12-hydroxy-5-8-10-14-eicosatetraenoic-acid and Skin-Neoplasms

12-hydroxy-5-8-10-14-eicosatetraenoic-acid has been researched along with Skin-Neoplasms* in 14 studies

Other Studies

14 other study(ies) available for 12-hydroxy-5-8-10-14-eicosatetraenoic-acid and Skin-Neoplasms

ArticleYear
12-Hydroxyeicosatetraenoic acid levels are increased in actinic keratoses and squamous cell carcinoma.
    Journal of the American Academy of Dermatology, 2018, Volume: 79, Issue:6

    Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Biopsy; Carcinoma, Squamous Cell; Celecoxib; Chemoprevention; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Glucuronosyltransferase; Humans; Keratosis, Actinic; Lipoxygenase Inhibitors; Neoplasms, Radiation-Induced; Skin Neoplasms

2018
Platelet-type 12-lipoxygenase accelerates tumor promotion of mouse epidermal cells through enhancement of cloning efficiency.
    Carcinogenesis, 2008, Volume: 29, Issue:2

    Accumulating evidence suggests that platelet-type 12-lipoxygenase (p12-LOX) plays an important role in tumor development. However, how p12-LOX contributes to tumorigenesis is still not understood. The role of p12-LOX was therefore examined in tumor promotion using mouse epidermal JB6 P+ cells that are sensitive to 12-O-tetradecanoylphorbol-13-acetate-induced transformation. The expression of p12-LOX was significantly higher in JB6 P+ cells than in JB6 P- cells that were resistant to transformation, and its expression was further increased by tumor necrosis factor (TNF)-alpha. Importantly, the inhibition of p12-LOX in JB6 P+ cells by baicalein, a specific inhibitor or small interfering RNA significantly suppressed TPA-induced transformation. Moreover, treatment with 12(S)-hydroxyeicosatetraenoic acid (HETE), a metabolite of p12-LOX, enhanced TPA-induced neoplastic transformation either in the presence or absence of baicalein. These results indicate that p12-LOX is required for tumor promotion of epidermal cells and that 12(S)-HETE functions as a rate-limiting factor. Notably, treatment with baicalein significantly suppressed the proliferation of JB6 P+ cells when cells were seeded at a low density in a culture plate. Moreover, the cloning efficiency of JB6 P+ cells was dramatically decreased by inhibition of p12-LOX. In contrast, baicalein treatment did not affect the cloning efficiency of most malignant cancer cells. These results indicate that p12-LOX is induced by the inflammatory cytokine TNF-alpha in the early stage of tumorigenesis, and is required for tumor promotion through enhancing efficient proliferation of a small number of initiated cells. The present results suggest that the p12-LOX pathway may be an effective target of chemoprevention for skin carcinogenesis.

    Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Animals; Arachidonate 12-Lipoxygenase; Blood Platelets; Cell Proliferation; Cell Transformation, Neoplastic; Cloning, Molecular; Enzyme Inhibitors; Epidermis; Epithelial Cells; Flavanones; Mice; Mice, Inbred BALB C; Skin Neoplasms; Tumor Necrosis Factor-alpha

2008
Modulation of epidermal tumor development caused by targeted overexpression of epidermis-type 12S-lipoxygenase.
    Cancer research, 2002, Aug-15, Volume: 62, Issue:16

    In contrast to other 12S-lipoxygenase (LOX) isoforms expressed in the skin of mice, epidermis-type (e) 12S-LOX was found to be transcriptionally down-regulated in the course of epidermal tumor development in NMRI mice. This may indicate that this enzyme is related to antitumorigenic rather than protumorigenic effects. To test this hypothesis, two transgenic mouse lines were generated that differentially expressed e12S-LOX under the control of the bovine keratin 6 promoter known to be constitutively up-regulated in mouse skin tumors. As compared with the wild-type, low transgene expression correlated with a decreased skin tumor response paralleled by an up-regulation of leukocyte-type 12S-LOX and an accumulation of the linoleic acid derivative 13S-hydroxyoctadecadienoic acid. In contrast, high transgene expression coincided with an increased tumor response paralleled by a strong keratin 6 promoter-driven up-regulation of the transgenic e12S-LOX and an accumulation of the arachidonic acid derivative 12S-hydroxyeicosatetraenoic acid as the predominant LOX product. These results indicate a complex interaction between different LOX isoforms and an opposite role of arachidonic acid and linoleic acid products in the modulation of skin carcinogenesis.

    Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; 9,10-Dimethyl-1,2-benzanthracene; Animals; Arachidonate 12-Lipoxygenase; Carcinogens; Down-Regulation; Female; Gene Expression; Isoenzymes; Linoleic Acids; Male; Mice; Mice, Inbred DBA; Mice, Transgenic; Papilloma; RNA, Messenger; Skin; Skin Neoplasms; Tetradecanoylphorbol Acetate; Transgenes

2002
Promutagenic etheno-DNA adducts in multistage mouse skin carcinogenesis: correlation with lipoxygenase-catalyzed arachidonic acid metabolism.
    Chemical research in toxicology, 2000, Volume: 13, Issue:8

    Formation of the lipoxygenase-catalyzed metabolites of arachidonic acid, 8-hydroxyeicosatetraenoic acid (8-HETE) and 12-hydroxyeicosatetraenoic acid (12-HETE), and of the exocyclic DNA adducts 1,N(6)-ethenodeoxyadenosine (epsilondA) and 3, N(4)-ethenodeoxycytidine (epsilondC) was investigated in NMRI mouse skin carcinogenesis induced by 7,12-dimethylbenz[a]anthracene (DMBA) and promoted by 12-O-tetradecanoylphorbol-13-acetate (TPA). In reversible papillomas obtained after 20 weeks of TPA treatment, 15- and 68-fold higher contents of 8-HETE and 12-HETE, respectively, were observed, which were paralleled by 12- and 9-fold increased amounts of epsilondA and epsilondC, respectively. When compared to the level in vehicle-treated control skin, these elevations were statistically significant. In irreversible papillomas harvested 20 weeks after the last TPA treatment, the levels of HETEs and etheno-DNA adducts were found to be slightly reduced, as compared to those in reversible papillomas, but were still increased over control levels in age-matched mice. Comparison of mean group values by simple regression analysis showed a close positive correlation between HETE and etheno-DNA adduct levels. Consistent with the miscoding properties of epsilondA causing mainly A --> T transversions, its increased formation in papillomas could thus contribute to this type of mutation in codon 61 of cHa-ras, shown to be a hallmark of DMBA-initiated and TPA-promoted mouse skin carcinogenesis. Although direct evidence that etheno adducts are derived from lipoxygenase-catalyzed metabolites of arachidonic acid is missing, our results implicate DNA damage by oxidative stress and lipid peroxidation as a cause of genetic instability observed at late stages of tumor promotion in mouse skin carcinogenesis.

    Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Animals; Arachidonic Acid; Chromatography, High Pressure Liquid; Deoxyadenosines; Deoxycytidine; DNA Adducts; DNA, Neoplasm; Female; Gas Chromatography-Mass Spectrometry; Hydroxyeicosatetraenoic Acids; Lipoxygenase; Mice; Mutagenesis; Papilloma; Skin Neoplasms; Up-Regulation

2000
Constitutive expression of 8-lipoxygenase in papillomas and clastogenic effects of lipoxygenase-derived arachidonic acid metabolites in keratinocytes.
    Molecular carcinogenesis, 1999, Volume: 24, Issue:2

    The expression pattern, enzymatic activity, and products of 8-lipoxygenase (LOX) were analyzed in normal and neoplastic skin of NMRI mice. While barely detectable in normal epidermis, 8-LOX was transiently induced by 12-O-tetradecanoylphorbol-13-acetate and constitutively expressed in papillomas but not carcinomas obtained by the initiation-promotion protocol of mouse skin carcinogenesis. The product profile and chirality of both the native and the recombinant protein produced the S enantiomers of 8-hydroxy-5Z,9E,11Z,14Z-eicosatetraenoic acid (8-HETE) and 9-hydroxy-10E,12Z-octadecadienoic acid (9-HODE) as the main arachidonic acid- and linoleic acid-derived metabolites. As compared with normal epidermis, papillomas exhibited 25- and 4-fold elevated levels of 8-HETE and 9-HODE, respectively. However, the varying S to R ratios of 8-HETE and the predominance of 9(R)-HODE indicated that in addition to 8(S)-LOX, other enzymes yet to be defined may be involved in 8-HETE and 9-HODE production. The massive accumulation of both 8-HETE and 12-hydroxy-5Z,8Z,10E,14Z-eicosatetraenoic acid (12-HETE) point to a critical role of these LOX pathways in epidermal tumor development, in particular in the papilloma stage. Here we showed that 8- and 12-hydroperoxyeicosatetraenoic acids and 8- and 12-HETE induce chromosomal alterations in cycling primary basal keratinocytes.

    Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Animals; Arachidonate Lipoxygenases; Arachidonic Acid; Female; Hydroxyeicosatetraenoic Acids; Keratinocytes; Linoleic Acids; Linoleic Acids, Conjugated; Male; Mice; Papilloma; Skin Neoplasms

1999
Monohydroxylated fatty acids in mouse epidermis papilloma quantification and stereochemical characterization.
    Advances in experimental medicine and biology, 1997, Volume: 400A

    Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Animals; Chromatography, High Pressure Liquid; Hydroxyeicosatetraenoic Acids; Linoleic Acids; Linoleic Acids, Conjugated; Mice; Papilloma; Skin Neoplasms

1997
Arachidonate has protumor-promoting action that is inhibited by linoleate in mouse skin carcinogenesis.
    The Journal of nutrition, 1996, Volume: 126, Issue:4 Suppl

    Previous studies demonstrated a requirement for arachidonic acid metabolites in tumor development in mouse skin. The goal of this study was to determine whether the arachidonate content of epidermal phospholipids could be altered by increasing dietary levels of linoleate and whether specific metabolites of linoleate and arachidonate have dissimilar biological effects. In a series of tumor studies in which the quantity of dietary linoleate was incrementally increased, a slight reduction in phospholipid levels of arachidonate was observed that correlated with an increased phospholipid level of linoleate and a suppression in tumor yield. A comparison of the arachidonate lipoxygenase metabolite 12-hydroxyeicosatetraenoic acid (12-HETE) with the 13-hydroxyoctadecadienoic acid (13-HODE) lipoxygenase metabolite of linoleate revealed that 12-HETE has biological activities that mimic the phorbol ester tumor promoters, whereas 13-HODE has antithetical effects. Specifically, 12(S)-HETE enhanced the activation of protein kinase C by phorbol esters, mimicked phorbol ester-induced adhesion of keratinocytes to fibronectin and mimicked phorbol ester repression of expression of a differentiation-related gene, keratin-1. 13-HODE blocked 12-HETE-induced cell adhesion and prevented 12-HETE-induced suppression of keratin-1 expression. Overall, these studies suggest that arachidonate and linoleate have opposing functions in the epidermis, particularly with regard to events involved in tumor development.

    Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Animals; Arachidonic Acid; Female; Hydroxyeicosatetraenoic Acids; Linoleic Acid; Linoleic Acids; Mice; Phospholipases A; Protein Kinase C; Skin Neoplasms

1996
12-Lipoxygenase isoenzymes in mouse skin tumor development.
    Molecular carcinogenesis, 1995, Volume: 14, Issue:2

    12-lipoxygenase-catalyzed arachidonic acid metabolism in normal and neoplastic mouse epidermis was assessed by cDNA cloning of the epidermal 12-lipoxygenases and by studying their expression patterns, enzyme activities, and product levels. Papillomas and squamous cell carcinomas induced by the initiation/promotion protocol contained 50- to 60-fold more 12-hydroxy-5,8,10,14-eicosatetraenoic acid (HETE) than normal epidermis. The ratio of S to R enantiomers was 9:1. This indicates that most of this eicosanoid was of enzymatic origin. Accordingly, cell-free preparations of the tumors exhibited about fivefold elevated 12-lipoxygenase activities. A papilloma-derived cDNA library was screened with human platelet-type 12-lipoxygenase cDNA probes. Two cDNA clones encoding the platelet-type and the leukocyte-type isoforms of murine 12-lipoxygenase were isolated, demonstrating the coexpression of the isoenzymes in the same tissue and species. When expressed in COS-7 cells, the recombinant enzymes showed the characteristic substrate selectivity and product profile, with the leukocyte-type enzyme metabolizing linoleic and arachidonic acid to 13-hydroxy-9,11-octadecadienoic acid and to 12- and 15-HETE, respectively, and the platelet-type enzyme oxygenating exclusively arachidonic acid to 12-HETE. In epidermis in vivo and in keratinocytes in culture, only the platelet-type 12-lipoxygenase (mRNA and protein) was detectable. In mouse epidermis both isoenzymes were induced transiently by phorbol esters. Most tumors showed constitutive overexpression of platelet-type mRNA, whereas leukocyte-type specific transcripts were detectable only in a few tumors. These data suggest that the platelet-type enzyme is the 12-lipoxygenase isoform of keratinocytes that is responsible for the generation of most of the 12-HETE found in neoplastic epidermis.

    Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; 9,10-Dimethyl-1,2-benzanthracene; Amino Acid Sequence; Animals; Arachidonate 12-Lipoxygenase; Base Sequence; Blood Platelets; Cloning, Molecular; Cytosol; DNA, Complementary; Epidermis; Female; Gene Expression Regulation, Neoplastic; Hydroxyeicosatetraenoic Acids; Isoenzymes; Leukocytes; Mice; Molecular Sequence Data; RNA, Neoplasm; Skin Neoplasms; Stereoisomerism; Tetradecanoylphorbol Acetate

1995
[Synthesis of arachidonic acid cascade eicosanoids in tumors of various histogenesis in mice].
    Vestnik Rossiiskoi akademii meditsinskikh nauk, 1995, Issue:4

    The investigation was undertaken to characterize the profile of arachidonic acid metabolites in different spontaneous and transplantable tumors in mice. The five metabolites via the cyclooxygenase pathway (PGE2, PGF2 alpha, PGD2, TxB2, 6-keto-PGF1 alpha), as well as the three lipoxygenase products (5-HETE, 12-HETE, and 15-HETE) were monitored by thin layer chromatography and high performance liquid chromatography after "ex vivo" metabolism of exogenous [1-C14]-arachidonic acid by homogenates of tumor tissues. It was shown that all tumors had a unique profile of eicosanoids. The most cyclooxygenase activity along with the significant synthesis of PGE2, PGF2 alpha, and 6-keto-PGF1 alpha was noted in lung tumors. The antitumor effect of indomethacin was directly related to the ability of tumors to produce PGE2. On the other hand, there were varying lipoxygenase activities in tumors. In some cases, the extremely high levels of 15- and 12-HETE synthesis in neoplastic tissue could indicate that there was a basic possibility of using lipoxygenase inhibitors for suppressing malignant tumors.

    Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Adenocarcinoma; Animals; Arachidonic Acid; Carcinoma, Lewis Lung; Carcinoma, Squamous Cell; Chromatography, High Pressure Liquid; Chromatography, Thin Layer; Dinoprostone; Eicosanoids; Hydroxyeicosatetraenoic Acids; In Vitro Techniques; Indomethacin; Leukemia L1210; Lipoxygenase Inhibitors; Mammary Neoplasms, Experimental; Melanoma, Experimental; Mice; Mice, Inbred C3H; Mice, Inbred C57BL; Mice, Inbred CBA; Mice, Inbred DBA; Neoplasm Transplantation; Neoplasms, Experimental; Skin Neoplasms

1995
Biosynthesis of 12(S)-hydroxyeicosatetraenoic acid by B16 amelanotic melanoma cells is a determinant of their metastatic potential.
    Laboratory investigation; a journal of technical methods and pathology, 1994, Volume: 70, Issue:3

    We have previously demonstrated that the metastatic potential of tumor cells can be increased by treatment with exogenous 12(S)hydroxyeicosatetraenoic acid [12(S)-HETE], a lipoxygenase metabolite of arachidonic acid. However, the biosynthesis of the authentic lipid mediator by tumor cells, and especially the correlation of its biosynthesis to tumor cell metastatic capacity have not been characterized. In addition, a role for other mono HETEs in influencing tumor cell metastatic behavior has been suggested, but conclusive evidence is lacking. In this study, we analyzed the biosynthesis of mono HETEs from arachidonic acid in tumor cells of different metastatic ability and correlated biosynthesis to metastatic potential.. The biosynthesis of mono HETEs by low and high metastatic subpopulations of B16 amelanotic melanoma (B16a) cells was analyzed by high performance liquid chromatography (HPLC). The identity of biosynthetic 12-HETE was confirmed by gas chromatography/mass spectrometry (GC/MS) and its stereochemical structure assigned by chiral phase HPLC. The effect of a lipoxygenase inhibitor on the biosynthesis of mono HETEs and its effect on metastatic behavior was examined.. HPLC analysis revealed that low (LM180) and high (HM340) metastatic B16a cells exhibited different profiles and efficiencies for conversion of arachidonic acid to mono HETEs. LM180 cells produced equal quantities of 12-HETE and 5-HETE. In contrast, HM340 cells synthesized predominantly 12-HETE and small amounts of 15-, 11- and 5-HETEs. At equal concentrations of substrate, four times more 12-HETE was synthesized by HM340 cells than by LM180 cells. The identity of biosynthetic 12-HETE was confirmed by gas chromatography/mass spectrometry and chiral phase HPLC demonstrated that it was the S enantiomer. The biosynthesis of 12(S)-HETE, but not other HETEs, was significantly inhibited by a lipoxygenase inhibitor, N-benzyl-N-hydroxy-5-phenylpentanamide. N-benzyl-N-hydroxy-5-phenylpentanamide, in a dose-dependent manner, decreased the adhesion of HM340 cells to murine pulmonary microvessel endothelium in vitro and lung colony formation in vivo. Furthermore, re-introduction of 12(S)-HETE, but not other mono HETEs, to HM340 cells pretreated with N-benzyl-N-hydroxy-5-phenylpentanamide, increased their adhesion to endothelium.. Biosynthesis of 12(S)-HETE by tumor cells is a determinant of their metastatic potential and inhibition of 12(S)-HETE biosynthesis in tumor cells may be a crucial target for intervening in metastasis.

    Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Animals; Arachidonic Acids; Cell Adhesion; Chromatography, High Pressure Liquid; Gas Chromatography-Mass Spectrometry; Humans; Hydroxamic Acids; Hydroxyeicosatetraenoic Acids; Lipoxygenase Inhibitors; Lung Neoplasms; Male; Melanoma, Amelanotic; Mice; Mice, Inbred C57BL; Molecular Conformation; Pentanoic Acids; Radioimmunoassay; Skin Neoplasms; Tumor Cells, Cultured

1994
PKC mediates 12(S)-HETE-induced cytoskeletal rearrangement in B16a melanoma cells.
    Cell motility and the cytoskeleton, 1993, Volume: 26, Issue:1

    The fatty acid 12(S)-HETE may be a new second messenger capable of activating PKC. In tumor cells 12(S)-HETE stimulates cytoskeleton-dependent cellular responses such as adhesion and spreading. Analysis of 12(S)-HETE effects on B16a melanoma cell cytoskeleton revealed reversible rearrangement of microtubules, microfilaments, the actin-binding proteins, vinculin, myosin heavy (MHC) and light chains (MLC), as well as bundling of vimentin intermediate filaments. The alterations in microfilaments and intermediate filaments occurred very rapidly, i.e., 5 min after exposure of tumor cells to 12(S)-HETE. The 12(S)-HETE-induced cytoskeletal alterations were accompanied by centrifugal organelle-translocation. Interestingly, MLC exhibited clear association with the cytoplasmic organelles. Biochemical analysis of the 12(S)-HETE effect indicated a PKC-mediated reversible hyperphosphorylation of MLC, vimentin, and a 130 kD cytoskeletal-associated protein. Optimal effects were obtained after 5 min treatment with 12(S)-HETE at 0.1 microM concentration. 12(S)-HETE pretreatment induced tumor cell spreading on a fibronectin matrix which required the intactness of all three major cytoskeletal components. The spreading process was dependent upon the activity of PKC. Our data suggest that 12(S)-HETE is a physiological stimulant of PKC. Further, it induces rearrangement of the cytoskeleton of tumor cells in interphase resulting in the stimulation of cytoskeleton-dependent cell activity such as spreading.

    Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Actin Cytoskeleton; Actins; Animals; Calcium; Cell Movement; Cytoskeletal Proteins; Cytoskeleton; Dose-Response Relationship, Drug; Fibronectins; Fluorescent Antibody Technique; Hydroxyeicosatetraenoic Acids; Immunohistochemistry; Intermediate Filaments; Melanoma, Experimental; Mice; Myosins; Organelles; Phospholipids; Phosphorylation; Protein Kinases; Skin Neoplasms; Tumor Cells, Cultured; Vimentin; Vinculin

1993
The lipoxygenase inhibitor 2-phenylmethyl-1-naphthol (DuP 654) is a 12(S)-hydroxyeicosatetraenoic acid receptor antagonist in the human epidermal cell line SCL-II.
    Skin pharmacology : the official journal of the Skin Pharmacology Society, 1993, Volume: 6, Issue:2

    The lipoxygenase inhibitor 2-phenylmethyl-1-naphthol (DuP 654) has been shown to be an active anti-inflammatory drug in a murine skin inflammation model. Since 12-HETE is assumed to have a pathophysiological role in inflammatory skin diseases, and epidermal cells possess high affinity binding sites for 12(S)-HETE, we studied the effect of DuP 654 on 12(S)-HETE binding to the human epidermal cell line SCL-II. DuP 654 antagonized 12(S)-HETE binding in a dose-dependent manner with a Ki of 3.41 +/- 0.23 nM. The antagonistic effect was reversible. After 1- and 24-hour preincubation, the drug had no more significant inhibitory effect at concentrations between 10(-10) and 10(-5) M on specific 12(S)-HETE binding (Bmax of 215,000 +/- 21,000 receptors per cell) or on receptor affinity (Kd of 3.25 +/- 0.42 nM). Our results show that DuP 654, in addition to its 5-lipoxygenase inhibitory activity, exhibits 12-HETE receptor antagonist effect, and therefore may be of benefit in skin diseases with elevated 12-HETE levels.

    Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Carcinoma, Squamous Cell; Epidermal Cells; Epidermis; Humans; Hydroxyeicosatetraenoic Acids; Naphthols; Receptors, Cell Surface; Receptors, Eicosanoid; Skin Neoplasms; Tumor Cells, Cultured

1993
Regulation of 12(S)-hydroxyeicosatetraenoic acid (12(S)-HETE) binding sites on human epidermal cells by interferon-gamma.
    Experimental cell research, 1990, Volume: 191, Issue:2

    We recently detected specific high-affinity binding sites for 12(S)-HETE, the main arachidonic acid metabolite in skin, on epidermal cells. The putative receptor is involved in keratinocyte chemotaxis toward 12(S)-HETE, which points to its participation in wound healing. In an effort to further characterize the 12(S)-HETE receptor, we investigated its regulation by various cytokines. Of the tested cytokines, only interferon (IFN)-gamma led to a massive induction of the 12(S)-HETE receptors. The effect was dose and time dependent and blocked by cycloheximide. The up-regulation of 12(S)-HETE receptors by IFN-gamma may represent an amplification mechanism of the assumed role of 12(S)-HETE in skin wound repair.

    Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Binding Sites; Carcinoma, Squamous Cell; Cell Line; Cycloheximide; Dose-Response Relationship, Drug; Epidermal Cells; Epidermis; Humans; Hydroxyeicosatetraenoic Acids; Interferon-gamma; Keratinocytes; Receptors, Cell Surface; Receptors, Eicosanoid; Skin Neoplasms; Time Factors; Up-Regulation

1990
Arachidonic acid metabolites in cutaneous carcinomas. Evidence suggesting that elevated levels of prostaglandins in basal cell carcinomas are associated with an aggressive growth pattern.
    Archives of dermatology, 1986, Volume: 122, Issue:4

    There is evidence suggesting a role of eicosanoids in the growth of certain tumors. In this study, tissue samples were collected from basal cell carcinomas (BCCs) and squamous cell carcinomas (SCCs) of the skin. Both BCCs and SCCs contained more prostaglandin E2 and F2 alpha (PGE2 and PGF2 alpha) than normal epidermis. In vitro incubation of tumor samples with arachidonic acid also resulted in PGE2 and PGF2 alpha formation. Basal cell carcinomas exhibiting a histologically aggressive growth pattern contained higher levels of prostaglandins than those with a nonaggressive growth pattern, both in vivo and after in vitro incubation. Lipoxygenase products (12- and 15-hydroxyeicosatetraenoic acid) were present in smaller amounts than cyclo-oxygenase products (PGE2 and PGF2 alpha) in vivo. Compared with normal epidermis, SCCs and, particularly, BCCs produced smaller amounts of 12-hydroxyeicosatetraenoic acid during in vitro incubation with arachidonic acid. The levels of lipoxygenase products were not related to the tumor growth pattern. These results indicate that excessive prostaglandin levels in BCCs may be associated with an aggressive growth pattern.

    Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Animals; Arachidonic Acids; Breast Neoplasms; Carcinoma, Basal Cell; Carcinoma, Squamous Cell; Chromatography, High Pressure Liquid; Dinoprost; Dinoprostone; Head and Neck Neoplasms; Humans; Hydroxyeicosatetraenoic Acids; In Vitro Techniques; Mice; Prostaglandins; Prostaglandins E; Prostaglandins F; Rabbits; Radioimmunoassay; Skin Neoplasms

1986
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