Polyphenols are naturally occurring compounds found primarily in fruits, vegetables, cereals, beverages, and dry beans. Polyphenols are secondary metabolites of plants and are usually involved in protection against ultraviolet (UV) radiation or against aggression from pathogens (Figure 1) (Singla et al., 2019; Reed and de Freitas, 2020). In food, polyphenols can contribute bitterness, astringency, color, taste, odor, and oxidative stability. Animal, human, and epidemiological studies indicate that various polyphenols have antioxidant and anti-inflammatory properties that may have preventive and/or therapeutic effects in cardiovascular disease, neurodegenerative disorders, fat metabolism disorders, and tumors (Yahfoufi et al., 2018; Potì et al., 2019). In recent years, interest in polyphenols has increased as they are the subject of scientific research due to their possible beneficial effects on human health. Also, the main advantage of polyphenolic compounds is their use as chemoprophylaxis due to low toxicity and high tolerability (Singla et al., 2019; Reed and de Freitas, 2020).

The main indicator in the use of polyphenols is bioavailability. Bioavailability is the proportion of a nutrient that is digested, absorbed, and metabolized through normal pathways. The bioavailability of each polyphenol is different, but their relationship between the amount of polyphenols in food and their bioavailability in the human body is not fully understood. It is important that the chemical structure of polyphenols, and not their concentration, determines the rate and extent of absorption, as well as the nature of the metabolites circulating in plasma. The most abundant polyphenols in the diet are not necessarily those that show the highest concentration of active metabolites in target tissues; therefore, the biological properties of polyphenols differ significantly from one polyphenol to another (Brglez Mojzer et al., 2016; Rogovskii, 2022). Evidence from preclinical and clinical studies indicates that the antioxidant and anti-inflammatory properties of polyphenols may potentially prevent or treat various tumors (Table 1) (Henning et al., 2015; Gee et al., 2017; Silva et al., 2019; Zeng et al., 2019; Basak et al., 2020; Lee et al., 2021; Mallet et al., 2021; Rojas-Ochoa et al., 2021; Shan et al., 2021; Wang et al., 2021). This review focuses on the current understanding of the biological effects of polyphenolic compounds and their importance in health and tumor prevention and therapy.

In Table 1, various types of tumors are reviewed for which polyphenolic compounds have been used as therapy and have been positive. From the indicators in Table 1, the dominant explanation for these benefits is the neutralization of free radicals, the formation of stabilized chemical complexes, thus preventing further reactions. There is also evidence of an additional mechanism by which polyphenols protect against oxidative stress by producing hydrogen peroxide (H2O2), which may then help regulate immune response actions such as cell growth. It is believed that polyphenols have an anticarcinogenic effect, inhibit cell growth, causing aging or apoptosis of tumor cells, and their differential redox status can selectively affect tumor cells.

The effect of polyphenols on tumor cells is most often protective. To date, many polyphenols, such as quercetin, catechins, isoflavones, lignans, flavanones, ellagic acid, red wine polyphenols, resveratrol, and curcumin, have been studied and tested for effectiveness (Brglez Mojzer et al., 2016; Rogovskii, 2022). All of them showed protective effects in experimental models with tumors, their mechanisms of action turned out to be different.

Oncogenesis is a multistage and microevolutionary process. There are three main stages of oncogenesis: initiation, promotion and progression. Initiated cells thus may have the ability to transform into a malignant tumor if further development follows. Development is influenced by factors that do not alter the DNA sequence and include the selection of initiated cells (Patterson et al., 2018; Peters and Gonzalez, 2018).

Several mechanisms of action have been identified for the chemopreventive action of polyphenols, including estrogenic/antiestrogen activity, antiproliferative activity, apoptosis induction, cell cycle inhibition, oxidation prevention, detoxification enzyme induction, regulation of the host immune system, and anti-inflammatory activity (Singh et al., 2021a; Bahrami et al., 2021; Weh et al., 2022) (Figure 2, Figure 3 and Figure 4). At the same time, polyphenols can affect the metabolism of pro-carcinogens and modulate the expression of cytochrome P450 enzymes involved in their activation into carcinogens. They may also facilitate their clearance by increasing the expression of phase II conjugating enzymes. This induction of phase II enzymes may be due to polyphenol toxicity (Diaz-Gerevini et al., 2016).

Polyphenols can form potentially toxic quinones in the body, which are themselves substrates for these enzymes. Consumption of polyphenols can then activate these enzymes to detoxify themselves and thus cause an overall increase in the body’s defenses against toxic xenobiotics (Erlank et al., 2011). It has been demonstrated that tea catechins in the form of capsules, when administered to men with high grade intraepithelial neoplasia of the prostate, have a prophylactic activity by inhibiting the transformation of high grade intraepithelial neoplasia lesions into tumors (Bettuzzi et al., 2006).

Theaflavins, thearubigins and black tea polyphenols also had strong antitumor properties. Black tea polyphenols have been found to inhibit proliferation and enhance apoptosis in prostate carcinoma DU 145 cell lines (Klein and Fischer, 2002). Higher levels of insulin like growth factor-1 (IGF-1) have been found to be associated with a higher risk of developing prostate cancer (Cao et al., 2015). The binding of IGF-1 to its receptor is part of the signal transduction pathway that causes cell proliferation. The addition of black tea polyphenols was found to block the progression of IGF-1-induced cell growth into the S-phase of the cell cycle at a dose of 40 mg/ml in prostate cancer.

Polyphenols act as generators of reactive oxygen species (ROS) that act as second messengers in cellular signal transduction. In tumor cells, there are many targets that polyphenolic compounds can act on. However, nuclear factor kappa B (NF-κB) can be considered a central target, since it controls the expression of genes responsible for tumor proliferation, apoptosis, and metastasis (Khan et al., 2020).

Resveratrol prevents all stages of tumor development and has been shown to be effective in most types of tumors, including lung cancer, melanoma, breast cancer, prostate cancer, gastric cancer, and colorectal cancer (Rauf et al., 2018). It has also been shown to inhibit angiogenesis and metastasis. Extensive data in vitro show that resveratrol can modulate multiple signaling pathways involved in cell growth, apoptosis, and inflammation (Wu et al., 2019). The anticarcinogenic effects of resveratrol appear to be closely related to its antioxidant activity, where it inhibits cyclooxygenase, hydroperoxidase, protein kinase C, B-cell lymphoma 2 (Bcl-2) phosphorylation, Akt-kinase with focal adhesion, NF-κB expression, expression of matrix metalloproteases (MMPs) and cell cycle regulators (Yousef et al., 2017; El-Readi et al., 2019; Buhrmann et al., 2020). These and other in vitro and in vivo studies justify the use of polyphenols in tumor chemoprophylaxis in a combinatorial approach with chemotherapeutic drugs or cytotoxic factors for the effective treatment of drug-resistant tumors (Patra et al., 2021).

Based on the literature data on the effects of polyphenolic compounds on tumors, it can be concluded that polyphenols have great potential for use in combination with chemotherapy. A suitable combination of polyphenols with existing chemotherapeutic agents will result in a reduction in side effects without reducing the therapeutic effects of chemotherapy drugs.

One of the promising sources of phytopreparations are medicinal plants containing flavonoids, which, due to their wide distribution in plants and great structural diversity, are currently in the focus of attention of researchers in the field of pharmacognosy, pharmacy and medicine. Flavonoids are the most numerous class of natural phenolic compounds, which are characterized by structural diversity, high and versatile activity and low toxicity. The wide range of biological activity of flavonoids is associated with the diversity of their chemical structures and the various physicochemical properties resulting from them (Figure 1). This interest is due to the fact that flavonoids cause antioxidant, angioprotective, hepatoprotective, and antitumor activity (Serafini et al., 2010; Wen et al., 2021). Moreover, it is the antitumor properties that attract scientists to the greatest extent in the field of creating new drugs in the fight against tumor.

Cell signaling systems are involved in the transmission of chemical signals from the cell surface to the cytoplasm, due to which the cell is able to respond to environmental changes. To do this, cells have specialized receptors on the surface of the plasma membrane that can recognize the presence of certain molecules in the environment, called extracellular signaling molecules. Flavonoids are able to influence the functioning of cytokine receptors, tyrosine kinase receptors (RTKs), tumor necrosis factor ligand superfamily member 10 (TRAIL), protein-coupled receptors (GRCRs), and a broad class of transmembrane signaling protein called integrins (Wiseman et al., 2001; Chen et al., 2018). The molecular mechanisms of this influence and signal propagation pathways are not well understood. In recent years, only scattered information has appeared indicating changes in the activity or expression of proteins of a particular signaling system in the presence of certain flavonoids. In this chapter, we will discuss the main mechanisms of action of flavonoids on the signaling pathways of oncogenesis.

In order to assess the potential of various polyphenolic compounds to have an effect on tumors of the central nervous system (CNS), it is first necessary to consider the ability of these substances to crossing the blood-brain barrier (BBB). The bioavailability of polyphenolic compounds for the CNS is very low. For example, direct administration of large amounts of EGCG into the stomach during the day made it possible to obtain very high concentrations of this substance in the blood plasma, but its concentration in the brain was 5–10% of the concentration in the blood in vivo (Ferri et al., 2015). Thus, in order to achieve therapeutic concentrations of EGCG in the brain, it was necessary to increase its concentration in the blood to excessively high values. The study of other flavonoids showed that quercetin penetrates poorly through the BBB, but after penetrating, it accumulates in such parts of the brain as the hippocampus, striatum, cerebellum, where its concentration can reach 1 mg per gram of brain tissue (Pervin et al., 2019). Kaempferol and isorhamnetin penetrate better, and the average concentration of these substances in the brain can reach several hundred nanograms per gram of healthy tissue (Rangel-Ordóñez et al., 2010). At present, doubts have arisen about the adequacy of estimates of the degree of penetration of polyphenolic compounds into the CNS, as well as the effectiveness of the action of low concentrations of these substances, since, despite the apparent low content of these substances in the tissues of the CNS, there is a lot of experimental evidence of their effective effect on behavioral reactions and cognitive functions of animals and humans. In addition, it was found that after penetration into the brain tissue, flavonoids can undergo significant modification. Thus, catechins are conjugated with glycosides and are present in the form of glucuronides, which also have the ability to protect cells from oxidative stress. Moreover, chemical modification of flavonoids and other plant polyphenols can be used to deliver these substances to the brain, where they can be highly active (Rudrapal et al., 2021; Zhou et al., 2022). Thus, it is proposed to use a fully acetylated form of EGCG as a drug precursor. It was shown that active EGCG is released in the cytoplasm of cells due to the action of intracellular esterases (Lambert et al., 2006). The use of flavonoids as building blocks for the creation of substances capable of penetrating the BBB and exhibiting drug activity is one of the most promising research strategies in the therapy of CNS tumors.

Prolonged intense exposure to UV radiation on the surface of the skin leads to the development of oxidative stress, damage to DNA molecules and the development of inflammatory processes (Aphalo et al., 2015). Exposure to ultraviolet light can cause various skin diseases, not only premature aging, but also serious diseases such as melanoma and non-melanoma skin cancers (Watson et al., 2016). Most polyphenolic compounds of plant origin are able to absorb radiation in the UV range and, therefore, can act as a screen. Indeed, it has been experimentally shown that when extracts from plants are applied to the surface of the skin, the reaction of the skin to ultraviolet light irradiation is significantly reduced (Cavinato et al., 2017). However, the protective effect of these substances is not limited to shielding tissues from the action of the ultraviolet part of the spectrum. Protection is also carried out due to the action on the regulatory systems of the cell.

It was found that the appearance of ROS is associated with the activation of the factor NF-kB and the subsequent expression of NADPH oxidase and cyclooxygenase-2 (COX-2), the activity of which is the cause of the accumulation of ROS in keratinocytes (Wang et al., 2019b). The activity of cyclooxygenase in the cytoplasm and the accumulation of products of lipid peroxidation (LPO) are associated with an increase in the concentration of calcium cations in the cytoplasm during ultraviolet irradiation. Antioxidants do not appear to be able to protect the skin from the effects of UV radiation (Sourivong et al., 2007). Thus, it was experimentally shown that the antioxidant ionol was not effective in protecting cells exposed to UV radiation, while the blocker of COX-2 cyclooxygenase aspirin reduced the concentration of lipid peroxidation in keratinocytes (Ponomareva et al., 1985). Due to the fact that UV radiation induces the activity of COX-2 cyclooxygenase, the concentration of prostaglandins formed from arachidonic acid increases in skin cells (De Leo et al., 1984). As a result, inflammation processes develop, edema is observed, keratinocyte proliferation accelerates, epidermal hyperplasia accelerates, oxidation products accumulate, which leads to oxidative damage to DNA. Therefore, as a result of chronic irradiation, mutations accumulate, which leads to malignant degeneration of keratinocytes and the development of oncogenesis (Leonardi et al., 2018). On the contrary, the action of COX-2 inhibitors or agents that interfere with the expression of this enzyme can significantly prevent the carcinogenic degeneration of epidermal cells (Leonardi et al., 2018).

The ability of some flavonoids to suppress the expression of COX-2 may underlie the mechanisms of the protective action of these substances against the action of UV radiation, as was shown for baicalein and wogonin, hesperetin, magniferin and tangeritin (Fischer et al., 2018; Farjadmand et al., 2021). It is possible that this regulation is carried out through the mitogen-activated protein kinase (MAPK) regulatory pathway, as was shown for luteolin (Aziz et al., 2018). Using the methylated flavonol 5,7-dimethoxyflavone as an example, it was shown that not only COX, but also other components of the regulatory chain, such as peroxisome proliferator-activated receptor (PPAR), NF-kB, can be regulated, resulting in a decrease in the concentration of IL-6 and IL-8 (Walle and Walle, 2007). In addition, there is a decrease in the expression of MMPs, a decrease in the concentration of oxidative stress components, and suppression of the activity of inflammation components through the regulatory pathways NF-kB and MAPK (Walle and Walle, 2007). As a result, damage to the skin and the subsequent possible development of oncology associated with the action of UV radiation are prevented.

Flavonoids may also affect other regulatory systems. Silibinin has recently been found to prevent damage to the epidermis after UV radiation by activating the tumor suppressor protein p53, resulting in the activation of the GADD45α protein, which contributes to the protection of cells under conditions of stress and DNA damage (Rigby et al., 2017). Chrysin protects epidermal keratinocytes from damage by UV irradiation, primarily by restoring the expression of aquaporin 3 (AQP-3), which ensures the normalization of the osmotic and salt balance of the cell, disturbed by irradiation. In a study on the protective effects of eriodictyol on keratinocytes, this flavanoid was found to act through activation of the p38/MAPK/Akt signaling pathway (Wu et al., 2011). Blackberry anthocyanins protect keratinocytes from UV radiation by significantly increasing the expression of antioxidant enzymes such as catalase, mitochondrial superoxide dismutase and glutathione peroxidase, thus preventing the development of oxidative stress (Murapa et al., 2012). Grape procyanidins also prevent the production of reactive oxygen species in cells, but using a different mechanism - suppression of p38 (MAPK14) and c-Jun NH1-terminal kinase/c-Jun NH2-terminal kinase (JNK1/2) (MAPK8) expression (Matito et al., 2011). The soy isoflavone metabolite daidzein, 7,3',4'-trihydroxy-isoflavone, prevents the development of melanoma induced by UV irradiation and by acting on the ATP-binding sites of protein kinases Cot and mitogen-activated protein (MAP) kinase kinase 4 (MKK4) (Ravindranath et al., 2004). It is noteworthy that the original daidzein molecule is not able to interact with these proteins and does not exhibit anticarcinogenic activity under these conditions.

According to current data, viruses are the etiological agents of about 15% of human tumors. These viruses include: human T-leukemia/lymphoma virus, human immunodeficiency virus (HIV), human papillomavirus (HPV), hepatitis B and C viruses, Epstein-Barr virus (EBV), and other (Cao and Li, 2018). It is important to note that some viruses are associated with tumors of only one localization, while others are associated with various malignant neoplasms, which is probably due to the tropism of viruses for certain types of cell systems. The virus-genetic theory of the occurrence of tumors, proposed back in the 40 s of the 20th century by Zilber, has received numerous confirmations over the years (Cao and Li, 2018; Haley et al., 2019). At present, it is clear that although viruses are not the only cause of tumors, they play a large role in the occurrence of malignant neoplasms (for instance, the presence of hepatitis B virus increases the risk of developing hepatocellular carcinoma) in both humans and animals. A characteristic feature of tumor diseases associated with viruses is a long latent period, years and even decades can pass from the moment of infection to the manifestation of the disease (Mui et al., 2019; Blackard and Sherman, 2021).

The creation of antiviral drugs based on natural compounds is undoubtedly one of the promising real directions. The expansion of the number of compounds used and the use of the synergism of their biological action provide a large reserve of therapeutic antiviral action and, along with the prevention of oncological diseases. Along with a number of different natural substances, polyphenolic compounds with antioxidant activity can also be used, in particular flavanoids, which occupies one of the leading positions in antioxidant activity. The mechanism of the antiviral action of polyphenolic compounds includes both direct interference with the mechanism of viral replication and suppression of cellular signaling pathways necessary for replication (Di Petrillo et al., 2022) (Figure 5). Numerous studies have shown that some polyphenols have an effect against influenza A, herpes virus, hepatitis B and C, HPV and others. Table 8 lists the polyphenols for which their antiviral activity has been confirmed (Docherty et al., 2004; Docherty et al., 2005; Yiu et al., 2010; Ciesek et al., 2011; Fatima et al., 2014; Pang et al., 2014; Rastogi et al., 2015; Sun et al., 2021).

Significant progress has been made in the use of plant polyphenolic compounds for the treatment of HIV infection. Flavonoids have been found to inhibit viral fusion, integration, and reverse transcription. Inhibition of protease, reverse transcriptase, replication, and maturation are among the anti-HIV mechanisms of some polyphenols (Yu and Zhao, 2012; Andrae-Marobela et al., 2013). Flavonoids, alkaloids, anthocyanins, chalcones, xanthones and homoisoflavonoids, which inhibit neuraminidase, are proposed to be used as anti-influenza agents (Bahramsoltani et al., 2016). Polyphenol, isochlorogenic acid, dehydrocheilantifoline and some other amide alkaloids have an effect against hepatitis B virus (Man et al., 2021). Curcumin inhibits the replication and expression of the hepatitis B virus gene (Thongsri et al., 2021). In cell model studies, it was found that quercetin inhibits the entry of the influenza virus at an early stage of infection, due to its pronounced anti-inflammatory properties, reduces the effects of pro-inflammatory cytokines and the risk of developing lung inflammation (Mehrbod et al., 2020; Nile et al., 2020). In addition, it enhances the effect of other drugs.

In general, polyphenols are able to interfere with different stages of the life cycle of viruses, which characterizes them as multipurpose drugs that act on vital proteins of the pathogen (Table 8). At the same time, many researchers pay attention to the fact that for the development of drugs based on polyphenols, it is necessary to overcome quite a lot of difficulties, since these compounds are characterized by complex structures, low bioavailability, and rapid excretion from the body. In addition, in-depth studies in vitro (ex vivo), in vivo, as well as multicenter clinical studies are required. Despite all the difficulties, polyphenols should eventually find their place as candidates for creating on their basis not only antiviral drugs, but also for the prevention of cancer.

The search for effective methods of treatment and prevention of tumors, despite the successes achieved in recent decades, remains one of the most urgent tasks in medicine. Antitumor therapies (e.g., chemotherapy) use approaches based on induction of cell death by increasing the intracellular concentration of ROS (Wang et al., 2017). Since ROS are formed in cells not only as a result of the action of external physicochemical factors, but also in the processes of cellular metabolism, pharmacological correction of the redox properties of tumor cells is a promising approach to improve the effectiveness of antitumor therapy. In chemotherapy, drugs that enhance the production of ROS by cells are widely used. In recent decades, it has been shown that ROS generation is an important step in the process of induction of apoptosis of tumor cells by such widely used chemotherapeutic agents as cisplatin and doxorubicin (Li et al., 2020; Xia et al., 2020).

To increase the effectiveness of chemotherapeutic agents, approaches are proposed aimed at inducing oxidative stress in tumor cells. Therefore, pharmacological correction of the redox properties of tumor cells is a promising approach to improve the effectiveness of antitumor therapy. Currently, natural polyphenolic compounds are considered as preparations for the development of selective chemosensitizers. Due to the large number and variety of phenolic compounds, the antitumor properties of many of them have not been studied. In recent years, the regulatory properties of EGCG, the main catechin in green tea, resveratrol, one of the main polyphenols contained in the skin of grapes and red wines, and curcumin, the main curcuminoid that is part of the turmeric root, have been most actively studied (NavaneethaKrishnan et al., 2019). Polyphenols at low micromolar concentrations cause a protective antioxidant effect. At high concentrations, polyphenolic compounds exhibit pro-oxidant and cytotoxic properties. At the same concentrations in tumor and normal cells, polyphenols can induce oppositely directed effects (Oalđe Pavlović et al., 2021).

EGCG inhibits ROS generation in normal epithelial cells but induces ROS generation in tumor cells. In transformed cells, EGCG activates a mitochondria-mediated pathway of cell death, accompanied by the generation of ROS, a decrease in the transmembrane mitochondrial potential, and the release of apoptotic proteins (Min and Kwon, 2014). Similar results have been obtained in pancreatic cancer, lung cancer, colon cancer, and melanoma cell lines, as well as in breast cancer xenograft animal models (Gan et al., 2018; Khan and Mukhtar, 2018; Ravindran Menon et al., 2021; Romano and Martel, 2021). At concentrations of 5–20 μM, EGCG induced apoptosis only in melanoma cells, without any toxic effect on normal melanocytes (Ravindran Menon et al., 2021). At concentrations of 10–80 mg/ml, EGCG induced apoptosis in hepatocellular carcinoma cells, but not in the normal liver cells (Sojoodi et al., 2020). Sensitization of EGCG tumor cells to the action of a number of antitumor drugs has been shown in both in vitro and in vivo studies. EGCG enhances the effects of doxorubicin, 5-fluorouracil, cisplatin, trizenox (As2O3), bortezomib, and etoposide (Lecumberri et al., 2013; Almatroodi et al., 2020; Huang et al., 2020). Among the proposed mechanisms of tumor cell chemosensitization, the key role is played by redox modulation as a result of increased intracellular ROS production. For example, in ovarian cancer cells, EGCG increased cisplatin toxicity three to six fold, including in cisplatin-resistant cells (Zhou et al., 2014). However, the selectivity of the action of the compound in relation to tumor cells is not justified.

Numerous in vitro and in vivo studies have shown high antitumor activity of curcumin (see section “THE EFFECTIVENESS OF POLYPHENOLS”). It has been shown that the antitumor properties of curcumin are realized with the participation of ROS (Wan et al., 2019). It is assumed that curcumin causes ROS-induced decrease in transmembrane mitochondrial potential, resulting in activation of apoptosis (Wan et al., 2019). A number of studies have shown the ability of curcumin to activate autophagy through increased intracellular production of ROS (Tang et al., 2021). When autophagy is activated, mitochondria are the main source of ROS. At the same time, it is known that the functional relationship between apoptosis and autophagy is complex, that is, in some cases, autophagy is part of the cellular adaptation mechanism that protects cells from apoptosis, while in other conditions, autophagy can cause cell death or initiate apoptosis (Maiuri et al., 2007). It has recently been found that the molecular mechanism of sensitization of MCF-7 cells to the action of paclitaxel and adrenomycin by curcumin involves inhibition of the flap structure-specific endonuclease 1 (Fen1) endonuclease with the participation of ROS and NF-E2–related factor 2 (Nrf2) (Chen et al., 2014).

During therapy, resveratrol sensitizes tumor cells to the action of radiation therapy, cisplatin, doxorubicin, paclitaxel, and bortezamib (Fu et al., 2021; Ren et al., 2021). Synergy of action has been observed with the combined use of resveratrol and curcumin in relation to breast cancer, colon cancer, lung cancer and hepatocellular cancer (Niedzwiecki et al., 2016; Pavan et al., 2016; Arena et al., 2021). An increase in intracellular ROS production also plays a key role in the mechanism of cell sensitization under the action of resveratrol. It has been shown that resveratrol increases the sensitivity of pancreatic cancer cells as a result of Nrf2 activation and increased ROS production (Cheng et al., 2018). It is important to note that during radio- and chemotherapy, resveratrol protects normal cells from radiation damage and the toxic effects of chemotherapy drugs.

Man consumes polyphenolic compounds throughout the evolutionary process, and these substances have been and remain a constantly present component of the internal environment of the body. Once in the body, they are involved in numerous processes of cell signaling, gene expression and various metabolic functions. Polyphenolic compounds, in particular flavonoids, are sometimes an inconspicuous but necessary link in the assembly and functioning of proteins, in the formation of biological membranes, and in the transmission of information in the cell. Being always available, they serve as helpers in many processes. It can be hoped that further research on polyphenols will make it possible to make many interesting discoveries, and the creation of artificial derivatives of flavonoids will make it possible to obtain new effective medicinal substances.

Targeting the stage of oncogenesis and development of tumors with polyphenolic compounds is a promising strategy for their use in both prevention and treatment (including increasing sensitivity to chemotherapy) of tumors. Data published in the literature that meet the requirements of evidence-based medicine confirm the beneficial effect of turmeric and rosemary with a high content of polyphenols, such as curcumin and carnazole acid, in pathological disorders in the body’s division processes, in particular, in oncological processes. Studies of the action of flavonoids show their ability to influence various life processes, both individual cells and the body as a whole. Although epidemiological studies of the relationship between the spread of cancer and the consumption of flavonoids have not yielded unambiguous results, in experimental conditions in vitro and in vivo, as well as in studies of volunteers, quite convincing evidence has been obtained of the promise of the use of certain flavonoids in the prevention and even in the treatment of tumors.