PMID- 8444009
OWN - NLM
STAT- MEDLINE
DCOM- 19930407
LR  - 20191023
IS  - 0262-0898 (Print)
IS  - 0262-0898 (Linking)
VI  - 11
IP  - 2
DP  - 1993 Mar
TI  - Human and murine Kupffer cell function may be altered by both intrahepatic and 
      intrasplenic tumor deposits.
PG  - 175-82
AB  - The liver is the most common site of hematogenous metastases from colorectal 
      carcinoma. Kupffer cells (KC), which line the hepatic sinusoids, may form the 
      first line of defense against circulating tumor cells. The purpose of this study 
      was to determine the effect of hepatic metastases and intra-abdominal tumor 
      growth on KC binding of human colorectal carcinoma (HCRC) cells. MIP-101, a 
      poorly metastatic cell line, and CX-1, a highly metastatic cell line, were 
      injected intrasplenically into nude mice and KC were isolated by collagenase 
      perfusion at varying intervals after injection. Conditioned media were collected 
      from MIP-101, CCL 188 and CX-1 to determine their in vitro effect on KC function. 
      KC from MIP-101 injected mice (14% liver metastases, 100% splenic tumors) bound a 
      significantly greater number of MIP-101 and clone A cells than CX-1 cells in 
      vitro. KC isolated from mice 5 weeks after CX-1 injection (100% liver metastases) 
      also showed increased binding of MIP-101 and clone A cells compared to CX-1 
      cells. Similar results were obtained when tumor cell binding to normal human 
      liver KC was compared to binding to KC from human livers from patients with 
      hepatic metastasis from colorectal cancer. In contrast KC obtained from mice 3 
      weeks after CX-1 injection (44% liver metastases) showed significantly decreased 
      binding of MIP-101 and clone A cells. The conditioned medium from CX-1 cells 
      significantly decreased the in vitro binding of both MIP-101 and CX-1 by KC. 
      These results indicate that the ability of KC to bind HCRC cells (which precedes 
      phagocytosis and tumor cell killing) is a dynamic function and affected by 
      concomitant tumor growth. HCRC cells may alter KC function via the production of 
      specific tumor-derived soluble factors. In order to devise new and more effective 
      therapeutic options in the treatment of liver metastases the nature of this tumor 
      cell-KC interaction must be better understood.
FAU - Meterissian, S
AU  - Meterissian S
AD  - Department of Surgery, New England Deaconess Hospital, Harvard Medical School, 
      Boston, MA 02115.
FAU - Steele, G D Jr
AU  - Steele GD Jr
FAU - Thomas, P
AU  - Thomas P
LA  - eng
GR  - CA44583/CA/NCI NIH HHS/United States
GR  - CA44704/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Clin Exp Metastasis
JT  - Clinical & experimental metastasis
JID - 8409970
RN  - 0 (Culture Media, Conditioned)
SB  - IM
MH  - Animals
MH  - Cell Adhesion
MH  - Colorectal Neoplasms/pathology
MH  - Culture Media, Conditioned
MH  - Humans
MH  - Kupffer Cells/cytology/metabolism/*physiology
MH  - Liver Neoplasms, Experimental/*physiopathology/*secondary
MH  - Macrophages/physiology
MH  - Mice
MH  - Mice, Nude
MH  - Splenic Neoplasms/physiopathology/*secondary
MH  - Tumor Cells, Cultured
EDAT- 1993/03/01 00:00
MHDA- 2001/03/28 10:01
CRDT- 1993/03/01 00:00
PHST- 1993/03/01 00:00 [pubmed]
PHST- 2001/03/28 10:01 [medline]
PHST- 1993/03/01 00:00 [entrez]
AID - 10.1007/BF00114975 [doi]
PST - ppublish
SO  - Clin Exp Metastasis. 1993 Mar;11(2):175-82. doi: 10.1007/BF00114975.