Hematopoietic switch from lymphoid to granulocytic development in 3LL tumor-bearing mice

In Vivo. 2001 Jul-Aug;15(4):255-63.

Abstract

A significant splenomegaly and lymphadenopathy develops during the progressive growth of Lewis Lung (3LL) tumors in mice. Enlarged spleen and lymph nodes occur because of a pronounced increase in granulocytes in these organs. This granulocytosis in spleen and lymph node was not simply due to recruitment of granulocytes from peripheral blood to spleen and lymph nodes, but also a result of development and/or differentiation of granulocytes from the bone marrow. There was a marked increase in development of myeloid lineage cells, whereas lymphoid populations including T cells and B cells, were dramatically decreased in bone marrow and peripheral blood of 3LL tumor-bearing mice. These data demonstrate that host hematopoiesis shifts from lymphoid to granulocytic development in the 3LL tumor-bearing mice. Interestingly, a somatic mutation of N-Ras gene was found in 3LL tumor cells at codon 61, suggesting that mutated N-Ras may contribute to induction of granulocytosis in 3LL tumor-bearing mice.

MeSH terms

  • Animals
  • Carcinoma, Lewis Lung / complications
  • Carcinoma, Lewis Lung / genetics
  • Carcinoma, Lewis Lung / metabolism
  • Carcinoma, Lewis Lung / pathology*
  • Cell Differentiation / genetics
  • Cell Lineage
  • Chemokines / biosynthesis
  • Chemokines / genetics
  • Codon / genetics
  • Gene Expression Regulation, Neoplastic
  • Genes, ras
  • Granulocytes / pathology*
  • Hematopoiesis*
  • Immunophenotyping
  • Interferon-gamma / deficiency
  • Interferon-gamma / genetics
  • Lymphatic Diseases / etiology
  • Lymphatic Diseases / pathology
  • Lymphocytes / pathology*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, SCID
  • Neoplasm Proteins / biosynthesis
  • Neoplasm Proteins / genetics
  • Neoplasm Transplantation
  • Neutrophils / pathology
  • Specific Pathogen-Free Organisms
  • Splenomegaly / etiology
  • Splenomegaly / pathology

Substances

  • Chemokines
  • Codon
  • Neoplasm Proteins
  • Interferon-gamma