Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1 Green tea is one of the few agents shown to consistently prevent a range of cancer types in rodents, even when consumed after carcinogen exposure. Digestive tract microbes may explain why it does not work to convincingly prevent cancer in people. + 3382 word(s) 3382 2020-10-21 05:12:29 |
2 update layout and reference -1765 word(s) 1617 2020-11-03 04:40:21 |

Video Upload Options

Do you have a full video?


Are you sure to Delete?
If you have any further questions, please contact Encyclopedia Editorial Office.
Adami, G.R.; Tangney, C.; Schwartz, J.L.; Dang, K.C. Green Tea Catechins. Encyclopedia. Available online: (accessed on 19 July 2024).
Adami GR, Tangney C, Schwartz JL, Dang KC. Green Tea Catechins. Encyclopedia. Available at: Accessed July 19, 2024.
Adami, Guy R., Christy Tangney, Joel L. Schwartz, Kim Chi Dang. "Green Tea Catechins" Encyclopedia, (accessed July 19, 2024).
Adami, G.R., Tangney, C., Schwartz, J.L., & Dang, K.C. (2020, November 03). Green Tea Catechins. In Encyclopedia.
Adami, Guy R., et al. "Green Tea Catechins." Encyclopedia. Web. 03 November, 2020.
Green Tea Catechins

Green tea and green tea catechins have been shown to be strongly inhibitory to cancer formation in rodents. They are believed to do this by altering cells after they have been initiated on the path toward cancer. Green tea and green tea catechin prevention of cancer in humans has been hard to detect. We discuss that the reason for this difference is likely to be the digestive tract microbiome. If green tea catechins are to be continue to be tested for cancer prevention properties in humans it will be necessary to take into account variable digestive tract microbiome metabolism in people so the dose can be optimized for each person thus avoiding toxicity. 

green tea polyphenols catechins cancer prevent

1. Green Tea Catechins

Green tea (GT) derived from the leaves of the Camellia sinensis plant is a rich source of the polyphenols known as catechins. A 240 mL or 8 ounce serving of GT contains, in solution, 300 mg catechins: (-)- epigallocatechin-3-gallate (EGCG), (-)-epigallocatechin, (EGC), (-)-epicatechin-3-gallate (ECG), (-)-epicatechin (EC) [1], and approximately 30 mg of the stimulant caffeine. The catechins are potent antioxidants that can react with and reduce many different reactive oxygen species [2]. While once thought to inhibit carcinogenesis chiefly by inactivation of dietary oxidants, catechins have been shown to have additional properties inside cells that may contribute to the perceived health benefits of drinking GT [3][4]. These include interactions with intracellular proteins so to alter: apoptosis, transformed cell proliferation, angiogenesis, DNA repair, and enzymatic detoxification of ROS, etc. [2][4][5].

2. GT Inhibition of Rodent Cancer

Published reviews detail the many rodent studies documenting the ability of GT extract or GT polyphenol consumption to prevent digestive tract tumors [6][7]. Studies of the oral cavity and the esophagus include usage of hamster, rat, and mouse models to show that GT extract or purified polyphenols in drinking water can inhibit the induction of tumors by various carcinogens at both sites [8][9][10][11][12][13]. At least five published studies alone have shown a cancer preventive effect of GT or GT polyphenols on oral cancer induced by 3 different carcinogens [8][9][12][20][21]. GT form or method of application may have differed, and dose may have had some species specificity, but all these studies saw a positive result as shown in Table 1.

Table 1. Extract/polyphenol effects on rodent oral squamous cell carcinoma models.


Catechin Mixture

Delivery of GT

Dose of GT Extract for
Equivalence in Polyphenols

Duration of GTE or
GTP Exposure

Inhibition of
Incidence 6,7

Decrease in
Tumor No.

Decrease in
Tumor Vol.


Wistar albino rats, Male 1

200 mg/kg GT polyphenol, daily

Drinking water

600 mg/kg GT

12 weeks





Syrian Golden Hamster, Male 2

600 mg/kg GT extract daily

Drinking water

600 mg/kg GT

18 weeks





Syrian Golden Hamster, Male 3

1500 mg/kg GT extract, daily

Drinking water

1500 mg/kg GT

17 weeks





C3H/HR syngeneic mouse 4

25 mg/kg GT polyphenol

IP injection

75 mg/kg GT

21 days





Swiss albino mice, Male 5

8 mg/kg GT polyphenol

Oral gavage

0.002 mg/kg GT

24 weeks





1 GT polyphenol given after 4-Nitroquinoline 1-oxide (4-NQO) oral application completed

2 GT extract given for 18 weeks, after 7,12-dimethylbenz[a]anthracene (DMBA) oral application completed

3 GT extract given 2 weeks before and then concurrent with 15 weeks DMBA oral application

4 ECGC injections after syngeneic mouse tumor cell injections

5 ECGC given daily for last 24 weeks of N-Nitrosodiethylamine (NDEA) oral application

6 Inhibition of incidence of OSCC; or for Swiss albino mice only, moderate to severe dysplasia of tongue

7 NS: not significant

3. GT Inhibition of Human Cancer

Human studies have not shown the same consistently high level of efficacy of GT or GT polyphenols in prevention of oral cancer or any other cancers [4][6][7]. Epidemiological studies of esophageal cancers revealed overall little or no association between GT drinking and cancer rates [20][21]. Interestingly, in cohort analyses stratified by sex, protective associations between GT and esophageal cancer were observed for Chinese women [21], and in a case-control study for non-tobacco/non-alcohol users and women users [20]. Studies of oral cancer are similarly variable with limited evidence for GT drinking being a cancer preventive based on epidemiology, though curiously there was a tendency for a benefit in females in a prospective cohort study [22]. An early randomized trial of oral squamous cell carcinoma (OSCC) prevention showed reduction in dysplastic lesions by consuming a GT extract in capsules combined with direct application of 1 g GT extract to the lesion [23] but a later trial showed no statistically significant benefit of GT in capsules as shown in Table 2 [24]. Notably, GT polyphenols are typically consumed in capsules when tested in recent clinical trials on cancer prevention, unlike human epidemiological studies, which may contribute to results [24][25][26]. Conflicting findings have also been seen for GT consumption and incidence rates for a number of other cancers, with modestly lower rates of liver and prostate cancer of self-reported tea drinkers based on meta-analysis [27][28][29][30]. Furthermore, recent trials designed to examine GT effects on breast cancer risk noted liver toxicity among 5% of the study subjects taking capsules with the equivalent of 5 cups decaffeinated GT daily [26]. Overall, a clear association between GT or GT polyphenol consumption and human cancer prevention has not been verified.

3.1. Does GT induce changes in gene expression in cell of the digestive tract?

Assaying RNA or protein level changes in tissue after consumption of potential bioactive compounds, such as GT, is a rapid method to show if the compound has an effect on the tissue, and may help discern if effects relevant to cancer inhibition occur. There are a limited number of studies published on GT polyphenol effects on epithelial gene expression (or RNA levels) under conditions of carcinogenesis  in vivo in rodents but they show clear cut differences in gene expression in rodent tissues after green tea extract is added to the drinking water.

Published studies of epithelial gene expression changes, induced by catechin or GT extract consumption, in humans, are rare. In a randomized placebo-controlled trial of subjects with oral premalignant changes, immunohistological examination of oral mucosa after 3 months of GT-extract consumption revealed no changes in a range of proteins after exposure. In a subset of those with reduced dysplasia, Cyclin D1 and Vascular Endothelial Growth Factor (VEGF) mucosal levels decreased [24]. Brush biopsy offers a noninvasive and validated method optimized for miRNA measurement of oral epithelial cells [50]. After 4 weeks of GT drinking, human tissue exposed to probably the highest concentration of undiluted tea in the body, the tongue epithelium, showed on average no changes in gene expression due to inter-subject variability in levels of miRNA. Only after differential co-expression analysis, which can correct for a lack of a response in some subjects, did GT-induced changes in miRNA expression become evident [51][52][53]. The question arises why doesn't catechin consumption cause clear cut, reproducible changes in gene expression in groups of people?

3.2. Gut and Oral Bacteria May Metabolize GT Polyphenols

It is clear that green tea drinking can change oral bacteria in people [53][54]. There is also much evidence that gut bacteria metabolize dietary polyphenols. This can, in theory, transform the polyphenols into more bioavailable forms and stimulate uptake into digestive tract epithelium [31][32][33][34]. Years ago, it was shown that GT catechins can be metabolized by intestinal bacterial enzymes. Some GT metabolites are more readily taken up by cells than the parent compounds and still retain biological activities relevant to carcinogenesis at least in vitro [35][36]. This could allow one to conclude that digestive tract bacteria may contribute to the bioavailability of green tea catechins.

3.3. Model for How Variable Gut and Oral Microbiota may Affect GT Studies on Humans

People who are non-cohabitating show a great variety of oral and gut microbiota which is reduced in those who live together [37][38]. Diet [39][40], gut/oral health [41][42], and drugs [43][44] may further influence gut and oral microbiota. Clinical studies on GT-based prevention do not normally account for variation of aerodigestive tract microbiota or the foods, beverages, and medications ingested. As a result, one would predict that responses to supplemental polyphenol and GT itself would be variable. Whether one is assaying changes in cell function [45] or histological changes in cancer-prone sites [24], rarely is a consistent net positive result seen across a sample of human subjects. This may be due to the differences in GT metabolizing digestive tract microbes that we suggest are crucial for catechin uptake, turnover, and/or function [29][46]. As a result, levels of GT extract that may be appropriate for most individual humans are much too high, for example, in subjects with gut/oral microbes most efficient at converting GT polyphenols to metabolites that are bioactive. Conversely, a study on a rodent cohort consuming GT polyphenols, with bioactivity dependent on digestive tract microbiota which vary little, would reveal consistent changes in gene expression. This would ease GT dosage optimization in a rodent study and make it fairly likely that changes in cancer incidence would be observed. In clinical trials, using humans with variable gut/oral microbiota, that would not be the case [47]. For example, humans with high levels of gut/oral bacteria that metabolize GT polyphenol to functional, readily absorbed metabolites might show toxicity, while those with gut/oral bacteria that lack this metabolic activity may show no effect [26]. With heterogeneous populations, a dosage would be chosen tolerable to all but the most sensitive subjects. It would vary little between studies and be on-average ineffective and that is what has been observed (Table 2). This is in contrast to rodent studies where levels of catechins given to experimental subjects vary between studies (Table 1). One possible solution is to artificially convert GT polyphenols to forms that are more readily absorbed by cells [35][48]. Another would be to characterize subject specific GT toxicity, possibly by measuring each subject’s gut/oral microbiota and its ability to activate and inactivate GT catechins, prior to entry in the trial, or more directly measuring GT metabolites after a trial run of drinking GT.


  1. Balentine, D.A.; Wiseman, S.A.; Bouwens, L.C. The chemistry of tea flavonoids. Rev. Food Sci. Nutr. 1997, 37, 693–704.
  2. Chen, L.; Mo, H.; Zhao, L.; Gao, W.; Wang, S.; Cromie, M.M.; Lu, C.; Wang, J.S.; Shen, C.L. Therapeutic properties of green tea against environmental insults. Nutr. Biochem. 2017, 40, 1–13.
  3. Halliwell, B.; Rafter, J.; Jenner, A. Health promotion by flavonoids, tocopherols, tocotrienols, and other phenols: Direct or indirect effects? Antioxidant or not? J. Clin. Nutr. 2005, 81, 268S–276S.
  4. Yang, C.S.; Wang, H. Cancer Preventive Activities of Tea Catechins. Molecules 2016, 21, 1679.
  5. Tao, L.; Park, J.Y.; Lambert, J.D. Differential prooxidative effects of the green tea polyphenol, (-)-epigallocatechin-3-gallate, in normal and oral cancer cells are related to differences in sirtuin 3 signaling. Nutr. Food Res. 2015, 59, 203–211.
  6. Yang, C.S.; Wang, X.; Lu, G.; Picinich, S.C. Cancer prevention by tea: Animal studies, molecular mechanisms and human relevance. Rev. Cancer 2009, 9, 429–439.
  7. Wang, L.X.; Shi, Y.L.; Zhang, L.J.; Wang, K.R.; Xiang, L.P.; Cai, Z.Y.; Lu, J.L.; Ye, J.H.; Liang, Y.R.; Zheng, X.Q. Inhibitory Effects of (-)-Epigallocatechin-3-gallate on Esophageal Cancer. Molecules 2019, 24, 954.
  8. Koh, Y.W.; Choi, E.C.; Kang, S.U.; Hwang, H.S.; Lee, M.H.; Pyun, J.; Park, R.; Lee, Y.; Kim, C.H. Green tea (-)-epigallocatechin-3-gallate inhibits HGF-induced progression in oral cavity cancer through suppression of HGF/c-Met. Nutr. Biochem. 2011, 22, 1074–1083.
  9. Li, N.; Chen, X.; Liao, J.; Yang, G.; Wang, S.; Josephson, Y.; Han, C.; Chen, J.; Huang, M.T.; Yang, C.S. Inhibition of 7,12-dimethylbenz[a]anthracene (DMBA)-induced oral carcinogenesis in hamsters by tea and curcumin. Carcinogenesis 2002, 23, 1307–1313.
  10. Morse, M.A.; Kresty, L.A.; Steele, V.E.; Kelloff, G.J.; Boone, C.W.; Balentine, D.A.; Harbowy, M.E.; Stoner, G.D. Effects of theaflavins on N-nitrosomethylbenzylamine-induced esophageal tumorigenesis. Cancer 1997, 29, 7–12.
  11. Srinivasan, P.; Suchalatha, S.; Babu, P.V.; Devi, R.S.; Narayan, S.; Sabitha, K.E.; Devi, C.S.S. Chemopreventive and therapeutic modulation of green tea polyphenols on drug metabolizing enzymes in 4-Nitroquinoline 1-oxide induced oral cancer. Biol. Interact. 2008, 172, 224–234.
  12. Sur, S.; Pal, D.; Roy, R.; Barua, A.; Roy, A.; Saha, P.; Panda, C.K. Tea polyphenols EGCG and TF restrict tongue and liver carcinogenesis simultaneously induced by N-nitrosodiethylamine in mice. Appl. Pharmacol. 2016, 300, 34–46.
  13. Yang, C.S.; Chen, J.X.; Wang, H.; Lim, J. Lessons learned from cancer prevention studies with nutrients and non-nutritive dietary constituents. Nutr. Food Res. 2016, 60, 1239–1250.
  14. Yang, C.S.; Wang, H. Mechanistic issues concerning cancer prevention by tea catechins. Nutr. Food Res. 2011, 55, 819–831.
  15. Fiala, E.S.; Sohn, O.S.; Wang, C.X.; Seibert, E.; Tsurutani, J.; Dennis, P.A.; El-Bayoumy, K.; Sodum, R.S.; Desai, D.; Reinhardt, J.; et al. Induction of preneoplastic lung lesions in guinea pigs by cigarette smoke inhalation and their exacerbation by high dietary levels of vitamins C and E. Carcinogenesis 2005, 26, 605–612.
  16. Hu, Y.; Le Leu, R.K.; Christophersen, C.T.; Somashekar, R.; Conlon, M.A.; Meng, X.Q.; Winter, J.M.; Woodman, R.J.; McKinnon, R.; Young, G.P. Manipulation of the gut microbiota using resistant starch is associated with protection against colitis-associated colorectal cancer in rats. Carcinogenesis 2016, 37, 366–375.
  17. Witschi, H. Successful and not so successful chemoprevention of tobacco smoke-induced lung tumors. Lung Res. 2000, 26, 743–755.
  18. Witschi, H.; Espiritu, I.; Yu, M.; Willits, N.H. The effects of phenethyl isothiocyanate, N-acetylcysteine and green tea on tobacco smoke-induced lung tumors in strain A/J mice. Carcinogenesis 1998, 19, 1789–1794.
  19. Li, N.; Han, C.; Chen, J. Tea preparations protect against DMBA-induced oral carcinogenesis in hamsters. Cancer 1999, 35, 73–79.
  20. Gao, Y.T.; McLaughlin, J.K.; Blot, W.J.; Ji, B.T.; Dai, Q.; Fraumeni, J.F., Jr. Reduced risk of esophageal cancer associated with green tea consumption. Natl. Cancer Inst. 1994, 86, 855–858.
  21. Zheng, P.; Zheng, H.M.; Deng, X.M.; Zhang, Y.D. Green tea consumption and risk of esophageal cancer: A meta-analysis of epidemiologic studies. BMC Gastroenterol. 2012, 12, 165.
  22. Ide, R.; Fujino, Y.; Hoshiyama, Y.; Mizoue, T.; Kubo, T.; Pham, T.M.; Shirane, K.; Tokui, N.; Sakata, K.; Tamakoshi, A.; et al. A prospective study of green tea consumption and oral cancer incidence in Japan. Epidemiol. 2007, 17, 821–826.
  23. Li, N.; Sun, Z.; Han, C.; Chen, J. The chemopreventive effects of tea on human oral precancerous mucosa lesions. Soc. Exp. Biol. Med. 1999, 220, 218–224.
  24. Tsao, A.S.; Liu, D.; Martin, J.; Tang, X.M.; Lee, J.J.; El-Naggar, A.K.; Wistuba, I.; Culotta, K.S.; Mao, L.; Gillenwater, A.; et al. Phase II randomized, placebo-controlled trial of green tea extract in patients with high-risk oral premalignant lesions. Cancer Prev. Res. 2009, 2, 931–941.
  25. Tang, G.Y.; Meng, X.; Gan, R.Y.; Zhao, C.N.; Liu, Q.; Feng, Y.B.; Li, S.; Wei, X.L.; Atanasov, A.G.; Corke, H.; et al. Health Functions and Related Molecular Mechanisms of Tea Components: An Update Review. J. Mol. Sci. 2019, 20, 6196.
  26. Yu, Z.; Samavat, H.; Dostal, A.M.; Wang, R.; Torkelson, C.J.; Yang, C.S.; Butler, L.M.; Kensler, T.W.; Wu, A.H.; Kurzer, M.S.; et al. Effect of Green Tea Supplements on Liver Enzyme Elevation: Results from a Randomized Intervention Study in the United States. Cancer Prev. Res. 2017, 10, 571–579.
  27. Almatroodi, S.A.; Almatroudi, A.; Khan, A.A.; Alhumaydhi, F.A.; Alsahli, M.A.; Rahmani, A.H. Potential Therapeutic Targets of Epigallocatechin Gallate (EGCG), the Most Abundant Catechin in Green Tea, and Its Role in the Therapy of Various Types of Cancer. Molecules 2020, 25, 3146.
  28. Boehm, K.; Borrelli, F.; Ernst, E.; Habacher, G.; Hung, S.K.; Milazzo, S.; Horneber, M. Green tea (Camellia sinensis) for the prevention of cancer. Cochrane Database Syst. Rev. 2009, CD005004, doi:10.1002/14651858.CD005004.pub2.
  29. Jacob, S.A.; Khan, T.M.; Lee, L.H. The Effect of Green Tea Consumption on Prostate Cancer Risk and Progression: A Systematic Review. Cancer 2017, 69, 353–364.
  30. Ni, Y.; Li, J.; Panagiotou, G. A Molecular-Level Landscape of Diet-Gut Microbiome Interactions: Toward Dietary Interventions Targeting Bacterial Genes. MBio 2015, 6, e01263-15.
  31. 68Cassidy, A.; Minihane, A.M. The role of metabolism (and the microbiome) in defining the clinical efficacy of dietary flavonoids. J. Clin. Nutr. 2017, 105, 10–22.
  32. Duenas, M.; Munoz-Gonzalez, I.; Cueva, C.; Jimenez-Giron, A.; Sanchez-Patan, F.; Santos-Buelga, C.; Moreno-Arribas, M.V.; Bartolome, B. A survey of modulation of gut microbiota by dietary polyphenols. Res. Int. 2015, 2015, 850902.
  33. Ozdal, T.; Sela, D.A.; Xiao, J.; Boyacioglu, D.; Chen, F.; Capanoglu, E. The Reciprocal Interactions between Polyphenols and Gut Microbiota and Effects on Bioaccessibility. Nutrients 2016, 8, 78.
  34. Williamson, G.; Clifford, M.N. Role of the small intestine, colon and microbiota in determining the metabolic fate of polyphenols. Pharmacol. 2017, 139, 24–39.
  35. Marquez Campos, E.; Stehle, P.; Simon, M.C. Microbial Metabolites of Flavan-3-Ols and Their Biological Activity. Nutrients 2019, 11, 2260
  36. Mena, P.; Bresciani, L.; Brindani, N.; Ludwig, I.A.; Pereira-Caro, G.; Angelino, D.; Llorach, R.; Calani, L.; Brighenti, F.; Clifford, M.N.; et al. Phenyl-gamma-valerolactones and phenylvaleric acids, the main colonic metabolites of flavan-3-ols: Synthesis, analysis, bioavailability, and bioactivity. Prod. Rep. 2019, 36, 714–752.
  37. Song, S.J.; Lauber, C.; Costello, E.K.; Lozupone, C.A.; Humphrey, G.; Berg-Lyons, D.; Caporaso, J.G.; Knights, D.; Clemente, J.C.; Nakielny, S.; et al. Cohabiting family members share microbiota with one another and with their dogs. Elife 2013, 2, e00458.
  38. Stahringer, S.S.; Clemente, J.C.; Corley, R.P.; Hewitt, J.; Knights, D.; Walters, W.A.; Knight, R.; Krauter, K.S. Nurture trumps nature in a longitudinal survey of salivary bacterial communities in twins from early adolescence to early adulthood. Genome Res. 2012, 22, 2146–2152.
  39. Hansen, T.H.; Kern, T.; Bak, E.G.; Kashani, A.; Allin, K.H.; Nielsen, T.; Hansen, T.; Pedersen, O. Impact of a vegan diet on the human salivary microbiota. Rep. 2018, 8, 5847.
  40. Wu, G.D.; Chen, J.; Hoffmann, C.; Bittinger, K.; Chen, Y.Y.; Keilbaugh, S.A.; Bewtra, M.; Knights, D.; Walters, W.A.; Knight, R.; et al. Linking long-term dietary patterns with gut microbial enterotypes. Science 2011, 334, 105–108.
  41. Frank, D.N.; Robertson, C.E.; Hamm, C.M.; Kpadeh, Z.; Zhang, T.; Chen, H.; Zhu, W.; Sartor, R.B.; Boedeker, E.C.; Harpaz, N.; et al. Disease phenotype and genotype are associated with shifts in intestinal-associated microbiota in inflammatory bowel diseases. Bowel Dis. 2011, 17, 179–184.
  42. Yamashita, Y.; Takeshita, T. The oral microbiome and human health. Oral Sci. 2017, 59, 201–206.
  43. Jackson, L.R.; Peterson, E.D.; McCoy, L.A.; Ju, C.; Zettler, M.; Baker, B.A.; Messenger, J.C.; Faries, D.E.; Effron, M.B.; Cohen, D.J.; et al. Impact of Proton Pump Inhibitor Use on the Comparative Effectiveness and Safety of Prasugrel Versus Clopidogrel: Insights from the Treatment with Adenosine Diphosphate Receptor Inhibitors: Longitudinal Assessment of Treatment Patterns and Events after Acute Coronary Syndrome (TRANSLATE-ACS) Study. Am. Heart Assoc. 2016, 5, e003824.
  44. Seto, C.T.; Jeraldo, P.; Orenstein, R.; Chia, N.; DiBaise, J.K. Prolonged use of a proton pump inhibitor reduces microbial diversity: Implications for Clostridium difficile susceptibility. Microbiome 2014, 2, 1–11.
  45. Ho, C.K.; Choi, S.W.; Siu, P.M.; Benzie, I.F. Effects of single dose and regular intake of green tea (Camellia sinensis) on DNA damage, DNA repair, and heme oxygenase-1 expression in a randomized controlled human supplementation study. Nutr. Food Res. 2014, 58, 1379–1383.
  46. Liu, Z.; Bruins, M.E.; Ni, L.; Vincken, J.P. Green and Black Tea Phenolics: Bioavailability, Transformation by Colonic Microbiota, and Modulation of Colonic Microbiota. Agric. Food Chem. 2018, 66, 8469–8477.
  47. Landberg, R.; Manach, C.; Kerckhof, F.M.; Minihane, A.M.; Saleh, R.N.M.; De Roos, B.; Tomas-Barberan, F.; Morand, C.; Van de Wiele, T. Future prospects for dissecting inter-individual variability in the absorption, distribution and elimination of plant bioactives of relevance for cardiometabolic endpoints. J. Nutr. 2019, 58, 21–36.
  48. Li, F.; Wang, Y.; Li, D.; Chen, Y.; Qiao, X.; Fardous, R.; Lewandowski, A.; Liu, J.; Chan, T.H.; Dou, Q.P. Perspectives on the recent developments with green tea polyphenols in drug discovery. Expert Drug Discov. 2018, 13, 643–660.
  49. Ozdal, T.; Sela, D. A.; Xiao, J.; Boyacioglu, D.; Chen, F.; Capanoglu, E., The Reciprocal Interactions between Polyphenols and Gut Microbiota and Effects on Bioaccessibility. Nutrients 2016, 8, (2), 78.
  50. Adami, G. R.; Tang, J. L.; Markiewicz, M. R., Improving accuracy of RNA-based diagnosis and prognosis of oral cancer by using noninvasive methods. Oral Oncol 2017, 69, 62-67.
  51. de la Fuente, A., From 'differential expression' to 'differential networking' - identification of dysfunctional regulatory networks in diseases. Trends Genet 2010, 26, (7), 326-33.
  52. Voigt, A.; Nowick, K.; Almaas, E., A composite network of conserved and tissue specific gene interactions reveals possible genetic interactions in glioma. PLoS Comput Biol 2017, 13, (9), e1005739.
  53. Adami, G. R.; Tangney, C. C.; Tang, J. L.; Zhou, Y.; Ghaffari, S.; Naqib, A.; Sinha, S.; Green, S. J.; Schwartz, J. L., Effects of green tea on miRNA and microbiome of oral epithelium. Sci Rep 2018, 8, (1), 5873.
  54. Yuan, X.; Long, Y.; Ji, Z.; Gao, J.; Fu, T.; Yan, M.; Zhang, L.; Su, H.; Zhang, W.; Wen, X.; et al. Green Tea Liquid Consumption Alters the Human Intestinal and Oral Microbiome. Nutr. Food Res. 2018, 62, 1800178.
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to : , , ,
View Times: 673
Revisions: 2 times (View History)
Update Date: 03 Nov 2020
Video Production Service