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  1. Article ; Online: Lidocaine

    Entaz Bahar / Hyonok Yoon

    Medicina, Vol 57, Iss 782, p

    A Local Anesthetic, Its Adverse Effects and Management

    2021  Volume 782

    Abstract: The most widely used medications in dentistry are local anesthetics (LA), especially lidocaine, and the number of recorded adverse allergic responses, particularly of hazardous responses, is quite low. However, allergic reactions can range from moderate ... ...

    Abstract The most widely used medications in dentistry are local anesthetics (LA), especially lidocaine, and the number of recorded adverse allergic responses, particularly of hazardous responses, is quite low. However, allergic reactions can range from moderate to life-threatening, requiring rapid diagnosis and treatment. This article serves as a review to provide information on LA, their adverse reactions, causes, and management.
    Keywords local anesthetics ; lidocaine ; adverse allergic responses ; Medicine (General) ; R5-920
    Language English
    Publishing date 2021-07-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Targeting the RAS/RAF/MAPK pathway for cancer therapy: from mechanism to clinical studies.

    Bahar, Md Entaz / Kim, Hyun Joon / Kim, Deok Ryong

    Signal transduction and targeted therapy

    2023  Volume 8, Issue 1, Page(s) 455

    Abstract: Metastatic dissemination of solid tumors, a leading cause of cancer-related mortality, underscores the urgent need for enhanced insights into the molecular and cellular mechanisms underlying metastasis, chemoresistance, and the mechanistic backgrounds of ...

    Abstract Metastatic dissemination of solid tumors, a leading cause of cancer-related mortality, underscores the urgent need for enhanced insights into the molecular and cellular mechanisms underlying metastasis, chemoresistance, and the mechanistic backgrounds of individuals whose cancers are prone to migration. The most prevalent signaling cascade governed by multi-kinase inhibitors is the mitogen-activated protein kinase (MAPK) pathway, encompassing the RAS-RAF-MAPK kinase (MEK)-extracellular signal-related kinase (ERK) pathway. RAF kinase is a primary mediator of the MAPK pathway, responsible for the sequential activation of downstream targets, such as MEK and the transcription factor ERK, which control numerous cellular and physiological processes, including organism development, cell cycle control, cell proliferation and differentiation, cell survival, and death. Defects in this signaling cascade are associated with diseases such as cancer. RAF inhibitors (RAFi) combined with MEK blockers represent an FDA-approved therapeutic strategy for numerous RAF-mutant cancers, including melanoma, non-small cell lung carcinoma, and thyroid cancer. However, the development of therapy resistance by cancer cells remains an important barrier. Autophagy, an intracellular lysosome-dependent catabolic recycling process, plays a critical role in the development of RAFi resistance in cancer. Thus, targeting RAF and autophagy could be novel treatment strategies for RAF-mutant cancers. In this review, we delve deeper into the mechanistic insights surrounding RAF kinase signaling in tumorigenesis and RAFi-resistance. Furthermore, we explore and discuss the ongoing development of next-generation RAF inhibitors with enhanced therapeutic profiles. Additionally, this review sheds light on the functional interplay between RAF-targeted therapies and autophagy in cancer.
    MeSH term(s) Humans ; Mitogen-Activated Protein Kinase Kinases ; Extracellular Signal-Regulated MAP Kinases/metabolism ; raf Kinases/genetics ; raf Kinases/metabolism ; Melanoma ; Lung Neoplasms
    Chemical Substances Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; raf Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2023-12-18
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2886872-9
    ISSN 2059-3635 ; 2095-9907
    ISSN (online) 2059-3635
    ISSN 2095-9907
    DOI 10.1038/s41392-023-01705-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Lidocaine: A Local Anesthetic, Its Adverse Effects and Management.

    Bahar, Entaz / Yoon, Hyonok

    Medicina (Kaunas, Lithuania)

    2021  Volume 57, Issue 8

    Abstract: The most widely used medications in dentistry are local anesthetics (LA), especially lidocaine, and the number of recorded adverse allergic responses, particularly of hazardous responses, is quite low. However, allergic reactions can range from moderate ... ...

    Abstract The most widely used medications in dentistry are local anesthetics (LA), especially lidocaine, and the number of recorded adverse allergic responses, particularly of hazardous responses, is quite low. However, allergic reactions can range from moderate to life-threatening, requiring rapid diagnosis and treatment. This article serves as a review to provide information on LA, their adverse reactions, causes, and management.
    MeSH term(s) Anesthesia, Local/adverse effects ; Anesthetics, Local/adverse effects ; Drug Hypersensitivity ; Drug-Related Side Effects and Adverse Reactions ; Humans ; Lidocaine/adverse effects
    Chemical Substances Anesthetics, Local ; Lidocaine (98PI200987)
    Language English
    Publishing date 2021-07-30
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2188113-3
    ISSN 1648-9144 ; 1010-660X
    ISSN (online) 1648-9144
    ISSN 1010-660X
    DOI 10.3390/medicina57080782
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Modeling and Predicting the Cell Migration Properties from Scratch Wound Healing Assay on Cisplatin-Resistant Ovarian Cancer Cell Lines Using Artificial Neural Network

    Entaz Bahar / Hyonok Yoon

    Healthcare, Vol 9, Iss 911, p

    2021  Volume 911

    Abstract: The study of artificial neural networks (ANN) has undergone a tremendous revolution in recent years, boosted by deep learning tools. The presence of a greater number of learning tools and their applications, in particular, favors this revolution. However, ...

    Abstract The study of artificial neural networks (ANN) has undergone a tremendous revolution in recent years, boosted by deep learning tools. The presence of a greater number of learning tools and their applications, in particular, favors this revolution. However, there is a significant need to deal with the issue of implementing a systematic method during the development phase of the ANN to increase its performance. A multilayer feedforward neural network (FNN) was proposed in this paper to predict the cell migration assay on cisplatin-sensitive and cisplatin-resistant (CisR) ovarian cancer (OC) cell lines via scratch wound healing assay. An FNN training algorithm model was generated using the MATLAB fitting function in a MATLAB script to accomplish this task. The input parameters were types of cell lines, times, and wound area, and outputs were relative wound area, percentage of wound closure, and wound healing speed. In addition, we tested and compared the initial accuracy of various supervised learning classifier and support vector regression (SVR) algorithms. The proposed ANN model achieved good agreement with the experimental data and minimized error between the estimated and experimental values. The conclusions drawn demonstrate that the developed ANN model is a useful, accurate, fast, and inexpensive method to predict cancerous cell migration characteristics evaluated via scratch wound healing assay.
    Keywords artificial neural network ; cell migration assay ; scratch wound healing assay ; ovarian cancer ; cisplatin-resistant ; Medicine ; R
    Subject code 006
    Language English
    Publishing date 2021-07-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article: Modeling and Predicting the Cell Migration Properties from Scratch Wound Healing Assay on Cisplatin-Resistant Ovarian Cancer Cell Lines Using Artificial Neural Network.

    Bahar, Entaz / Yoon, Hyonok

    Healthcare (Basel, Switzerland)

    2021  Volume 9, Issue 7

    Abstract: The study of artificial neural networks (ANN) has undergone a tremendous revolution in recent years, boosted by deep learning tools. The presence of a greater number of learning tools and their applications, in particular, favors this revolution. However, ...

    Abstract The study of artificial neural networks (ANN) has undergone a tremendous revolution in recent years, boosted by deep learning tools. The presence of a greater number of learning tools and their applications, in particular, favors this revolution. However, there is a significant need to deal with the issue of implementing a systematic method during the development phase of the ANN to increase its performance. A multilayer feedforward neural network (FNN) was proposed in this paper to predict the cell migration assay on cisplatin-sensitive and cisplatin-resistant (CisR) ovarian cancer (OC) cell lines via scratch wound healing assay. An FNN training algorithm model was generated using the MATLAB fitting function in a MATLAB script to accomplish this task. The input parameters were types of cell lines, times, and wound area, and outputs were relative wound area, percentage of wound closure, and wound healing speed. In addition, we tested and compared the initial accuracy of various supervised learning classifier and support vector regression (SVR) algorithms. The proposed ANN model achieved good agreement with the experimental data and minimized error between the estimated and experimental values. The conclusions drawn demonstrate that the developed ANN model is a useful, accurate, fast, and inexpensive method to predict cancerous cell migration characteristics evaluated via scratch wound healing assay.
    Language English
    Publishing date 2021-07-19
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2721009-1
    ISSN 2227-9032
    ISSN 2227-9032
    DOI 10.3390/healthcare9070911
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Regulation of Cell Cycle Progression through RB Phosphorylation by Nilotinib and AT-9283 in Human Melanoma A375P Cells.

    Pham, Trang Minh / Ahmed, Mahmoud / Lai, Trang Huyen / Bahar, Md Entaz / Hwang, Jin Seok / Maulidi, Rizi Firman / Ngo, Quang Nhat / Kim, Deok Ryong

    International journal of molecular sciences

    2024  Volume 25, Issue 5

    Abstract: BCR-ABL tyrosine kinase inhibitors are commonly employed for the treatment of chronic myeloid leukemia, yet their impact on human malignant melanoma remains uncertain. In this study, we delved into the underlying mechanisms of specific BCR-ABL tyrosine ... ...

    Abstract BCR-ABL tyrosine kinase inhibitors are commonly employed for the treatment of chronic myeloid leukemia, yet their impact on human malignant melanoma remains uncertain. In this study, we delved into the underlying mechanisms of specific BCR-ABL tyrosine kinase inhibitors (imatinib, nilotinib, ZM-306416, and AT-9283) in human melanoma A375P cells. We first evaluated the influence of these inhibitors on cell growth using cell proliferation and wound-healing assays. Subsequently, we scrutinized cell cycle regulation in drug-treated A375P cells using flow cytometry and Western blot assays. Notably, imatinib, nilotinib, ZM-306416, and AT-9283 significantly reduced cell proliferation and migration in A375P cells. In particular, nilotinib and AT-9283 impeded the G1/S transition of the cell cycle by down-regulating cell cycle-associated proteins, including cyclin E, cyclin A, and CDK2. Moreover, these inhibitors reduced RB phosphorylation, subsequently inhibiting E2F transcriptional activity. Consequently, the expression of the E2F target genes (
    MeSH term(s) Humans ; Imatinib Mesylate ; Phosphorylation ; Melanoma ; Fusion Proteins, bcr-abl/genetics ; Tyrosine Kinase Inhibitors ; Pyrimidines/pharmacology ; Protein Kinase Inhibitors/pharmacology ; Cell Division ; Benzimidazoles ; Urea/analogs & derivatives
    Chemical Substances 1-cyclopropyl-3-(3-(5-morpholin-4-ylmethyl-1H-benzoimidazol-2-yl)-1H-pyrazol-4-yl)urea ; Imatinib Mesylate (8A1O1M485B) ; Fusion Proteins, bcr-abl (EC 2.7.10.2) ; Tyrosine Kinase Inhibitors ; Pyrimidines ; Protein Kinase Inhibitors ; Benzimidazoles ; Urea (8W8T17847W)
    Language English
    Publishing date 2024-03-03
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms25052956
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Chemotherapy Resistance: Role of Mitochondrial and Autophagic Components.

    Bahar, Entaz / Han, Sun-Young / Kim, Ji-Ye / Yoon, Hyonok

    Cancers

    2022  Volume 14, Issue 6

    Abstract: Cancer chemotherapy resistance is one of the most critical obstacles in cancer therapy. One of the well-known mechanisms of chemotherapy resistance is the change in the mitochondrial death pathways which occur when cells are under stressful situations, ... ...

    Abstract Cancer chemotherapy resistance is one of the most critical obstacles in cancer therapy. One of the well-known mechanisms of chemotherapy resistance is the change in the mitochondrial death pathways which occur when cells are under stressful situations, such as chemotherapy. Mitophagy, or mitochondrial selective autophagy, is critical for cell quality control because it can efficiently break down, remove, and recycle defective or damaged mitochondria. As cancer cells use mitophagy to rapidly sweep away damaged mitochondria in order to mediate their own drug resistance, it influences the efficacy of tumor chemotherapy as well as the degree of drug resistance. Yet despite the importance of mitochondria and mitophagy in chemotherapy resistance, little is known about the precise mechanisms involved. As a consequence, identifying potential therapeutic targets by analyzing the signal pathways that govern mitophagy has become a vital research goal. In this paper, we review recent advances in mitochondrial research, mitophagy control mechanisms, and their implications for our understanding of chemotherapy resistance.
    Language English
    Publishing date 2022-03-12
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers14061462
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Regulation of TGF-

    Hwang, Jin Seok / Lai, Trang Huyen / Ahmed, Mahmoud / Pham, Trang Minh / Elashkar, Omar / Bahar, Entaz / Kim, Deok Ryong

    Cancers

    2022  Volume 14, Issue 19

    Abstract: Metastasis is associated with poor prognosis and is the major cause of death in cancer patients. The epithelial to mesenchymal transition (EMT) is essential for cancer cells to acquire a highly migratory phenotype. Metabolic reprogramming is required to ... ...

    Abstract Metastasis is associated with poor prognosis and is the major cause of death in cancer patients. The epithelial to mesenchymal transition (EMT) is essential for cancer cells to acquire a highly migratory phenotype. Metabolic reprogramming is required to meet the energy demands during this process. Recent studies have indicated that autophagy is involved in EMT, during which cancer cells depend on autophagy activation for survival. However, accumulating evidence indicates that autophagy's involvement in cancer is context-dependent, acting as either promoter or inhibitor. In this study, we investigated the role of autophagy in supplying energy to support EMT. We induced EMT in Non-small cell lung cancer A549 cells using TGF-β1 with and without autophagy inhibition. Suppression of autophagy activity by knocking down of
    Language English
    Publishing date 2022-10-04
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers14194845
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Chemotherapy Resistance Explained through Endoplasmic Reticulum Stress-Dependent Signaling.

    Bahar, Entaz / Kim, Ji-Ye / Yoon, Hyonok

    Cancers

    2019  Volume 11, Issue 3

    Abstract: Cancers cells have the ability to develop chemotherapy resistance, which is a persistent problem during cancer treatment. Chemotherapy resistance develops through different molecular mechanisms, which lead to modification of the cancer cells signals ... ...

    Abstract Cancers cells have the ability to develop chemotherapy resistance, which is a persistent problem during cancer treatment. Chemotherapy resistance develops through different molecular mechanisms, which lead to modification of the cancer cells signals needed for cellular proliferation or for stimulating an immune response. The endoplasmic reticulum (ER) is an important organelle involved in protein quality control, by promoting the correct folding of protein and ER-mediated degradation of unfolded or misfolded protein, namely, ER-associated degradation. Disturbances of the normal ER functions causes an accumulation of unfolded or misfolded proteins in the ER lumen, resulting in a condition called "ER stress (ERS)." ERS triggers the unfolded protein response (UPR)-also called the ERS response (ERSR)-to restore homeostasis or activate cell death. Although the ERSR is one emerging potential target for chemotherapeutics to treat cancer, it is also critical for chemotherapeutics resistance, as well. However, the detailed molecular mechanism of the relationship between the ERSR and tumor survival or drug resistance remains to be fully understood. In this review, we aim to describe the most vital molecular mechanism of the relationship between the ERSR and chemotherapy resistance. Moreover, the review also discusses the molecular mechanism of ER stress-mediated apoptosis on cancer treatments.
    Language English
    Publishing date 2019-03-08
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers11030338
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Establishment of Acquired Cisplatin Resistance in Ovarian Cancer Cell Lines Characterized by Enriched Metastatic Properties with Increased Twist Expression

    Entaz Bahar / Ji-Ye Kim / Hyun-Soo Kim / Hyonok Yoon

    International Journal of Molecular Sciences, Vol 21, Iss 7613, p

    2020  Volume 7613

    Abstract: Ovarian cancer (OC) is the most lethal of the gynecologic cancers, and platinum-based treatment is a part of the standard first-line chemotherapy regimen. However, rapid development of acquired cisplatin resistance remains the main cause of treatment ... ...

    Abstract Ovarian cancer (OC) is the most lethal of the gynecologic cancers, and platinum-based treatment is a part of the standard first-line chemotherapy regimen. However, rapid development of acquired cisplatin resistance remains the main cause of treatment failure, and the underlying mechanism of resistance in OC treatment remains poorly understood. Faced with this problem, our aim in this study was to generate cisplatin-resistant (CisR) OC cell models in vitro and investigate the role of epithelial–mesenchymal transition (EMT) transcription factor Twist on acquired cisplatin resistance in OC cell models. To achieve this aim, OC cell lines OV-90 and SKOV-3 were exposed to cisplatin using pulse dosing and stepwise dose escalation methods for a duration of eight months, and a total of four CisR sublines were generated, two for each cell line. The acquired cisplatin resistance was confirmed by determination of 50% inhibitory concentration (IC 50 ) and clonogenic survival assay. Furthermore, the CisR cells were studied to assess their respective characteristics of metastasis, EMT phenotype, DNA repair and endoplasmic reticulum stress-mediated cell death. We found the IC 50 of CisR cells to cisplatin was 3–5 times higher than parental cells. The expression of Twist and metastatic ability of CisR cells were significantly greater than those of sensitive cells. The CisR cells displayed an EMT phenotype with decreased epithelial cell marker E-cadherin and increased mesenchymal proteins N-cadherin and vimentin. We observed that CisR cells showed significantly higher expression of DNA repair proteins, X-ray repair cross-complementing protein 1 (XRCC1) and poly (ADP-ribose) polymerases 1 (PARP1), with significantly reduced endoplasmic reticulum (ER) stress-mediated cell death. Moreover, Twist knockdown reduced metastatic ability of CisR cells by suppressing EMT, DNA repair and inducing ER stress-induced cell death. In conclusion, we highlighted the utilization of an acquired cisplatin resistance model to identify the potential role of Twist as a therapeutic target to reverse acquired cisplatin resistance in OC.
    Keywords ovarian cancer ; cisplatin resistance ; Twist ; metastasis ; epithelial–mesenchymal transition ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 610
    Language English
    Publishing date 2020-10-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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