Human renal cancers resistant to IFN's antiproliferative action exhibit sensitivity to IFN's gene-inducing and antiviral actions

Lawrence Pfeffer, Chiang Wang, Stefan N. Constantinescu, Ed Croze, Lawrence M. Blatt, Anthony P. Albino, David M. Nanus

Research output: Contribution to journalArticle

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Abstract

Purpose: Although treatment with interferon-α (IFNα) results in tumor regression in a subset (<20%) of patients with renal cell carcinoma, the underlying mechanisms for the resistance of renal cancer (RC) cells to IFNα is unknown. Materials and Methods: We examined 5 RC lines resistant and 5 RC lines sensitive to the antiproliferative effects of IFNα for differences in: 1) the number of IFN binding sites, 2) the number of signal-transducing IFNAR-1 chains of the IFNα receptor, 3) IFNα receptor structure, 4) IFN- stimulated gene (ISG) expression and 5) IFNα sensitivity in antiviral assays. Results: No structural alterations in the IFNα receptor were detected in any RC line examined, although varying numbers of ligand binding sites and IFNAR-1 signal transducer chains were present. All 5 IFN-sensitive, and 4 of 5 IFN-resistant RC lines were sensitive to the antiviral and gene- inducing actions of IFNα. Conclusions: The resistance of RC lines to IFN's antiproliferative action is not due to defects in ligand binding or in IFN- receptor structure. Our results indicate that the defective antiproliferative response in most RC cells is not due to their failure to induce the gene- inducing and antiviral effects of IFNα.

Original languageEnglish (US)
Pages (from-to)1867-1871
Number of pages5
JournalJournal of Urology
Volume156
Issue number5
DOIs
StatePublished - Jan 1 1996

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Kidney Neoplasms
Interferons
Antiviral Agents
Interferon Receptors
Genes
Renal Cell Carcinoma
Binding Sites
Ligands
Transducers
Gene Expression

All Science Journal Classification (ASJC) codes

  • Urology

Cite this

Human renal cancers resistant to IFN's antiproliferative action exhibit sensitivity to IFN's gene-inducing and antiviral actions. / Pfeffer, Lawrence; Wang, Chiang; Constantinescu, Stefan N.; Croze, Ed; Blatt, Lawrence M.; Albino, Anthony P.; Nanus, David M.

In: Journal of Urology, Vol. 156, No. 5, 01.01.1996, p. 1867-1871.

Research output: Contribution to journalArticle

Pfeffer, Lawrence ; Wang, Chiang ; Constantinescu, Stefan N. ; Croze, Ed ; Blatt, Lawrence M. ; Albino, Anthony P. ; Nanus, David M. / Human renal cancers resistant to IFN's antiproliferative action exhibit sensitivity to IFN's gene-inducing and antiviral actions. In: Journal of Urology. 1996 ; Vol. 156, No. 5. pp. 1867-1871.
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abstract = "Purpose: Although treatment with interferon-α (IFNα) results in tumor regression in a subset (<20{\%}) of patients with renal cell carcinoma, the underlying mechanisms for the resistance of renal cancer (RC) cells to IFNα is unknown. Materials and Methods: We examined 5 RC lines resistant and 5 RC lines sensitive to the antiproliferative effects of IFNα for differences in: 1) the number of IFN binding sites, 2) the number of signal-transducing IFNAR-1 chains of the IFNα receptor, 3) IFNα receptor structure, 4) IFN- stimulated gene (ISG) expression and 5) IFNα sensitivity in antiviral assays. Results: No structural alterations in the IFNα receptor were detected in any RC line examined, although varying numbers of ligand binding sites and IFNAR-1 signal transducer chains were present. All 5 IFN-sensitive, and 4 of 5 IFN-resistant RC lines were sensitive to the antiviral and gene- inducing actions of IFNα. Conclusions: The resistance of RC lines to IFN's antiproliferative action is not due to defects in ligand binding or in IFN- receptor structure. Our results indicate that the defective antiproliferative response in most RC cells is not due to their failure to induce the gene- inducing and antiviral effects of IFNα.",
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T1 - Human renal cancers resistant to IFN's antiproliferative action exhibit sensitivity to IFN's gene-inducing and antiviral actions

AU - Pfeffer, Lawrence

AU - Wang, Chiang

AU - Constantinescu, Stefan N.

AU - Croze, Ed

AU - Blatt, Lawrence M.

AU - Albino, Anthony P.

AU - Nanus, David M.

PY - 1996/1/1

Y1 - 1996/1/1

N2 - Purpose: Although treatment with interferon-α (IFNα) results in tumor regression in a subset (<20%) of patients with renal cell carcinoma, the underlying mechanisms for the resistance of renal cancer (RC) cells to IFNα is unknown. Materials and Methods: We examined 5 RC lines resistant and 5 RC lines sensitive to the antiproliferative effects of IFNα for differences in: 1) the number of IFN binding sites, 2) the number of signal-transducing IFNAR-1 chains of the IFNα receptor, 3) IFNα receptor structure, 4) IFN- stimulated gene (ISG) expression and 5) IFNα sensitivity in antiviral assays. Results: No structural alterations in the IFNα receptor were detected in any RC line examined, although varying numbers of ligand binding sites and IFNAR-1 signal transducer chains were present. All 5 IFN-sensitive, and 4 of 5 IFN-resistant RC lines were sensitive to the antiviral and gene- inducing actions of IFNα. Conclusions: The resistance of RC lines to IFN's antiproliferative action is not due to defects in ligand binding or in IFN- receptor structure. Our results indicate that the defective antiproliferative response in most RC cells is not due to their failure to induce the gene- inducing and antiviral effects of IFNα.

AB - Purpose: Although treatment with interferon-α (IFNα) results in tumor regression in a subset (<20%) of patients with renal cell carcinoma, the underlying mechanisms for the resistance of renal cancer (RC) cells to IFNα is unknown. Materials and Methods: We examined 5 RC lines resistant and 5 RC lines sensitive to the antiproliferative effects of IFNα for differences in: 1) the number of IFN binding sites, 2) the number of signal-transducing IFNAR-1 chains of the IFNα receptor, 3) IFNα receptor structure, 4) IFN- stimulated gene (ISG) expression and 5) IFNα sensitivity in antiviral assays. Results: No structural alterations in the IFNα receptor were detected in any RC line examined, although varying numbers of ligand binding sites and IFNAR-1 signal transducer chains were present. All 5 IFN-sensitive, and 4 of 5 IFN-resistant RC lines were sensitive to the antiviral and gene- inducing actions of IFNα. Conclusions: The resistance of RC lines to IFN's antiproliferative action is not due to defects in ligand binding or in IFN- receptor structure. Our results indicate that the defective antiproliferative response in most RC cells is not due to their failure to induce the gene- inducing and antiviral effects of IFNα.

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