PMID- 10697636
OWN - NLM
STAT- MEDLINE
DCOM- 20000310
LR  - 20041117
IS  - 0250-7005 (Print)
IS  - 0250-7005 (Linking)
VI  - 19
IP  - 6C
DP  - 1999 Nov-Dec
TI  - Ovarian cancer-induced immunosuppression: relationship to tumor necrosis 
      factor-alpha (TNF-alpha) release from ovarian tissue.
PG  - 5657-62
AB  - Cytokines have been reported to be potential biological markers of, disease 
      status in cancer patients. Tumor necrosis factor-alpha (TNF-alpha) is a key 
      cytokine released from monocytes and macrophages. TNF-alpha is involved in 
      essential biological functions such as immunoregulation, modulation of cell 
      growth and differentiation. In this work, the role of TNF-alpha release in 
      ovarian cancer patients was investigated. Fifty-five patients with ovarian cancer 
      and 20 controls of matched age and parity were included in this study. TNF-alpha 
      concentrations were measured in sera and cytosolic fractions of both groups. The 
      results demonstrated a significant increase in TNF-alpha concentrations among 
      patients compared to the control subjects (P < 0.001). Furthermore, a 
      non-significant increase (P = 0.05, was observed between the different types 
      (serous, Mucinous, and endometrioid) of epithelial ovarian cancers. Also 
      TNF-alpha concentrations did not correlate with the disease stage. Moreover, 
      immunohistochemical analysis of tissue specimens stained for TNF-alpha was 
      positive in malignant lesions and negative for the normal ovarian tissue. These 
      findings confirmed the TNF-alpha kinetics obtained by ELISA assays. 
      Interestingly, TNF-alpha levels were also elevated in culture supernatants of 
      PBMC stimulated by cytosolic fractions from malignant ovarian tissues. 
      Blastogenic assays using cytosolic fractions from malignant ovarian specimens to 
      stimulate healthy donor peripheral blood mononuclear cells (PBMC) showed a marked 
      decrease in 3H-thymidine uptake compared to the cells stimulated by normal 
      cytosols. To establish a cause-effect relationship between TNF-alpha release and 
      inhibition of cell proliferation, the experiments showed that 3H-thymidine uptake 
      by PBMC was markedly inhibited by recombinant human TNF-alpha (rh TNF-alpha) and 
      that inhibition was significantly reversed when TNF-alpha monoclonal antibody was 
      added to the cells. The data presented in this work indicate that TNF-alpha may 
      play an important role in the biology of ovarian cancer and hence, tumor 
      pathogenesis.
FAU - Hassan, M I
AU  - Hassan MI
AD  - Biochemistry Department, Ain Shams Faculty of Medicine, Egypt.
FAU - Kassim, S K
AU  - Kassim SK
FAU - Saeda, L
AU  - Saeda L
FAU - Laban, M
AU  - Laban M
FAU - Khalifa, A
AU  - Khalifa A
LA  - eng
PT  - Journal Article
PL  - Greece
TA  - Anticancer Res
JT  - Anticancer research
JID - 8102988
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Antibodies, Monoclonal/pharmacology
MH  - Cell Division/drug effects
MH  - Cytosol/metabolism
MH  - Female
MH  - Humans
MH  - *Immune Tolerance
MH  - Immunohistochemistry
MH  - Leukocytes, Mononuclear/metabolism/physiology
MH  - Middle Aged
MH  - Neoplasms, Glandular and Epithelial/blood/immunology/metabolism
MH  - Ovarian Neoplasms/blood/*immunology/metabolism
MH  - Ovary/immunology
MH  - Recombinant Proteins/immunology/pharmacology
MH  - Tumor Necrosis Factor-alpha/biosynthesis/*immunology
EDAT- 2000/03/04 09:00
MHDA- 2000/03/18 09:00
CRDT- 2000/03/04 09:00
PHST- 2000/03/04 09:00 [pubmed]
PHST- 2000/03/18 09:00 [medline]
PHST- 2000/03/04 09:00 [entrez]
PST - ppublish
SO  - Anticancer Res. 1999 Nov-Dec;19(6C):5657-62.