title: Mechanism for the recruitment of macrophages to cancer site. In vivo concentration gradient of monocyte chemotactic activity.
abstract: BACKGROUND
  Tumor stroma is characterized by the development of new blood vessels, an inflammatory cell infiltration, and a fibrotic reaction. The inflammatory component of tumor stroma plays an important role in the modulation of tumor expansion. In this respect, macrophages constitute a major part of the inflammatory cell infiltration and can exert cytotoxic activity against tumor cells. The accumulation of macrophages in the vicinity of the tumor suggests their recruitment from circulating blood monocytes through the local release of chemotactic factors for monocytes.
  
  
  METHODS
  To detect the existence of a concentration gradient of monocyte chemotactic activity (MCA) between the tumor vicinity and blood vessels, malignant pleural effusions defined by the local presence of cancer cells were evaluated for quantification of MCA.
  
  
  RESULTS
  Unlike nonmalignant pleural effusions, malignant pleural effusions were characterized by the presence of increased levels of MCA, and in lung adenocarcinoma (a cancer with high inflammatory cell infiltration), pleural levels of MCA were significantly greater than in small cell lung carcinoma (a cancer with low inflammatory cell reaction). An MCA concentration gradient between pleural fluid and plasma was present in malignant effusions because pleural MCA levels in all cancer types were significantly greater than MCA levels in the plasma of the same patients.
  
  
  CONCLUSIONS
  Thus, an increased local level of MCA is a feature of cancers with high inflammatory cell infiltration, and the presence of an in vivo concentration gradient of MCA suggests the direct role of this biologic activity in recruiting blood monocytes to the cancer site.
authors.affiliation: Inserm U14, Vandoeuvre-lès-Nancy, France.
authors.forename: N
authors.initials: N
authors.lastname: Martinet
authors.forename: G
authors.initials: G
authors.lastname: Beck
authors.forename: V
authors.initials: V
authors.lastname: Bernard
authors.forename: F
authors.initials: F
authors.lastname: Plenat
authors.forename: P
authors.initials: P
authors.lastname: Vaillant
authors.forename: F
authors.initials: F
authors.lastname: Schooneman
authors.forename: J M
authors.initials: JM
authors.lastname: Vignaud
authors.forename: Y
authors.initials: Y
authors.lastname: Martinet
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism* / Q000473:pathology; D000368:Aged; D001706:Biopsy; D018288:Carcinoma, Small Cell / Q000378:metabolism* / Q000473:pathology; D018932:Chemokine CCL2; D002630:Chemotactic Factors / Q000096:biosynthesis / Q000097:blood / Q000378:metabolism*; D002633:Chemotaxis / Q000502:physiology*; D004801:Eosine Yellowish-(YS); D005260:Female; D006416:Hematoxylin; D006801:Humans; D007249:Inflammation / Q000473:pathology; D008175:Lung Neoplasms / Q000378:metabolism* / Q000473:pathology; D008264:Macrophages / Q000187:drug effects / Q000502:physiology*; D008297:Male; D008654:Mesothelioma / Q000378:metabolism / Q000473:pathology; D008875:Middle Aged; D010996:Pleural Effusion / Q000378:metabolism; D016066:Pleural Effusion, Malignant / Q000378:metabolism* / Q000473:pathology; D014407:Tumor Cells, Cultured / Q000378:metabolism
chemical_list: D018932:Chemokine CCL2; D002630:Chemotactic Factors; D004801:Eosine Yellowish-(YS); D006416:Hematoxylin