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L. Jiang
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P1.03 - Poster Session with Presenters Present (ID 455)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Radiology/Staging/Screening
- Presentations: 1
- Moderators:
- Coordinates: 12/05/2016, 14:30 - 15:45, Hall B (Poster Area)
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P1.03-062 - Lung Cancer Screening with Low-Dose CT in China: Study Design and Baseline Results from the First Round Screening Arm (ID 5639)
14:30 - 14:30 | Author(s): L. Jiang
- Abstract
Background:
Lung cancer screening with low-dose CT (LDCT) was shown to reduce lung cancer mortality by 20% in the National Lung Screening Trial. However, several other trails have reported that there was no reduction in lung cancer mortality with a LDCT screening strategy. Meanwhile, whether LDCT screens could decrease healthcare costs is yet insufficiently explored. The objectives of the present study was to investigate whether LDCT screening is capable to reduce the lung cancer mortality by at least 20% and analyze the healthcare costs of the lung cancer LDCT screening in China.
Methods:
The present study is a randomized controlled trial of LDCT screening for lung cancer versus usual care. Eligible participants were those aged 45–70 years, and with either of the following risk factors: 1) history of cigarette smoking ≥ 20 pack-years, and, if former smokers, had quit within the previous 15 years; 2) malignant tumors history in immediate family members; 3) personal cancer history; 4) professional exposure to carcinogens; 5) long term exposure to second-hand smoke; 6) long term exposure to cooking oil fumes. All the participants were randomized into a screening arm with three rounds of alternate years LDCT screens and a control arm with three rounds of alternate years questionnaire inquiries. Management of positive screening test was carried out by a prespecified protocol.
Results:
From November 2013 to November 2014, 5933 participants were enrolled in our trail, of which 2933 were assigned to LDCT screening arm, and 3000 to control arm. In the first screening round, 2892 participants (98.6%) undergo LDCT after randomization. At baseline 742 subjects (25.7%) showed noncalcified nodules (NCN) larger than 4 mm. 69 cases were highly suspected of lung cancer according to the suggestion of three experienced experts. The highly suspected cases were accounting for 9.30% of all NCN subjects and 2.39% of all the screening arm participants. By March 2016, 26 cases underwent surgical resections, including 23 lung adenocarcinoma, 1 lung squamous cell carcinoma and 2 benign lesions, representing a positive lung cancer detection rate with low-dose CT screening of 0.83%(24/2892). Among all the lung cancer cases, 23/24 (95.8%) had stage I disease, and 1/24 (4.2%) had stage II disease. The second round screening was still ongoing since May 2016.
Conclusion:
Screening with LDCT increases the detection rate of early stage lung cancers (stage I and II) in a high risk population.
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P2.01 - Poster Session with Presenters Present (ID 461)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Biology/Pathology
- Presentations: 1
- Moderators:
- Coordinates: 12/06/2016, 14:30 - 15:45, Hall B (Poster Area)
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P2.01-082 - Transcriptional Profiling Identified the Anti-Proliferative Effect of Mitofusin-2 Deficiency and Its Risk in Lung Adenocarcinoma (ID 6011)
14:30 - 14:30 | Author(s): L. Jiang
- 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, without investigating the changes in regulatory network or addressing the underlying mechanisms.
Methods:
We performed expression profiling in MFN2 knock-down A549 cells. Furthermore, we compared the expression profiling of a cohort consisting of 61 pairs of tumor-normal match samples from The Cancer Genome Atlas(TCGA).
Results:
The expression profiling in MFN2 knock-down cells suggested that cancer related pathways were among the most susceptible pathways to MFN2 deficiency. Next, we teased out the specific pathways to address the impact that MFN2 ablation had on A549 cells, as well as identified a few genes whose expression level associated with clinicopathologic parameters. In addition, transcriptional factor target enrichment analysis identified E2F as a potential transcription factor that was deregulated in response to MFN2 deficiency. Figure 1 Figure 2
Conclusion:
The anti-proliferative effect of MFN2 deficiency and its risk in lung adenocarcinoma were found by transcriptional profiling.