Anupam Bishayee

Prof. Dr. Anupam Bishayee

Professor of Pharmacology, Lake Erie College of Osteopathic Medicine, 5000 Lakewood Ranch Boulevard, Bradenton, FL 34211, USA
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Research Focus & Metrics

Academic Career Length

16Years (2011-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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13 November 2019 in Biomolecules
Verified
Journal Article
Open access
PDF file
VAVaishali Aggarwal
Vaishali Aggarwal
HTHardeep Singh Tuli
Hardeep Singh Tuli
AVAyşegül Varol
Ayşegül Varol
FTFalak Thakral
Falak Thakral
Mükerrem Betül YererMükerrem Betül Yerer
Mükerrem Betül Yerer
Gautam SethiGautam Sethi
Gautam Sethi
Reactive oxygen species (ROS) play a pivotal role in biological processes and continuous ROS production in normal cells is controlled by the appropriate regulation between the silver lining of low and high ROS concentration mediated effects. Interestingly, ROS also dynamically influences the tumor microenvironment and is known to initiate cancer angiogenesis, metastasis, and survival at different concentrations. At moderate concentration, ROS activates the cancer cell survival signaling cascade involving mitogen-activated protein kinase/extracellular signal-regulated protein kinases 1/2 (MAPK/ERK1/2), p38, c-Jun N-terminal kinase (JNK), and phosphoinositide-3-kinase/ protein kinase B (PI3K/Akt), which in turn activate the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), matrix metalloproteinases (MMPs), and vascular endothelial growth factor (VEGF). At high concentrations, ROS can cause cancer cell apoptosis. Hence, it critically depends upon the ROS levels, to either augment tumorigenesis or lead to apoptosis. The major issue is targeting the dual actions of ROS effectively with respect to the concentration bias, which needs to be monitored carefully to impede tumor angiogenesis and metastasis for ROS to serve as potential therapeutic targets exogenously/endogenously. Overall, additional research is required to comprehend the potential of ROS as an effective anti-tumor modality and therapeutic target for treating malignancies.

Verified
Journal Article
Open access
PDF file
JKJeong-Hyeon Ko
Jeong-Hyeon Ko
Gautam SethiGautam Sethi
Gautam Sethi
Jae-Young UmJae-Young Um
Jae-Young Um
EZEastern Zhuang
Eastern Zhuang
FAFrank Arfuso
Frank Arfuso
KAKwang Seok Ahn
Kwang Seok Ahn
: Natural product compounds have recently attracted significant attention from the scientific community for their potent effects against inflammation-driven diseases, including cancer. A significant amount of research, including preclinical, clinical, and epidemiological studies, has indicated that dietary consumption of polyphenols, found at high levels in cereals, pulses, vegetables, and fruits, may prevent the evolution of an array of diseases, including cancer. Cancer development is a carefully orchestrated progression where normal cells acquires mutations in their genetic makeup, which cause the cells to continuously grow, colonize, and metastasize to other organs such as the liver, lungs, colon, and brain. Compounds that modulate these oncogenic processes can be considered as potential anti-cancer agents that may ultimately make it to clinical application. Resveratrol, a natural stilbene and a non-flavonoid polyphenol, is a phytoestrogen that possesses anti-oxidant, anti-inflammatory, cardioprotective, and anti-cancer properties. It has been reported that resveratrol can reverse multidrug resistance in cancer cells, and, when used in combination with clinically used drugs, it can sensitize cancer cells to standard chemotherapeutic agents. Several novel analogs of resveratrol have been developed with improved anti-cancer activity, bioavailability, and pharmacokinetic profile. The current focus of this review is resveratrol’s in vivo and in vitro effects in a variety of cancers, and intracellular molecular targets modulated by this polyphenol. This is also accompanied by a comprehensive update of the various clinical trials that have demonstrated it to be a promising therapeutic and chemopreventive agent.

1 May 2022 in Seminars in Cancer Biology
Verified
Journal Article
Closed access
DTDevesh Tewari
Devesh Tewari
PPPooja Patni
Pooja Patni
ABAnusha Bishayee
Anusha Bishayee
ASArchana N Sah
Archana N Sah
Anupam BishayeeAnupam Bishayee
Anupam Bishayee

1 April 2014 in Biochimica et Biophysica Acta (BBA) - Reviews on Cancer
Verified
Journal Article
Closed access
KSKodappully Sivaraman Siveen
Kodappully Sivaraman Siveen
SSSakshi Sikka
Sakshi Sikka
RSRohit Surana
Rohit Surana
XDXiaoyun Dai
Xiaoyun Dai
JZJingwen Zhang
Jingwen Zhang
Anupam BishayeeAnupam Bishayee
Anupam Bishayee

1 March 2019
Verified
Journal Article
Open access
NKNiloofar Kahkeshani
Niloofar Kahkeshani
FFFatemeh Farzaei
Fatemeh Farzaei
MFMaryam Fotouhi
Maryam Fotouhi
SASeyedeh Shaghayegh Alavi
Seyedeh Shaghayegh Alavi
RBRoodabeh Bahramsoltani
Roodabeh Bahramsoltani
Anupam BishayeeAnupam Bishayee
Anupam Bishayee
Objective(s): Gallic acid is a natural phenolic compound found in several fruits and medicinal plants. It is reported to have several health-promoting effects. This review aims to summarize the pharmacological and biological activities of gallic acid in vitro and animal models to depict the pharmacological status of this compound for future studies. Materials and Methods: All relevant papers in the English language were collected up to June 2018. The keywords of gallic acid, antioxidant, anticancer, antimicrobial, gastrointestinal-, cardiovascular-, metabolic-, neuropsychological-, and miscellaneous-diseases were searched in Google Scholar, PubMed, and Scopus. Results: Several beneficial effects are reported for gallic acid, including antioxidant, anti-inflammatory, and antineoplastic properties. This compound has been reported to have therapeutic activities in gastrointestinal, neuropsychological, metabolic, and cardiovascular disorders. Conclusion: Current evidence confirms the pharmacological and therapeutic interventions of gallic acid in multiple health complications; however, available data are limited to just cellular and animal studies. Future investigations are essential to further define the safety and therapeutic efficacy of gallic acid in humans.

6 December 2019 in Frontiers in Pharmacology
Verified
Journal Article
Open access
PDF file
HTHardeep Singh Tuli
Hardeep Singh Tuli
MTMuobarak Jaber Tuorkey
Muobarak Jaber Tuorkey
FTFalak Thakral
Falak Thakral
Katrin SakKatrin Sak
Katrin Sak
(Dr.)Manoj Kumar(Dr.)Manoj Kumar
(Dr.)Manoj Kumar
Anupam BishayeeAnupam Bishayee
Anupam Bishayee
Background: Genistein is one among the several other known isoflavones that is found in different soybeans and soy products. The chemical name of genistein is 4′,5,7-trihydroxyisoflavone. Genistein has drawn attention of scientific community because of its potential beneficial effects on human grave diseases, such as cancer. Mechanistic insight of genistein reveals its potential for apoptotic induction, cell cycle arrest, as well as antiangiogenic, antimetastatic, and anti-inflammatory effects. Objective: The purpose of this review is to unravel and analyze various molecular mechanisms of genistein in diverse cancer models. Data sources: English language literature was searched using various databases, such as PubMed, ScienceDirect, EBOSCOhost, Scopus, Web of Science, and Cochrane Library. Key words used in various combinations included genistein, cancer, anticancer, molecular mechanisms prevention, treatment, in vivo, in vitro, and clinical studies. Study selection: Study selection was carried out strictly in accordance with the statement of Preferred Reporting Items for Systematic Reviews and Meta-analyses. Data extraction: Four authors independently carried out the extraction of articles. Data synthesis: One hundred one papers were found suitable for use in this review. Conclusion: This review covers various molecular interactions of genistein with various cellular targets in cancer models. It will help the scientific community understand genistein and cancer biology and will provoke them to design novel therapeutic strategies.