Virtual Library
Start Your Search
J. Xu
Author of
-
+
Imaging and locally advanced NSCLC (ID 41)
- Event: ELCC 2017
- Type: Poster Discussion session
- Track:
- Presentations: 1
- Moderators:H. Prosch, S. Senan, P. Van Schil
- Coordinates: 5/06/2017, 14:45 - 15:45, Room W
-
+
61PD - Recurrence risk-scoring model for resected stage I lung adenocarcinoma with solid component (ID 326)
14:45 - 15:45 | Author(s): J. Xu
- Abstract
Background:
The presence of solid histologic pattern in lung adenocarcinoma (ADC) is associated with early recurrence. However, individualized prognosis in patients with solid component is still unclear. This study aimed to develop a nomogram predicting the recurrence probability in stage I lung ADC patients with solid component.
Methods:
A total of 5904 patients with stage I lung ADC who underwent curative surgical resection from January 2008 through December 2014 at Shanghai Chest Hospital were retrospectively reviewed. Tumors were subtyped by using the IASCL/ATS/ERS classification. Of these patients, 708 contained a solid component. Prognostic value of gender, age at diagnosis, smoking history, operation type, tumor location, tumor size, pathological subtype, cell differentiation, lymphovascular and visceral pleural invasion were investigated. Multivariate Cox regression analysis of recurrence-free survival (RFS) in patients with solid component was performed and a nomogram to predict RFS was constructed. The nomogram was internally validated.
Results:
The overall recurrence rate in patients with solid component was 25.0% (177/708), with predominant solid subtype and minor solid component in 49.2% (87/177) and 50.8% (90/177) of cases, respectively. Larger tumor size (P = 0.002), predominant solid component (P = 0.003), advanced age at diagnosis (P = 0.015), and visceral pleural invasion (P = 0.040) were associated with an increased risk of recurrence and were included in the nomogram. The predictive model had a concordance index of 0.643 (95% confidence interval, 0.601-0.685) and showed good calibration.
Conclusions:
The nomogram model including identified risk factors for RFS is applicable in treatment decision-making for early stage lung ADC with pathological solid component. External validation is required to recommend this nomogram in routine practice.
Clinical trial identification:
Legal entity responsible for the study:
Shanghai Chest Hospital
Funding:
Shanghai Chest Hospital
Disclosure:
All authors have declared no conflicts of interest.
-
+
Poster Display Session (ID 63)
- Event: ELCC 2017
- Type: Poster Display Session
- Track:
- Presentations: 2
- Moderators:
- Coordinates: 5/07/2017, 12:30 - 13:00, Hall 1
-
+
62P - Risk factors associated with early vs late recurrence in stage I lung adenocarcinoma (ID 436)
12:30 - 13:00 | Author(s): J. Xu
- Abstract
Background:
Patients with stage I lung adenocarcinoma (ADC) develop recurrences after complete surgical resection, both early and over the long term. This study aimed to identify and compare risk factors for early and late recurrence after surgery in stage I lung ADC patients.
Methods:
We analyzed recurrences among 5904 patients with stage I lung ADC who underwent curative operations at Shanghai Chest Hospital between January 1, 2008 and December 31, 2014. Recurrences were classified as within 2 years (early), and more than 2 years (late) after surgery. The clinicopathologic findings were compared between patients with early and late recurrences. Both univariate and multivariate analyses were performed, incorporating factors of gender, age at diagnosis, operation type, tumor location and size, pathologic subtype, cell differentiation, lymphovascular invasion, visceral pleural invasion, and smoking history.
Results:
Recurrence occurred in totally 628 (10.6%) patients, with early and late recurrence in 300 and 328 patients, respectively. Early and late recurrences shared common risk factors of advanced age at diagnosis (P = 0.013 and P = 0.006, respectively), poorly cell differentiation (both P = 0.000), larger tumor size (both P = 0.000), and visceral pleural invasion (both P = 0.000). Early recurrence was additionally associated with male (HR, 1.327; 95%CI, 1.042-1.690; P = 0.022), sublobar resection (HR, 2.353; 95%CI, 1.634-3.387; P = 0.000), tumor located in the right middle lobe (HR, 1.711; 95%CI, 1.634-3.387; P = 0.005) and solid, micropapillary or variant subtypes (HR, 5.437; 95%CI, 1.258-23.509; P = 0.023).
Conclusions:
These findings suggest the existence of different risk factors accounting for early vs late recurrences among patients with stage I lung ADC.
Clinical trial identification:
Legal entity responsible for the study:
Shanghai Chest Hospital
Funding:
Shanghai Chest Hospital
Disclosure:
All authors have declared no conflicts of interest.
-
+
9P - Knockdown of MFN2 gene expression inhibits lung adenocarcinoma cell proliferation (ID 254)
12:30 - 13:00 | Author(s): J. Xu
- Abstract
Background:
Mitofusin-2(MFN2) was initially identified as a hyperplasia suppressor in hyper-proliferative vascular smooth muscle cells of hypertensive rat arteries, which has also been implicated in various cancers. There exists a controversy in whether it is an oncogene or exerting anti-proliferative effect on tumor cells. Our previous cell cycle analysis and MTT assay showed that cell proliferation was inhibited in MFN2 deficient A549 human lung adenocarcinoma cells. MFN2-knockdown induced gene expression changes in A549 cells was analyzed by microarray assay and then functional pathway enrichment analysis revealed that six pathways were enriched in deregulated genes including Cell cycle, DNA replication, ECM-receptor interaction, Focal adhesion, MAPK signaling pathway and Chemokine signaling pathway, as we previously reported.
Methods:
MFN2 expression at protein level was examined in 30 pair lung adenocarcinoma/adjacent normal lung samples with immunohistochemistry staining. Then MFN2 knockdown was performed in human lung adenocarcinoma cells A549 with lentiviral-mediated shRNA strategy. The expression changes of downstream factors were determined in A549 cells by western blot. Furthermore, tumor models in nude mice were generated and tumor formation and progression in these mice were analysed.
Results:
As compared to adjacent normal lung tissues, MFN2 expression was significantly higher in lung adenocarcinoma tissues with positive MFN2 signals in 90% (27/30) lung adenocarcinoma tissues and only in 26.7% (8/30) adjacent normal tissues. The downregulation of RAP1A and upregulation of RALB and ITGA2 identified in MFN2-knockdown cells by microarray analysis were confirmed by western blot. In vivo, tumor models in nude mice were generated. Tumor formation and progression in nude mice suggested that MFN2 knockdown reduced tumorigenesis of A549 cells.
Conclusions:
The current study confirmed the anti-proliferative effect of MFN2 deficiency and its risk in lung adenocarcinoma.
Clinical trial identification:
Legal entity responsible for the study:
Shanghai Chest Hospital
Funding:
This work was supported by the National Natural Science foundation of China (81572249 and 81201839).
Disclosure:
All authors have declared no conflicts of interest.
