Head and Neck Cancer Prevention by Phytochemicals: Current Status and Challenges

Nimbalkar, Vaishnavi K.; Manna, Subhakankha; Maru, Girish B.; Mahimkar, Manoj B.

doi:10.1007/s40495-020-00213-w

Cited by 3 publications

(16 citation statements)

References 130 publications

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“…Extensive preclinical research has been performed on the stages of carcinogenesis, and the findings play a key role in understanding the tumorigenesis process in HNC-related organ sites. In the literature from the last twenty years, several key in vivo and in vitro scientific works have studied whether carcinogens and/or carotenoids, and other phytochemicals, modulate the proliferation of CSC stem cells or HNSCC cells [ 38 ].…”

Section: Resultsmentioning

confidence: 99%

“…Many experimental studies are incapable of replicating the complexity of the host system and that of the administered carcinogens, e.g., tobacco, alcohol, and HPV, as well as the habits and doses of the user. It is also very difficult to include the range of exposure sites in the head and neck region in a study; preclinical studies therefore cannot accurately identify the structural and functional differences in metabolic competences and pathways/biomarkers associated with tumorigenesis process affected by chemopreventive factors [ 38 ].…”

Section: Resultsmentioning

confidence: 99%

“…In recent years, researchers have used chemically induced, spontaneously developed, transgenic and co-carcinogenic models of oral cancer derived from hamster buccal pouch to examine the development of HNSCC [ 53 , 102 , 145 , 146 ]. The first mentioned cellular systems of HNSCC related to the use of popular carcinogens such as 4-nitroquinoline-1-oxide (4NQO), nicotine-derived nitrosamine ketone (NNK), acrylamide, 7,12-dimethylbenz(a)anthracene (DMBA), bovine serum albumin (BSA), bromophenol blue, hydroxyurea, 2-mercaptoethanol, sodium dodecyl sulphate (SDS) N , N , N′ , N′ -tetramethylene diamine (TEMED), trizol and N-nitrosonornicotine (NNN), cigarette smoke, betel nut/leaf extract, 3-(methylnitrosamino) propionitrile (MNPN), alcohol, and tumour-promoting agents such as 12- O -tetradecanoylphorbol-13-acetate (TPA), as they mimic human phases of tumorigenesis in animals [ 38 , 102 ].…”

Section: Resultsmentioning

confidence: 99%

“…Summing up the research on animal models, it is important to emphasize that such carcinogen-induced well-established cancer models are popular and labour-intensive but have many limitations [ 38 , 147 ]. Importantly, while such studies allow prolonged carcinogen exposure, they have limited implications: they prevent the analysis of particular genes in HNSCC progression, and transgenic and xenograft systems do not present an actual picture of human tumorigenesis.…”

Section: Resultsmentioning

confidence: 99%

“…Interestingly, each of the carcinogenesis steps is known to be affected by dietary chemicals, including carotenoids. CTDs, as natural compounds present in food and beverages, are known for their intracellular antioxidant activities [ 38 ]. Several plant-derived phytochemicals, such as carotenoids, prevent and delay the primary carcinogenesis steps and have been found to decrease the risk and/or local progression and expansion of carcinogen-induced tumours in head and neck oncogenesis models [ 38 ].…”

Section: Introductionmentioning

confidence: 99%

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Dietary Carotenoids in Head and Neck Cancer—Molecular and Clinical Implications

Starska

2022

Nutrients

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Head and neck cancer (HNC) is one of the most common cancers in the world according to GLOBCAN. In 2018, it was reported that HNC accounts for approximately 3% of all human cancers (51,540 new cases) and is the cause of nearly 1.5% of all cancer deaths (10,030 deaths). Despite great advances in treatment, HNC is indicated as a leading cause of death worldwide. In addition to having a positive impact on general health, a diet rich in carotenoids can regulate stages in the course of carcinogenesis; indeed, strong epidemiological associations exist between dietary carotenoids and HNS, and it is presumed that diets with carotenoids can even reduce cancer risk. They have also been proposed as potential chemotherapeutic agents and substances used in chemoprevention of HNC. The present review discusses the links between dietary carotenoids and HNC. It examines the prospective anticancer effect of dietary carotenoids against intracellular cell signalling and mechanisms, oxidative stress regulation, as well as their impact on apoptosis, cell cycle progression, cell proliferation, angiogenesis, metastasis, and chemoprevention; it also provides an overview of the limited preclinical and clinical research published in this arena. Recent epidemiological, key opinion-forming systematic reviews, cross-sectional, longitudinal, prospective, and interventional studies based on in vitro and animal models of HNC also indicate that high carotenoid content obtained from daily supplementation has positive effects on the initiation, promotion, and progression of HNC. This article presents these results according to their increasing clinical credibility.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Dietary Carotenoids in Head and Neck Cancer—Molecular and Clinical Implications

Starska

2022

Nutrients

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Exploring the potential of site-specific co-delivery of Berberine alongside 5-fluorouracil in oral cancer: Formulation development, in-vitro apoptosis, ex-vivo permeability and in-vivo biocompatibility studies

Mahadik

Tamane

2022

Journal of Drug Delivery Science and Technology

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Prevention of carcinogen-induced oral cancers by polymeric black tea polyphenols via modulation of EGFR-Akt-mTOR pathway

Nimbalkar

Gangar

Shai

et al. 2022

Sci Rep

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The overexpression of Epidermal Growth Factor Receptor (EGFR) and dysregulation of its downstream effector pathways are important molecular hallmarks of oral cancers. Present study investigates the chemopreventive potential of polymeric black tea polyphenols (PBPs)/thearubigins (TRs) in the hamster model of oral carcinogenesis as well as determine the effect of PBPs on EGFR and the molecular players in the EGFR pathway. In dose-dependent manner, pre and concurrent treatment with PBPs (1.5%, 5%, 10%) decreased the number and volume of macroscopic tumors as well as the number and area of microscopic lesions. Interestingly, at 10% dose of PBPs, no macroscopic or microscopic tumors were observed. We observed PBPs mediated dose-dependent decrease in oxidative DNA damage (8OHdG); inflammation (COX-2); proliferation (PCNA, Cyclin D1); expression of EGFR, and its downstream signaling kinases (pAkt, Akt, and mTOR); hypoxia (HIF1α) and angiogenesis (VEGF). There was also a PBPs mediated dose-dependent increase in apoptosis (Bax). Thus, our data clearly indicate that the observed chemopreventive potential of PBPs was due to modulation in the EGFR pathway associated with cell proliferation, hypoxia, and angiogenesis. Taken together, our results demonstrate preclinical chemopreventive efficacy of PBPs and give an insight into its mechanistic role in the chemoprevention of experimental oral cancer.

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Head and Neck Cancer Prevention by Phytochemicals: Current Status and Challenges

Cited by 3 publications

References 130 publications

Dietary Carotenoids in Head and Neck Cancer—Molecular and Clinical Implications

Dietary Carotenoids in Head and Neck Cancer—Molecular and Clinical Implications

Exploring the potential of site-specific co-delivery of Berberine alongside 5-fluorouracil in oral cancer: Formulation development, in-vitro apoptosis, ex-vivo permeability and in-vivo biocompatibility studies

Prevention of carcinogen-induced oral cancers by polymeric black tea polyphenols via modulation of EGFR-Akt-mTOR pathway

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