Panax ginseng is a plant that has been used in traditional medicine in China for thousands of years. It is used as a general tonic or adaptogen with chronically ill patients and is frequently featured in traditional medicine prescriptions from China, Japan, and Korea used by cancer patients. The putative active compounds are the ginsenosides, of which there are more than two dozen. These compounds are found in both Panax ginseng and in other Panax species that are used in herbal medicine. Analysis of ginsenosides is being used in developing quality control assessments for ginseng, which has frequently been adulterated due to its high cost; many currently available standardized extracts do appear to contain the amounts of ginsenosides listed on package labeling. The toxicity of ginseng appears to be low: some of the reports of toxic episodes of ginseng may actually pertain to other components of multicomponent preparations. Very low incidence of toxicity has been observed in ginseng clinical trials using well-characterized preparations. Numerous pharmacological activities of ginseng and the ginsenosides have been explored: the authors review here the activities relating to cancer. Immune system modulation, antistress activities, and antihyperglycemic activities are among the most notable features of ginseng noted in laboratory and clinical analyses. Much testing has been done in humans to explore ginseng's purported antifatigue properties, but this area remains controversial. A number of investigations point to antitumor properties and other pharmacological activities related to cancer, but no trials have yet confirmed a clinically significant anticancer activity. Cancer patients may empirically find ginseng to be useful when they are fatigued, although clinical trials should be conducted to confirm its benefits.

We demonstrate an atomic layer deposition of TiO2 thin films on self-assembled monolayers of ω-functionalized alkanethiolates. The TiO2 thin films were grown on OH-terminated alkanethiolate monolayer-coated gold by atomic layer deposition at 100 °C. The atomic layer deposition of the TiO2 thin films is self-controlled and extremely linear relative to the number of cycles. Selective deposition of the TiO2 thin film using atomic layer deposition was accomplished with patterned self-assembled monolayers as templates. Microcontact printing was done to prepare the patterned monolayers of the alkanethiolates on gold substrates. The selective atomic layer deposition is based on the fact that the TiO2 thin film is selectively deposited only on the regions exposing OH-terminated alkanethiolate monolayers of the gold substrates, because the regions covered with CH3-terminated monolayers do not have any functional group to react with precursors.

A new cinnamylphenol, macharistol (1), along with a known pterocarpan, (+)-medicarpin (2), were isolated as cytotoxic constituents from the stems of Machaerium aristulatum. In addition, a known pterocarpan, (+)-maackiain (3), and a known isoflavone, formononetin (4), were identified as inactive constituents. Compound 1 was evaluated in the in vivo hollow fiber assay with KB, Col-2, and hTERT-RPE1 cells and found to be inactive at the highest dose (25 mg/kg body weight) tested.

Vatdiospyroidol (1), a novel cytotoxic resveratrol tetramer, was isolated from the stems of Vatica diospyroides Sym. (Dipterocarpaceae) by bioassay-guided fractionation monitored with a human oral epidermoid carcinoma (KB) cell line. Another novel resveratrol tetramer, vaticaphenol A (2), was obtained as a noncytotoxic constituent, along with the known compounds, bergenin, betulin, betulinic acid, mangiferonic acid, and (E)-resveratrol 3-O-β-d-glucopyranoside. The structures of compounds 1 and 2 were elucidated by spectral analysis, including 1D and 2D NMR experiments, and by molecular modeling.

The potential antitumor activity of timosaponin A-III (1), a steroidal saponin from the rhizomes of Anemarrhena asphodeloides, was investigated in human colorectal cancer HCT-15 cells both in cell culture and in an in vivo murine xenograft model. Compound 1 inhibited the proliferation of cancer cells with cell-cycle arrest and induction of apoptosis. Cell-cycle arrest in the G0/G1 and G2/M phase by 1 was correlated with the down-regulation of cyclin A, cyclin B1, cyclin-dependent kinase 2 (CDK2), CDK4, proliferating cell nuclear antigen, and c-Myc. The increase of the sub-G1 peak by 1 was also closely related to the induction of apoptosis, which was evidenced by the induction of DNA fragmentation, activation of caspases, induction of cleaved poly-(ADP ribose) polymerase, and suppression of Bcl-xL and Bcl-2 expression. In an in vivo xenograft model, treatment with 1 (2 or 5 mg/kg body weight, three times/week, ip administration) for four weeks significantly suppressed tumor growth in athymic nude mice bearing HCT-15 cells, without any overt toxicity. Cell-cycle arrest and induction of apoptosis might be plausible mechanisms of actions for the observed antineoplastic activity of 1.

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