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PubMed2000

Melphalan and other anticancer modalities up-regulate B7-1 gene expression in tumor cells.

In this study, we show that administration of low-dose melphalan (l -PAM, l -phenylalanine mustard) to mice bearing a large MOPC-315 plasmacytoma led to a rapid up-regulation of B7-1 (CD80), but not B7-2 (CD86), expression on the surface of MOPC-315 tumor cells. This l -PAM-induced preferential up-regulation of B7-1 surface expression was due, at least in part, to a direct effect of l -PAM on the tumor cells, as in vitro exposure of MOPC-315 tumor cells to l -PAM led to the preferential up-regulation of B7-1 surface expression. Moreover, in vitro exposure of MOPC-315 tumor cells to two other anticancer modalities, gamma-irradiation and mitomycin C, resulted in the preferential up-regulation of B7-1 surface expression. This effect was not restricted to MOPC-315 tumor cells, as preferential up-regulation of B7-1 surface expression was observed also following in vitro exposure of the P815 mastocytoma (that is negative for both B7-1 and B7-2 surface expression) to any of the three anticancer modalities. The up-regulation of B7-1 surface expression following in vitro exposure of tumor cells to l -PAM, gamma-irradiation, or mitomycin C required de novo protein and RNA synthesis, and was associated with the accumulation of mRNA for B7-1 within 4-8 h, indicating that the regulation of B7-1 expression is at the RNA transcriptional level. These results have important implications for an additional immune-potentiating mechanism of these anticancer modalities in clinical setting.

Animals↗

PubMed2006

Studies of anticancer and antipyretic activity of Bidens pilosa whole plant.

Screening of different extracts and fractions from the plant Bidens pilosa Linn. var. (Asteraceae) has been conducted using the in-vitro comet assay for anticancer and the antipyretic action, which was done with in-vivo models. The extract from whole plant was extracted with n-hexane, chloroform and methanol extract (E1 - E3). The extracts were fractioned by column chromatography method and fractioned with ethyl acetate, acetone and water (F1 - F3). All the extracts and fractions were tested for anticancer and antipyretic activity. Among extracts E1 shows remarkable anticancer activity and E3 bears maximum antipyretic activity. In the antipyretic activity, paracetamol was used as the standard test drug. The most promising material (LC50 < 1500 microg/ml) was F1 ethyl acetate fractions of methanolic extract and methanolic crude extract of whole plants. However, little correlation was observed in the degree of antipyretic activity between the test drug and standard drug. In conclusion, the extract obtained from the whole plant of Bidens pilosa showed a significant cytotoxic effect to methanolic extract against Hela cells by in vitro method and showed a comparable antipyretic activity effect to paracetamol in rabbit pyrogen test.

Acetates↗

PubMed1990

[Preoperative adjuvant therapy for urinary bladder cancer--preoperative intra-arterial anticancer drugs infusion using artificial liver, and preoperative radiotherapy].

One hundred patients with carcinoma of the urinary bladder were treated with preoperative intra-arterial anticancer drug infusion in combination with an active carbon-based artificial liver or preoperative radiotherapy (400 rad X 5 days, total 2000 rad) in order to alleviate systemic side effects after preoperative adjuvant therapy and to perform radical cystectomy as soon as possible. Five-year survival was 69.8% in the artificial liver combined preoperative intra-arterial anticancer drug infusion group, and that of the no-pretreatment group and the preoperative irradiated group was 48.6% and 45.8%, respectively. In particular, the CDDP treated group had a higher 5-year survival of 77.4% than did the without CDDP treated group. This was attributable mostly to improved prognosis of T2, whereas either of these preoperative adjuvant therapies failed to ameliorate the prognosis of T3 or T4 stage patients. Therefore, systemic preoperative anticancer chemotherapies such as M-VAC are necessary to destroy "micrometastases" and to improve the prognosis of highly advanced bladder cancer.

Adult↗

PubMed1991

[The anticancer effects of high energy shock waves on rat bladder cancer induced by BBN].

The in vivo anticancer effects of high energy shock waves (HESW), on bladder cancer induced by N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN), were studied in the rat using the Siemens lithotriptor (Lithostar). There was no significant difference in the anticancer effects in delaying tumor growth, measured as the whole bladder weight including the weight of the cancer, between the groups with and without exposure to HESW. However, light microscopic examination revealed extensive submucosal bleeding and exfoliation of mucosa, and electron microscopic examination revealed degeneration of pleomorphic microvilli, swelling of mitochondria, and destruction of mitochondrial cristae in the cancer cells in bladders exposed to HESW. Flow cytometric determination of DNA content in the cancer cells exposed to HESW indicated a selective diminution of cells in the G2 and M phases and an increase of cells in the G0 and G1 phases of the cell cycle. While the mechanism of HESW-induced anticancer effect could not be determined on the basis of this study, these changes in the morphology and the cell cycle of cancer cells induced by HESW exposure suggest some kind of biological effects following exposure to HESW. It is expected that HESW be an effective method for the treatment of human cancer in combination with chemotherapy and radiation.

Animals↗

PubMed1999

Activation of the transforming growth factor beta signaling pathway and induction of cytostasis and apoptosis in mammary carcinomas treated with the anticancer agent perillyl alcohol.

The mechanisms of action of the anticancer agent perillyl alcohol (POH), presently in Phase II clinical trials, were investigated in advanced rat mammary carcinomas. Gross and ultrastructural morphology of POH-mediated tumor regression indicated that apoptosis accounted for the marked reduction in the epithelial compartment. Characterization of cell growth and death indices revealed that apoptosis was induced within 48 h of chemotherapy, before the induction of cytostasis. RNA expression studies, based on a multiplexed-nuclease protection assay, demonstrated that cell cycle- and apoptosis-related genes were differentially expressed within 48 h of POH treatment; p21(Cip1/WAF1), bax, bad, and annexin I were induced; cyclin E and cyclin-dependent kinase 2 were repressed; and bcl-2 and p53 were unchanged. Next, a potential role for transforming growth factor beta (TGF-beta) signaling in POH-mediated carcinoma regression was explored. RNA expression studies, again based on a multiplexed-nuclease protection assay, showed that TGF-beta-related genes were induced and temporally regulated during POH treatment: (a) c-jun and c-fos were transiently induced within 12 h of chemotherapy; (b) TGF-beta1 was induced within 24 h of chemotherapy; (c) the mannose 6-phosphate/insulin-like growth factor II receptor and the TGF-beta type I and II receptors were induced within 48 h of chemotherapy; and (d) smad3 was induced during active carcinoma regression. In situ protein expression studies, based on fluorescence-immunohistochemistry in concert with confocal microscopy, confirmed up-regulation and demonstrated colocalization of TGF-beta1, the mannose 6-phosphate/insulin-like growth factor II receptor, the TGF-beta type I and II receptors, and Smad2/Smad3 in epithelial cells. Nuclear localization of Smad2/Smad3 indicated that the TGF-beta signaling pathway was activated in regressing carcinomas. Subpopulations of Smad2/Smad3-positive and apoptotic nuclei colocalized, indicating a role for Smads in apoptosis. Thus, Smads may serve as a potential biomarker for anticancer activity. Importantly, none of the POH-mediated anticancer activities were observed in normal mammary gland.

Animals↗

PubMed1999

Anticancer drugs induce caspase-8/FLICE activation and apoptosis in the absence of CD95 receptor/ligand interaction.

Proteases of the caspase family are the critical executioners of apoptosis. Their activation has been mainly studied upon triggering of death receptors, such as CD95 (Fas/APO-1) and tumor necrosis factor-R1, which recruit caspase-8/FLICE as the most proximal effector to the receptor complex. Because apoptosis induced by anticancer drugs has been proposed to involve CD95/CD95 ligand interaction, we investigated the mechanism of caspase activation by daunorubicin, doxorubicin, etoposide, and mitomycin C. In Jurkat leukemic T cells, all drugs induced apoptosis and the cleavage of procaspase-8 to its active p18 subunit. However, cells resistant to CD95 were equally susceptible to anticancer drugs and activated caspase-8 with a similar kinetic and dose response as CD95-sensitive cells. The broad caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone prevented apoptosis and caspase-8 activation in response to CD95 and drug treatment, whereas a neutralizing CD95 decoy as well as a dominant-negative FADD construct selectively abrogated CD95, but not drug-induced effects. A potent activation of caspase-8 was also induced by cycloheximide, indicating that it was independent of protein synthesis. Our data, therefore, show that (1) anticancer drug-induced apoptosis does not require de novo synthesis of death ligands or CD95 interaction, and (2) that caspase-8 can be activated in the absence of a death receptor signaling.

Amino Acid Chloromethyl Ketones↗

PubMed1998

Role of bio-metal Fe(III) in anticancer effect of dacarbazine.

Physicochemical, Microbial and Pharmacological studies on Fe(III)-Dacarbazine complex have been done in solid and aqueous phase. On the basis of elemental analysis, polarographic studies, amperometric titrations and IR spectral studies the probable formula for the complex has been worked out to be 1:1, Fe(III)-Dacarbazine. The metal ligand interaction has been studied using polarographic method at 25 +/- 1 degrees C and at ionic strength of mu = 1.0 (KCl). Microbial studies on the complex was done against various pathogenic bacteria viz. Pseudomonas mangiferae, Staphylococcus aureus, Salmonella typhi and Vibrio cholarae and fungi i.e. Trichothecium and Chrysosporium sp. using Raper's method. Mouse sarcoma cell line 180 and Balb/C mice were used for the anticancer screening of solid complex in vitro and in vivo respectively. The observed polarographic data, on lingane treatment revealed the formation of single (1:1) (M:L) complex with Fe(III) and dacarbazine ligands. The results of amperometric titrations of Fe(III) with dacarbazine in IM KCl supporting electrolyte pH 7.0 +/- 0.1 supported the above findings the IR data speaks of the complex formation between the metal and the dacarbazine ligand through the two nitrogen one each of primary amide and trizo groups. The results of microbial and pharmacological studies with the M:Drug complex revealed that the anticancer activity of the drug metal complex is nearly doubled as compared to the pure drug. As such Fe(III) dacarbazine complex may be recommended to the therapeutic experts for its possible use as more potent anticancer drug.

Animals↗

PubMed1999

Bis-benzimidazole anticancer agents: targeting human tumour helicases.

Certain DNA minor groove binding agents, distamycin, netropsin, and a series of anticancer bis-benzimidazoles can block DNA helicase activity by binding to duplex DNA at specific base sequences. DNA helicases are crucial to cell DNA replication, transcription and repair because these enzymes separate double-stranded DNA, thereby preparing the strands for enzymatic manipulation. From our studies we have developed a hypothesis that focuses on cellular DNA helicase action as a mechanistic site where these minor groove binders can act. A crucial aspect for modulation of DNA activity by drugs is for specificity and selectivity. A series of DNA-interactive bis-benzimidazole analogues of Hoechst 33258 was also prepared to explore the potential for anticancer activity mediated for certain of the drugs via bioreductive activation by endogenous NADH or NADPH. The biological endpoints examined included intracellular distribution in euoxic and hypoxic conditions observed by fluorescence microscopy; relative efficacy as antimetabolites determined by the MTT [tetrazolium salt, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] assay in euoxic and hypoxic conditions; and relative inhibitory activities on human DNA helicase, as determined by degree of dissociation of GC B6486 DNA. The intracellular distribution was unique to each of the test compounds. Compounds V-93 and V-153, the respective semiquinone and quinone derivatives, demonstrated the predicted enhanced cytotoxicity and anti-helicase activities, supporting the concept that preferential binding of DNA at 5'-CG and TG sequences provides a novel approach to anticancer drug development.

Animals↗

PubMedDate not supplied

Anticancer potential of N,N-diethylaminoethyl ethers of flavanone oximes: a comparison with mitoxantrone action on rat Yoshida sarcoma cells in vivo.

This study was performed to evaluate the anticancer abilities of four biologically active N,N-diethylaminoethyl ethers of flavanone oximes against rat Yoshida Sarcoma cells in vivo, and to investigate the mechanism(s) involved. The effects were compared with those of anthraquinone drug (mitoxantrone) action. The presented results provide the first evidence that all the investigated substances induce programmed cell death (apoptosis) of Yoshida Sarcoma cells in vivo. On interpretative grounds, the administration of investigated flavanone derivatives in the promotion phase of the disease led to both growth inhibition (cell cycle perturbation) and apoptosis. A correlation was found between structure of the substituent(s) at B-ring of substances and the revealed anticancer activity. The data suggest that flavanone derivatives (oxime ethers) besides their antiradical, antioxidant and radioprotector properties observed before, may act as promising anticancer agents acting in the promotion phase of disease. This finding prompted us to consider the development of a new strategy: modulation of effects using combination therapy involving mitoxantrone and flavanone oximes.

Animals↗

PubMed1998

Antisense expression of protein kinase C alpha improved sensitivity to anticancer drugs in human lung cancer LTEPa-2 cells.

AIM: To study the role of protein kinase C alpha (PKC alpha) in sensitivity to some clinical anticancer drugs in human lung cancer LTEPa-2 cells. METHODS: Human lung cancer cell model expressing antisense PKC alpha was established and characterized by gene transfection and immunoblotting. Northern blotting was used to analyze the expression of multiple drug resistance (mdr-1) gene and antisense PKC alpha mRNA. IC50 for some anticancer drugs in cultured cells were measured. RESULTS: Expression of antisense PKC alpha mRNA inhibited mdr-1 gene expression in lung cancer cells and improved sensitivity to anticancer drugs (harringtonine, carboplatin, bleomycin A5, vincristine and doxorubicin) in lung cancer cells. IC50 for harringtonine, carboplatin, bleomycin A5, vincristine, and doxorubicin was decreased by 46.4%, 42.1%, 79%, 69.9%, and 61.6% respectively. CONCLUSION: PKC alpha plays an important regulation role of mdr-1 gene expression and drug sensitivity in human lung cancer cells.

Adenocarcinoma↗

PubMed1999

Penetration of anticancer drugs through solid tissue: a factor that limits the effectiveness of chemotherapy for solid tumors.

Penetration of anticancer agents to cells distant from the vascular system is required for efficacy of cancer chemotherapy against solid tumors. Many solid tumors have a poorly formed blood vascular system with variable rates of blood flow and much larger intercapillary distances than those found in normal tissues. The requirement for drugs to penetrate several layers of tissue might pose a barrier to the effective treatment of solid tumors. Multicellular layers (approximately 200 microm thick) were grown in vitro on Teflon membranes from EMT6 murine and MCF7 human tumors and have been used to quantitate the penetration of four widely used anticancer drugs through solid tissue. The penetration of doxorubicin and mitoxantrone was limited and very slow (<10% of the rate of penetration through the Teflon membrane alone). The penetration of methotrexate and 5-FU was more rapid (approximately 30-50% of the rate of penetration through the Teflon membrane alone), but remains a substantial barrier to the effectiveness of these drugs. Strategies to improve the penetration of anticancer drugs through poorly vascularized tumor tissue have considerable potential to improve the outcome of chemotherapy for solid tumors.

Animals↗

PubMedDate not supplied

Introduction of gadd153 gene into gastric cancer cells can modulate sensitivity to anticancer agents in association with apoptosis.

Gadd 153 gene is known as one of the growth arrest and DNA damage inducible genes that may play an important role in signal transduction pathway(s) in response to DNA damage. We have investigated whether the introduction of gadd153 gene into gastric cancer cells could modulate the sensitivity to anticancer agents in association with apoptosis. The transfection of gadd153 gene into MKN45 gastric cancer cells (MKN45gadd153) increased the sensitivity to a variety of anticancer agents, compared to that of neo gene-transfected cells (MKN45neo). The sensitivity to CDDP and VP-16 was increased to a greater extent, whereas the sensitivity to 5-FU and taxotere was increased to a lesser extent. The increase of sensitivity to these drugs was associated with the increase of the formation of internucleosomal DNA ladders in apoptosis. The basal level of gadd153 mRNA was overexpressed in MKN45gadd153 cells, and its induction following the treatment of VP-16 and taxotere was found to a greater extent than that of MKN45neo cells. The analysis of mRNA expression in drug resistance-related genes including mdr1, mrp, topoisomerase II alpha showed that the increase of drug-sensitivity in MKN45gadd153 cells was not due to the changes in expression of drug resistance genes. These results suggest that the introduction of gadd153 gene into gastric cancer cells may modulate the sensitivity to certain anticancer agents by activating AP-1-associated signal transduction pathway(s) leading to apoptosis.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed1999

Tricyclic pyrone analogs: a new synthetic class of bifunctional anticancer drugs that inhibit nucleoside transport, microtubule assembly, the viability of leukemic cells in vitro and the growth of solid tumors in vivo.

Tricyclic pyrones (TPs) may represent a novel synthetic class of microtubule (MT) de-stabilizing anticancer drugs previously shown by us to inhibit macromolecule synthesis, tubulin polymerization, and the proliferation of leukemic and mammary tumor cells in vitro. A linear skeleton with a N-containing aromatic ring attached at C3 of the top A-ring, a central pyran B-ring and a six-membered bottom C-ring with no alkylation at C7 are required for the antitumor activities of the lead compounds, a 3-pyridyl benzopyran (code name H10) and its somewhat weaker 2-pyridyl regioisomer (code name H19). Increasing concentrations of H10 do not alter the binding of [3H]vinblastine and [3H]GTP to tubulin but mimic the ability of unlabeled colchicine (CLC) to reduce the amount of [3H]CLC bound to tubulin, suggesting that TPs may interact with the CLC binding site to inhibit tubulin polymerization. Exogenous Mg2+ cations absolutely required for the binding of GTP to tubulin and MT assembly cannot overcome the antitubulin action of H10. H10 reduces the viability of L1210 cells in vitro (IC50: 0.5 microM) but its antitumor activity may be related to its ability to inhibit tubulin polymerization and rapidly increase the mitotic index rather than to induce DNA cleavage and apoptosis. The anticancer potential of TPs in vivo is demonstrated by the fact that i.p. injections of the water-soluble H10-HCl decrease the growth of solid tumors in mice inoculated s.c. with Lewis lung carcinoma. A critical finding is that the antimitotic H10 is a bifunctional anticancer drug, which also blocks the cellular transport of nucleosides (IC50: 6 microM) to inhibit DNA synthesis. Since few CLC site-binding antimitotic agents are active in solid tumor models in vivo, the ability of these new MT destabilizing TPs to totally block nucleoside transport might be valuable in polychemotherapy to arrest tumor cells at several phases of their cycle, potentiate the action of antimetabolites and sensitize multidrug-resistant tumor cells.

Animals↗

PubMed1999

Role of bio-metal Fe(III) in anticancer behaviour of tamoxifen.

Physicochemical, microbial and pharmacological studies on Fe (III)--Tamoxifen complex have been carried out in solid and aqueous phases. On the basis of elemental analysis, polarographic studies, amperometric titrations and IR spectral studies the probable formula for the complex has been worked out to be 1:1, Fe(III)--Tamoxifen. A tentative structure has been suggested to the complex. The metal ligand interaction has been studied using polarographic method at 27 degrees +/- 1 degree C and at ionic strength of mu = 1.0 (KCl). Microbial studies on the complex was carried out against various pathogenic bacteria and fungi using Raper's method. Mouse sarcoma cell line 180 and Balb/C mice were used for the anticancer screening of solid complex, in vitro and in vivo, respectively. The results of microbial and pharmacological studies with the M:Drug complex revealed that the complex is more potent as compared to the pure drug as regards to its anticancer activity. As such Fe (III) Tamoxifen complex may be recommended to the therapeutic experts for its possible use as more potent anticancer drug.

Animals↗

PubMed1999

Establishment and characterization of human ovarian clear cell adenocarcinoma cell line (SMOV-2), and its cytotoxity by anticancer agents.

A novel cell line derived from a surgically resected ovarian clear cell adenocarcinoma of 46 year-old Japanese woman was established and designated SMOV-2. Cells of this lineage were continuously propagated in vitro over 44 months and were grown in a mono-layered sheet with a doubling time of 48.2 hours. The histopathology of the transplanted tumor in nude mice showed two distinctive cell types, hobnail cells and clear cells, which demonstrated recognizable characteristics of clear cell adenocarcinoma, as compared to resected original tumors. At the molecular level, SMOV-2 cells had the wild type p53 genes that were free from missence mutations. Anticancer agents (cisplatin and paclitaxel) were examined for cytotoxity against these SMOV-2 cells in vitro. These examinations revealed that the chemotherapy-treated cells had decreased proliferation, cell cycle arrests, and induction of apoptosis by the anticancer agents. As can be gleaned from this research, SMOV-2 is a valuable model to study the mechanism of apoptotic responses of solid tumors to future anticancer agents.

Adenocarcinoma, Clear Cell↗

PubMed2000

Differential cytotoxic pathways of topoisomerase I and II anticancer agents after overexpression of the E2F-1/DP-1 transcription factor complex.

The transcription factor complex E2F-1/DP-1 regulates the G1-to-S-phase transition and has been associated with sensitivity to the S-phase-specific anticancer agents camptothecin and etoposide, which poison DNA topoisomerase I and II, respectively. To investigate the relationship between E2F-1 and drug sensitivity in detail, we established human osteosarcoma U-20S-TA cells expressing full-length E2F-1/ DP-1 under the control of a tetracycline-responsive promoter, designated UE1DP-1 cells. Topoisomerase I levels and activity as well as the number of camptothecin-induced DNA single- and double-strand breaks were unchanged in UEIDP-1/tc- cells with >10-fold E2F-1/DP-1 overexpression. However, UE1DP-1/tc- cells were hypersensitive to camptothecin in both a clonogenic assay and four different apoptotic assays. This indicates that camptothecin-induced toxicity in this model is due to the activation of an E2F-1/ DP-1-induced post-DNA damage pathway rather than an increase in the number of replication forks caused by the S-phase initiation. In contrast, topoisomerase IIalpha levels (but not topoisomerase IIbeta levels), together with topoisomerase IIalpha promoter activity, increased 2--3-fold in UE1DP-1/tc-cells. Furthermore, the number of etoposide-induced DNA single- and double-strand breaks increased in UE1DP-1/tc-cells together with a rise in clonogenic sensitivity to etoposide, but an equal apoptotic sensitivity to etoposide. The increase in topoisomerase IIalpha promoter activity in UE1DP-1/tc--cells was shown to be due to S-phase initiation per se because it was blocked by ectopic expression of dominant negative cyclin-dependent kinase 2. In conclusion, overexpression of E2F-1/DP-1 in U-20S-TA cells is sufficient to increase clonogenic sensitivity to both topoisomerase I- and II-targeted anticancer drugs. However, the mechanism by which this occurs appears to be qualitatively different. The UE1DP-1 cell model may be used to elucidate post-DNA damage mechanisms of cell death induced by topoisomerase I-directed anticancer agents.

Antineoplastic Agents↗

PubMed2000

Inhibition of translation initiation mediates the anticancer effect of the n-3 polyunsaturated fatty acid eicosapentaenoic acid.

Eicosapentaenoic acid (EPA), an n-3 polyunsaturated fatty acid that is abundant in the fish-based diets of populations that exhibit a remarkably low incidence of cancer, exerts anticancer activity in vitro and in animal models of experimental cancer. Here we define the molecular basis for the anticancer effects of EPA. EPA inhibits cell division by inhibiting translation initiation. This is a consequence of the ability of EPA to release Ca2+ from intracellular stores while inhibiting their refilling via capacitative Ca2+ influx that results in partial emptying of intracellular Ca2+ stores and thereby activation of protein kinase R. Protein kinase R phosphorylates and inhibits eukaryotic initiation factor 2alpha, resulting in inhibition of protein synthesis at the level of translation initiation, preferentially reducing the synthesis and expression of growth-regulatory proteins, including G1 cyclins, and causes cell cycle arrest in G1. In a KLN-205 squamous cell carcinoma mouse model, daily oral administration of EPA resulted in a significant reduction of tumor size and expression of cyclin D1 in the tumor tissues. Furthermore, EPA-treated tumors showed a significant increase in the proportion of diploid cells, indicative of cell cycle arrest in G0-G1, and a significant reduction of malignant hypertetraploid cells. These results characterize EPA as a member of an emerging new class of anticancer compounds that inhibit translation initiaton.

3T3 Cells↗

PubMed1975

Proliferation-dependent cytotoxicity of anticancer agents: a review.

One of the factors of importance in determining the killing of mammalian cells following exposure to a variety of anticancer agents is the proliferative state of the cell population. Generally, proliferating cells are much more sensitive to anticancer agents than are nonproliferating cells. In this review, the cellular aspects of this differential sensitivity are discussed with the hemopoietic stem cell population and tissue culture cells as the focus for the analysis. This phenomenon is not only of concern to the cell biologist but also has implications with regard to scheduling of anticancer agents against human tumors.

Animals↗