations were associated with the acinar type of prostate cancer, but they were not associated with the ductal type. No significant correlation was found between mutation change and the hormone sensitive or refractory status. However, the time to convert to HRPC was significantly shorter in the patients with a mutation in the EGFR gene (p=0.017). There were no HER-2 gene amplifications or mutations found in any of the samples. CONCLUSONS: EGFR gene mutation and amplification occurred frequently in these advanced prostate cancer cases, but EGFR mutations do not appear to play a significant role in the hormone refractory pathway. However, EGFR gene mutation is closely associated with the time to convert to HRPC.
Epidermal Growth Factor ; Exons ; Fluorescence ; Gene Amplification ; Genes, erbB-1 ; Genes, erbB-2 ; Humans ; Prostate ; Prostatic Neoplasms ; Receptor, Epidermal Growth Factor ; Sequence Deletion

BACKGROUND: Glioblastomas may develop de novo (primary glioblastomas, P-GBLs) or through progression from lower-grade astrocytomas (secondary glioblastomas, S-GBLs). The aim of this study was to compare the immunohistochemical classification of glioblastomas with clinically determined P-GBLs and S-GBLs to identify the best combination of antibodies for immunohistochemical classification. METHODS: We evaluated the immunohistochemical expression of epidermal growth factor receptor (EGFR), p53, and isocitrate dehydrogenase 1 (IDH-1) in 150 glioblastoma cases. RESULTS: According to clinical history, the glioblastomas analyzed in this study consisted of 146 P-GBLs and 4 S-GBLs. Immunohistochemical expression of EGFR, p53, and IDH-1 was observed in 62.6%, 49.3%, and 11.1%, respectively. Immunohistochemical profiles of EGFR(+)/p53(-), IDH-1(-)/EGFR(+)/p53(-), and EGFR(-)/p53(+) were noted in 41.3%, 40.2%, and 28.7%, respectively. Expression of IDH-1 and EGFR(-)/p53(+) was positively correlated with young age. The typical immunohistochemical features of S-GBLs comprised IDH-1(+)/EGFR(-)/p53(+), and were noted in 3.6% of clinically P-GBLs. The combination of IDH-1(-) or EGFR(+) was the best set of immunohistochemical stains for identifying P-GBLs, whereas the combination of IDH-1(+) and EGFR(-) was best for identifying S-GBLs. CONCLUSIONS: We recommend a combination of IDH-1 and EGFR for immunohistochemical classification of glioblastomas. We expect our results to be useful for determining treatment strategies for glioblastoma patients.
Antibodies ; Astrocytoma ; Classification* ; Coloring Agents ; Genes, erbB-1 ; Genes, p53 ; Glioblastoma* ; Humans ; Immunohistochemistry ; Isocitrate Dehydrogenase ; Receptor, Epidermal Growth Factor

OBJECTIVE: To establish a rapid and accurate "on/off" switch technique consisted of 3'-phosphorothioate-modified allele-specific primers and exo+ polymerase to screen the G719S and T790M mutations of epidermal growth factor receptor (EGFR) gene. The switch was used to identify cervical cancer patients who are sensitive to tyrosine kinase inhibitor (TKI). METHODS: Allele-specific primers targeting recombinant wild-type and mutation-type templates were designed with 3' terminal phosphorothioate modification. Two-directional primer extension was carried out using Pfu polymerase. The G719S and T790M mutations were detected by the technique among cervical cancer tissues. The results were verified by Sanger sequencing. RESULTS: No mutation was detected among the 80 cervical cancer cases, and the results were consistent with that of Sanger sequencing. No significant difference was found between the frequencies of the G719S and T790M mutations between the patient and the control groups (P> 0.05). CONCLUSION A sensitive "on/off" switch technique for detecting the two EGFR mutations was established. The G719S and T790M mutations are not associated with cervical cancer.
Carcinoma, Non-Small-Cell Lung ; Drug Resistance, Neoplasm ; ErbB Receptors ; genetics ; Female ; Genes, erbB-1 ; Humans ; Lung Neoplasms ; Mutation ; Protein Kinase Inhibitors ; Uterine Cervical Neoplasms ; genetics