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Tumor Markers in Lung Cancer: DCAMLK-1LK-1

This study has been completed.
Information provided by (Responsible Party):
Gary Kinasewitz, University of Oklahoma Identifier:
First received: April 11, 2012
Last updated: August 8, 2012
Last verified: August 2012

DCAMLK1 is a Ca2+ - ca/modulin (CaM) - dependent protein kinase that is a marker of stem cells in colonic crypts. Mutations within the stem cell population are thought to be responsible for the development of most colorectal carcinomas and studies have shown that DCAMLK1 is highly expressed in these tumors. Since the lung is an embryological development of the foregut, the investigators speculate that DCAMLK1 will also be upregulated in lung cancers.

The aim of this pilot study is to measure DCAMLK1 levels in the blood of patients with suspected malignant and benign lung diseases, and to correlate DCAMKL1 levels with smoking status.

Condition Intervention
Lung Cancer
Other: Measure DCAM levels in blood
Other: DCAM levels in blood

Study Type: Interventional
Study Design: Allocation: Non-Randomized
Intervention Model: Parallel Assignment
Masking: Open Label
Primary Purpose: Diagnostic
Official Title: Tumor Markers in Lung Cancer: DCAMLK-1LK-1: A Pilot Study

Resource links provided by NLM:

Further study details as provided by Gary Kinasewitz, University of Oklahoma:

Primary Outcome Measures:
  • Tumor Markers in Lung Cancer: [ Time Frame: 6 months ]
    DCAMLK-1LK-1 levels will be measured in the blood of patients with Lung Cancer and compared to that of controls with other lung diseases.

Enrollment: 49
Study Start Date: December 2011
Study Completion Date: July 2012
Primary Completion Date: July 2012 (Final data collection date for primary outcome measure)
Arms Assigned Interventions
Lung Cancer
Other: Measure DCAM levels in blood
Measure DCAM levels in blood
Other Name: Lung Cancer
Lung Disease
Other: DCAM levels in blood
DCAM levels in blood
Other Name: Lung Disease

Detailed Description:

In the investigators' preliminary study DCAMKL1 antigen was detected not only in malignant tissue, but also in BAL fluid from patients with benign lung disease. This suggests that DCAMKL1 expression might be induced by smoking or benign lung diseases. To examine this hypothesis, the investigators will compare DCAMLK1 expression in blood from patients with lung cancer to controls who are current or former smokers with benign lung disease.

Previous work has showed that DCAMLK1 is not detectable in the blood of healthy non smoking individuals. To determine whether smoking and or pulmonary inflammation induce DCAMLK1 expression, the investigators will obtain serum samples from 20 control patients with lung disease who are seen in the Chest Clinic at the Oklahoma City VAMC. Smoking histories will be obtained for all participants and DCAMLK1 levels will be correlated with smoking status.


Ages Eligible for Study:   45 Years and older   (Adult, Senior)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   Yes

Inclusion Criteria:

  • >45 years of age

Exclusion Criteria:

  • Unable to provide informed consent
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Please refer to this study by its identifier: NCT01578018

United States, Oklahoma
Oklahoma City, Oklahoma, United States, 73104
Sponsors and Collaborators
University of Oklahoma
Principal Investigator: Kellie Jones, MD University of Oklahoma
  More Information

Responsible Party: Gary Kinasewitz, Principal Investigator, University of Oklahoma Identifier: NCT01578018     History of Changes
Other Study ID Numbers: 16249
Study First Received: April 11, 2012
Last Updated: August 8, 2012

Keywords provided by Gary Kinasewitz, University of Oklahoma:
lung cancer

Additional relevant MeSH terms:
Lung Neoplasms
Respiratory Tract Neoplasms
Thoracic Neoplasms
Neoplasms by Site
Lung Diseases
Respiratory Tract Diseases processed this record on May 25, 2017