|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Preincubation of tumor cells with IFN-gamma, IFN-alpha or TNF-alpha significantly decreased the susceptibility of each tumor cell line to lysis by LAK cells, and the change in sensitivity did not correlate with the expression of HLA antigens or intercellular adhesion molecule-I (ICAM-I) on the surface of tumor cells.
|
1355757 |
1992 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Tumor areas which were class II positive also express class II associated invariant chain and the adhesion molecules lymphocyte function antigen 3 and intercellular adhesion molecule 1.
|
1377602 |
1992 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Furthermore, tumors expressed human LFA-1/ICAM-1 and the tumor blood vessels strongly expressed murine ICAM-1, but not MECA 79.
|
1684402 |
1991 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In positive samples, ICAM-1 was expressed on differentiated neuroblasts and Schwann cells, but negative on ganglion cells; however, most of the differentiated tumors were ICAM-1-negative, suggesting ICAM-1 induction by unknown local signal.
|
1710608 |
1991 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In B-lymphoid malignancies, CD54 expression appears to correlate with the differentiation stage of malignant cells, since B-origin acute lymphoblastic leukemias and conventional B-chronic lymphocytic leukemias (B-CLL; ie, "dim SIg" CLL) expressed lower levels of CD54 than more mature lymphoproliferative disorders ("bright SIg" CLL, prolymphocytic leukemias, and lymphoplasmacytic tumors).
|
1974471 |
1990 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The inducibility of ICAM-I expression on cultured fibroblasts by several lymphokines suggests that the expression of ICAM-I in the vicinity of carcinoma cells is effected by lymphokines produced by activated lymphocytes/macrophages within the tumor.
|
2654024 |
1989 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
All squamous cell carcinomas consisted of intercellular adhesion molecule-1-positive neoplastic cells infiltrated by lymphocyte function-associated antigen-1-positive tumor infiltrating lymphomononuclear and CD-la-positive Langerhans cells, whereas only a minor number of adenocarcinomas displayed a consistent number of intercellular adhesion molecule-1-positive neoplastic cells.
|
7519825 |
1994 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The expression of ICAM-1 and CD44 was determined by fluorescence-activated cell sorter (FACS) analysis, the tumor cell binding affinity to ECM components was measured by cell attachment assay, the degree of homotypic aggregation was quantified by cell aggregation assay, and the mRNA levels of c-myc, EGF-R, TGF-beta, and collagenase were analyzed by a quantitative polymerase chain reaction analysis.
|
7521786 |
1994 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Several mechanisms appear to be involved in the escape of melanoma from immunologic control, 1) downregulation of surface-expressed major histocompatibility complex class I molecules and the failure of tumor cells to process endogenously synthesized proteins for antigen presentation, 2) inhibition of the interaction of cytotoxic T cells with melanoma cells, eg, by soluble adhesion molecules (intercellular adhesion molecule 1), and 3) induction and maintenance of clonal anergy in tumor cell-specific T cells.
|
7912108 |
1994 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Increased ICAM-1 expression corresponds to greater binding of human leukocyte functional antigen-1 (CD11a/CD18)-expressing peripheral blood mononuclear cells (PBMC) to C8161 monolayers, suggesting that cytokine-treated melanoma cells would be more metastatic due to PBMC-tumor cell emboli.
|
7915992 |
1994 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
ICAM-1 was frequently expressed in higher stage tumors, especially in those with abundant immune cells scattered within tumor.
|
8100398 |
1993 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The expression of the human tumor associated antigen CEA (carcinoembryonic antigen), HLA classes I and II, and ICAM-1 antigens in the transfected HT-29 cells were also analyzed by flow cytometry.
|
8102353 |
1993 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
A human/mouse chimeric monoclonal antibody against intercellular adhesion molecule-1 for tumor radioimmunoimaging.
|
8641973 |
1996 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Most importantly, administration of tumor cells genetically modified with genes encoding xenogeneic ICAM-1 can facilitate an immunological response to genetically unaltered pre-existing tumors.
|
8789803 |
1996 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Overexpression of growth factor receptors (EGF receptor, c-erbB2, c-erbB3, TGF beta receptor I-III), growth factors (EGF, TGF alpha, TGF beta-1-3, aFGF, bFGF), adhesion molecules (ICAM-1, ELAM-1) and gene mutations (p53, K-ras, DCC, APC) are present in a significant number of these tumors.
|
8834768 |
1996 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The pattern of expression of cell adhesion molecules, i.e., leucocyte function associated antigen 3 (LFA-3) and intercellular adhesion molecule 1 (ICAM-1) on human bladder tumour biopsy specimens was investigated.
|
8903546 |
1996 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The up-modulation of cell-adhesion molecules (NCAM, ICAM-1 and Thy1) and immune recognition molecules (NCAM, ICAM-1 and MHC class I), associated with reduced growth and tumour cell differentiation, suggests that RA may have a potential role in regulating the growth and development of retinoblastoma tumours.
|
9222276 |
1997 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Decreased expression of ICAM-1 was observed in 12 out of 34 (35%) tumour specimens and de novo expression of HLA-DR (HLA class II) by carcinoma cells in 13 out of 34 (38%) cases.
|
9328140 |
1997 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In this study, to investigate the relationship between the alteration in ICAM-1 and MHC expression with the tumor grade and/or cell differentiation, we examined the expression of ICAM-1 and HLA-DR before and after treatment with IFN-gamma in 4 human bladder cancer cell lines.
|
9392053 |
1997 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Therefore, ICAM-1 regulation on tumor cells might be a mechanism of immune escape.
|
9434632 |
1997 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Over-expression of ICAM-I might prevent cell-cell disruption and, hence, tumor dissemination.
|
9495363 |
1998 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
ICAM-1 expression in LD1-20 D metastatic liver cancer had a positive correlation with tumor size and the time after implantation.
|
10037274 |
1999 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
RCC cells were incubated with and without IFN-gamma, then analyzed by flow cytometry for the percent positive and mean intensity fluorescence (MIF), a measurement of mean antigen density, of HLA-I, HLA-II, ICAM-1, and tumor antigens (URO-2, URO-3, and URO-4).
|
10048768 |
1999 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Altogether, our results suggest that (i) the extent of sICAM-1 release is distinctive for individual melanomas and can be independent of ICAM-1 expression; (ii) tumor endothelia may sustain levels of sICAM-1 in selected melanomas; (iii) melanoma-released VEGF does not affect ICAM-1 expression and sICAM-1 release by HUVEC.
|
10414467 |
1999 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Increased tumor expression of ICAM-1 represents a promising immune anti-cancer strategy.
|
10551902 |
1999 |