The Correlation Between Lung Cancer Susceptibility, Drug Response and Genetic Polymorphism

The recruitment status of this study is unknown because the information has not been verified recently.
Verified January 2011 by Taipei Medical University WanFang Hospital.
Recruitment status was  Active, not recruiting
Sponsor:
Information provided by:
Taipei Medical University WanFang Hospital
ClinicalTrials.gov Identifier:
NCT01280448
First received: January 19, 2011
Last updated: NA
Last verified: January 2011
History: No changes posted
  Purpose

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.


Condition
Lung Cancer

Study Type: Observational
Study Design: Observational Model: Case Control
Time Perspective: Prospective
Official Title: The Correlation Between Lung Cancer Susceptibility, Drug Response and Genetic Polymorphism

Resource links provided by NLM:


Further study details as provided by Taipei Medical University WanFang Hospital:

Biospecimen Retention:   Samples With DNA

genes


Estimated Enrollment: 600
Study Start Date: September 2010
Estimated Study Completion Date: September 2013
Groups/Cohorts
Case Group
Control Group

Detailed Description:

The current study is a matched case-control study. The experimental group is the patients diagnosed as lung cancer at Taipei Medical University- Wanfang Hospital from January 2010 to December 2013, and one healthy patient will be matched to each case as the control group. The purpose of the current study is to investigate the association between genetic polymorphisms and lung cancer in the Taiwanese population and to analyze the correlation.

  Eligibility

Ages Eligible for Study:   20 Years and older
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   Yes
Sampling Method:   Non-Probability Sample
Study Population

Lung Cancer patients

Criteria

Inclusion Criteria:

  • 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.

    1. Case group - Patients with the pathology diagnosed as the primary lung cancer patients.
    2. Control group - Patients without any cancer or disease history of cancers.

Exclusion Criteria:

  • 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 -

    1. With other cancers.
    2. With COPD induced by smoking or the genetic factors.
    3. With familial adenomatous polyposis
    4. With HIV infection, hepatitis B or hepatitis C
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT01280448

Locations
Taiwan
Taipei Medical University - WanFang Hospital
Taipei, Taiwan
Sponsors and Collaborators
Taipei Medical University WanFang Hospital
Investigators
Principal Investigator: Hsin-Gjin Eugene Liu Taipei Medical University WanFang Hospital
  More Information

No publications provided

Responsible Party: Hsingjin Eugene Liu, MD PhD, Department of Hematology-oncology, WanFang Hospital
ClinicalTrials.gov Identifier: NCT01280448     History of Changes
Other Study ID Numbers: 99054
Study First Received: January 19, 2011
Last Updated: January 19, 2011
Health Authority: Taiwan: Department of Health

Keywords provided by Taipei Medical University WanFang Hospital:
Lung Cancer
Tobacco Smoking
gene polymorphism

Additional relevant MeSH terms:
Disease Susceptibility
Lung Neoplasms
Disease Attributes
Lung Diseases
Neoplasms
Neoplasms by Site
Pathologic Processes
Respiratory Tract Diseases
Respiratory Tract Neoplasms
Thoracic Neoplasms

ClinicalTrials.gov processed this record on October 29, 2014