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[DNA damage and anticancer effect].

In a sense, cancer chemotherapy is similar to antibacterial chemotherapy. The main target for both chemotherapies is on DNA and its precursors. Whenever anticancer drugs exhibit its activity on cancer cells, damage or metabolic abnormality of DNA is usually accompanied. Among various anticancer drugs, the main cellular target of alkylating agents or anticancer antibiotics is DNA strand, and many of newly introduced anticancer drugs exert effect on DNA strand or DNA synthesis. The mechanism of action of quinocarmycin, KT 6149, which is a derivative of mitomycin C, YM534, which shows thrombocyte agglutination activity, and MCNU, a nitrosourea, were studied for their antitumor action and damage to DNA strand. It was found that there was a close relationship between anticancer effect and single strand scission of DNA in all the agents tested.

Animals↗

[Problems in the development of analogs of anticancer drugs].

Undoubtedly the progress of cancer chemotherapy is supported by the development of new anticancer drugs. In Japan, there is a tendency to develop anticancer drugs by both chemical modification of the known anticancer drugs (analogues) and finding new structures. However, we have to be cautious to develop analogues of the known anticancer drugs. Before we consider to put these drugs into the clinical trials, several points must be clarified: that is, the new compounds would have any merit or superior points compared to the mother compounds. Especially, we should observe whether or not the new compounds possess any reduction of major toxicities of the mother compounds, how about the situation of cross resistance, anticancer efficacies and particularly the results of toxicology studies. We have limited cancer patients for testing new drugs, and also from ethical view, some easy consideration for developing analogues having minor differences from the mother compounds, must be abandoned.

Antineoplastic Agents↗

[Anticancer activities of a new mitomycin derivative KW 2149, against human tumors xenografted into nude mice].

Anticancer activity of KW 2149, a new derivative of mitomycin C (MMC), was investigated using 4 human tumors xenografted into nude mice. The basic methodology was essentially the same with NCI's therapeutic protocol. For the comparative study, KW 2149 or MMC was administered intraperitoneally at a schedule of q4d X 3. Daily doses were determined as a 1/3, 1/4 and 1/5 of LD50 value of each anticancer agent (7.5 mg/kg, 5.6 mg/kg and 4.5 mg/kg for KW 2149, and 2.7 mg/kg, 2.1 mg/kg and 1.7 mg/kg for MMC). Anticancer activity of KW 2149 seemed to be dependent on the doses. Comparing with MMC, KW 2149 produced higher response rates at the doses of 1/3 and 1/4 of LD50 and was less toxic judging from the decrease of the body weight. This study may indicate an utility of KW 2149, as a new anticancer agents, or suggest the difference of anticancer activities between these two agents.

Adenocarcinoma↗

[Drug interactions with anticancer agents].

Each anticancer agent has its own pharmacologic activities. Effect of anticancer agent may be influenced by the concomitant administration of another drug. In addition, patients with advanced cancer occasionally require other medications as well. These drugs can alter both the effects and adverse reactions of anticancer agents. Therefore, much attention must be placed on the interaction with anticancer agents. This paper summarizes drug interactions between anticancer agents and other drugs. Furthermore, clinical significance of these interactions will be discussed. It is hoped that this paper will provide more attention for the study of this problem.

Allopurinol↗

Separation of hemolytic substances from anticancer preparations of hemolytic streptococci.

Preparations 60F and 50F isolated from the cell-free extract of anticancer hemolytic streptococci possessed not only anticancer activity but hemolytic activity. Thus, the experiment to separate hemolytic substances from 60F and 50F were carried out. Three kinds of fractions were obtained from 60F or 50F by dissolving them in ammonium sulfate solutions of various concentrations. These fractions were named 60F-I, 60F-II and 60F-III, and 50F-I, 50F-II and 50F-III, respectively. 60F-I and 50F-I possessed neither anticancer activity nor hemolytic activity. 60F-II and 50F-II possessed only anticancer activity, and 60F-III and 50F-III possessed only hemolytic activity. Thus, hemolytic substances were separated from 60F and 50F, and it was demonstrated that the anticancer activity of hemolytic streptococci was not due to their hemolysins or hemolytic activity.

Ammonium Sulfate↗

[Clinical effects of total-body hyperthermia combined with anticancer chemotherapy for far-advanced cancer].

We treated 27 patients with far-advanced cancer with extracorporeally induced total-body hyperthermia combined with anticancer chemotherapy (TBHC). All of them under went unsuccessful anticancer chemotherapy. Excluding 7 patients who could not be evaluated, a partial response was obtained in 7 of 20 patients (35%). Considering that the patients in our series were in the terminal stage of cancer, our results are encouraging. However, despite the regression of the mass in some patients, the survival time after TBHC was not always prolonged. A characteristic complication of TBHC was the weakness of the muscles in the lower extremities. The occurrence of muscle weakness could be prevented by administration of phosphate. To improve the therapeutic effects of TBHC, there are some problems to be solved. In combined anticancer chemotherapy, the selection of anticancer drugs and the timing of their administration are of importance. Thus, the optimal heating method and the combined anticancer chemotherapy are the areas requiring further study to determine the clinical efficacy of TBHC in patients.

Animals↗

Assessment of anti-tumor cell effect of human leukocyte interferon in combination with anticancer agents by a convenient assay system in monolayer cell culture.

Cell growth inhibition by anticancer agents was determined by a simple dye-uptake method. This technique could be performed more easily and rapidly than the cell counting method, the method for measurement of 3H-thymidine incorporation, or other dye-uptake methods. The number of viable cells was linearly correlated with the amount of dye taken by the surviving cells, so that the method described in this article could be applied to the assessment of anti-tumor cell effects of human leukocyte interferon (Hu IFN-alpha) in combination with anticancer agents. In combinations of Hu IFN-alpha with anticancer agents such as bleomycin, mitomycin C, and cytosine arabinoside in certain concentration ranges, antagonism was noticed when Hu IFN-alpha and anticancer agents were added simultaneously to the cell culture. However, outside those ranges of concentration, additive effects were observed. Furthermore, the treatment of the cell with IFN followed by the anticancer agents and vice versa showed additive effects.

Antibiotics, Antineoplastic↗

[A study on sensitivity testing of ovarian cancer cells to anticancer chemotherapy - with special reference to the use of LDH and its isozymes as indicators (author's transl)].

The malignant ovarian cancer cells removed on operation were cultured and exposed to the anticancer drug (either 5-fluorouracil or mitomycin C) for 30 minutes or 24 hours respectively. The activity of the LDH and LDH isozyme in the culture medium was measured. Also the activity of the LDH and its isozyme was determined in the patients undergoing chemotherapy with either 5-fluorouracil or mitomycin C. The results are summarized as follows: 1) The LDH isozyme pattern of the culture medium prior to exposure of malignant cells to the anticancer drugs was classified into 2 types i.e., M type which is characterized by a predominance of LDH4,5 (referred hereinafter to as group M) and H type with a predominance of LDH1,2 (referred to as group H). 2) Of 11 cases studied, 7 were classified as group M and 4 were categorized as group H. there was no distinct relationship between histological type and LDH isozyme pattern. 3) In the group with exposure to anticancer drugs the total LDH activity in both group H and group M was lower than in the control group. Control specimens in group H showed increased total LDH activity. 4) The H/M ratio based on subunits of LDH isozyme was virtually unchanged by exposure to anticancer drugs in group M, while rapidly lowered by the same treatment in group H. 5) The death rate of malignant cells as estimated by dye exclusion methods was higher with exposure to anticancer drugs than without it. 6) The serum LDH was more markedly lowered after treatment in group H than in group M. However, there was no substantial difference between the two groups in M/H ratio before and after treatment.

Antineoplastic Agents↗

[Treatment of cancer by intraperitoneal infusion of anticancer drugs using an anti-adhesion sheet connected with a subcutaneously implanted reservoir].

Intraperitoneal infusion of anticancer drugs via a catheter fitted with a subcutaneously implanted reservoir, when repeated frequently, usually becomes increasingly more difficult to perform owing to the catheter's becoming more and more clogged. Moreover, intraperitoneally administered anticancer drugs give rise to severe intestinal adhesions, which in turn interfere with rapid, even and widespread diffusion of the infused drugs in the peritoneal cavity. With the aim of overcoming the difficulties and inconveniences with conventionally used apparatuses for the intraperitoneal administration of drugs, we tentatively manufactured a new apparatus for intraperitoneal drug infusion. A special protective sheet, devised by Tanaka, for the prevention of postoperative intestinal adhesion following abdominal surgery, is connected with a reservoir to be implanted in the subcutis. The apparatus is inserted into the peritoneal cavity of gastric patients with peritoneal dissemination to allow it to remain in place therein. Treatment with anticancer drugs administered intraperitoneally with the use of this device proved apparently more successful than without it, resulting in improvement of QOL, disappearance of ascites, shrinkage in the size of tumor mass and depressed serum levels of a tumor marker, CA 19-9. The sheet was thus found to have the advantages of permitting safe repeated administration of anticancer drugs, even and extensive drug delivery to the peritoneal cavity, sampling of intraperitoneal cancer cells and ascitic fluid without inconvenience, and easy-to-perform continual infusion of anticancer drugs at the outpatient service.

Adenocarcinoma↗

An anticancer drug-sensitive murine erythroleukemia clone: implications for the mechanism of action of antineoplastic drugs.

The mechanism(s) by which anticancer drugs kill tumor cells remains obscure. The studies reported here were undertaken with the view that the mechanism may be understood in part through an analysis of anticancer drug-sensitive clones. We have isolated a murine (Friend) erythroleukemia clone in which drug sensitivity was correlated with increased differentiation, suggesting that anticancer drug-induced cell death may be based on differentiation or a differentiation-dependent mechanism. In addition, this clone showed a high propensity for constitutive differentiation and frequent appearance of large multinucleate cells. Morphologically similar large aberrant cells were observed after the treatment of parental (745A) cells with Adriamycin (or bleomycin). We attribute these morphological defects occurring in clone 3-1 or in the parental cell line after anticancer drug treatment to a defective or inhibited cell cycle function. We suggest that the putative cell cycle defect in clone 3-1 is coupled to the increased drug-induced differentiation and resulting cell death. From a broader perspective, the studies reported here suggest that the search for and design of new anticancer drugs be directed at agents that modulate differentiation functions.

Animals↗

Induction of apoptosis in HL60 leukemic cells by anticancer drugs in combination with anti-Fas monoclonal antibody.

Some anticancer drugs kill tumor cells through the mechanism of apoptosis. Fas antigen has been generally noticed as an apoptosis-signalling receptor molecule on the surface of different cells. Recently, it has become clear that some tumor cells express Fas antigen on their surface, and apoptosis is induced in those cells by IgM-anti-Fas monoclonal antibody (IgM-anti-Fas MoAb). If it is possible to induce apoptosis in tumor cells effectively by anticancer drugs in combination with IgM-anti-Fas MoAb, then we may be able to develop a new strategy for cancer chemotherapy. HL60 human leukemic cell line was incubated with anticancer drugs adriamycin (ADM) or cytosine arabinoside (Ara-C) at different doses alone and in combination with IgM-anti-Fas MoAb. We then observed the morphologic changes of tumor cells, the DNA fragmentation by agarose gel electrophoresis, and the changes in the amount of Fas antigen expression in their cell surface by using flow cytometry. In ADM- or Ara-C-treated tumor cells, apoptotic cells increased in number time- and dose-dependently. By the combination of ADM or Ara-C with IgM-anti-Fas MoAb, the induction of apoptosis in HL60 cells was enhanced significantly. The DNA electrophoresis supported those results. The amount of Fas antigen expression was slightly increased only in cells treated with a low dose of Ara-C, not in others. Our results suggest that apoptosis is a major process of leukemic cell death induced by anticancer drugs. Furthermore, it has become clear that the combination of anticancer drugs with IgM-anti-Fas MoAb enhances leukemic cell death through apoptosis in vitro, though the mechanism remains to be resolved.

Antibodies, Monoclonal↗

Artificial intelligence for anticancer drug discovery from natural products of macroalgae and sponges: A systematic review.

Marine natural products (MNPs) from macroalgae and marine sponges have inspired clinically important anticancer agents, including the cytarabine pharmacophore and the eribulin scaffold, while cyanobacterial dolastatin chemistry supplies the auristatin payloads of several marine-inspired antibody-drug conjugates (ADCs) such as brentuximab vedotin. Artificial intelligence (AI) methods, encompassing both classical machine learning (ML) with hand-engineered features and modern deep learning (DL) with many-layered neural networks, are increasingly supporting key decisions in natural-product anticancer drug discovery, including bioactivity prediction, target identification, absorption, distribution, metabolism, excretion and toxicity (ADMET) filtering, generative analogue design, and the selection of preclinical candidates. DL architectures relevant to this field include graph neural networks, transformer-based molecular generators, diffusion models for protein-ligand docking, and convolutional networks for mass spectrometry, while classical ML contributes interpretable fingerprint-based bioactivity models and molecular networking for dereplication. This review follows a systematic literature review methodology to organize the landscape of AI methods now applied to MNP anticancer discovery, distinguishing ML and DL approaches where relevant, situating them within the chemical context of macroalgal and sponge-derived oncology leads, and critically examining published case studies, including validation level (computational, in vitro, in vivo, clinical). The principal bottleneck for medical translation has shifted partly from algorithmic capability toward data infrastructure and experimental validation. Sparse, heterogeneous, and taxonomically biased bioactivity records limit what current models can learn and reduce the reliability of AI-prioritized candidates entering the preclinical pipeline. A roadmap is proposed that prioritizes open MNP-specific benchmarks, symbiont-aware modeling, and active learning loops with synthesizability and ADMET constraints. These AI workflows may accelerate the prioritization of marine-derived anticancer leads and support earlier, more evidence-based translational decisions in oncology drug development.

Biological Products↗

Anticancer drug activity in human bladder tumor cell lines.

A panel of ten human bladder tumor cell lines were tested for drug sensitivity to ten standard or investigational anticancer drugs using a tumor colony assay. The activity of these anticancer agents in vitro was then compared with the clinical activity of these agents in bladder cancer. Drug activity was found in only five of the ten cell lines. In only 9 of 100 drug assays was the inhibition of colony growth lower than 30% of the controls. The activity of the more active anticancer drugs in bladder cancer (i.e., methotrexate and cisplatin) was not predicted using the tumor colony assay. Overall, the low level of activity of most anticancer drugs tested paralleled the clinical experience of drug resistance found in human bladder cancer.

Antineoplastic Agents↗

Recent advances in understanding the cell death pathways activated by anticancer therapy.

Over the past two decades, the role of apoptosis in the cytotoxicity of anticancer drugs has become clear. Apoptosis may occur via a death receptor-dependent (extrinsic) or independent (intrinsic or mitochondrial) pathway. Mitochondria play a central role in cell death in response to DNA damage, and mediate the interaction(s) of various cytoplasmic organelles, including the endoplasmic reticulum, Golgi apparatus, and lysosomes. The mitochondrial pathway of cell death is mediated by Bcl-2 family proteins, a group of antiapoptotic and proapoptotic proteins that regulate the passage of small molecules, such as cytochrome c, Smac/Diablo, and apoptosis-inducing factor, which activates caspase cascades, through the mitochondrial transition pore. In addition, apoptosis can induce autophagic cell death via crosstalk between the two pathways upon treatment with anticancer drugs. The current review focused on recent advances surrounding the mechanism(s) of cell death induced by anticancer agents and discussed potential molecular targets for enhancing the chemotherapeutic effect(s) of anticancer agents.

Animals↗

Platinum-based anticancer agents: innovative design strategies and biological perspectives.

The impact of cisplatin on cancer chemotherapy cannot be denied. Over the past 20 years, much effort has been dedicated to discover new platinum-based anticancer agents that are superior to cisplatin or its analogue, carboplatin. Most structural modifications are based on changing one or both of the ligand types coordinated to platinum. Altering the leaving group can influence tissue and intracellular distribution of the drug, whereas the carrier ligand usually determines the structure of adducts formed with DNA. DNA-Pt adducts produced by cisplatin and many of its classical analogues are almost identical, and would explain their similar patterns of tumor sensitivity and susceptibility to resistance. Recently some highly innovative design strategies have emerged, aimed at overcoming platinum resistance and/or to introduce novel mechanisms of antitumor action. Platinum compounds bearing the 1,2-diaminocyclohexane carrier ligand; and those of multinuclear Pt complexes giving rise to radically different DNA-Pt adducts, have resulted in novel anticancer agents capable of circumventing cisplatin resistance. Other strategies have focused on integrating biologically active ligands with platinum moieties intended to selectively localizing the anticancer properties. With the rapid advance in molecular biology, combined with innovation, it is possible new Pt-based anticancer agents will materialize in the near future.

Animals↗

Involvement of c-Jun NH(2)-terminal kinase pathway in differential regulation of heat shock proteins by anticancer drugs.

In the present study, we examined the modulation of heat shock factor 1 (HSF1) activity and expression of heat shock proteins (HSPs) after exposure to anticancer drugs. Anticancer drugs induced HSF1 DNA-binding activity, and this was followed by an increase of mitochondrial HSP75 and HSP60 levels and concurrent decrease of cytoplasmic HSP70 levels. Unlike heat shock-induced full phosphorylation, HSF1 was partially phosphorylated after exposure to vincristine, and this result was tightly correlated with the kinetics of JNK/SAPK activation, and up-regulation of mitochondrial HSP75 level and concurrent down-regulation of HSP70. Furthermore, the dominant-negative mutant of SEK1 blocked the phosphorylation of HSF1 and up-regulation of mitochondrial HSP75 in response to vincristine or vinblastine. These data suggest that anticancer drugs regulate the HSF1 transcriptional activity differently from heat shock, and JNK/SAPK pathway appears to be involved in anticancer drug-induced HSF1 phosphorylation and consequently differential regulation of mitochondrial HSP75 and HSP60 and cytoplasmic HSP70.

Animals↗

Antitumor efficacy of seventeen anticancer drugs in human breast cancer xenograft (MX-1) transplanted in nude mice.

To validate the usefulness of a human tumor-nude mice xenograft system as a potential model in the secondary screening of anticancer agents, the antitumor activity of 17 anticancer drugs has been studied in the treatment of a human breast cancer tumor (MX-1) transplanted to nude mice. For evaluation of the antitumor activity of the drugs we employed the LD10 predetermined in BDF1 mice as a standard therapeutic dose. Drugs were administered IV, IP, or PO, and antitumor activity was assessed by drug-induced growth inhibition measured by caliper. Among the 17 anticancer drugs, the most active compounds (maximum inhibition rate of tumor growth: greater than or equal to 90%) are mitomycin C, chromomycin A3, vincristine, vinblastine, vindesine, and hexamethylmelamine. Another group of compounds showed moderate activity (maximum inhibition rate of tumor growth: 89%-50%), these being adriamycin, daunomycin, mitoxantrone, bleomycin, 5-FU, 6-TG, and ftorafur. The remaining four drugs (peplomycin, cytosine arabinoside, 6-MP, and methotrexate) were inactive against the MX-1 tumor. These results suggested that in the nude mouse-human tumor xenograft system of the MX-1 tumor there was a good correlation between the antitumor activity of various anticancer drugs and their clinical efficacy; this system is therefore expected to be a useful model for the secondary screening system.

Animals↗

Enhanced radioinduced cytotoxicity of cultured human bladder cancer cells using 43 degrees C hyperthermia or anticancer drugs.

Using a colony-forming technique and 2 human bladder cancer cell lines, T24 and KK-47, the enhanced radioinduced cytotoxicity in combination with 43 degrees C hyperthermia (HPT) or 4 anticancer drugs; bleomycin (BLM), cis-dichlorodiammineplatinum (II) (CDDP), mitomycin C (MMC), carbazilquinone (CQ), has been studied. In the series of both cell lines, the combination of 43 degrees C hyperthermia and irradiation resulted in exceedingly enhanced cytotoxicity. This was characterized by a marked decline of the slope of the radiation dose-survival curve as compared with slope in the combination of each of the anticancer drugs and irradiation. Among the 4 anticancer drugs, BLM was thought to be the most promising agent as a potentiator of the radiotherapy, on the basis of a remarkable decrease in the shoulder portion of the radiation dose-survival curve. The other 3 anticancer drugs showed a certain degree of potentiation of radiosensitivity.

Antineoplastic Agents↗