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Article ; Online: Two new flavonoids and anticancer activity of Hymenosporum flavum

Rehab Fikry Taher / Ahmed A. Al-Karmalawy / Ahmed I. Abd El Maksoud / Hany Khalil / Amr Hassan / Ezzel-Din A. El-Khrisy / Walaa El-Kashak

Journal of HerbMed Pharmacology, Vol 10, Iss 4, Pp 443-

in vitro and molecular docking studies

2021 Volume 458

Abstract: Introduction: Hymenosporum flavum (Hook.) F. Muell. is the sole species within the genus Hymenosporum is known for its antimicrobial activity. The current study aims to examine the prospective activity of H. flavum as a safe supporter of sorafenib (as a ... ...

Abstract	Introduction: Hymenosporum flavum (Hook.) F. Muell. is the sole species within the genus Hymenosporum is known for its antimicrobial activity. The current study aims to examine the prospective activity of H. flavum as a safe supporter of sorafenib (as a reference standard) against hepatocellular carcinoma (HCC). Methods: Isolation and identification of compounds were made by chromatographic and spectroscopic methods. A fingerprint for the plant extract was done using HPLC-MS/MS spectrometric analysis. The total plant extract was examined in vitro for HCC activity. The isolated flavonoids were examined for their cytotoxic activities using molecular docking studies against both RAF-1 and ERK-2, and the promising compounds were further examined in vitro using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Results: Two new flavonols were isolated from the leaf extract of H. flavum (Hook.) F. Muell., quercetin-3-O-(glucopyranosyl 1→2 ribopyranoside) (1) and kaempferol-3-O-(glucopyranosyl 1→2 ribopyranoside) (2), accompanying other six known flavonoids (3-8), and identified via spectroscopic analysis. Moreover, HPLC- PDA/MS/MS spectrometric analysis revealed the presence of seventy phenolic metabolites. The cytotoxic activity of the plant extract confirmed its potential action on HepG2 cells indicated by the production level of lactate dehydrogenase (LDH) upon treatment compared with the normal cells. The isolated flavonoids were examined for their cytotoxic activity using molecular docking studies against both RAF-1 and ERK-2 as proposed mechanisms of their anticancer activities. Furthermore, compounds 1 and 3, which showed the best in silico results, were further examined in vitro using qRT-PCR. They exhibited promising inhibitory activities against both RAF-1 and ERK-2 gene expression. Moreover, they showed promising cytotoxic activities indicated by the MTT assay. Also, both of them improved the efficiency of sorafenib in targeting both RAF-1 and ERK-2 pathways suggesting synergistic ...
Keywords	flavonoids ; molecular docking ; raf-1 ; erk-2 ; hplc/ms/ms ; sorafenib ; Medicine (General) ; R5-920 ; Therapeutics. Pharmacology ; RM1-950
Subject code	540
Language	English
Publishing date	2021-10-01T00:00:00Z
Publisher	Shahrekord University of Medical Sciences
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Predicting fluorouracil toxicity: can we finally do it?

Ezzeldin, Hany H / Diasio, Robert B

Journal of clinical oncology : official journal of the American Society of Clinical Oncology

2008 Volume 26, Issue 13, Page(s) 2080–2082

MeSH term(s)	Antimetabolites, Antineoplastic/adverse effects ; Diarrhea/chemically induced ; Diarrhea/etiology ; Diarrhea/genetics ; Dihydrouracil Dehydrogenase (NADP)/genetics ; Fluorouracil/adverse effects ; Genetic Predisposition to Disease ; Genetic Testing ; Humans ; Leucovorin/adverse effects ; Leukopenia/chemically induced ; Leukopenia/etiology ; Leukopenia/genetics ; Logistic Models ; Methylenetetrahydrofolate Reductase (NADPH2)/genetics ; Mucositis/chemically induced ; Mucositis/etiology ; Mucositis/genetics ; Odds Ratio ; Patient Selection ; Polymorphism, Genetic ; Predictive Value of Tests ; Risk Assessment ; Risk Factors ; Severity of Illness Index ; Thymidylate Synthase/genetics ; Vitamin B Complex/adverse effects
Chemical Substances	Antimetabolites, Antineoplastic ; Vitamin B Complex (12001-76-2) ; Dihydrouracil Dehydrogenase (NADP) (EC 1.3.1.2) ; Methylenetetrahydrofolate Reductase (NADPH2) (EC 1.5.1.20) ; Thymidylate Synthase (EC 2.1.1.45) ; Leucovorin (Q573I9DVLP) ; Fluorouracil (U3P01618RT)
Language	English
Publishing date	2008-05-01
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	604914-x
ISSN	1527-7755 ; 0732-183X
ISSN (online)	1527-7755
ISSN	0732-183X
DOI	10.1200/JCO.2007.15.5481
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Article: Genetic testing in cancer therapeutics.

Ezzeldin, Hany H / Diasio, Robert B

Clinical cancer research : an official journal of the American Association for Cancer Research

2006 Volume 12, Issue 14 Pt 1, Page(s) 4137–4141

MeSH term(s)	Antineoplastic Agents/pharmacology ; Epigenesis, Genetic ; Genetic Predisposition to Disease ; Genetic Testing ; Genotype ; Humans ; Medical Oncology/methods ; Models, Biological ; Neoplasms/diagnosis ; Neoplasms/drug therapy ; Neoplasms/genetics ; Pharmacogenetics/methods
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2006-07-15
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-06-0707
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Article ; Online: Histone deacetylase inhibitors: current status and overview of recent clinical trials.

Ma, Xujun / Ezzeldin, Hany H / Diasio, Robert B

Drugs

2009 Volume 69, Issue 14, Page(s) 1911–1934

Abstract: Histone deacetylase (HDAC) inhibitors are a new group of anticancer agents that have a potential role in the regulation of gene expression, induction of cell death, apoptosis and cell cycle arrest of cancer cells by altering the acetylation status of ... ...

Abstract	Histone deacetylase (HDAC) inhibitors are a new group of anticancer agents that have a potential role in the regulation of gene expression, induction of cell death, apoptosis and cell cycle arrest of cancer cells by altering the acetylation status of chromatin and other non-histone proteins. In clinical trials, HDAC inhibitors have demonstrated promising antitumour activity as monotherapy in cutaneous T-cell lymphoma and other haematological malignancies. In solid tumours, several HDAC inhibitors have been shown to be efficacious as single agents; however, results of most clinical trials were in favour of using HDAC inhibitors either prior to the initiation of chemotherapy or in combination with other treatments. Currently, the molecular basis of response to HDAC inhibitors in patients is not fully understood. In this review, we summarize the current status of HDAC inhibitors, as single agents or in combination with other agents in different phases of clinical trials. In most of the clinical trials, HDAC inhibitors were tolerable and exerted biological or antitumor activity. HDAC inhibitors have been studied in phase I, II and III clinical trials with variable efficacy. The combination of HDAC inhibitors with other anticancer agents including epigenetic or chemotherapeutic agents demonstrated favourable clinical outcome.
MeSH term(s)	Acetylation/drug effects ; Antineoplastic Agents/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Clinical Trials as Topic ; Enzyme Inhibitors/therapeutic use ; Epigenesis, Genetic/drug effects ; Forecasting ; Gene Expression/drug effects ; Histone Acetyltransferases/antagonists & inhibitors ; Histone Acetyltransferases/metabolism ; Histone Deacetylase Inhibitors ; Histone Deacetylases/metabolism ; Humans ; Models, Biological ; Neoplasms/drug therapy ; Neoplasms/enzymology ; Neoplasms/genetics
Chemical Substances	Antineoplastic Agents ; Enzyme Inhibitors ; Histone Deacetylase Inhibitors ; Histone Acetyltransferases (EC 2.3.1.48) ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2009-09-10
Publishing country	New Zealand
Document type	Journal Article ; Review
ZDB-ID	120316-2
ISSN	1179-1950 ; 0012-6667
ISSN (online)	1179-1950
ISSN	0012-6667
DOI	10.2165/11315680-000000000-00000
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Article: Dihydropyrimidine dehydrogenase deficiency, a pharmacogenetic syndrome associated with potentially life-threatening toxicity following 5-fluorouracil administration.

Ezzeldin, Hany / Diasio, Robert

Clinical colorectal cancer

2004 Volume 4, Issue 3, Page(s) 181–189

Abstract: Dihydropyrimidine dehydrogenase (DPD) deficiency is a pharmacogenetic syndrome associated with potentially life-threatening toxicity following the administration of standard doses of 5-fluorouracil. This syndrome derives its importance from the fact that ...

Abstract	Dihydropyrimidine dehydrogenase (DPD) deficiency is a pharmacogenetic syndrome associated with potentially life-threatening toxicity following the administration of standard doses of 5-fluorouracil. This syndrome derives its importance from the fact that approximately 2 million patients receive the drug worldwide each year. Population studies have suggested that 4%-7% of the American population exhibit dose-limiting toxicity that might be associated with a genetic defect in the DPYD gene that encodes for the DPD enzyme. During the past several years it has become increasingly clear that genetics is a major determinant of the variability in drug response, accounting for the probability of drug efficacy and the likelihood of toxic drug reactions. This article briefly discusses the clinical presentation, laboratory diagnosis, pharmacokinetics, inheritance, and the clinical management options of DPD deficiency. The variability of DPD enzyme activity in population studies and the different DPYD alleles together with new phenotypic and genotypic methods of screening for DPD deficiency will also be reviewed.
MeSH term(s)	Antimetabolites, Antineoplastic/adverse effects ; Antimetabolites, Antineoplastic/pharmacokinetics ; Antimetabolites, Antineoplastic/therapeutic use ; Diagnosis, Differential ; Dihydropyrimidine Dehydrogenase Deficiency ; Dihydrouracil Dehydrogenase (NADP)/genetics ; Dihydrouracil Dehydrogenase (NADP)/pharmacology ; Fluorouracil/adverse effects ; Fluorouracil/pharmacokinetics ; Fluorouracil/therapeutic use ; Genotype ; Humans ; Inheritance Patterns ; Metabolic Diseases/complications ; Metabolic Diseases/diagnosis ; Metabolic Diseases/genetics ; Phenotype ; Syndrome
Chemical Substances	Antimetabolites, Antineoplastic ; Dihydrouracil Dehydrogenase (NADP) (EC 1.3.1.2) ; Fluorouracil (U3P01618RT)
Language	English
Publishing date	2004-06-30
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2112638-0
ISSN	1533-0028
ISSN	1533-0028
DOI	10.3816/ccc.2004.n.018
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Article ; Online: Wave Front-Guided Photorefractive Keratectomy Using a High-Resolution Aberrometer After Corneal Collagen Cross-Linking in Keratoconus.

Shaheen, Mohamed Shafik / Shalaby Bardan, Ahmed / Piñero, David P / Ezzeldin, Hani / El-Kateb, Mohamed / Helaly, Hany / Khalifa, Mounir A

Cornea

2016 Volume 35, Issue 7, Page(s) 946–953

Abstract: Purpose: To evaluate the clinical outcomes of wave front-guided (WFG) photorefractive keratectomy (PRK) using a high-definition aberrometer in corneas with keratoconus at least 1 year after corneal collagen cross-linking (CXL).: Methods: Prospective ... ...

Abstract	Purpose: To evaluate the clinical outcomes of wave front-guided (WFG) photorefractive keratectomy (PRK) using a high-definition aberrometer in corneas with keratoconus at least 1 year after corneal collagen cross-linking (CXL). Methods: Prospective uncontrolled interventional case series study including a total of 34 consecutive eyes of 25 patients with keratoconus previously treated with CXL. All cases underwent WFG PRK using the VISX STAR S4 IR excimer laser and the iDesign system. All eyes had keratoconus grade I or II according to the Amsler-Krumeich classification. Visual, refractive, and ocular aberrometric outcomes were evaluated during a 12-month follow-up. Astigmatic changes were analyzed with the Alpins vector method. Results: A significant improvement was observed in the uncorrected and corrected distance visual acuities (P < 0.001). The mean efficacy and safety indices at 12 months postoperatively were 1.58 ± 1.11 and 1.96 ± 1.52, respectively. Manifest sphere and cylinder were reduced significantly (P < 0.001), with 76.5% of the eyes having a spherical equivalent within ±1.00 D at 12 months postoperatively. The mean difference vector and magnitude of error were 1.06 ± 0.92 and 0.43 ± 0.86 D, respectively. Some corneal irregularity indices were reduced significantly with surgery (P ≤ 0.005) as well as the level of ocular higher order aberrations, primary coma, and trefoil (P < 0.001). Conclusions: Sequential WFG PRK using the iDesign system and the STAR S4 IR excimer laser after CXL is an effective option to correct the spherocylindrical error and to minimize the level of higher order aberrations in mild and moderate keratoconus if the maximum intended ablation depth does not exceed 15% of the minimal corneal thickness.
MeSH term(s)	Aberrometry/methods ; Adult ; Collagen/metabolism ; Corneal Stroma/metabolism ; Corneal Topography ; Cross-Linking Reagents ; Female ; Humans ; Keratoconus/drug therapy ; Keratoconus/metabolism ; Keratoconus/surgery ; Keratoconus/therapy ; Lasers, Excimer/therapeutic use ; Male ; Photorefractive Keratectomy/methods ; Photosensitizing Agents/therapeutic use ; Prospective Studies ; Riboflavin/therapeutic use ; Surgery, Computer-Assisted ; Ultraviolet Rays ; Visual Acuity/physiology ; Young Adult
Chemical Substances	Cross-Linking Reagents ; Photosensitizing Agents ; Collagen (9007-34-5) ; Riboflavin (TLM2976OFR)
Language	English
Publishing date	2016-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	604826-2
ISSN	1536-4798 ; 0277-3740
ISSN (online)	1536-4798
ISSN	0277-3740
DOI	10.1097/ICO.0000000000000888
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Article: Dihydropyrimidine dehydrogenase deficiency: impact of pharmacogenetics on 5-fluorouracil therapy.

Lee, Adam / Ezzeldin, Hany / Fourie, Jeanne / Diasio, Robert

Clinical advances in hematology & oncology : H&O

2004 Volume 2, Issue 8, Page(s) 527–532

Abstract: Through the use of pharmacogenetic studies, interindividual variability in response (efficacy and toxicity) to 5-fluorouracil (5-FU) chemotherapy has been linked to the rate-limiting enzyme in the drug's catabolic pathway, known as dihydropyrimidine ... ...

Abstract	Through the use of pharmacogenetic studies, interindividual variability in response (efficacy and toxicity) to 5-fluorouracil (5-FU) chemotherapy has been linked to the rate-limiting enzyme in the drug's catabolic pathway, known as dihydropyrimidine dehydrogenase (DPD). This pharmacogenetic syndrome, known as "DPD deficiency," results in excessive amounts of 5-FU available to be anabolized to its active metabolites and is relatively undetectable by clinical observation prior to 5-FU administration. Extensive studies have associated both profound and partial deficiency in DPD activity with severe, unanticipated toxicity after 5-FU administration, while research on the molecular basis behind DPD deficiency has been linked to various sequence variants of the DPYD gene. Due to the widespread use of 5-FU, the severity of toxicity associated with DPD deficiency, and the prevalence of DPD deficiency in the population, extensive research is continually being performed to develop quick and accurate phenotypic and genotypic assays suitable for clinical settings that would allow clinicians to identify patients susceptible to adverse 5-FU reactions.
MeSH term(s)	Antidotes/therapeutic use ; Antimetabolites, Antineoplastic/adverse effects ; Antimetabolites, Antineoplastic/pharmacokinetics ; Antimetabolites, Antineoplastic/therapeutic use ; Biotransformation ; DNA Mutational Analysis ; Deoxyuracil Nucleotides/metabolism ; Diarrhea/chemically induced ; Dihydropyrimidine Dehydrogenase Deficiency ; Dihydrouracil Dehydrogenase (NADP)/genetics ; Dihydrouracil Dehydrogenase (NADP)/metabolism ; Drug Eruptions/etiology ; Fever/chemically induced ; Floxuridine/analogs & derivatives ; Floxuridine/metabolism ; Fluorouracil/adverse effects ; Fluorouracil/pharmacokinetics ; Fluorouracil/therapeutic use ; Humans ; Inactivation, Metabolic/genetics ; Mass Screening ; Mucositis/chemically induced ; Mutation ; Prodrugs/pharmacokinetics ; Pyrimidine Nucleosides/therapeutic use ; Thymidylate Synthase/metabolism ; Uridine Triphosphate/analogs & derivatives ; Uridine Triphosphate/metabolism
Chemical Substances	Antidotes ; Antimetabolites, Antineoplastic ; Deoxyuracil Nucleotides ; Prodrugs ; Pyrimidine Nucleosides ; fluorodeoxyuridine triphosphate ; Floxuridine (039LU44I5M) ; 5-fluorouridine 5'-triphosphate (3828-96-4) ; Dihydrouracil Dehydrogenase (NADP) (EC 1.3.1.2) ; Thymidylate Synthase (EC 2.1.1.45) ; Fluorouracil (U3P01618RT) ; Uridine Triphosphate (UT0S826Z60)
Language	English
Publishing date	2004-08
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2271951-9
ISSN	1543-0790
ISSN	1543-0790
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Article ; Online: (13)C-5-FU breath test current status and future directions: a comprehensive review.

Ezzeldin, Hany H / Acosta, Edward P / Mattison, Lori K / Fourie, Jeanne / Modak, Anil / Diasio, Robert B

Journal of breath research

2009 Volume 3, Issue 4, Page(s) 47002

Abstract: Breath tests (BTs) represent a safe non-invasive alternative strategy that could provide valuable diagnostic information in conditions like fat malabsorption, carbohydrate (lactose and fructose) malabsorption, liver dysfunction, impaired gastric emptying, ...

Abstract	Breath tests (BTs) represent a safe non-invasive alternative strategy that could provide valuable diagnostic information in conditions like fat malabsorption, carbohydrate (lactose and fructose) malabsorption, liver dysfunction, impaired gastric emptying, abnormal small bowel transit time, small intestinal bacterial overgrowth and Helicobacter pylori infection. To date, despite the availability of a number of breath tests, only three have gained approval by the FDA for application in a clinical setting ((13)C-urea breath test for the detection of H. pylori; NO breath test for monitoring asthma and alkane breath test for heart transplant rejection). Unfortunately, none of these tests investigate cancer patients or response to cancer chemotherapy. Several years ago it was realized that the presence of a reliable non-invasive approach could assist in the detection of patients at risk of developing severe life-threatening toxicities prior to the administration of fluoropyrimidines (e.g. 5-FU) or related cancer chemotherapy. 5-FU toxicity results mainly from deficient uracil catabolism. This review discusses the development of a BT that utilizes an orally administered pyrimidine ([2-(13)C]-uracil) which is metabolized via the same catabolic pathway as 5-FU. This ([2-(13)C]-uracil) breath test could provide a valuable addition to the patients' standard of care.
Language	English
Publishing date	2009-12
Publishing country	England
Document type	Journal Article
ZDB-ID	2381007-5
ISSN	1752-7163 ; 1752-7155
ISSN (online)	1752-7163
ISSN	1752-7155
DOI	10.1088/1752-7155/3/4/047002
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Article: Methylation of the DPYD promoter: an alternative mechanism for dihydropyrimidine dehydrogenase deficiency in cancer patients.

Ezzeldin, Hany H / Lee, Adam M / Mattison, Lori K / Diasio, Robert B

Clinical cancer research : an official journal of the American Association for Cancer Research

2005 Volume 11, Issue 24 Pt 1, Page(s) 8699–8705

Abstract: Purpose: Dihydropyrimidine dehydrogenase (DPD) deficiency, a known pharmacogenetic syndrome associated with 5-fluorouracil (5-FU) toxicity, has been detected in 3% to 5% of the population. Genotypic studies have identified >32 sequence variants in the ... ...

Abstract	Purpose: Dihydropyrimidine dehydrogenase (DPD) deficiency, a known pharmacogenetic syndrome associated with 5-fluorouracil (5-FU) toxicity, has been detected in 3% to 5% of the population. Genotypic studies have identified >32 sequence variants in the DPYD gene; however, in a number of cases, sequence variants could not explain the molecular basis of DPD deficiency. Recent studies in cell lines indicate that hypermethylation of the DPYD promoter might down-regulate DPD expression. The current study investigates the role of methylation in cancer patients with an unexplained molecular basis of DPD deficiency. Experimental design: DPD deficiency was identified phenotypically by both enzyme assay and uracil breath test, and genotypically by denaturing high-performance liquid chromatography. The methylation status was evaluated in PCR products (209 bp) of bisulfite-modified DPYD promoter, using a novel denaturing high-performance liquid chromatography method that distinguishes between methylated and unmethylated alleles. Clinical samples included five volunteers with normal DPD enzyme activity, five DPD-deficient volunteers, and five DPD-deficient cancer patients with a history of 5-FU toxicity. Results: No evidence of methylation was detected in samples from volunteers with normal DPD. Methylation was detected in five of five DPD-deficient volunteers and in three of five of the DPD-deficient cancer patient samples. Of note, one of the two samples from patients with DPD-deficient cancer with no evidence of methylation had the mutation DPYD2A, whereas the other had DPYD13. Discussion: Methylation of the DPYD promoter region is associated with down-regulation of DPD activity in clinical samples and should be considered as a potentially important regulatory mechanism of DPD activity and basis for 5-FU toxicity in cancer patients.
MeSH term(s)	Adult ; Antimetabolites, Antineoplastic/toxicity ; Chromatography, High Pressure Liquid ; CpG Islands/genetics ; DNA Methylation ; Dihydropyrimidine Dehydrogenase Deficiency ; Dihydrouracil Dehydrogenase (NADP)/genetics ; Down-Regulation ; Female ; Fluorouracil/toxicity ; Genotype ; Humans ; Male ; Middle Aged ; Mutation ; Neoplasms/enzymology ; Nucleic Acid Denaturation ; Phenotype ; Promoter Regions, Genetic/genetics
Chemical Substances	Antimetabolites, Antineoplastic ; Dihydrouracil Dehydrogenase (NADP) (EC 1.3.1.2) ; Fluorouracil (U3P01618RT)
Language	English
Publishing date	2005-12-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-05-1520
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Article: Methylation of the DPYD promoter and dihydropyrimidine dehydrogenase deficiency.

Yu, Jinsheng / McLeod, Howard L / Ezzeldin, Hany H / Diasio, Robert B

Clinical cancer research : an official journal of the American Association for Cancer Research

2006 Volume 12, Issue 12, Page(s) 3864; author reply 3864

MeSH term(s)	DNA Methylation ; Dihydropyrimidine Dehydrogenase Deficiency ; Dihydrouracil Dehydrogenase (NADP)/genetics ; Humans ; Promoter Regions, Genetic
Chemical Substances	Dihydrouracil Dehydrogenase (NADP) (EC 1.3.1.2)
Language	English
Publishing date	2006-06-15
Publishing country	United States
Document type	Comment ; Letter
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-06-0549
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