scholarly journals Small Cell Architecture—A Histological Equivalent of EGFR Amplification in Glioblastoma Multiforme?

2001 ◽  
Vol 60 (11) ◽  
pp. 1099-1104 ◽  
Author(s):  
Peter C. Burger ◽  
Dennis K. Pearl ◽  
Kenneth Aldape ◽  
Allan J. Yates ◽  
Bernd W. Scheithauer ◽  
...  
Keyword(s):  
Glioblastoma Multiforme ◽  
Small Cell ◽  
Egfr Amplification ◽  
Cell Architecture

Molecular profiling of small cell bladder cancer.

2015 ◽  
Vol 33 (7_suppl) ◽  
pp. 338-338
Author(s):  
Jue Wang ◽  
David Arguello ◽  
Zoran Gatalica ◽  
Sandeep K. Reddy
Keyword(s):  
Bladder Cancer ◽  
Sanger Sequencing ◽  
Small Cell ◽  
Egfr Amplification ◽  
Surface Receptors ◽  
Response To Chemotherapy ◽  
Cell Bladder Cancer ◽  
Underlying Mechanisms ◽  
Next Generation Sequencing Ngs ◽  
Tumor Profiling

338 Background: Small cell bladder cancer (SCBC), a malignancy indistinguishable from small cell lung cancer (SCLC), is a rare and aggressive subtype of bladder cancer. Response to chemotherapy in SCBC is poor, yet the standard therapy remains cisplatin and etoposide. Novel therapies based on a better understanding of the underlying mechanisms of transformation are needed. The purpose of this study is to identify potential targets and therapeutic options for this disease, using multiplatform tumor profiling. Methods: In total, 19 small cell bladder cancer specimenswere tested via a multiplatform profiling service (Caris Life Sciences, Phoenix, AZ) consisting of gene sequencing (Sanger or next generation sequencing [NGS]), protein expression (immunohistochemistry [IHC]) and gene amplification (CISH or FISH). Results: Loss of RRM1 (22.2%, 4/18), MGMT (83.3%, 15/18), and TS (26.3%, 5/19) by IHC are associated with potential benefit to traditional chemotherapy. High expression of ERCC1, associated with resistance to platinum-based therapy, was 37.5% (3/8). MRP1, a drug pump associated with resistance to various chemotherapies, was present in 100% (5/5) of specimens. PD-L1 (0%, 0/6) was not expressed. EGFR amplification was detected in 25.0% of patients (1/4). NGS aberrations included TP53 (90.0%), cMET (20.0%, 2/10), RB1 (11.1%), FBXW7 (10%, 1/10), PTEN (10%, 1/10). Sanger sequencing also detected KRAS (100%, 1/1) and PIK3CA (33.3%, 1/3) mutations. Conclusions: Multiplatform tumor profiling identified biomarkers which may clarify treatment dilemmas with this rare cancer. MRP1 overexpression and TP53 loss help explain this cancer’s resistance to traditional chemotherapy and its aggressive course. This approach identified potential therapies, some of which are not typically considered, like temozolomide. Immunotherapy may not be as beneficial in SCBC based on absent PD-L1 expression. NGS and Sanger sequencing identified cell surface receptors and downstream molecules that could be candidates for therapeutic strategies.

scholarly journals Adjuvant Erlotinib Versus Placebo in Patients With Stage IB-IIIA Non–Small-Cell Lung Cancer (RADIANT): A Randomized, Double-Blind, Phase III Trial

2015 ◽  
Vol 33 (34) ◽  
pp. 4007-4014 ◽  
Author(s):  
Karen Kelly ◽  
Nasser K. Altorki ◽  
Wilfried E.E. Eberhardt ◽  
Mary E.R. O'Brien ◽  
David R. Spigel ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Adverse Events ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Hazard Ratio ◽  
Phase Iii ◽  
Small Cell Lung ◽  
Double Blind ◽  
Egfr Amplification

Purpose Epidermal growth factor receptor (EGFR) –tyrosine kinase inhibitors have proven efficacy in advanced non–small-cell lung cancer (NSCLC). We hypothesized that erlotinib would be efficacious in the adjuvant setting. Patients and Methods An international randomized, double-blind, placebo-controlled study was conducted in patients with completely resected IB to IIIA NSCLC whose tumors expressed EGFR protein by immunohistochemistry or EGFR amplification by fluorescence in situ hybridization. Patients were assigned 2:1 to erlotinib 150 mg once per day or placebo for 2 years. Stratification factors were stage, histology, previous adjuvant chemotherapy, smoking status, EGFR amplification status, and country. The primary end point was disease-free survival (DFS); key secondary end points were overall survival (OS) and DFS and OS in patients whose tumors had EGFR-activating mutations (EGFRm-positive). Results A total of 973 patients were randomly assigned (November 26, 2007, to July 7, 2010). There was no statistically significant difference in DFS (median, 50.5 months for erlotinib and 48.2 months for placebo; hazard ratio, 0.90; 95% CI, 0.74 to 1.10; P = .324). Among the 161 patients (16.5%) in the EGFRm-positive subgroup, DFS favored erlotinib (median, 46.4 v 28.5 months; hazard ratio, 0.61; 95% CI, 0.38 to 0.98; P = .039), but this was not statistically significant because of the hierarchical testing procedure. OS data are immature. Rash and diarrhea were common adverse events occurring in 528 (86.4%) and 319 (52.2%) patients treated with erlotinib, respectively, versus 110 (32.1%) and 54 (15.7%) patients receiving placebo. The most common grade 3 adverse events in patients treated with erlotinib were rash (22.3%) and diarrhea (6.2%). Conclusion Adjuvant erlotinib did not prolong DFS in patients with EGFR-expressing NSCLC or in the EGFRm-positive subgroup. Further evaluation of erlotinib is warranted in the EGFRm-positive subgroup.

scholarly journals A Cloud-Enabled Small Cell Architecture in 5G Networks for Broadcast/Multicast Services

2019 ◽  
Vol 65 (2) ◽  
pp. 414-424 ◽  
Author(s):  
Michail-Alexandros Kourtis ◽  
Begona Blanco ◽  
Jordi Perez-Romero ◽  
Dimitris Makris ◽  
Michael J. Mcgrath ◽  
...  
Keyword(s):  
Small Cell ◽  
5G Networks ◽  
Cell Architecture ◽  
Multicast Services

scholarly journals Phase I/II Trial of Erlotinib and Temozolomide With Radiation Therapy in the Treatment of Newly Diagnosed Glioblastoma Multiforme: North Central Cancer Treatment Group Study N0177

2008 ◽  
Vol 26 (34) ◽  
pp. 5603-5609 ◽  
Author(s):  
Paul D. Brown ◽  
Sunil Krishnan ◽  
Jann N. Sarkaria ◽  
Wenting Wu ◽  
Kurt A. Jaeckle ◽  
...  
Keyword(s):  
Glioblastoma Multiforme ◽  
Phase I ◽  
Recursive Partitioning ◽  
Growth Factor Receptor ◽  
Treatment Resistance ◽  
Class Iii ◽  
Egfr Amplification ◽  
Phosphatase And Tensin Homolog ◽  
End Point ◽  
Tensin Homolog

Purpose Epidermal growth factor receptor (EGFR) amplification in glioblastoma multiforme (GBM) is a common occurrence and is associated with treatment resistance. Erlotinib, a selective EGFR inhibitor, was combined with temozolomide (TMZ) and radiotherapy (RT) in a phase I/II trial. Patients and Methods Adults not taking enzyme-inducing anticonvulsants after resection or biopsy of GBM were treated with erlotinib (150 mg daily) until progression. Erlotinib was delivered alone for 1 week, then concurrently with TMZ (75 mg mg/m2 daily) and RT (60 Gy), and finally, concurrently with up to six cycles of adjuvant TMZ (200 mg/m2 daily for 5 days every 28 days). The primary end point was survival at 1 year. Results Ninety-seven eligible patients were accrued with a median follow-up time of 22.2 months. By definition, the primary end point was successfully met with a median survival time of 15.3 months. However, there was no sign of benefit in overall survival when comparing N0177 with the RT/TMZ arm of the European Organisation for Research and Treatment of Cancer/National Cancer Institute of Canada trial 26981/22981 (recursive partitioning analysis [RPA] class III, 19 v 21 months; RPA class IV, 16 v 16 months; RPA class V, 8 v 10 months, respectively). Presence of diarrhea, rash, and EGFRvIII, p53, phosphatase and tensin homolog (PTEN), combination EGFR and PTEN, and EGFR amplification status were not predictive (P > .05) of survival. Conclusion Although the primary end point was successfully met using nitrosourea-based (pre-TMZ) chemotherapy era historic controls, there was no sign of benefit compared with TMZ era controls. Analyses of molecular subsets did not reveal cohorts of patients sensitive to erlotinib. TMZ chemotherapy combined with RT resulted in improved outcomes compared with historical controls who received nitrosourea-based chemotherapies.

scholarly journals Effects of chemoradiotherapy on acute-phase protein levels in glioblastoma multiforme and locally advanced non-small cell lung cancer

2018 ◽  
Vol 43 (2) ◽  
pp. 159-166
Author(s):  
Çiğdem Damla Deniz ◽  
Mehmet Gürbilek ◽  
Mehmet Koç
Keyword(s):  
Lung Cancer ◽  
Prognostic Factors ◽  
Glioblastoma Multiforme ◽  
Small Cell Lung Cancer ◽  
Acute Phase ◽  
Cell Lung Cancer ◽  
Locally Advanced ◽  
Small Cell ◽  
Small Cell Lung ◽  
Nsclc Patients

Abstract Objective: Chemoradiotherapy (CRT) is a commonly used therapeutic modality. We investigated CRT effects on acute phase reactants (APRs). The aim of this study was to assess possible changes in APR levels during radiotherapy and to determine the usefulness of APRs as prognostic factors in patients with non-small cell lung cancer (NSCLC) and glioblastoma multiforme (GBM). Methods: We prospectively evaluated 30 patients and 30 healthy controls. Plasma levels of APRs were measured. Post-CRT and pre-CRT levels were compared. Survival of patients were also followed up for a period of 3 years. Results: In NSCLC patients, post-CRT albumin, transferrin (Trf), and ceruloplasmin (Cp) levels were significantly lower, and post-CRT ferritin (FER) levels were significantly higher, than their pre-CRT levels. In GBM patients, post-CRT Trf and prealbumin (Prealb) levels were significantly higher than pre-CRT levels. Pre-CRT C-reactive protein (CRP) and FER levels in NSCLC patients and Cp levels in GBM patients were associated with patient survival. Conclusion: This study suggests that APRs may be useful for monitoring response to treatment during CRT in NSCLC and GBM patients. Bearing in mind their accessibility and clinical value, plasma CRP and FER in NSCLC patients and Cp in GBM patients can be considered candidate prognostic factors.

Dynamic TDD Support in Macrocell-Assisted Small Cell Architecture

2015 ◽  
Vol 33 (6) ◽  
pp. 1201-1213 ◽  
Author(s):  
Bo Yu ◽  
Liuqing Yang ◽  
Hiroyuki Ishii ◽  
Sayandev Mukherjee
Keyword(s):  
Small Cell ◽  
Dynamic Tdd ◽  
Cell Architecture
Sign in / Sign up

Export Citation Format

Share Document