Macrophage-like-cell-lnduced growth regulation of lymphoma cells

K. C. Komanduri, D. J. Tomes, H. J. Gabius, Shantaram S Joshi

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Since hematopoietic stromal cells play a major role in regulating the growth and differentiation of hematopoietic cells, we have studied the effects of stromal cells on the in vitro growth of highly malignant murine RAW117-H10 lymphoma cells. These cells, when grown on a preformed layer of syngeneic Balb/c macrophage/monocyte cell line, J774A.1, stop proliferating 48 h after coculture. This stromal-cell-mediated growth regulation appears to require cell-to-cell contact between stromal cells and RAW117-H10 cells, since the J774A.1 cell supernatant did not significantly inhibit the in vitro growth of RAW117-H10 cells. Because one of the cytokines produced by the macrophages is tumor necrosis factor (TNF)-α, which is known to inhibit certain tumor cells, we also studied the effects of various concentrations of TNF-α on the in vitro growth of RAW117-H10 lymphoma cells. TNF-α did not significantly affect the growth of these cells in vitro. However, TNF-α induced significant morphologic changes in these cells similar to those seen in plasma cytoid differentiation. Thus, our results indicate that the macrophage-like stromal cells regulate the in vitro growth of malignant lymphoma cells, and that direct cell surface contact between stromal and lymphoma cells is necessary for the growth regulation, and the growth inhibition is not due to TNF-α secreted by the macrophages. TNF-α is associated with differentiation of these lymphoma cells.

Original languageEnglish (US)
Pages (from-to)196-201
Number of pages6
JournalOncology (Switzerland)
Volume52
Issue number3
DOIs
StatePublished - Jan 1 1995

Fingerprint

Lymphoma
Macrophages
Growth
Stromal Cells
Tumor Necrosis Factor-alpha
Cell Differentiation
Coculture Techniques
Monocytes
In Vitro Techniques
Cytokines
Cell Line

Keywords

  • Endogenous lectins
  • Growth inhibition
  • Lymphoma cells
  • Stromal cells
  • Tumor necrosis factor-α

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Macrophage-like-cell-lnduced growth regulation of lymphoma cells. / Komanduri, K. C.; Tomes, D. J.; Gabius, H. J.; Joshi, Shantaram S.

In: Oncology (Switzerland), Vol. 52, No. 3, 01.01.1995, p. 196-201.

Research output: Contribution to journalArticle

Komanduri, K. C. ; Tomes, D. J. ; Gabius, H. J. ; Joshi, Shantaram S. / Macrophage-like-cell-lnduced growth regulation of lymphoma cells. In: Oncology (Switzerland). 1995 ; Vol. 52, No. 3. pp. 196-201.
@article{4400c972e8794528a433397871bea498,
title = "Macrophage-like-cell-lnduced growth regulation of lymphoma cells",
abstract = "Since hematopoietic stromal cells play a major role in regulating the growth and differentiation of hematopoietic cells, we have studied the effects of stromal cells on the in vitro growth of highly malignant murine RAW117-H10 lymphoma cells. These cells, when grown on a preformed layer of syngeneic Balb/c macrophage/monocyte cell line, J774A.1, stop proliferating 48 h after coculture. This stromal-cell-mediated growth regulation appears to require cell-to-cell contact between stromal cells and RAW117-H10 cells, since the J774A.1 cell supernatant did not significantly inhibit the in vitro growth of RAW117-H10 cells. Because one of the cytokines produced by the macrophages is tumor necrosis factor (TNF)-α, which is known to inhibit certain tumor cells, we also studied the effects of various concentrations of TNF-α on the in vitro growth of RAW117-H10 lymphoma cells. TNF-α did not significantly affect the growth of these cells in vitro. However, TNF-α induced significant morphologic changes in these cells similar to those seen in plasma cytoid differentiation. Thus, our results indicate that the macrophage-like stromal cells regulate the in vitro growth of malignant lymphoma cells, and that direct cell surface contact between stromal and lymphoma cells is necessary for the growth regulation, and the growth inhibition is not due to TNF-α secreted by the macrophages. TNF-α is associated with differentiation of these lymphoma cells.",
keywords = "Endogenous lectins, Growth inhibition, Lymphoma cells, Stromal cells, Tumor necrosis factor-α",
author = "Komanduri, {K. C.} and Tomes, {D. J.} and Gabius, {H. J.} and Joshi, {Shantaram S}",
year = "1995",
month = "1",
day = "1",
doi = "10.1159/000227457",
language = "English (US)",
volume = "52",
pages = "196--201",
journal = "Oncology",
issn = "0890-9091",
publisher = "UBM Medica Healthcare Publications",
number = "3",

}

TY - JOUR

T1 - Macrophage-like-cell-lnduced growth regulation of lymphoma cells

AU - Komanduri, K. C.

AU - Tomes, D. J.

AU - Gabius, H. J.

AU - Joshi, Shantaram S

PY - 1995/1/1

Y1 - 1995/1/1

N2 - Since hematopoietic stromal cells play a major role in regulating the growth and differentiation of hematopoietic cells, we have studied the effects of stromal cells on the in vitro growth of highly malignant murine RAW117-H10 lymphoma cells. These cells, when grown on a preformed layer of syngeneic Balb/c macrophage/monocyte cell line, J774A.1, stop proliferating 48 h after coculture. This stromal-cell-mediated growth regulation appears to require cell-to-cell contact between stromal cells and RAW117-H10 cells, since the J774A.1 cell supernatant did not significantly inhibit the in vitro growth of RAW117-H10 cells. Because one of the cytokines produced by the macrophages is tumor necrosis factor (TNF)-α, which is known to inhibit certain tumor cells, we also studied the effects of various concentrations of TNF-α on the in vitro growth of RAW117-H10 lymphoma cells. TNF-α did not significantly affect the growth of these cells in vitro. However, TNF-α induced significant morphologic changes in these cells similar to those seen in plasma cytoid differentiation. Thus, our results indicate that the macrophage-like stromal cells regulate the in vitro growth of malignant lymphoma cells, and that direct cell surface contact between stromal and lymphoma cells is necessary for the growth regulation, and the growth inhibition is not due to TNF-α secreted by the macrophages. TNF-α is associated with differentiation of these lymphoma cells.

AB - Since hematopoietic stromal cells play a major role in regulating the growth and differentiation of hematopoietic cells, we have studied the effects of stromal cells on the in vitro growth of highly malignant murine RAW117-H10 lymphoma cells. These cells, when grown on a preformed layer of syngeneic Balb/c macrophage/monocyte cell line, J774A.1, stop proliferating 48 h after coculture. This stromal-cell-mediated growth regulation appears to require cell-to-cell contact between stromal cells and RAW117-H10 cells, since the J774A.1 cell supernatant did not significantly inhibit the in vitro growth of RAW117-H10 cells. Because one of the cytokines produced by the macrophages is tumor necrosis factor (TNF)-α, which is known to inhibit certain tumor cells, we also studied the effects of various concentrations of TNF-α on the in vitro growth of RAW117-H10 lymphoma cells. TNF-α did not significantly affect the growth of these cells in vitro. However, TNF-α induced significant morphologic changes in these cells similar to those seen in plasma cytoid differentiation. Thus, our results indicate that the macrophage-like stromal cells regulate the in vitro growth of malignant lymphoma cells, and that direct cell surface contact between stromal and lymphoma cells is necessary for the growth regulation, and the growth inhibition is not due to TNF-α secreted by the macrophages. TNF-α is associated with differentiation of these lymphoma cells.

KW - Endogenous lectins

KW - Growth inhibition

KW - Lymphoma cells

KW - Stromal cells

KW - Tumor necrosis factor-α

UR - http://www.scopus.com/inward/record.url?scp=0028929409&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028929409&partnerID=8YFLogxK

U2 - 10.1159/000227457

DO - 10.1159/000227457

M3 - Article

VL - 52

SP - 196

EP - 201

JO - Oncology

JF - Oncology

SN - 0890-9091

IS - 3

ER -