NCT01280448

Brief Summary

Lung cancer is the leading cause of cancer deaths in Taiwan. The carcinogen in the environment is a key role in the development of lung cancer, and one of its main resource is tobacco. Activated carcinogens in the organism lead to mutations of crucial oncogenes resulting in tumor development. Genes such as Cytochrome P-450 family, GST (glutathione S-transferase) family, UGT (UDP-Glucuronosyltransferase) family, ERCC-1(excision repair cross-complementing rodent repair deficiency),ERCC-4 and ERCC-5,are encoding antioxidant enzymes or involving in the DNA repair process and the production of some transcription factors. In recent years, many studies have shown the correlation between these genes and the susceptibility of lung cancer. Each gene has a different role in the tumor development pathway. CYP, UGT, GST, NAT2 (N-acetyltransferase 2) and NQO1(NAD(P)H:quinono oxidoreductase 1) involve in the production of antioxidant enzymes. The antioxidant enzymes can detoxificate hydrogen peroxide or defense against oxidative stress. However, the genetic polymorphisms may influence the function of detoxification, which cause the increase in the susceptibility of lung cancer. P53 and MDM2 genes play important roles in the production of tumor-suppression proteins and the regulation of transcription factors, which may regulate the growth and the apoptosis of cell cycle and influence the susceptibility of lug cancer. The polymorphisms in ERCC genes may cause the damage in the DNA repair process which might also cause increase in lung cancer susceptibility. The overexpression of epidermal growth factor receptor is highly correlated with increasing risk of the non-small cell lung cancers. The overexpression may induce the proliferation of cancer cells and the inhibition of the apatosis. Therefore, in recent years, EGFR has been widely studied as the new target of the drugs and the susceptibility of the lung cancer. In addition,the genetic polymorphisms in drug metabolism channel proteins, like OCT2 (organic cation transporter), ATP7A, ATP7B and ABC (ATP-binding cassette) transporter may have influence on the metabolism, the efficacy and the toxicity of the drugs.

Trial Health

43
At Risk

Trial Health Score

Automated assessment based on enrollment pace, timeline, and geographic reach

Trial has exceeded expected completion date
Enrollment
600

participants targeted

Target at P75+ for all trials

Timeline
Completed

Started Sep 2010

Typical duration for all trials

Geographic Reach
1 country

1 active site

Status
unknown

Health score is calculated from publicly available data and should be used for screening purposes only.

Trial Relationships

Click on a node to explore related trials.

Study Timeline

Key milestones and dates

Study Start

First participant enrolled

September 1, 2010

Completed
5 months until next milestone

First Submitted

Initial submission to the registry

January 19, 2011

Completed
1 day until next milestone

First Posted

Study publicly available on registry

January 20, 2011

Completed
2.6 years until next milestone

Study Completion

Last participant's last visit for all outcomes

September 1, 2013

Completed
Last Updated

January 20, 2011

Status Verified

January 1, 2011

First QC Date

January 19, 2011

Last Update Submit

January 19, 2011

Conditions

Keywords

Lung CancerTobacco Smokinggene polymorphism

Study Arms (2)

Case Group

Control Group

Eligibility Criteria

Age20 Years+
Sexall
Healthy VolunteersYes
Age GroupsAdult (18-64), Older Adult (65+)
Sampling MethodNon-Probability Sample
Study Population

Lung Cancer patients

You may qualify if:

  • This study has two groups, the case group and the control group. The match criteria is patients with the same gender and the age is ± 5 years.
  • Case group - Patients with the pathology diagnosed as the primary lung cancer patients.
  • Control group - Patients without any cancer or disease history of cancers.

You may not qualify if:

  • Case group - Patients with the pathology diagnosed as the non-primary lung cancer patients or the patients with lung cancer induced by other cancer metastasis.
  • Control group -
  • With other cancers.
  • With COPD induced by smoking or the genetic factors.
  • With familial adenomatous polyposis
  • With HIV infection, hepatitis B or hepatitis C

Contact the study team to confirm eligibility.

Sponsors & Collaborators

Study Sites (1)

Taipei Medical University - WanFang Hospital

Taipei, Taiwan

Location

Biospecimen

Retention: SAMPLES WITH DNA

genes

MeSH Terms

Conditions

Lung NeoplasmsTobacco Smoking

Condition Hierarchy (Ancestors)

Respiratory Tract NeoplasmsThoracic NeoplasmsNeoplasms by SiteNeoplasmsLung DiseasesRespiratory Tract DiseasesSmokingBehaviorTobacco Use

Study Officials

  • Hsin-Gjin Eugene Liu

    Taipei Medical University WanFang Hospital

    PRINCIPAL INVESTIGATOR

Study Design

Study Type
observational
Observational Model
CASE CONTROL
Time Perspective
PROSPECTIVE
Sponsor Type
OTHER

Study Record Dates

First Submitted

January 19, 2011

First Posted

January 20, 2011

Study Start

September 1, 2010

Study Completion

September 1, 2013

Last Updated

January 20, 2011

Record last verified: 2011-01

Locations