Concentration, Structure and Iron Saturation of Ferritins from Normal Human Lung and Lung Tumors with Graded Histopathology

Enzyme ◽  
1982 ◽  
Vol 27 (3) ◽  
pp. 189-198 ◽  
Author(s):  
Maria C. Linder ◽  
Kristine Wright ◽  
James Madara
Keyword(s):  
Human Lung ◽  
Lung Tumors ◽  
Iron Saturation ◽  
Normal Human

scholarly journals Distribution of peptidyl-glycine alpha-amidating mono-oxygenase (PAM) enzymes in normal human lung and in lung epithelial tumors.

1996 ◽  
Vol 44 (1) ◽  
pp. 3-12 ◽  
Author(s):  
L Saldise ◽  
A Martínez ◽  
L M Montuenga ◽  
A Treston ◽  
D R Springall ◽  
...  
Keyword(s):  
Human Lung ◽  
Regulatory Peptides ◽  
Lung Tumors ◽  
Normal Lung ◽  
Post Translational Modification ◽  
Human Lung Tissue ◽  
Lung Epithelial ◽  
Normal Human ◽  
Myelinated Nerves ◽  
Intrinsic Ganglia

C-terminal alpha-amidation is a post-translational modification necessary for the biological activity of many regulatory peptides produced in the respiratory tract. This modification is a two-step process catalyzed by two separate enzyme activities, both derived from the peptidyl-glycine alpha-amidating mono-oxygenase (PAM) precursor. The distribution of these two enzymes, peptidyl-glycine alpha-hydroxylating monoxygenase (PHM) and peptidyl-alpha-hydroxyglycine a amidating lyase (PAL), was studied in the normal lung and in lung tumors using immunocytochemical methods and in situ hybridization. In normal lung the enzymes were located in some cells of the airway epithelium and glands, the endothelium of blood vessels, some chondrocytes of the bronchial cartilage, the alveolar macrophages, smooth muscle cells, neurons of the intrinsic ganglia, and in myelinated nerves. A total of 24 lung tumors of seven different histological types were studied. All cases contained PAM-immunoreactive cells with various patterns of distribution. All immunoreactive cells were positive for the PHM antiserum but only some of them for the PAL antiserum. The distribution of PAM co-localizes with some other previously described amidated peptides, suggesting that amidation is an important physiological process taking place in the normal and malignant human lung tissue.

scholarly journals Isolation of tumor-resident CD8+ T cells from human lung tumors

2021 ◽  
Vol 2 (1) ◽  
pp. 100267
Author(s):  
Stéphanie Corgnac ◽  
Yann Lecluse ◽  
Fathia Mami-chouaib
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Human Lung ◽  
Lung Tumors

Secretion of autocrine growth factors by cultured human lung tumors: Effects on neoplastic lung epithelial cells

Lung Cancer ◽  
1988 ◽  
Vol 4 (3-4) ◽  
pp. 205-209 ◽  
Author(s):  
Jill M. Siegfried ◽  
Suzanne K. Hansen ◽  
Vickie Y. Lawrence ◽  
Sara E. Owens
Keyword(s):  
Growth Factors ◽  
Epithelial Cells ◽  
Human Lung ◽  
Lung Tumors ◽  
Lung Epithelial Cells ◽  
Autocrine Growth ◽  
Autocrine Growth Factors ◽  
Lung Epithelial

scholarly journals Parathyroid hormone-related protein regulates the growth of orthotopic human lung tumors in athymic mice

Cancer ◽  
2001 ◽  
Vol 92 (6) ◽  
pp. 1402-1410 ◽  
Author(s):  
Randolph H. Hastings ◽  
Douglas W. Burton ◽  
Rick A. Quintana ◽  
Elana Biederman ◽  
Aneeta Gujral ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Human Lung ◽  
Lung Tumors ◽  
Athymic Mice ◽  
Related Protein ◽  
Parathyroid Hormone Related Protein

Surfactant downregulates synthesis of DNA and inflammatory mediators in normal human lung fibroblasts

1996 ◽  
Vol 270 (1) ◽  
pp. L159-L163 ◽  
Author(s):  
M. J. Thomassen ◽  
J. M. Antal ◽  
B. P. Barna ◽  
L. T. Divis ◽  
D. P. Meeker ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Inflammatory Mediators ◽  
Human Lung ◽  
Thymidine Incorporation ◽  
Interleukin 1 ◽  
S Phase ◽  
Lung Fibroblast ◽  
Lung Fibroblasts ◽  
Human Lung Fibroblast ◽  
Normal Human

The initial inflammatory event in the adult respiratory distress syndrome (ARDS) is followed by fibroproliferation and a cascade of fibroblast-derived mediators. Because lung fibroblasts may be exposed to surfactant as well as inflammatory cytokines during ARDS, we hypothesized that surfactant might modulate fibroblast activity. We previously demonstrated that surfactant inhibited production of inflammatory cytokines from endotoxin-stimulated human alveolar macrophages. In the current study the effects of surfactant on normal human lung fibroblast proliferative capacity and mediator production were examined. Both synthetic (Exosurf) and natural (Survanta) surfactant inhibited fibroblast [3H]thymidine incorporation. Examination of pre-S-phase events indicated stimulation of the immediate response gene, c-fos, and no effect on the G1/S cyclin, cyclin D1, suggesting that the surfactant block occurred elsewhere before S phase. The antioxidant N-acetyl-L-cysteine (NAC), like surfactant, inhibited [3H]thymidine incorporation. Furthermore, menadione, a generator of intracellular H2O2, stimulated fibroblast [3H]thymidine incorporation, and this was inhibited by surfactant. Interleukin-1 (IL-1)-stimulated secretion of the inflammatory mediators, IL-6 and prostaglandin E2, was also inhibited by surfactant. These data suggest that surfactant may modify lung fibroblast participation in ARDS sequelae by downregulating DNA synthesis and secondary inflammatory mediator production.

p53 mutations in primary human lung tumors and their metastases

1994 ◽  
Vol 9 (2) ◽  
pp. 105-109 ◽  
Author(s):  
Martin B. Reichel ◽  
Hiroko Ohgaki ◽  
Iver Petersen ◽  
Paul Kleihues
Keyword(s):  
Human Lung ◽  
Lung Tumors ◽  
P53 Mutations
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