PMID- 10501846
OWN - NLM
STAT- MEDLINE
DCOM- 19991102
LR  - 20240426
IS  - 0340-7004 (Print)
IS  - 1432-0851 (Electronic)
IS  - 0340-7004 (Linking)
VI  - 48
IP  - 7
DP  - 1999 Oct
TI  - Signaling defects in T lymphocytes of patients with malignancy.
PG  - 346-52
AB  - In patients with cancer, alterations in the expression of T-cell 
      receptor-associated molecules in tumor-infiltrating lymphocytes (TIL) as well as 
      in circulating lymphocytes have been reported. By quantitative flow cytometry 
      analysis, decreased or absent expression of the zeta chain in CD4(+) or CD8(+) T 
      cells as well as in natural killer (NK) cells was demonstrated in patients with 
      malignancies. Changes in the expression of zeta are biologically significant, 
      because the absence or low expression of this signaling molecule in TIL of 
      patients with stage III or IV head and neck cancer predicts a significantly 
      shorter 5-year survival than that of patients with normal zeta expression in TIL. 
      Preliminary evidence indicates that expression of zeta in TIL may not only 
      influence survival but also predicts a favorable response to biologic therapies. 
      Patients with cancer also show significantly greater spontaneous ex vivo 
      apoptosis in peripheral blood mononuclear cells (PBMC) compared to normal 
      controls, as measured by a terminal deoxynucleotide transferase-mediated dUTP 
      nick end labeling (TUNEL) assay. While no correlation could be established 
      between the proportions of cells with low zeta chain expression and those that 
      spontaneously apoptose ex vivo, the zeta chain has been shown to be cleaved by 
      caspases in T cells coincubated with tumor cells or with T cells exposed to CH-11 
      antibody, which induces apoptosis upon crosslinking Fas on the cell surface. The 
      results suggest that low/absent zeta chain expression and lymphocyte apoptosis 
      may be manifestations of negative effects of the tumor on the host immune system.
FAU - Whiteside, T L
AU  - Whiteside TL
AD  - Department of Pathology and Otolaryngology, University of Pittsburgh School of 
      Medicine, Pittsburgh, PA 15213, USA. whitesidetl@msx.upmc.edu
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Germany
TA  - Cancer Immunol Immunother
JT  - Cancer immunology, immunotherapy : CII
JID - 8605732
RN  - 0 (Membrane Proteins)
RN  - 0 (Receptors, Antigen, T-Cell)
RN  - 0 (antigen T cell receptor, zeta chain)
SB  - IM
CIN - Cancer Immunol Immunother. 1999 Oct;48(7):343-5. PMID: 10501845
MH  - Animals
MH  - Apoptosis
MH  - DNA Fragmentation
MH  - Down-Regulation
MH  - Humans
MH  - Lymphocyte Subsets/*immunology
MH  - Lymphocytes, Tumor-Infiltrating/*immunology
MH  - Membrane Proteins/biosynthesis/metabolism
MH  - Mice
MH  - Neoplasms/*immunology/metabolism
MH  - Receptors, Antigen, T-Cell/biosynthesis/metabolism
MH  - Signal Transduction/*immunology
MH  - T-Lymphocytes/*immunology
PMC - PMC11037126
EDAT- 1999/09/29 00:00
MHDA- 1999/09/29 00:01
PMCR- 1999/09/01
CRDT- 1999/09/29 00:00
PHST- 1999/09/29 00:00 [pubmed]
PHST- 1999/09/29 00:01 [medline]
PHST- 1999/09/29 00:00 [entrez]
PHST- 1999/09/01 00:00 [pmc-release]
AID - 90480346.262 [pii]
AID - 10.1007/s002620050585 [doi]
PST - ppublish
SO  - Cancer Immunol Immunother. 1999 Oct;48(7):346-52. doi: 10.1007/s002620050585.