The Effect on Cognition of Mitochondrial Respiratory System Proteins in Peripheral Blood Mononuclear Cells in the Course of Lung Cancer

2016 ◽  
pp. 45-52 ◽  
Author(s):  
S. Michalak ◽  
J. Rybacka-Mossakowska ◽  
J. Gazdulska ◽  
I. Gołda-Gocka ◽  
R. Ramlau
Keyword(s):  
Lung Cancer ◽  
Peripheral Blood Mononuclear Cells ◽  
Respiratory System ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells ◽  
Mitochondrial Respiratory

scholarly journals The Effect of Lung Cancer on Cytokine Expression in Peripheral Blood Mononuclear Cells

PLoS ONE ◽  
2013 ◽  
Vol 8 (6) ◽  
pp. e64456 ◽  
Author(s):  
David H. Chang ◽  
John R. Rutledge ◽  
Ankur A. Patel ◽  
Barbara G. Heerdt ◽  
Leonard H. Augenlicht ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Cytokine Expression ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells

Phase I Study of G3139, a bcl-2 Antisense Oligonucleotide, Combined With Carboplatin and Etoposide in Patients With Small-Cell Lung Cancer

2004 ◽  
Vol 22 (6) ◽  
pp. 1110-1117 ◽  
Author(s):  
Charles M. Rudin ◽  
Mark Kozloff ◽  
Philip C. Hoffman ◽  
Martin J. Edelman ◽  
Robyn Karnauskas ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Small Cell ◽  
Time To Progression ◽  
Small Cell Lung ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells ◽  
Extensive Stage

Purpose Bcl-2 is expressed in the majority of cases of small cell lung cancer (SCLC) and may contribute to chemotherapeutic resistance. Bcl-2 suppression by G3139 (oblimersen sodium), a phosphorothioate oligonucleotide complementary to the bcl-2 mRNA, has the potential to enhance the antitumor efficacy of standard cytotoxic chemotherapy. A dose-finding study was performed evaluating the combination of G3139, carboplatin, and etoposide in patients with previously untreated extensive stage SCLC. Patients and Methods Sixteen patients were treated in three consecutive cohorts. Cohort 1 (n = 5) received G3139 5 mg/kg/d on days 1 to 8 of a 21 day cycle, with carboplatin area under the curve (AUC) = 6 on day 6, and etoposide 80 mg/m2/d on days 6 to 8. In cohort 2 (n = 4), carboplatin dose was reduced to AUC = 5. In cohort 3 (n = 7), G3139 dose was escalated to 7 mg/kg/d. G3139 plasma concentrations and Bcl-2 protein levels in peripheral blood mononuclear cells were evaluated. Results Two of three assessable patients in cohort 1 experienced cycle 1 dose-limiting toxicity (grade 4 neutropenia). No cycle 1 dose-limited toxicity was observed in cohorts 2 or 3. Of 14 patients assessable for response, partial response was documented in 12 patients (86%), and stable disease in two. Median time to progression was 5.9 months. Carboplatin and etoposide administration did not appear to alter G3139 pharmacokinetics. No evidence of Bcl-2 suppression in peripheral blood mononuclear cells was observed. Conclusion The combination of G3139, carboplatin, and etoposide is well tolerated and results in an encouraging response rate and time to progression in patients with extensive stage SCLC.

scholarly journals Monitoring DNA Damage and Repair in Peripheral Blood Mononuclear Cells of Lung Cancer Radiotherapy Patients

Cancers ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2517
Author(s):  
Pavel N. Lobachevsky ◽  
Nicholas W. Bucknell ◽  
Joel Mason ◽  
Diane Russo ◽  
Xiaoyu Yin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Dna Damage ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Ex Vivo ◽  
Predictive Biomarkers ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells

Thoracic radiotherapy (RT) is required for the curative management of inoperable lung cancer, however, treatment delivery is limited by normal tissue toxicity. Prior studies suggest that using radiation-induced DNA damage response (DDR) in peripheral blood mononuclear cells (PBMC) has potential to predict RT-associated toxicities. We collected PBMC from 38 patients enrolled on a prospective clinical trial who received definitive fractionated RT for non-small cell lung cancer. DDR was measured by automated counting of nuclear γ-H2AX foci in immunofluorescence images. Analysis of samples collected before, during and after RT demonstrated the induction of DNA damage in PBMC collected shortly after RT commenced, however, this damage repaired later. Radiation dose to the tumour and lung contributed to the in vivo induction of γ-H2AX foci. Aliquots of PBMC collected before treatment were also irradiated ex vivo, and γ-H2AX kinetics were analyzed. A trend for increasing of fraction of irreparable DNA damage in patients with higher toxicity grades was revealed. Slow DNA repair in three patients was associated with a combined dysphagia/cough toxicity and was confirmed by elevated in vivo RT-generated irreparable DNA damage. These results warrant inclusion of an assessment of DDR in PBMC in a panel of predictive biomarkers that would identify patients at a higher risk of toxicity.

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