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PubMed2000

Intranuclear localization of proliferating cell nuclear antigen during the cell cycle in renal cell carcinoma.

OBJECTIVE: To investigate, with laser scanning cytometry (LSC), proliferating cell nuclear antigen (PCNA) expression during the cell cycle in renal cell carcinoma. STUDY DESIGN: DNA ploidy and intracellular localization of PCNA in renal cell carcinoma were determined using LSC and immunohistochemistry. The subjects were nine patients who had received surgery for renal cell carcinoma. After DNA ploidy analysis, the glass slides were restained by immunohistochemistry of PCNA. LSC allowed direct observation of PCNA localization during the cell cycle because we could obtain immunohistochemical staining of PCNA as a function of cell cycle phase for individual cells. RESULTS: PCNA was not demonstrated in the nuclei of G0/G1 cells. PCNA expression increased from the S phase of the cell cycle. PCNA rapidly degraded at the end of the G2 phase. In the late G2 and M phase, PCNA was not detected in almost any nucleus. CONCLUSION: LSC allows morphologic observation of the intracellular distribution of PCNA during the cell cycle in renal cell carcinoma.

Adult↗
PubMed1990

Quantitative analysis of cytoskeletal proteins throughout the cell cycle of the MRC-5 fibroblastic cell line.

Fluorescent dyes were used to stain actin, vimentin, tubulin and DNA in the same MRC-5 fibroblastic cells. Cytofluorometry and image analysis were then used to quantitatively evaluate the F actin, vimentin and tubulin content throughout the cell cycle. The results showed that different cells can have the same DNA content while their cytoskeletal protein content is variable. The data also showed that cytoskeletal protein content variations exist throughout the cell cycle of the fibroblastic cell line. The F actin content increased during the cell cycle from G1 to G2 phases and decreased in M phase. The amount of tubulin in the G2 was about twice as much as that in the G1 phase, before decreasing in the M phase; there was a threshold of tubulin content for G2 cells entering S phase.

Actins↗
PubMed1994

Maintenance of meiotic arrest by a phosphorylated p34cdc2 is independent of cyclic adenosine 3',5'-monophosphate.

The meiotic division in oocytes is arrested in the G2 phase of the cell cycle. Resumption of meiosis, also known as oocyte maturation, entails a G2 to M transition and is associated with a drop in intraoocyte concentrations of cAMP. Recent studies imply that tyrosine dephosphorylation of p34cdc2 is a prerequisite for entry into the M-phase of the cell cycle. Our study was designed to test the involvement of protein tyrosine phosphatase (PTPase)-regulated dephosphorylation of p34cdc2 in resumption of meiosis in rat oocytes and to explore the possible control of this event by the intraoocyte concentrations of cAMP. Isolated rat oocytes undergoing meiotic maturation spontaneously in vitro served as our experimental model. We found that sodium metavanadate, an inhibitor of PTPase, reversibly blocked the spontaneous maturation in vitro of rat oocytes (ED50 = 0.26 mM). We further demonstrated that the vanadate-sensitive event is completed by 2 h after reinitiation of meiosis. Immunoblot analysis using specific antiphosphotyrosine antibodies revealed that vanadate caused accumulation of phosphotyrosine on a 34-kDa protein, also recognized by anti-p34cdc2 antibodies. The phosphorylated form of p34cdc2 was also detected in oocytes arrested in the G2 phase by the phosphodiesterase inhibitor isobutyl methylxanthine (IBMX). Intraoocyte concentrations of cAMP in vanadate-inhibited oocytes were similar to those in oocytes that resumed meiosis spontaneously in vitro and lower than those in oocytes maintained in meiotic arrest by IBMX (0.73 +/- 0.08, 0.84 +/- 0.09, and 1.42 +/- 0.3 fmol/oocyte, respectively) [corrected]. We conclude that a PTPase that regulates the phosphorylation state of p34cdc2 participates in the control of meiosis in rat oocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed2005

P element excision and repair by non-homologous end joining occurs in both G1 and G2 of the cell cycle.

P element excision generates a DNA double-strand break at the transposon donor site. Genetic studies have demonstrated a strong bias toward repair of P element-induced DNA breaks by homologous recombination with the sister chromatid, suggesting that P element excision occurs after DNA replication, in G2 of the cell cycle. We developed methods to arrest Drosophila tissue culture cells and assay P element excision in either G1- or G2-arrested cells. Dacapo or tribbles transgene expression arrests cells in either G2 or G2, respectively. RNA-mediated gene interference (RNAi) directed against cyclin E or cyclin A arrests cells in G1 or G2, respectively. P element excision occurs efficiently in both G1- and G2-arrested cells, suggesting that cell cycle regulation of P element transposase does not occur in our somatic cell system. DNA double-strand break repair occurs by two predominant mechanisms: homologous recombination (HR) and non-homologous end joining (NHEJ). HR is thought to be restricted to the post-replicative, G2, phase of the cell cycle, while NHEJ may occur throughout the cell cycle. Our results indicate that NHEJ repair of an extrachromasomal plasmid substrate occurs at least as efficiently in G2-arrested cells as in asynchronous cells or in G1-arrested cells.

Animals↗
PubMed1999

Involvement of p21 in the PKC-induced regulation of the G2/M cell cycle transition.

Activation of protein kinase C (PKC) inhibits cell cycle progression at the G1/S and G2/M transitions. We found that phorbol 12-myristate 13-acetate (PMA) induced upregulation of p21, not only in MCF-7 cells arrested in the G1 phase as previously shown, but also in cells delayed in the G2 phase. This increase in p21 in cells accumulated in the G1 and G2/M phases of the cell cycle after PMA treatment was inhibited by the PKC inhibitor GF109203X. This indicates that PKC activity is required for PMA-induced p21 upregulation and cell cycle arrest in the G1 and G2/M phases of the cell cycle. To further assess the role of p21 in the PKC-induced G2/M cell cycle arrest independently of its G1 arrest, we used aphidicolin-synchronised MCF-7 cells. Our results show that, in parallel with the inhibition of cdc2 activity, PMA addition enhanced the associations between p21 and either cyclin B or cdc2. Furthermore, we found that after PMA treatment p21 was able to associate with the active Tyr-15 dephosphorylated form of cdc2, but this complex was devoid of kinase activity indicating that p21 may play a role in inhibition of cdc2 induced by PMA. Taken together, these observations provide evidence that p21 is involved in integrating the PKC signaling pathway to the cell cycle machinery at the G2/M cell cycle checkpoint.

Aphidicolin↗
PubMed1996

DNA damage and p53-mediated cell cycle arrest: a reevaluation.

Most mammalian cells exhibit transient delays in the G1 and G2 phases of the cell cycle after treatment with radiation or radiomimetic compounds. p53 is required for the arrest in G1, which provides time for DNA repair. Recently, a role of p53 in the G2/M transition has also been suggested. However, it has been reported that the presence of functional p53 does not always correlate with the induction of these checkpoints. To precisely assess the role of p53 in activating cell cycle checkpoints and in cell survival after radiation, we studied the response of two isogenic human fibrosarcoma cell lines differing in their p53 status (wild type or mutant). We found that when irradiated cells undergo a wild-type p53-dependent G1 arrest, they do not subsequently arrest in G2. Moreover, wild-type p53 cells irradiated past the G1 checkpoint arrest in G2 but do not delay in the subsequent G1 phase. Furthermore, in these cell lines, which do not undergo radiation-induced apoptosis, the wild-type p53 cell line exhibited a greater radioresistance in terms of clonogenic survival. These results suggest that the two checkpoints may be interrelated, perhaps through a control system that determines, depending on the extent of the damage, whether the cell needs to arrest cell cycle progression at the subsequent checkpoint for further repair. p53 could be a crucial component of this control system.

Animals↗
PubMed2004

[Radiosensitization by pentoxifylline in human hepatoma cell line HepG2 and its mechanism].

OBJECTIVE: To investigate the radiosensitization by pentoxifylline (PTX) in human hepatoma cell line HepG2 and its possible mechanism. METHODS: MTT assay was used to evaluate the cytotoxicity of PTX and clonogenic assay employed to observe its effects on the radiosensitivity of the cells quantified by calculating the sensitive enhancement ratio (SER). Flow cytometry was performed to observe the changes in the cell cycle of HepG2 cells in response to X-ray irradiation and the effect of PTX intervention. RESULTS: The cytotoxicity of PTX increased in a dose-dependent manner following a 24-hour treatment, with the optimal dose range of 1-5 mmol/L. A sub-toxic dose of PTX at 2 mmol/L was used in the subsequent experiments. PTX significantly reduced the clonogenic activity and enhanced the radiosensitivity of HepG2 cells with a SER of 1.3+/-0.16 at the dose of 2 mmol/L. Irradiation resulted in cell cycle arrest at G2 phase in HepG2 cells, and the percentages of HepG2 cells in G2-M phase were 32.15% and 19.52% respectively after exposure to 6 Gy radiation alone and to 6 Gy plus 2 mmol/L PTX at 20 h, demonstrating the effectiveness of PTX in resolving radiation-induced G2 arrest. CONCLUSION: Radiosensitization by PTX is possibly associated with the abrogation of G2 arrest in HepG2 cells following radiation exposure.

Carcinoma, Hepatocellular↗
PubMed2000

Arrest of S-phase progression is impaired in Fanconi anemia cells.

Fanconi anemia (FA) is an inherited cancer-susceptibility disorder, characterized by genomic instability, hypersensitivity to DNA cross-linking agents, and a prolonged G2 phase of the cell cycle. We observed a marked dose-dependent accumulation of FA cells in the G2 compartment after treatment with 4,5',8-trimethylpsoralen (Me(3)Pso) in combination with 365 nm irradiation. Using bivariate DNA distribution methodology, we determined the proportion of replicating and arresting S-phase cells and observed that, whereas normal cells arrested DNA replication in the presence of Me(3)Pso cross-links and monoadducts, FA lymphoblasts failed to arrest DNA synthesis. Taken together, the above data suggest that, in response to damage induced by DNA cross-linking agents, the S-phase checkpoint is inefficient in FA cells. This would lead to accumulation of secondary lesions, such as single- and double-strand breaks and gaps. The prolonged time in G2 phase seen in FA cells therefore exists in order to allow the cells to remove lesions which accumulated during the preceding abnormal S phase.

Cell Line↗
PubMed1991

Camptothecin, teniposide, or 4'-(9-acridinylamino)-3-methanesulfon-m-anisidide, but not mitoxantrone or doxorubicin, induces degradation of nuclear DNA in the S phase of HL-60 cells.

Short-term (2-6 h) exposure of human promyelocytic HL-60 cell cultures to the DNA topoisomerase I inhibitor camptothecin (0.05-0.5 microgram/ml) or to the topoisomerase II inhibitor, teniposide (VM-26; 0.3-3.0 micrograms/ml) or 4'-(9-acridinylamino)methanesulfon-m-anisidide (amsacrine; 0.8 microgram/ml) triggered rapid degradation of DNA specifically in S-phase cells. As a result of the selective death of S-phase cells, only G1 cells remained in these cultures. On the other hand, mitoxantrone (0.02-0.4 microgram/ml) or doxorubicin (adriamycin; 0.4-10.0 micrograms/ml) did not induce DNA degradation in S phase but arrested HL-60 cells in S and G2 phases. In contrast to HL-60 cells, human lymphocytic leukemic MOLT-4 cells responded to all of these drugs (camptothecin, teniposide, amsacrine, mitoxantrone, and adriamycin) at all concentrations tested, invariably by being arrested in G2 and S phases and also by entering a higher DNA ploidy cycle. The data illustrate the differences in the sensitivity of S-phase cells in myelogenous versus lymphocytic leukemic lines to both DNA topoisomerase I and II inhibitors and emphasize the tissue (leukemia type)-specific factors that modulate the cytostatic and cytotoxic effects of these inhibitors. The qualitatively different response of HL-60 cells to camptothecin, teniposide, or amsacrine (by rapidly triggered DNA degradation in S phase) as compared to mitoxantrone or adriamycin (by cell arrest in G2 and S) suggests that, despite the generally assumed common mode of action attributed to these drugs (i.e., via stabilization of the cleavable DNA-topoisomerase complexes), there are significant differences in the mechanisms by which they exert cytostatic/cytotoxic effects.

Amsacrine↗
PubMed1998

DNA topoisomerase II sites in the histone H4 gene during the highly synchronous cell cycle of Physarum polycephalum.

The nearly perfect synchrony of nuclear division in a plasmodium of Physarum polycephalum provides a powerful system to analyze topoisomerase II cleavage sites in the course of the cell cycle. The histone H4 locus, whose schedule of replication and transcription is precisely known, was chosen for this analysis. Drug-induced topoisomerase II sites are clustered downstream of the histone H4 gene and appear highly dependent on cell cycle stage. They were only detected in mitosis and at the very beginning of S phase, precisely at the time of replication of the histone H4 region. The sites, which were absent in G2 phase, reappeared at the next mitosis. Remarkably, DNase I hypersensitive sites occurred in nearly the same location, but their schedule was totally different: they were absent in mitosis and present in G2. This schedule follows H4 transcription, which peaks in mid-S phase and in the second part of G2 phase and is off during mitosis. These results suggest that topoisomerase II may not be involved in transcription, but plays a role in remodeling chromatin structure, both during chromosome condensation in prophase/metaphase to allow their decatenation and during chromosome decondensation after metaphase to allow replication fork passage throughout the region.

Animals↗
PubMed1996

Initial triggering of M-phase in starfish oocytes: a possible novel component of maturation-promoting factor besides cdc2 kinase.

G2-phase-arrested immature starfish oocytes contain inactive cdc2 kinase and cdc25 phosphatase, and an inactivator for cdc2 kinase. In this system, we have studied how the regulatory balance is apped toward the initial activation of cdc2 kinase. During the hormone-dependent period (Guerrier, P., and M. Doree, 1975. Dev. Biol. 47:341-348), p34cdc2 and cdc25 protein are already converted, though not fully, to active forms, whereas the inactivators for cdc2 kinase and cdc25 phosphatase are able to exhibit their activities if the hormone were removed. We produced "triggered oocytes," in which due to a neutralizing anticdc25 antibody, the activation of cdc2 kinase is prevented out cdc25 protein is phosphorylated slightly after the maturation-inducing hormonal stimulus. In contrast to control immature oocytes, in triggered oocytes the injected cdc2 kinase is not inactivated, and accordingly the level of cdc2 kinase activity required for meiosis reinitiation is much less. These results imply the presence of a cdc2 kinase activity-independent process(es) that suppresses the inactivator for cdc2 kinase and initially phosphorylates cdc25 protein, although this process is reversible during the initial activation of cdc2 kinase. At the most initial triggering of M-phase, the cdc2 kinase activity-independent process might trip the switch leading to the initial activation of cdc2 kinase. Thereafter, in parallel, the cdc2 kinase-dependent feedback loops described by others may cause further increase in cdc2 kinase activity. We propose that a putative suppressor, which downregulates the inactivator for cdc2 kinase independently of nuclear components, might be a previously unrecognized component of maturation-promoting factor.

Adenine↗
PubMed1999

Antisense blockade of p21/WAF1 decreases radiation-induced G2 arrest in esophageal squamous cell carcinoma.

Introduction. The p21 cyclin-dependent kinase inhibitor arrests the cell cycle following DNA damage at the G1-S checkpoint. Recent literature has also demonstrated a role for p21 in G2 arrest. Studies with esophageal squamous cell carcinoma (ESSC) lines have shown that radiation-induced p21 protein induction is associated with G2 arrest. The aim of this study was to determine if p21 blockade would affect this G2 arrest pattern. Method. We transfected the ESSC line KYSE 170 with antisense p21 mRNA oligonucleotides or scrambled 20-mer p21 control oligonucleotides using a lipofectant reagent. Cells were exposed to 6 Gy or used as controls. p21 levels were determined by ELISA. Cell cycle arrest pattern was determined via flow cytometry. Student's t test and ANOVA were used to compare p21 levels and percentages of G2 arrest. Results. Irradiated/scrambled cells expressed 10.1 ng/ml of p21 protein compared to irradiated/antisense cells at 2.1 ng/ml (P < 0.05), demonstrating successful blockade of p21. Irradiated cells displayed prominent G2 arrest following 6 Gy doses, but there was a decrease from 65 to 44% G2 phase when p21 was blocked (P < 0.05). Conclusions. We have demonstrated that G2 arrest accompanying irradiation of ESSC cells decreases when p21 protein production is blocked via antisense oligonucleotides. These data support a role for p21 in mediating G2 arrest in these cells.

Carcinoma, Squamous Cell↗
PubMed1978

[The mode of action of bleomycin-cell kinetic investigations (author's transl)].

Chemotherapy of malignant ENT tumours with Bleomycin (BLM) alone is not very successful. In the last time however several authors pointed out much better therapeutic results when BLM therapy has been combined with radiation treatment It is farly unknown why this combination should cause a greater therapeutic effect. Therefore we investigated the following questions: 1. In what manner does BLM influence the kinetics of cell proliferation of malignant tissues? 2. Does BLM synchronize the tumour cells or is the greater therapeutic success of a combination of BLM and X rays only depending an an additional effect? 3. Can we find a connection between the effect of BLM and the histology of the tumour? With cell kinetic methods (authoradiography, cytophotometry, mitotic index) and histological technics we examined these problems in 5 human ENT tumours and got the following results: 1. BLM initially causes a partial synchronization of the tumour cells (blockade in the S-phase). During a continuous therapy with BLM however the tumour cells will be collected in the late S- and mainly in the G2-phase. But this peak of cells in G2 is not the expression of synchronization because a lot of these cells are blocked irreversible and will leave the cell cycle (hyperceratotic cells). Ffrom those cells which thereupon have entered the mitotic phase a further part of them will by endomitosis or endoreduplication. Only a small group of the cells originally collected in the G2-phase will devide and enter the G1-phase again. Furthermore we observed a distinct recruitment of G0-cells back into the cell cycle (for details see fig. 9). 2. The greater effect of radiation therapy following the application of BLM is not the result of synchronization but of an additional destruction of premitotic G2-cells which properly would have undergone mitosis. BLM and X rays therefore act additionally. 3. The greater therapeutic success of the combination of BLM and radiation treatment comes true only in keratinizing squamous cell carcinoma. The reason is that BLM destroys the tumour cells by hyperkeratosis and polyploidy. Thus BLM must be ineffective in carcinoma without the ability of keratinizing.

Bleomycin↗
PubMed1991

The concentration-dependent diversity of effects of DNA topoisomerase I and II inhibitors on the cell cycle of HL-60 cells.

Exposure of promyelocytic leukemic HL-60 cells to 3-60 nM of the DNA topoisomerase I inhibitor camptothecin (CAM) or to 30-450 nM and 0.12-1.5 microM of DNA topoisomerase II inhibitors teniposide (TN) and 4-(9-acridynylamino)-3-methanesulfon-m-anisidide (m-AMSA), respectively, resulted in two distinct kinetic effects: (1) the cells entered S phase but the rate of DNA replication was reduced in proportion to the inhibitor concentration; (2) the transition from G2 to M was impaired, approximately 1 h after addition of the inhibitor. As a consequence, the cells accumulated in the S (preferentially in early S) and in G2 phases of the cell cycle. Whereas CAM was more efficient in suppressing cell progression through S phase, TN and m-AMSA were more potent G2 blockers. At these low inhibitor concentrations no signs of immediate cytotoxicity or DNA degradation were apparent. However, above 145 nM of CAM, 900 nM of TN, or 2 microM of m-AMSA extensive DNA degradation in nuclei of S phase cells was evident within 6 h of addition of the inhibitor, resulting in the loss of S and G2 + M cells from these cultures. The data indicate that depending on concentration, mechanisms mediating the cytostatic/cytotoxic activity of both DNA topoisomerase I and II inhibitors may be quite different. Suppression of the DNA replication and the G2 to M transition, seen at low inhibitor concentrations, is compatible with the assumption that the inhibitor-induced stabilization of the topoisomerase-DNA cleavable complexes interferes with DNA replication and chromosome condensation/segregation, respectively. Above the threshold concentration for each inhibitor, an endonucleolytic activity is triggered, resulting in rapid DNA degradation in nuclei of S and G2 phase cells. The endonucleolytic effect is not only cell cycle phase-specific but is also modulated by tissue-specific factors because it cannot be observed, e.g., in the lymphocytic leukemic cell lines.

Amsacrine↗
PubMed1993

Increasing effect of tri-n-butyltins and triphenyltins on the frequency of chemically induced chromosome aberrations in cultured Chinese hamster cells.

Organotins have been widely used as anti-fouling coatings for fishing nets and ship bottoms, and marine pollution by them has become a serious environmental problem. In this communication, the potentiating effects of three kinds of tri-n-butyltins and three thiphenyltins on chromosome aberrations were studied in Chinese hamster CHO K1 cells. None of the organotins studied showed any clastogenic activity under the experimental conditions without rat liver S9. Post-treatment with organotins, however, increased the number of breakage-type (but not exchange-type) chromatid aberrations induced by five kinds of S-phase-dependent clastogens: MMC, cisPt, 4NQO, MMS, and AMD). Enhancement of the induction of chromosome aberrations by MMC was observed when cells were treated with organotins during the G2 phase. These results suggest that organotin G2 effect causes potentiating effects. Organotins also enhanced the induction of breakage-type chromatid aberrations by clastogenic pollutants in chlorinated tap water, indicating their potential for a more realistic health risk.

Animals↗
PubMed1999

Differentiation of human malignant melanoma cells that escape apoptosis after treatment with 9-nitrocamptothecin in vitro.

After in-vitro exposure to 0.05 micromol/L 9-nitrocamptothecin (9NC) for periods of time longer than 5 days, 65% to 80% of the human malignant melanoma SB1B cells die by apoptosis, whereas the remaining cells are arrested at the G2-phase of the cell cycle. Upon discontinuation of exposure to 9NC the G2-arrested cells resume cell cycling or remain arrested depending on the duration of 9NC exposure. In contrast to cycling malignant cells, the cells irreversibly arrested at G2 exhibit features of normal-like cells, the melanocytes, as assessed by the appearance of dendrite-like structures; loss of proliferative activity; synthesis of the characteristic pigment, melanin; and, particularly, loss of tumorigenic ability after xenografting in immunodeficient mice. Further, the expression of the cyclin-dependent kinase inhibitor p16 is upregulated in the 9NC-treated, G2-arrested, but downregulated in density G1-arrested cells, whereas the reverse is observed in the expression of another cyclin-dependent kinase inhibitor, p21. These results suggest that malignant melanoma SB1B cells that escape 9NC-induced death by apoptosis undergo differentiation toward nonmalignant, normal-like cells.

Animals↗
PubMed2003

An overactivated ATR/CHK1 pathway is responsible for the prolonged G2 accumulation in irradiated AT cells.

Induction of checkpoint responses in G1, S, and G2 phases of the cell cycle after exposure of cells to ionizing radiation (IR) is essential for maintaining genomic integrity. Ataxia telangiectasia mutated (ATM) plays a key role in initiating this response in all three phases of the cell cycle. However, cells lacking functional ATM exhibit a prolonged G2 arrest after IR, suggesting regulation by an ATM-independent checkpoint response. The mechanism for this ataxia telangiectasia (AT)-independent G2-checkpoint response remains unknown. We report here that the G2 checkpoint in irradiated human AT cells derives from an overactivation of the ATR/CHK1 pathway. Chk1 small interfering RNA abolishes the IR-induced prolonged G2 checkpoint and radiosensitizes AT cells to killing. These results link the activation of ATR/CHK1 with the prolonged G2 arrest in AT cells and show that activation of this G2 checkpoint contributes to the survival of AT cells.

Alkaloids↗
PubMed1991

Cytostatic synergism between bromodeoxyuridine, bleomycin, cisplatin and chlorambucil demonstrated by a sensitive cell kinetic assay.

Bromodeoxyuridine/Hoechst flow cytometry was used to analyse the interference of common cytostatic agents with cell activation and cell cycle progression of human B-cell lines. Bleomycin impaired both cell activation and G2 transit, the latter effect being oxygen dependent. The DNA alkylating agents cyclophosphamide, chlorambucil and mitomycin C caused G2 arrest, whereas cisplatin arrested cells in both the S and G2 phase of the cell cycle. Vinblastin interfered with mitosis, but in addition arrested cells in all phases of the cell cycle. The growth inhibitory action of bleomycin, cisplatin and chlorambucil was dependent upon the bromodeoxyuridine (BrdU) concentration in the culture medium. No interaction was found between BrdU and cyclophosphamide, mitomycin C and vinblastin. The cell cycle kinetic mechanism of the interaction between BrdU and bleomycin, cisplatin and chlorambucil was a potentiation of the G2 arrest. In conclusion, BrdU may be useful in clinical chemotherapy as a chemosensitizer for selected cytostatic agents.

Bleomycin↗