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Assessment of the intestinal permeability after a gastrectomy and the oral administration of anticancer drugs in rats: nitric oxide release in response to gut injury.

BACKGROUND: Although intestinal permeability is known to increase in conditions of stress (such as endotoxemia, septic shock, and ischemia-reperfusion), the mechanism of gut barrier dysfunction during chemotherapy remains to be elucidated. We designed an experiment in which a gastrectomy and anticancer drugs were administered to rats to assess the extent of damage or an increase in permeability of the intestinal mucosa. METHODS: The rats were separated into the following groups: group A, no operation without an anticancer drug (control rats); group B, a gastric operation; group C, chemotherapy; and group D, a gastric operation followed by chemotherapy. Six rats were placed in each group. The groups that were given the anticancer drug received 45 mg/kg for 7 and 14 days, respectively. Intestinal permeability was determined by an injection of fluorescein isothiocyanate-dextran (FITC-D) intravenously and the measurement of the amount of FITC-D leakage in the luminal lavage. The plasma nitric oxide concentrations were measured spectrophotometrically by the Griess reaction. The cell surface expression of CD44 in the rat small intestine was evaluated immunohistochemically. RESULTS: During the entire experimental period, the FITC-D levels in the anticancer drug that was administrated to rats (groups C and D) were significantly higher than the levels in groups A and B (P <.001). Similarly, the plasma nitric oxide concentration increased significantly not only in groups C and D but also in group B (P <.05). A linear regression analysis revealed a positive significant correlation between FITC-D and the plasma nitric oxide levels (r = 0.617; P <.001). When the anticancer drug was administered, the intestine histologically revealed so-called mucosal atrophy and a decreased expression of CD44 within the intestinal mucosa. CONCLUSIONS: The administration of anticancer drugs impairs the gut barrier function, possibly by reducing the cell-cell and cell-matrix interactions. This may contribute to the development of hyperpermeability that is induced by an overexpression of nitric oxide.

Administration, Oral↗

Requirement of caspase-3(-like) protease-mediated hydrogen peroxide production for apoptosis induced by various anticancer drugs.

Caspase-3(-like) proteases play important roles in controlling mammalian apoptosis. However, the downstream events from the caspase-3(-like) protease activation to death of cells are still unclear. Previously, we reported that hydrogen peroxide (H2O2) was generated by the activation of caspase-3(-like) proteases in the process of tyrosine kinase inhibitor-induced apoptosis in human small cell lung carcinoma Ms-1 cells. In the present study, we examined whether generation of H2O2 is a critical event for the apoptotic pathway downstream of caspase-3(-like) protease activation by various anticancer drugs. Anticancer drugs such as camptothecin, vinblastine, inostamycin, and adriamycin induced activation of caspase-3(-like) proteases and apoptosis. Generation of H2O2 was commonly detected after treatment with each of the four anticancer drugs, and scavenging of H2O2 caused cells to fail to undergo apoptosis. Moreover, anticancer drug-induced H2O2 production was inhibited not only by an inhibitor of caspase-3(-like) proteases but also by diphenyleneiodonium chloride, an inhibitor of flavonoid-containing enzymes such as NADPH oxidase. However, activation of caspase-3(-like) proteases was not inhibited by diphenyleneiodonium chloride. These findings suggest that activation of caspase-3(-like) proteases by various anticancer drugs causes generation of H2O2 presumably through the activation of NADPH oxidase, thereby inducing apoptosis. Therefore, H2O2 may function as a common mediator for apoptosis induced by various anticancer drugs.

Acetylcysteine↗

Preparation and characterization of a biodegradable drug targeting system for anticancer drug delivery: microsphere-antibody conjugate.

Targeted delivery of anticancer drugs is one of the most actively pursued goals in anticancer chemotherapy. A major disadvantage of anticancer drugs is their lack of selectivity for tumour tissue, which causes severe side effects and results in low cure rates. Any strategy by which a cytotoxic drug is targeted to the tumour, thus increasing the therapeutic index of the drug, is a way of improving cancer chemotherapy and minimizing systematic toxicity. This study covers the preparation of the gelatin microsphere (GM)-anti-bovine serum albumin (anti-BSA) conjugate for the development of a drug targeting approach for anticancer drug delivery. Microspheres of 5% (w/v) gelatin content were prepared by crosslinking with glutaraldehyde (GTA) at 0.05 and 0.50% (v/v) concentration. Microspheres were in the size range of 71-141?microm. The suitability of these microspheres as drug carriers for anticancer drug delivery was investigated in vitro by studying the release profiles of loaded methotrexate (MTX) and 5-fluorouracil (5-FU) and the cytotoxicities on cancer cell lines. The in vitro MTX release profiles (approximately 22-46% released in 24 h depending on the amount of GTA used) were much slower compared to 5-FU (approximately 42-91% released in 24 h). Both drugs demonstrated an initial fast release, which was followed by gradual, sustained drug release. The MTT cytotoxicity test results of GMs loaded with 5-FU and MTX showed approximately 54-70% and approximately 52-67% cytotoxicities in 4 days. In general, incorporation of MTX and 5-FU in microspheres enhanced the cytotoxic effect in a more prolonged manner compared to the free drugs. Gelatin micospheres were chemically conjugated to anti-BSA and the antigen-antibody activities were studied by immunofluorescence. Results indicated approximately 80% binding with conjugated anti-BSA and BSA-FITC. Based on their low cytotoxicity and the high antigen binding efficiencies, anti-BSA conjugated gelatin microspheres could be suitable targeted drug carrier systems for selective and long-term delivery of anticancer drugs to a specific body compartment (i.e. bladder cancer).

Antibodies↗

Modulating blood-brain barrier interactions of amino acid-based anticancer agents.

The large neutral amino acid (LNAA) transporter at the blood-brain barrier (BBB) mediates brain uptake of amino acid-based anticancer agents (e.g., melphalan and acivicin). In this study, we blocked the amino acid terminus of the anticancer agents using a bioreductive drug delivery system (TDDS). This molecular modification of the anticancer agents is expected to prevent LNAA carrier-mediated transport across the BBB. In this study, we demonstrate that the parent amino acid containing anticancer agents are substrates for the LNAA transporter at the BBB, whereas the TDDS is not recognized by the LNAA transporter. An in situ rat brain perfusion technique was used to determine competition for LNAA carrier-mediated transport at the BBB using [14C]L-leucine. The BBB capillary permeability-surface area (PA) product for the radiotracer [14C]L-leucine (control) was determined to be 5.18 +/- 0.32 x 10(-2) ml/s/g (100%). The control PA value for [14C]L-leucine was competitively inhibited (down to 7-18% of control) by excess L-phenylalanine as well as by excess concentration of the anticancer amino acids, melphalan and acivicin, showing competition for the LNAA transporter at the BBB. In contrast, brain perfusion of [14C]L-leucine in presence of excess TDDS resulted in no competition for brain uptake of [14C]L-leucine via the LNAA transporter. Thus, bioreversible derivatization of the parent anticancer amino acids resulted in blocking the amino acid functional group, thereby leading to loss of recognition for the cerebrovascular LNAA transporter at the BBB.

Algorithms↗

Correlation between expression of oncogene products and resistance to anticancer drugs in cultured ovarian cancer cell lines.

Despite recent advances in the application of chemotherapy to ovarian cancer, the development of alternative therapies that retain activity against drug-resistant-tumors remains a high priority. We analyzed a number of cultured ovarian cancer cell lines of different tissue types for the presence or absence of sensitivity to various anticancer drugs as well as expression patterns of oncogene products (erbB-2, EGFR, bcl-2). As a result, we identified oncogene products that were related to resistance. Using 9 cultured cell lines of ovarian cancers (serous, mucinous, endometrioid, clear, undifferentiated), sensitivities to anticancer drugs were investigated using the MTT assay. The phenotypes of oncogene products expressed by the above cultured cell lines were analyzed by Western blotting. The oncogene products involved in resistance to anticancer drugs were identified by multivariate analysis. Positive correlation between the resistance to anticancer drugs and the oncogene products was obtained by multivariate analysis for (a) CDDP and erbB-2 (b) x p-16 and erbB-2, and (c) MMC and EGFR. Correlation between resistance to anticancer drugs and expression of certain oncogene products was obtained in ovarian cancers, suggesting that sensitivity to anticancer drugs could be predicated prior to chemotherapy.

Adenocarcinoma, Clear Cell↗

Selective modulation of the therapeutic efficacy of anticancer drugs by selenium containing compounds against human tumor xenografts.

PURPOSE: Studies were carried out in athymic nude mice bearing human squamous cell carcinoma of the head and neck (FaDu and A253) and colon carcinoma (HCT-8 and HT-29) xenografts to evaluate the potential role of selenium-containing compounds as selective modulators of the toxicity and antitumor activity of selected anticancer drugs with particular emphasis on irinotecan, a topoisomerase I poison. EXPERIMENTAL DESIGN: Antitumor activity and toxicity were evaluated using nontoxic doses (0.2 mg/mouse/day) and schedule (14-28 days) of the selenium-containing compounds, 5-methylselenocysteine and seleno-L-methionine, administered orally to nude mice daily for 7 days before i.v. administration of anticancer drugs, with continued selenium treatment for 7-21 days, depending on anticancer drugs under evaluation. Several doses of anticancer drugs were used, including the maximum tolerated dose (MTD) and toxic doses. Although many chemotherapeutic agents were evaluated for toxicity protection by selenium, data on antitumor activity were primarily obtained using the MTD, 2 x MTD, and 3 x MTD of weekly x4 schedule of irinotecan. RESULTS: Selenium was highly protective against toxicity induced by a variety of chemotherapeutic agents. Furthermore, selenium increased significantly the cure rate of xenografts bearing human tumors that are sensitive (HCT-8 and FaDu) and resistant (HT-29 and A253) to irinotecan. The high cure rate (100%) was achieved in nude mice bearing HCT-8 and FaDu xenografts treated with the MTD of irinotecan (100 mg/kg/week x 4) when combined with selenium. Administration of higher doses of irinotecan (200 and 300 mg/kg/week x 4) was required to achieve high cure rate for HT-29 and A253 xenografts. Administration of these higher doses was possible due to selective protection of normal tissues by selenium. Thus, the use of selenium as selective modulator of the therapeutic efficacy of anticancer drugs is new and novel. CONCLUSIONS: We demonstrated that selenium is a highly effective modulator of the therapeutic efficacy and selectivity of anticancer drugs in nude mice bearing human tumor xenografts of colon carcinoma and squamous cell carcinoma of the head and neck. The observed in vivo synergic interaction is highly dependent on the schedule of selenium.

Administration, Oral↗

Clinical characteristics and treatment responses of tuberculosis in patients with malignancy receiving anticancer chemotherapy.

STUDY OBJECTIVES: The aim of this study was to elucidate the clinical characteristics and treatment responses of tuberculosis developing in patients receiving anticancer chemotherapy. DESIGN: Retrospective case-control study. SETTING: The Seoul National University Hospital, a tertiary referral hospital in South Korea. PATIENTS: From January 1, 2000, to July 31, 2004, patients with tuberculosis detected during the course of anticancer chemotherapy were enrolled as cases. Age- and sex-matched tuberculosis patients without any malignant disease were selected as control subjects. MEASUREMENTS AND RESULTS: Twenty-four patients and 48 control subjects were enrolled. Their mean +/- SD age was 56.3 +/- 14.3 years, and the male-to-female ratio was 3:1. The most common malignancy was gastric cancer (43%). Lymphoma (17%), lung cancer (8%), and head and neck cancer (8%) were also common. In both groups, the lung was the most common site of tuberculosis involvement (87.8% and 79.2%, retrospectively). The presence of scar tissue suggesting old tuberculosis on radiography was more common in patients with tuberculosis receiving anticancer chemotherapy (66.7% vs 43.8%, p = 0.07). No difference in radiographic severity was observed between groups. A regimen based on first-line antituberculosis drugs was started in all subjects. Frequency of completion of the expected antituberculosis chemotherapy was lower in patients with tuberculosis developing with anticancer chemotherapy (58.3% vs 79.2%, p = 0.02), but it was not different after excluding the loss due to progression of underlying malignancies. Bacteriologic/radiographic responses to treatment and toxicity of antituberculosis medication sufficient to change or stop treatment were not different in both groups. CONCLUSIONS: With regard to radiographic and clinical responses to antituberculosis treatment, tuberculosis developing during anticancer chemotherapy is not clinically different from tuberculosis developing in ordinary situations. Findings in this study suggest that anticancer chemotherapy is not an obstacle in treating tuberculosis.

Adult↗

Marine-derived anticancer agents in clinical trials.

Anticancer agents may be derived either from the isolation of an active lead compound occurring spontaneously in nature or by novel chemical synthesis in the laboratory. There are examples of successful drugs being derived from both sources, which have had a profound impact on the natural history of various types of cancer. The treatment of lymphomas and acute leukaemias with the use of combination chemotherapy, including anthracyclines and vinca alkaloids, are examples of the contribution of nature. In contrast, agents such as 5-fluorouracil, methotrexate and more recently, the humanised anti-CD20 antibody rituximab and the tyrosine kinase inhibitor imatinib are examples of synthetic compounds, which were designed with a clear rationale, that are routinely used in patients with solid tumours and haematological malignancies. Until recently, the tradition in natural product-derived anticancer drug development was to rely almost exclusively on the screening of terrestrial sources (plant extracts and fermentation products) for their cytotoxic properties. Although C-nucleosides obtained from Caribbean sponge were the initial inspiration for the synthesis of antiviral substituted nucleosides and the successful anticancer agent citarabine, active against leukaemias and lymphomas, the contribution of marine compounds as a source of anticancer agents was modest. In recent years, the improvements in the technology of deep-sea collection and aquaculture added to the growing recognition of the tremendous biodiversity present in the marine world, and has contributed to the growing interest of exploring the oceans as a potential source of new anticancer candidates. This is reflected in the number of marine-derived compounds undergoing preclinical and early clinical development. In this paper, the authors discuss the available literature on anticancer agents that have reached clinical trials, such as didemnin B, aplidine, dolastatin-10, bryostatin-1 and ecteinascidin-743 (ET-743, trabectedin), as well as other promising compounds still undergoing tests in the laboratory.

Animals↗

Sensitization for anticancer drug-induced apoptosis by betulinic Acid.

We previously described that betulinic acid (BetA), a naturally occurring pentacyclic triterpenoid, induces apoptosis in tumor cells through the mitochondrial pathway. Here, for the first time, we provide evidence that BetA cooperated with anticancer drugs to induce apoptosis and to inhibit clonogenic survival of tumor cells. Combined treatment with BetA and anticancer drugs acted in concert to induce loss of mitochondrial membrane potential and the release of cytochrome c and Smac from mitochondria, resulting in activation of caspases and apoptosis. Overexpression of Bcl-2, which blocked mitochondrial perturbations, also inhibited the cooperative effect of BetA and anticancer drugs, indicating that cooperative interaction involved the mitochondrial pathway. Notably, cooperation of BetA and anticancer drugs was found for various cytotoxic compounds with different modes of action (e.g., doxorubicin, cisplatin, Taxol, VP16, or actino-mycin D). Importantly, BetA and anticancer drugs cooperated to induce apoptosis in different tumor cell lines, including p53 mutant cells, and also in primary tumor cells, but not in human fibroblasts indicating some tumor specificity. These findings indicate that using BetA as sensitizer in chemotherapy-based combination regimens may be a novel strategy to enhance the efficacy of anticancer therapy, which warrants further investigation.

Antineoplastic Combined Chemotherapy Protocols↗

Adaptive control methods for the dose individualisation of anticancer agents.

Numerous studies have found a clear relationship between systemic exposure and the toxicity or (more rarely) the efficacy of anticancer agents. Moreover, the clearance of most of these drugs differs widely between patients. These findings, combined with the narrow therapeutic index of anticancer drugs, suggest that patient outcome would be improved if doses were individualised to achieve a target systemic exposure. Bayesian maximum a posteriori probability (MAP) forecasting is an efficient and robust method for the optimisation of drug therapy, but its use for anticancer drugs is not yet extensive. The aim of this paper is to review the application of population pharmacokinetics and MAP to anticancer drugs and to evaluate whether and when MAP Bayesian estimation improves the clinical benefit of anticancer chemotherapy. For each drug, the relationships between pharmacokinetic variables [e.g. plasma concentration or the area under the concentration-time curve] and pharmacodynamic effects are described. Secondly, the methodologies employed are considered and, finally, the results are analysed in terms of predictive performance as well as, where possible, the impact on clinical end-points. Some studies were retrospective and intended only to evaluate individual pharmacokinetic parameter values using very few blood samples. Among the prospective trials, a few studied the pharmacokinetic/pharmacodynamic relationships which provided the basis for routine pharmacokinetic monitoring. Others were performed in clinical context where MAP Bayesian estimation was used to determine maximum tolerated systemic exposure (e.g. for carboplatin, topotecan, teniposide) or for pharmacokinetic monitoring (e.g. for methotrexate or platinum compounds). Indeed, its flexibility in blood sampling times makes this technique much more applicable than other limited sampling strategies. These examples demonstrate that individual dose adjustment helps manage toxicity. The performance of pharmacokinetic monitoring is linked to the methodology used at each step of its design and application. Moreover, a limitation to the use of pharmacokinetic monitoring for certain anticancer drugs has been the difficulty in obtaining pharmacokinetic or pharmacodynamic data. Recent progress in analytical methods, as well as the development of noninvasive methods (such as positron emission tomography) for evaluating the effects of chemotherapy, will help to define pharmacokinetic-pharmacodynamic relationships. Bayesian estimation is the strategy of choice for performing pharmacokinetic studies, as well as ensuring that a given patient benefits from the desired systemic exposure. Together, these methods could contribute to improving cancer chemotherapy in terms of patient outcome and survival.

Animals↗

Cytochrome P450 and anticancer drugs.

Cytochrome P450 (CYP) is involved in the metabolism of a variety of anticancer drugs. CYP activities are known to be modified by several factors including genetic polymorphisms, changes in physiological conditions such as age, disease status or intake of certain drugs or foods or environmental factors such as smoking. These factors may cause interindividual differences in the pharmacokinetic profiles of anticancer drugs, leading to the variations of efficacy or toxicity of the drugs. Genetic polymorphisms present in CYPs sometimes result in the reduced activity of the enzymes causing low metabolic clearance of drugs or low production of active metabolites. For example, the formation of endoxifen, which is an active metabolite of tamoxifen, was less in patients with inactive polymorphic CYP2D6 than those with the wild type enzyme. CYP3A is the most abundant CYP expressed in the human liver and the small intestine that is involved in the metabolism of various anticancer drugs. The catalytic activity of CYP3A shows a large interindividual variability giving rise to large interindividual differences in the pharmacokinetic profiles of some anticancer drugs. So far, many attempts have been made to monitor the phenotypic activity of CYP3A in order to reduce the pharmacokinetic variations of anticancer drugs. Erythromycin, midazolam and cortisol are commonly used to monitor in vivo hepatic CYP3A activity. These methods have been applied to reduce the pharmacokinetic variations of docetaxel. Drug-drug interactions related to CYPs also modulate the pharmacokinetic profiles of anticancer drugs. These factors should be considered when trying to optimize and individualize chemotherapy.

Animals↗

Flavonoids as anticancer agents: structure-activity relationship study.

The protection against some forms of cancer provided by many common foods has been observed in multiple epidemiological studies. Non-nutritive dietary compounds, such as flavonoids, have been considered as the responsible agents for such observations and since then, much research activity has been done about their potential anticancer effect. As a result, these compounds have been shown to regulate proliferation and cell death pathways leading to cancer. Thus, flavonoids such as the synthetic flavone, flavopiridol; the soy isoflavonoid, genistein; the tea catechin epigallocatechin gallate; or the common dietary flavonol, quercetin, are emerging as prospective anticancer drug candidates and some of them have already entered in clinical trials. In view of the therapeutic potential of flavonoids, many researchers have tried to elucidate possible structure-activity relationships that might lead to new drug discovery. However, and possibly due to the information being very scattered, there is very little understanding about a possible relationship between the flavonoid structure and their anticancer activity. Besides their therapeutic potential, since lots of flavonoids are present in our diet, a greater understanding of their anticancer properties might also modify our dietary habits in order to attack cancer with an effective weapon, prevention. This paper seeks to show, in a brief but comprehensive way, the anticancer properties of flavonoids. Through an understanding of the cancer process and its treatment, flavonoids are studied as possible useful compounds in cancer prevention and cancer therapy. Furthermore, this review attempts to compile and discuss the literature studying structure-activity relationships, in order to show structural requirements implicated in the anticancer activity of flavonoids, which might help to rationalize their development as antitumor agents.

Animals↗

Betulinic acid derivatives as anticancer agents: structure activity relationship.

Betulinic acid, a pentacyclic triterpene, is widely distributed throughout the tropics. It possesses several biological properties such as anticancer, anti-inflammatory, antiviral, antiseptic, antimalarial, spermicidal, antimicrobial, antileshmanial, antihelmentic and antifeedent activities. However, betulinic acid was highly regarded for its anticancer and anti-HIV activities. Anticancer role of betulinic acid appeared by inducing apoptosis in cells irrespective of their p53 status. Due to high order safety in betulinic acid, a number of structural modifications carried out to improve its potency and efficacy. The C-1, C-2, C-3, C-4, C-20 and C-28 positions are the diversity centers in betulinic acid, and the derivatives resulted on various structural modifications at these positions screened for their anticancer activity. This review presents the structure activity relationship carried out on C-1, C-2, C-3, C-4, C-20, C-28, A-ring, D-ring and E-ring modified betulinic acid derivatives. We have compiled the most active betulinic acid derivatives along with their activity profile in each series. Structure activity relationship studies revealed that C-28 carboxylic acid was essential for the cytotoxicity. The halo substituent at C-2 position in betulinic acid enhanced the cytotoxicity. Though the relation of the cytotoxicity with the nature of substituents at C-3 position could not be generalized but the ester functionality appeared to be a better substituent for enhancing the cytotoxicity. An interesting observation is that the three rings skeleton (A, B and C rings) had played an important role in eliciting anticancer activity, which could be a new molecular skeleton to design new anticancer drugs.

Antineoplastic Agents, Phytogenic↗

Dose-dependent metabolism, therapeutic effect, and toxicity of anticancer drugs in man.

Dose-dependent metabolism is seen for a number of anticancer drugs, and they provide examples of several different types of dose-dependent metabolic processes. Arabinosyl cytosine and 5-fluorouracil are drugs whose catabolism is saturated at high doses. Therapeutic response to both drugs has been linked to plasma concentration of parent compound, and a nonlinear dose-response relationships might exist at high doses. L-Alanosine also appears to exhibit saturable metabolism at high doses, and this might be responsible for the rapid onset of L-alanosine toxicity as the dose is increased. Isophosphamide is a drug which requires metabolic activation to exert its biological effect, and saturation of metabolism seen at high dose could lead to a plateau in the dose-response relationship. Thymidine exhibits saturation of metabolism at high doses due in part to product inhibition of metabolism. Product inhibition of metabolism has also been suggested for arabinosyl cytosine. Plasma elimination of thymidine and possible elimination of 6-diazo-5-oxo-L-norleucine exhibit characteristics of a dose-dependent "memory" effect. Dose-dependent metabolism of methotrexate is unusual in that formation of the presumed toxic metabolite increases with increase in dose and is associated with a qualitative change in the pattern of drug toxicity at high compared to low doses of drug. The relationship between dose and toxicity of drugs and other foreign compounds is poorly understood in man. Anticancer drugs are one of the few classes of compounds where the relationship of toxicity to dose is reasonably well documented in human subjects. Saturation of metabolism leading to dose-dependent pharmacokinetics occurs with several anticancer drugs, and different types of dose-dependent metabolism have been covered in this review. An attempt has been made to show how dose-dependent metabolism of anticancer drugs might relate to their toxicity. Principles of dose-dependent toxicity seen with anticancer drugs might usefully be applied to other classes of compounds, particularly compounds exhibiting cytotoxicity but also other forms of toxicity. Dose-dependent metabolism could also be important in determining the therapeutic effect of anticancer drugs, and application of principles of dose-dependent metabolism to the development of new chemotherapeutic regimens migh lead to more effective cancer chemotherapy.

Alanine↗

A rapid in vitro screening system for the identification and evaluation of anticancer drugs.

We report the development of an in vitro screening system that can be used to identify new anticancer drugs that are specifically cytotoxic for dividing cells. The screening system takes advantage of the potential of many cell lines, including tumor cells, to stop dividing when they are plated at high cell density. The cytotoxic effects of anticancer drugs on dividing (i.e., cells plated at low cell density) and nondividing cells (i.e., cells plated at high cell density) is measured by the incorporation of 51Cr. This in vitro system was evaluated by measuring the cytotoxic effects of the anticancer drugs cisplatin, thiotepa, doxorubicin, methotrexate, and vinblastine on the cell lines B/C-N, ME-180, and MCF-7. In this in vitro system the concentrations of the anticancer drugs that produced significant cytotoxicity on only dividing cells are similar to the concentrations that are used clinically. The fact that this in vitro system is rapid, simple, applicable to many cell types, and able to predict effective concentrations of anticancer drugs should make it useful for the screening of new anticancer drugs and for the design of preclinical studies.

Animals↗

Alteration of CDKN2/p16 in human astrocytic tumors is related with increased susceptibility to antimetabolite anticancer agents.

A slowly proliferating cell fraction in tumors shows reduced sensitivity to cell cycle-dependent anticancer agents. To understand the molecular basis of drug resistance observed in brain tumors, we examined the relationship between alteration of p16, a cyclin dependent kinase inhibitor whose functions are frequently lost in many human gliomas, and chemosensitivity of tumor cells to various kinds of anticancer agents. Alterations of the p16 gene that include mutation(s) and homozygous deletion as well as p16 protein expression level, were examined in 56 specimens of astrocytic tumors. Their in vitro chemosensitivities to 30 kinds of anticancer agents were analyzed with flow cytometry which detects drug-induced cell death. We found that the alterations were correlated with increased sensitivity to antimetabolite anticancer agents but not with other kinds of agents, including alkylating agents, antibiotics, topoisomerase inhibitors and antimicrotubule agents. The present results suggest that p16 plays a role in determining chemosensitivity of brain tumors, depending on pharmacological mechanisms of anticancer agents. Proper understanding of the molecular machinery which regulates the chemosensitivity may contribute to the choice of anticancer agents for individual patients.

Antimetabolites, Antineoplastic↗

Effect of inhibitors of cysteine and serine proteases in anticancer drug-induced apoptosis in gastric cancer cells.

Activation of proteases can play an important role in apoptotic cell death induced by anticancer drugs. To assess involvement of activation of cysteine and serine proteases in anticancer drug-induced apoptosis, we tested effect of inhibitors of cysteine and serine proteases on sensitivity to anticancer drugs in MKN45 gastric cancer cells. Cytotoxic effect by adriamycin (ADM), SN-38 (active form of irrinotecan) and cisplatin (CDDP) was significantly prevented by cotreatment with Z-Val-Ala-Asp-fluoromethylketone (Z-VAD-fmk) (p<0.01), a pancaspase inhibitor compared with drug alone using MTT assay. In contrast, cotreatment with N-acetyl-Tyr-Val-Ala-Asp aldehyde (AC-YVAD-CHO), a caspase 1 inhibitor did not prevent any cytotoxic effect of these drugs. Cotreatment of N-acetyl-Asp-Glu-Val-Asp aldehyde (AC-DEVD-CHO), a caspase 3 inhibitor prevented cytotoxic effect of VP-16 and SN-38 (p<0.01). Prevention of these cytotoxic effects by caspase inhibitors was not dose-dependent. Cotreatment of N-tosyl-L-lysyl chloromethylketone (TLCK), a serine protease inhibitor significantly prevented cytotoxic effect of ADM, SN-38, 5-fluorouracil (5-FU) and CDDP in a slight dose-dependent manner (p<0.01) except for etoposide (VP-16) and docetaxel (TXT), while an other serine protease inhibitor, N-tosyl-L-phenylalanyl chloromethylketone (TPCK) did not prevent any anticancer drug-induced cytotoxic effect. These effects were associated with prevention of internucleosomal DNA ladder formation in apoptosis. Further, protease inhibitors did not block induction of cytochrome c, that can explain the partial effect of prevention by anticancer-induced cell death. These results suggest that anticancer drug-induced cytotoxic effect is mediated by activation of serine protease (caspase-independent) as well as caspase-dependent pathway leading to apoptotic cell death, and that protease-independent pathway may also be involved in apoptotic pathways. The involvement of protease in signal transduction pathways may differ in cytotoxic action of drugs in gastric cancer cells.

Antineoplastic Agents↗

Anticancer Drug Development: The Way Forward.

Cancer chemotherapy celebrated its fiftieth anniversary last year. It was in 1945 that wartime research on the nitrogen mustards, which uncovered their potential use in the treatment of leukaemias and other cancers, was first made public. Fifty years later, more than sixty drugs have been registered in the USA for the treatment of cancer, but there are still lessons to be learnt. One problem, paradoxically, is that many anticancer agents produce a response in several different classes of the disease. This means that once a new agent has been shown to be effective in one cancer, much effort is devoted to further investigations of the same drug in various combinations for different disorders. While this approach has led to advances in the treatment of many childhood cancers and some rare diseases, a plethora of studies on metastatic colon cancer, for example, has yielded little benefit. 5-fluorouracil continues to be used in trials, yet there is no evidence for an increase in survival. The lesson to be learnt is that many common cancers are not adequately treated by present-day chemotherapy, and most trials of this sort are a waste of time. Significant increases in survival will only occur if the selectivity of present-day anticancer agents can be increased or new classes of more selective agents can be discovered. There are two fundamental problems in drug development: a lack of suitable laboratory tests and the difficulty of conducting early clinical trials. Firstly, no existing laboratory method can accurately predict which chemical will be effective against a particular class of human cancer. At best, tests can demonstrate a general 'anticancer' property. This is well exemplified by the discovery of cisplatin. The fact that cisplatin caused regression in a number of transplanted rodent tumours created no great excitement amongst chemotherapists. It was only later when it was tested clinically against ovarian cancer that results were sufficiently positive to encourage others to investigate. Only then was it discovered that metastatic teratoma was extraordinarily sensitive to the drug. This finding was made as a result of phase II trials and no laboratory model could have predicted it. The lesson to be learnt is that new drugs should be tested extensively in phase II trials before they are discarded. The second problem concerns early clinical trials. Because new drugs can only be tested against advanced and usually heavily pretreated disease, it is unlikely that dramatic responses will occur. The methods used to detect responses in solid tumours and metastases are crude, and it is likely that many useful drugs are missed. New techniques are needed to detect small but important responses. In addition to these technical problems, clinical trials are expensive and the time required for preclinical pharmacology and toxicology is lengthy. In the early days, drugs could enter clinical trials after fairly simple toxicological studies. The thalidomide disaster in the 1960s, however, led to the setting up of regulatory bodies to scrutinize drugs before clinical trials. This proved detrimental for cancer drug development because a series of fairly long-term tests is now required. These must be carried out in both rodents and one other species, usually the dog. This approach was probably a good thing for most medicines where a large margin of safety is required between the therapeutic dose and the dose which causes side effects, but was inappropriate for anticancer agents which are tested at the maximum possible dose which gives manageable side effects. These new regulations meant that the cost of one clinical trial after the 1970s was equivalent to the cost of ten before that time. Solutions to these problems are available, although to put them into practice would require the cooperation of government regulatory authorities, the pharmaceutical industry and other organisations such as the US National Cancer Institute (NCI), the UK Cancer Research Campaign (CRC) and the European Organisation for Research and Treatment of Cancer (EORTC). Firstly, it is important to switch from clinical trials of analogues and combinations of standard drugs to trials of new classes of anticancer agents. Further, an international effort should be launched whereby these new agents can be rapidly tested in phase II trials against common solid cancers using new techniques to detect small but significant tumour responses. Lead chemicals discovered in this way could then be taken back to the laboratory for further development. There is no shortage of new drugs which act by mechanisms quite different from present-day agents, and new approaches can greatly increase the amount of cytotoxic agents delivered to solid tumours. As long ago as 1980, the CRC introduced protocols which enabled early clinical trials to be carried out rapidly and with minimal cost. These procedures used short-term tests only in rodents to determine a safe starting dose. The test can be completed within six months and around fifty clinical trials using this protocol have been successfully carried out in collaboration with the EORTC. Despite this, the American Food and Drug Administration (FDA), regulatory authorities in many other countries and many drug companies still insist on using a second animal species before a phase I clinical trial is permitted instead of using the money spent to develop several agents with minimal toxicology testing. The EORTC and CRC also plan to introduce positron emission tomographic scanning into early clinical trials as a highly sensitive method of measuring tumour response. Cancer mortality has changed little over the past forty years, mainly because of our failure to develop curative chemotherapy for the common solid cancers. The way forward is to carry out extensive phase I and II clinical trials of the many new types of anticancer agent that have become available as a result of increased knowledge about cancer cells and how they differ from normal tissues. In order to do this, the regulatory authorities must recognize that minimal toxicology protocols are adequate, and drug companies must be persuaded to give more emphasis to the search for new chemotherapeutic agents. A coordinated effort to achieve these aims would be a wonderful way to mark the fiftieth anniversary of modern chemotherapy. Unfortunately the regulatory authorities find it less risky to stick with extensive safety testing rather than to use shortcuts, however well-validated clinically. Many but not all drug companies, mindful of profits, prefer the easy way out and concentrate on analogues, while most clinicians opt for trials of combinations of known agents, being aware that they are worth a publication or two. Reprinted with permission from Helix, Volume V, Issue 1, 1996, pp. 20-21.

Journal Article↗