Mapping the Grounds for Mortalities in Acute Myeloid Leukemia Through Registry Analyses: A Retrospective Cohort Study of Children, Adolescents, and Young Adults Patients.

Background: Our objective was to identify non-malignant factors that contribute to mortality in children, adolescents and young adults, aiming to improve patient follow-up and reduce mortality rates to achieve better survival outcomes.

Methods: We analyzed 8,239 acute myeloid leukemia (AML) cases diagnosed between 2000 and 2019 in the USA. Using version 8.

[Subcutaneous nephrovesical bypass in ureteral obstruction].

We performed subcutaneous bypass draining (SBD) of the upper urinary tract (UUT) in 12 patients (3 males, 9 females, mean age 64 years) in 2006-2008. Ureteral obstruction was caused by a tumor in 11 patients, one patient had extended obliteration of the left ureter after resection of the abdominal aorta aneurysm and two plastic operations on the UUT. All the patients with ureteral tumor obstruction had only one functional kidney.

Effect of tea polyphenols on growth of oral squamous carcinoma cells in vitro.

Epidemiologic evidence indicates that both black and green tea is a rich source of flavonoids and other polyphenolic antioxidants which protects against heart disease and cancer. In the current investigation, utilizing human oral squamous carcinoma cell line SCC-25, we have evaluated the effect of three major tea constituents, (-)-epigallocatechin-3-gallate (EGCG), (-)-epicatechin-3-gallate (ECG) and (-)-epigallocatechin (EGC) on cell growth and DNA synthesis. Test agents in concentrations of 50, 80, 100 and 200 microM were incubated in triplicates in DMEM-HAM's F-12 (50: 50) supplemented with 10% calf serum and antibiotics in an atmosphere of 5% CO2 in air for 72 hrs.

The inhibitory effect of curcumin, genistein, quercetin and cisplatin on the growth of oral cancer cells in vitro.

Epidemiological evidence indicates that plant derived flavonoids and other phenolic antioxidants protect against heart disease and cancer. In the current investigation utilizing human oral squamous carcinoma cell line (SCC-25), we have evaluated the potency of three different plant phenolics, viz., curcumin, genistein and quercetin in comparison with that of cisplatin on growth and proliferation of SCC-25.

The effect of red wine and its components on growth and proliferation of human oral squamous carcinoma cells.

Epidemiologic evidence indicates that red wine may contain phenolic compounds which protect against heart disease and cancer. Resveratrol and quercetin are wine phenolics which possess antioxidant and antimutagenic effects. Resveratrol at 10 and 100 microM induced significant dose-dependent inhibition in human oral squamous carcinoma cell (SCC-25) growth and DNA synthesis.

Biphasic action of vitamin E on the growth of human oral squamous carcinoma cells.

Treatment of human tongue squamous carcinoma cell, SCC-25, with physiological concentrations of vitamin E succinate (VES) which varied from 0.001 to 50 mumoles/L resulted in significant dose-dependent stimulation of cell growth. Whereas, pharmacological doses of the vitamin (100-154 microM) induced significant inhibition in cell growth.

Modulating effect of resveratrol and quercetin on oral cancer cell growth and proliferation.

Resveratrol and quercetin are polyphenols which have been detected in significant amounts in green vegetables, citrus fruits and red grape wines. Beneficial effects attributed to these compounds include anti-inflammatory, antiviral and antitumor properties. The effect of resveratrol and quercetin on growth of human oral cancer cells is unknown.

Inhibition of growth in oral squamous carcinoma cells by cyclopentenone prostaglandins: comparison with chemotherapeutic agents.

Four cyclopentenone prostaglandins (CPPGs) and PGE2 caused significant dose-dependent inhibition in growth of human oral squamous carcinoma cells (SCC-15). The rank order of their potency was PGJ2>PGA1>16, 16-dimethyl PGA1>PGA2>PGE2. In a follow-up experiment it was found that the mean per cent inhibition in cell growth by PGJ2 and delta12-PGJ2 at 10(-5) M was 61.

Vitamin E succinate potentiates the inhibitory effect of prostaglandins on oral squamous carcinoma cell proliferation.

Previous studies have shown that prostaglandin E2 (PGE2) and vitamin E succinate can act in an additive manner to inhibit the proliferation of human oral squamous carcinoma cells (SCC-25). The initial studies on the additive anticancer activity of PGE2 and vitamin E succinate have been extended to include antineoplastic PGs, delta 12-PGJ2 and PGJ2. Treatment of oral squamous carcinoma cells (SCC-15) with delta 12-PGJ2, PGJ2, and vitamin E succinate, individually, caused significant concentration-dependent inhibition of cell proliferation to various degrees.

Prostaglandin E2 antagonizes gingival fibroblast proliferation stimulated by interleukin-1 beta.

Treatment of human gingival fibroblasts with prostaglandin E2 (PGE2) resulted in significant concentration-dependent inhibition in deoxyribonucleic acid (DNA) synthesis (8.40-37.89%), while indomethacin (INDO) (PG inhibitor), interleukin-1 beta (IL-1 beta) or IL-1 beta+INDO caused a significant and dose-dependent increase in DNA synthesis.

Inhibition of human oral squamous carcinoma cell (SCC-25) proliferation by prostaglandin E2 and vitamin E succinate.

The primary objective of this investigation was to study the effect of D-alpha-tocopherol acid succinate (vitamin E succinate) and prostaglandin E2 (PGE2), individually and in combination, on the proliferation of human tongue squamous carcinoma cells (SCC-25) in vitro. Test compounds in varying concentrations were incubated with cells in serum-free Dulbecco's Modified Eagle's Medium-Ham's F-12 Medium (50:50), supplemented with 0.1% albumin for sixteen hours.

Effect of retinoids and carotenoids on prostaglandin formation by oral squamous carcinoma cells.

Several studies have correlated the excessive production of prostaglandins (PGs) with tumor promotion and the suppression of the immune response. Inhibition of PGs by pharmacological agents has been demonstrated to enhance immunocompetence, and to suppress growth of tumors in animals and humans. In this study we examined the effect of retinol (I), all-trans-retinoic acid (II), N-(4-Hydroxyphenyl) retinamide (N-4-HPR) (III), canthaxanthin (CTX) (IV), and beta-carotene (beta-CT) (V) on the bioconversion of 14C-arachidonic acid (AA) to PGE2 by squamous carcinoma cells of the tongue, SCC-25.

Comparison of the inhibitory effect of polyunsaturated fatty acids on prostaglandin synthesis. II. Fibroblasts.

In a previous publication we reported that PUFAs of the n-6 and n-3 series caused significant inhibition of synthesis of both PGE2 (28.4-92.8%) and PGF2 alpha (24.

In vitro inhibition of prostaglandin biosynthesis in squamous cell carcinoma by retinoids.

The aim of this study was to evaluate the effect of four natural and synthetic retinoids: Ro 12-7310 (I), Ro 13-7410 (II), 13-cis-retinoic acid (III), and Ro 13-7652 (IV) on the synthesis of PGE2 in human squamous cell carcinoma (SCC) of the tongue (SCC-25). 5 X 10(6) cells were plated and labeled with 0.2 microCi of (14C)-arachidonic acid (AA) in 2 ml of DMEM/F12 containing 0.

Comparison of the inhibitory effect of polyunsaturated fatty acids on prostaglandin synthesis I oral squamous carcinoma cells.

Polyunsaturated fatty acids (PUFAs) have been shown to suppress the growth rate of human osteogenic sarcoma cells and to have selective cytotoxic activity against human cancer cells. The purpose of this study was to investigate the efficacy of various PUFAs on inhibition of prostaglandin (PG) synthesis by oral squamous carcinoma cells (SCC-25). A significant inhibition of PGE2 and PGF2 alpha synthesis in SCC-25 was observed by all PUFAs tested except in the case of linoleic acid (LA) at 10 microM level.

Effect of effervescent buffered aspirin on prostaglandin synthesis by human gingival fibroblasts.

Cultured human gingival fibroblasts were incubated with 14C-arachidonic acid (AA) at 37 degrees C for 2 hours. The metabolites formed were extracted from the cell-free medium in methanol, separated and identified by thin layer chromatography, using two solvent systems that allowed resolution of cyclooxygenase and lipoxygenase products. The predominant cyclooxygenase products were PGE2 and 6-keto-PGF1 alpha.

Cancer and the prostaglandins: a mini review on cancer research.

This review article has explored the relationship between PGs and cancer. The experimental exploitation of PG compounds and inhibitors has disclosed many possible applications. The potential for pharmacologic manipulation of the "Arachidonic Acid Cascade" system to benefit the cancer patient is promising, and it will require close collaboration of the pathologist, the biochemist, the pharmacologist, and the clinician.

Arachidonic acid metabolism in inflamed gingiva and its inhibition by anti-inflammatory drugs.

Prostaglandin (PG) synthetase inhibitors are tissue-selective. Therefore, the action of four nonsteroidal anti-inflammatory drugs (NSAID) was tested against PG synthesis from 14C-arachidonic acid by gingival homogenate. Suprofen and tolmetin sodium did not significantly inhibit PGs at any of the three concentration levels used (10(-7), 10(-5), 10(-3) M), whereas flurbiprofen and zomepirac sodium did significantly inhibit PG formation at millimolar concentration.

The effect of non-steroidal anti-inflammatory drugs on the metabolism of 14C-arachidonic acid by human gingival tissue in vitro.

We investigated the effect of non-steroidal anti-inflammatory drugs on prostaglandins (PGs) and 12-hydroxyeicosatetraenoic acid (12-HETE) formation by inflamed human gingival tissues. Gingival tissue homogenates were incubated with 14C-arachidonic acid in the presence of indomethacin, piroxicam, or ibuprofen, and the organic solvent extracts were chromatographed on silica gel plates with standards for radiometric assay. There was a significant negative trend between the doses (10(-7)-10(-3) M) of each of indomethacin, piroxicam, and ibuprofen, and the amounts of PGF2 alpha, PGE2, PGD2, and 15-keto-PGE2 produced.

Testosterone inhibits prostaglandin formation by human gingival connective tissue: relationship to 14C-arachidonic acid metabolism.

The relationship between various concentrations of the male sex steroid, testosterone, and the formation of radioactive prostaglandins (PGs) from 14C-arachidonic acid by human gingival homogenate has been investigated. There were statistically significant (combined) linear and quadratic trends between hormone treatment at concentrations of 10(-9), 10(-7), 10(-5) and 10(-3)M and the amounts of PGF2, PGE2, PGD2 and 15-keto-PGE2 formed. The mean amount of each PG formed at the various concentrations of testosterone was statistically significantly less than the corresponding control level.

The relationship between the concentration of female sex steroids and prostaglandins production by human gingiva in vitro.

The relationship between various concentrations of estradiol-17 beta and progesterone, alone and in combination, and the formation of radioactive prostaglandins (PGs) from 14C-arachidonic acid by gingival homogenate has been investigated. There was a statistically significant negative linear trend between each of the hormone treatments at concentrations of 10(-9), 10(-7), 10(-5) and 10(-3)M and the amounts of 6-keto-PGF1a, PGF2a, PGE2, PGD2 and 15-keto-PGE2 formed. Each of estradiol-17 beta and progesterone at 10(-9) and 10(-7)M exerted stimulatory effect, whereas at higher concentrations they had an inhibitory effect on all PGs tested.

Effect of epinephrine on prostaglandin E2 and cyclic AMP levels in gingiva of patients with chronic periodontitis.

The levels of prostaglandin E2 (PGE2) and cyclic AMP (cAMP) in human gingival samples were determined by means of radioimmunoassay after incubation with epinephrine (10(-6)M) at different time intervals. The levels of PGE2 and cAMP reached a maximum in the control and hormone treated samples after 80 and 40 minutes, respectively. Epinephrine seemed to affect a lesser increase in PGE2 and a greater increase in cAMP values in gingival tissues when compared with control samples.