**2. Pathophysiology of cancer**

**Plant Family**

Olea europrae (Olive)

Panax quinquefolius (North American Ginseng)

Plantago lanceolata (Ribwort plantain)

Podophyllum peltatum (Mayapple)

Polygonatum multiflorum (Tuber fleece flower)

Pyrus malus (Apple)

Rhodiola rosea (Golden root)

Saponaria vaccaria (Cowherb)

Silybum marianum (Milk thistle)

Sonchus arvensis (Perennial sowthistle)

Tanacetum vulgare

(Tansy)

Taraxacum officinale (Dandelions) **Parts**

oil

Leaf

parts

plant

fruit

fruit, seed

plant

parts

leaf

Oleaceae Leaf and

162 Using Old Solutions to New Problems - Natural Drug Discovery in the 21st Century

Araliaceae Root,

Plantaginaceae Aerial

Polygonaceae Whole

Rosaceae Bark and

Asteraceae Dried

Asteraceae Whole

Asteraceae Aerial

Asteraceae Root and

**used Major bioactive compounds Growing**

Ginsenosides and saponins Eastern North

Phenolics and flavonoids Canada, USA 38

Saponin and flavonoid and vitamin A USA 20, 21, 40

Oleuropein, hydroxytyrosol, hydroxytyrosol acetate, luteolin-7-Oglucoside, luteolin-4'-O-glucoside and luteolin, oleic acid and polyphenol

Berberidaceae Rhizome Podophyllotoxins Eastern North

Quercetin, catechin, flavonoid, coumaric and gallic acids, phloridzin

glycosides, cyanogenic glycosides, aryl glycosides, phenylethanoids, phenylpropanoids and their glycosides, flavonoids, flavonlignans, proanthocyanidins and gallic acid

and procyanidin

derivatives

bisdesmosidic saponins

Silymarin-polyphenoic flavolignans (silybin, isosilybin, silychristin, silydianin and taxifoline)

Alkanes, n-alkenes, n-aldehydes and nalcohols, shikimate metabolites, carotenoid-derived compounds, terpenoids, steroids, and phenols

Monoterpenes, sesqueterpenes, and oxygenated sesqueterpenes

Sesquiterpene lactones, triterpenoids, sterols, tannins, alkaloids, inulin, caffeic acid, and flavonoids

Crassulaceae Rhizome Monoterpene alcohols and their

Caryophyllaceae Seed Flavonoids, cyclopeptides, and

**regions**

America

America

North America

Eastern Canada

Western Canada

**Ref**

35, 36, 37

20, 21

39

21

41, 42

43

49

Canada, USA 44, 45

Canada 46, 47

Canada, USA 48

North America

USA 33, 34,

Cancer is a population of abnormal cells which divide without control, with the ability to invade other tissues. Cancer and some of the other chronic diseases share common pathogen‐ esis mechanisms, such as DNA damage, oxidative stress, and chronic inflammation [10]. It is understood that both environmental factors and chemical carcinogens play a key role in the initiation and progression of cancer. Among the major environmental factors are asbestos, polluted air near industrial emission sources, exposure to secondary tobacco smoke, indoor air pollution such as radon, drinking water containing arsenic, chlorination by-products, and other pollutants [11]. Chemicals with carcinogenic activity can be classified as DNA reactive (e.g.: nitrogen mustards, chlorambucil, epoxides, aliphatic halides, aromatic amines), epige‐ netic (e.g.: chlordane, pentachlorophenol, hormones, cyclosporin, purine analogs), dichloro‐ diphenyltrichloroethane, phenobarbital, minerals (e.g.: asbestos), metals (e.g.: arsenic, beryllium, cadmium) and unclassified carcinogens (e.g.: acrylamide, acrylonitrile, dioxane) [12]. DNA-reactive carcinogens act in the target cells of tissue(s) of their carcinogenicity to form DNA adducts that are the basis for neoplastic transformation [12]. Epigenetic carcinogens lack chemical reactivity and hence, do not form DNA adducts. These carcinogens are produced in the target cells of tissue(s) of their carcinogenicity. Effects of epigenetic carcinogens indirectly lead to neoplastic transformation or enhance the development of tumors from cryptogenically transformed cells [12].

Carcinogenesis is a multi-step process consisting of tumor initiation, promotion and progres‐ sion [13]. Cancer initiation can be blocked by activating protective mechanisms, either in the extracellular environment or intracellular environment by modifying trans-membrane transport, modulating metabolism, blocking reactive oxygen and nitrogen species, maintain‐ ing DNA structure, modulating DNA metabolism and repair, and controlling gene expression [10]. Tumor promotion is the second stage of carcinogenesis and is followed by tumor progression. Both stages can be suppressed by inhibiting genotoxic effects, favoring antioxi‐ dant and anti-inflammatory activity, inhibiting proteases and cell proliferation, inducing cell differentiation, modulating apoptosis and signal transduction pathways and protecting intercellular communications [10]. In addition, tumor progression can also be inhibited by affecting the hormonal status and the immune system in various ways and by inhibiting tumor angiogenesis [10].
