The Impact of M1/M2 Tumor Associated Macrophage (TAM) Polarization on Cancer Progression and Prognosis Prediction

The recruitment status of this study is unknown because the information has not been verified recently.
Verified May 2008 by National Taiwan University Hospital.
Recruitment status was  Recruiting
Sponsor:
Collaborator:
National Science Council, Taiwan
Information provided by:
National Taiwan University Hospital
ClinicalTrials.gov Identifier:
NCT00690261
First received: June 1, 2008
Last updated: June 3, 2008
Last verified: May 2008
  Purpose

The purpose of this study is to evaluate the correlation between M1/M2 phenotype of tumor associated macrophage (TAM) in lung cancer patients and clinical outcome.


Condition
Tumor
Lung Cancer

Study Type: Observational
Study Design: Observational Model: Case Control
Time Perspective: Prospective
Official Title: The Impact of M1/M2 Tumor Associated Macrophage (TAM) Polarization on Cancer Progression and Prognosis Prediction

Resource links provided by NLM:


Further study details as provided by National Taiwan University Hospital:

Primary Outcome Measures:
  • outcome (treatment response and mortality) [ Time Frame: 3 years ] [ Designated as safety issue: No ]

Secondary Outcome Measures:
  • clinical presentation [ Time Frame: at enrollement ] [ Designated as safety issue: No ]

Biospecimen Retention:   Samples Without DNA

Pleural effusions and lung cancer tissue


Estimated Enrollment: 100
Study Start Date: September 2007
Estimated Study Completion Date: August 2010
Groups/Cohorts
lung cancer
patients diagnosed of lung cancer with malignant pleural effusions

Detailed Description:

Inflammatory response in the tumor micro-environment may facilitate the metastatic process (1). Macrophages are pivotal members of the inflammatory cells and the innate immune system within the tumor stroma. Tumor-associated macrophages can release growth factors, cytokines and inflammatory mediators that may facilitate cancer cell invasion, migration, angiogenesis, tumor progression or metastasis (1-5). A lot of studies showed TAM encounter factors that most frequently polarize them toward M2 type macrophage (1,4-5). It is interesting that in vitro studies macrophages have the potential to kill tumor by appropriate stimulation but these macrophage belonged to M1 and were not present in most tumor tissue (6). Some drugs target to suppress TAM have the promising results in animal models (7-9). Switching the TAM phenotype from M2 to M1 may promote anti-tumor activity (10). In this study we will correlate TAM M1/M2 ratio and patients' prognosis, the gene expression pattern of TAM.

References

  1. Coussens LM, Werb Z. Inflammation and cancer. Nature 2002;420(6917):860-867.
  2. Crowther M, Brown NJ, Bishop ET, Lewis CE. Microenvironmental influence on macrophage regulation of angiogenesis in wounds and malignant tumors. J Leukoc Biol 2001;70(4):478-490.
  3. Lin EY, Nguyen AV, Russell RG, Pollard JW. Colony-stimulating Factor 1 Promotes Progression of Mammary Tumors to Malignancy. J. Exp. Med. 2001;193(6):727-740.
  4. Mantovani A. Cancer Inflammation by remote control. Nature 2005;435(7043):752-753.
  5. Pollard JW. Tumor-educated macrophages promote tumour progression and metastasis. Nature Reviews Cancer 2004;4(1):71-78.
  6. Sica A, Schippa T, Mantovani A, Allavena P. Tumor-associated macrophage are distinct M2 polarized population promoting tumor progression: potential targets of anti-tumor therapy. Eur J of Cancer 2006;42:717-27
  7. Sessa C, De Braud F, Perotti A, et al. Trabectedin for women with ovarian carcinoma after treatment with platinum and taxanes fails. J Clin Oncol 2005;23:1867-74.
  8. Wahl L, Kleinman HK. Tumor-associated macrophages as targets for cancer therapy. J Natl Cancer Inst 1998;90:1583-4.
  9. Giraudo E, Inoue M, Hanahan D. An amino-bisphosphonate targets MMP-9-expressing macrophages and angiogenesis to impair cervical carcinogenesis. J Clin Invest 2004;114:623-33.
  10. Guiducci C, Vicari AP, Sangaletti S, Trinchieri G, Colombo MP. Redirecting in vivo elicited tumor infiltrating macrophages and dendritic cells towards tumor rejection. Cancer Res 2005;65:3437-46.
  Eligibility

Ages Eligible for Study:   18 Years to 90 Years
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
Sampling Method:   Probability Sample
Study Population

patients diagnosed of lung cancer with malignant pleural effusions

Criteria

Inclusion Criteria:

  • lung cancer with malignant pleural effusions

Exclusion Criteria:

  • None
  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: NCT00690261

Contacts
Contact: Chao-Chi Ho, Ph.D. 886-2-2356-2905 ccho1203@ntu.edu.tw
Contact: Ang Yuan, Ph.D. navyyuan@ntu.edu.tw

Locations
Taiwan
National Taiwan University Hospital Recruiting
Taipei, Taiwan, 100
Contact: Chao-Chi Ho    886-2-2356-2905    ccho1203@ntu.edu.tw   
Sponsors and Collaborators
National Taiwan University Hospital
National Science Council, Taiwan
Investigators
Principal Investigator: Chao-Chi Ho Department of Internal Medicine and Emergency Medicine, National Taiwan University Hospital
  More Information

No publications provided

Responsible Party: Chao-Chi Ho, National Taiwan University Hospital
ClinicalTrials.gov Identifier: NCT00690261     History of Changes
Other Study ID Numbers: 200709004R
Study First Received: June 1, 2008
Last Updated: June 3, 2008
Health Authority: Taiwan: Department of Health

Keywords provided by National Taiwan University Hospital:
tumor associated macrophage
lung cancer
outcome

Additional relevant MeSH terms:
Lung Neoplasms
Neoplastic Processes
Respiratory Tract Neoplasms
Thoracic Neoplasms
Neoplasms by Site
Neoplasms
Lung Diseases
Respiratory Tract Diseases
Pathologic Processes

ClinicalTrials.gov processed this record on August 21, 2014