scholarly journals Circulating progastrin-releasing peptide in the diagnosis of Small Cell Lung Cancer (SCLC) and in therapeutic monitoring

2021 ◽  
Vol 10 ◽  
pp. 9-13
Author(s):  
Vittoria Barchiesi ◽  
Vittorio Simeon ◽  
Claudia Sandomenico ◽  
Monica Cantile ◽  
Dionigio Cerasuolo ◽  
...  

Introduction: Progastrin-releasing peptide (proGRP), a precursor of GRP, has been recently reported as a putative circulating biomarker for differential diagnosis between non–small cell lung cancer (NSCLC) and SCLC. We evaluated the diagnostic effectiveness of proGRP to differentiate patients with NSCLC and SCLC and the usefulness of combined measurement of proGRP and neuron-specific enolase (NSE) for diagnosing SCLC. Methods: Serum proGRP, NSE, cytokeratin 19 fragment 21-1 (CYFRA 21.1), squamous cell carcinoma antigen (SCC Ag) and carcinoembryonic antigen (CEA) were prospectively collected and measured in patients with a new diagnosis of lung cancer. Serum proGRP was also measured in healthy subjects. The serum proGRP, NSE, CYFRA 21.1 and CEA concentrations were determined by an electrochemiluminescence immunoassay and the serum SCC Ag concentration was determined by an automated immunofluorescence assay. Differences between proGRP and NSE in patients with SCLC and NSCLC were evaluated and compared using Mann-Whitney test. Results: A total of 77 patients affected by SCLC (n = 17) and NSCLC (n = 60) were enrolled in the present study. Moreover, 50 cases of healthy subjects were analyzed for proGRP. SCLC patients showed a significantly higher proGRP (1,484 pg/mL; range 168-3,777) levels compared to NSCLC patients (45 pg/mL; range 31.7-60.6), p<0.0001. In healthy subjects the median proGRP level was 36.1 (28.8-43.5) pg/mL, significantly lower than SCLC patients. ProGRP showed a higher specificity when compared to NSE, with a difference in proportion of 47.5% (95% confidence interval 32.5% to 62.5%, p<0.001). Serial measurements of proGRP in SCLC patients showed a decrease in responsive chemotherapy patients.

1997 ◽  
Vol 12 (1) ◽  
pp. 22-26 ◽  
Author(s):  
L. Giovanella ◽  
R. Piantanida ◽  
L. Ceriani ◽  
M. Bandera ◽  
R. Novario ◽  
...  

NSE is a biochemical marker for small cell lung cancer (SCLC) diagnosis and management. CYFRA 21.1 is a newly developed immunoassay to detect the serum fragments of cytokeratin 19 which are also expressed in SCLC with or without neurofilaments. The aim of this study was to evaluate the diagnostic performance and prognostic role of the two markers in SCLC and their contribution to chemotherapy monitoring and patient follow-up. We studied 62 patients with pathologically proven SCLC: 28 with limited disease (LD) and 34 with extensive disease (ED), and 100 patients with non-malignant pulmonary disease. Immunoradiometric assays (IRMA) were employed to test NSE and CYFRA 21.1 in patients and control subjects. For each patient subset results were expressed as median and interquartile distribution range. NSE and CYFRA 21.1 sensitivity was 0.52 (33/62) and 0.56 (35/62), respectively. In the group of patients with LD, NSE and CYFRA 21.1 sensitivity was 0.42 (12/28) and 0.54 (15/28) and in patients with ED, NSE and CYFRA 21.1 were positive in 0.62 (21/34) and 0.59 (20/34) of cases, respectively. Combining the two markers, a sensitivity of 0.78 (22/28) in LD, 0.82 (28/34) in ED and a global sensitivity of 0.80 (50/62) was obtained. Only NSE was significantly linked to the extension of disease (Mann-Whitney U test p = 0.002) while CYFRA 21.1 did not correlate. The analysis of survival and the evaluation of the two markers at diagnosis showed CYFRA 21.1 to be strongly linked to the patients’ outcome, independently of both clinical prognostic factors and NSE levels (log rank and Cox's model). The markers’ performance during chemotherapy was tested in a group of 33 patients with at least one marker above cut-off. NSE can be considered a reliable marker of tumor mass modifications under chemotherapy, while CYFRA 21.1 expression seems to be relatively independent of tumor volume modifications. An applicable model of biomarkers in SCLC could be the concurrent assay of NSE and CYFRA 21.1 in pre-therapeutic assessment and therapy planning. CYFRA 21.1 does not play an important role during therapy monitoring and follow-up; in these phases NSE alone may be employed.


2012 ◽  
Vol 27 (2) ◽  
pp. 139-146 ◽  
Author(s):  
Mohamed A. Alm El-Din ◽  
Gihan Farouk ◽  
Hala Nagy ◽  
Ayman Abd Elzaher ◽  
Gehan H. Abo El-Magd

Aim To investigate the reduction in the serum level of cytokeratin-19 fragments (CYFRA 21–1), nucleosomes and neuron-specific enolase (NSE) as early measures of the response to chemotherapy in non-small cell lung cancer (NSCLC). Methods Forty-two consecutive patients with locally advanced NSCLC were included. All patients received platinum-based chemotherapy. Staging investigations and quantification of CYFRA 21–1, nucleosomes and NSE (using enzyme-linked immunosorbent assay, ELISA) were performed before the start of treatment and after the second cycle of chemotherapy. According to the response to chemotherapy, patients were classified into 3 groups: (I) disease regression, (II) stable disease, and (III) progressive disease. The reduction in the levels of tumor markers was correlated with the response to chemotherapy. Results After the second cycle of chemotherapy, groups I and II had significantly decreased serum levels of CYFRA 21–1 (p<0.05). Similarly, the concentration of nucleosomes was significantly lower than the baseline levels in groups I (p=0.0008) and II (p=0.003). The reduction of both CYFRA 21–1 and nucleosome levels was not significant for patients in group III. In all groups the reduction of NSE levels in response to chemotherapy was not significant. As a marker of response to chemotherapy, CYFRA 21–1 showed the highest sensitivity (88.9%) and specificity (77.4%) compared with nucleosomes (77.8% and 58.1% respectively) and NSE (66.7% and 51.8% respectively). Conclusion The reduction in the serum level of CYFRA 21–1 and nucleosomes may be used for early identification of NSCLC patients with good response to chemotherapy.


2020 ◽  
Vol 20 (8) ◽  
pp. 982-988 ◽  
Author(s):  
Le-Le Zhang ◽  
Han Bao ◽  
Yu-Lian Xu ◽  
Xiao-Ming Jiang ◽  
Wei Li ◽  
...  

Background: Cassane-type diterpenoids are widely distributed in the medical plants of genus Caesalpinia. To date, plenty of cassane diterpenoids have been isolated from the genus Caesalpinia, and some of them were documented to exhibit multiple biological activities. However, the effects of these compounds on autophagy have never been reported. Objective: To investigate the effects and mechanisms of the cassane diterpenoids including Phanginin R (PR) on autophagy in Non-Small Cell Lung Cancer (NSCLC) A549 cells. Methods: Western blot analysis and immunofluorescence assay were performed to investigate the effects of the compounds on autophagic flux in A549 cells. The pathway inhibitor and siRNA interference were used to investigate the mechanism of PR. MTT assay was performed to detect cell viability. Results: PR treatment upregulated the expression of phosphatidylethanolamine-modified microtubule-associated protein Light-Chain 3 (LC3-II) in A549 cells. Immunofluorescence assay showed that PR treatment increased the production of red-fluorescent puncta in mRFP-GFP-LC3 plasmid-transfected cells, indicating PR promoted autophagic flux in A549 cells. PR treatment activated the c-Jun N-terminal Kinase (JNK) signaling pathway while it did not affect the classical Akt/mammalian Target of Rapamycin (mTOR) pathway. Pretreatment with the JNK inhibitor SP600125 or siRNA targeting JNK or c-Jun suppressed PR-induced autophagy. In addition, cotreatment with the autophagy inhibitor Chloroquine (CQ) or inhibition of the JNK/c-Jun signaling pathway increased PR-induced cytotoxicity. Conclusion: PR induced cytoprotective autophagy in NSCLC A549 cells via the JNK/c-Jun signaling pathway, and autophagy inhibition could further improve the anti-cancer potential of PR.


The Lancet ◽  
1982 ◽  
Vol 319 (8272) ◽  
pp. 583-585 ◽  
Author(s):  
DesmondN Carney ◽  
DanielC Ihde ◽  
MartinH Cohen ◽  
PaulJ Marangos ◽  
PaulA Bunn ◽  
...  

2006 ◽  
Vol 32 ◽  
pp. S28
Author(s):  
S. Mizuguchi ◽  
N. Nishiyama ◽  
T. Iwata ◽  
T. Nishida ◽  
N. Izumi ◽  
...  

2018 ◽  
Vol 22 (1) ◽  
pp. 55-62 ◽  
Author(s):  
Ae Rin Baek ◽  
Hyun Jung Seo ◽  
June Hyuk Lee ◽  
Sung Woo Park ◽  
An Soo Jang ◽  
...  

2020 ◽  
Vol 2020 (4-5) ◽  
Author(s):  
Naoko Miura ◽  
Taichi Matsubara ◽  
Shinkichi Takamori ◽  
Naoki Haratake ◽  
Ryo Toyozawa ◽  
...  

Abstract The transformation of adenocarcinoma to small cell lung cancer has been reported as acquisition of resistance to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors. We here report a patient who presented histologically confirmed transformation of adenocarcinoma to small cell lung cancer after treatment with immune checkpoint inhibitor. A 65-year-old man was treated with pembrolizumab as first-line therapy and achieved temporarily a stable disease with progression after six cycles of this agent. At that stage, a transbronchial biopsy showed small cell lung cancer, and he was found to have high serum concentrations of neuron-specific enolase despite concentrations of numerous tumor markers, including neuron-specific enolase, having been within normal limits at the time of presentation. The patient thereafter was treated as a small cell carcinoma patient using cisplatin plus irinotecan and amrubicin.


Sign in / Sign up

Export Citation Format

Share Document