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PubMed1985

Mitomycin C extravasation ulcers.

In a four-year period, eight patients with mitomycin C extravasation ulcers were encountered. Mitomycin C extravasation produces a painful indolent ulcer that does not have any tendency to heal. If extravasation of the drug is recognized, infusion should be stopped immediately, and the site of infusion should be changed. The ulcers should be excised, and primary closure is recommended; if it is not possible then the defect is covered by a partial thickness skin graft.

Extravasation of Diagnostic and Therapeutic Materi↗
PubMed1989

Efficacy of intravesical mitomycin C in the treatment of superficial transitional cell carcinoma of the urinary bladder.

We treated 47 patients with recurrent transitional cell carcinoma of the bladder with intravesical chemotherapy. Twenty milligrams of mitomycin C per treatment was introduced 7 days after transurethral resection (TUR) or diagnostic cystoscopy, and was repeated at 2-week intervals for five times followed again by cystoscopy. Two more similar courses were administered for a total of 36 weeks. Clinical data revealed no toxicity-related symptoms. Cystoscopic follow-up showed a gradual decline in the presence of tumor to a complete response rate of 87.1% at 36 weeks. Thirteen patients who were previously treatment failures with other drugs responded to mitomycin C.

Administration, Intravesical↗
PubMed1988

Postimplantation development of mitomycin C-treated mouse blastocysts.

Treatment of morula-stage mouse embryos with mitomycin C (0.004-0.5 microgram/ml) in vitro resulted in a decrease in the number of inner cell mass (ICM) cells at the blastocyst stage. The trophectoderm population was reduced only at the highest dosage (0.5 microgram/ml) tested. Postblastocyst development in vitro was retarded: Fewer embryos formed trophoblastic outgrowth, and the ICM was poorly developed. The embryo transfer experiments demonstrated that a reduction in ICM cell numbers diminished the potential of embryogenesis. The presence of a sufficient number of trophoblasts and ICM cells in the blastocyst is therefore a prerequisite for successful implantation and embryogenesis. The mitomycin-treated blastocysts with only 70% of normal ICM cells developed to egg cylinders that were about half normal size, but by days 12-14 the body size of the surviving embryo was similar to that of the control embryo. Morphogenesis was retarded during the early organogenesis stages, but only a slight delay was seen in the treated embryo on day 12. Such observation strongly suggests that a restorative phase of growth and morphogenesis has occurred during the immediate postimplantation period.

Animals↗
PubMed1989

Phase II study of combination 4'-epidoxorubicin and mitomycin C in recurrent epithelial ovarian cancer.

Thirty-three evaluable patients who had epithelial ovarian cancer that had not responded to treatment were entered into a phase II study of combination epirubicin and mitomycin C. Epirubicin (65 mg/m2) and mitomycin C (4 mg/m2) were administered separately, each as an i.v. bolus every 4 weeks. Ten patients (30%) had a complete or partial responses. The median duration of response was 20 weeks (range, 9-53). The regimen was well tolerated. Myelotoxicity occurred in four patients requiring hospitalization for septicaemia. Eleven patients had a blood transfusion. Alopecia was common, and nausea and vomiting, though frequent, usually mild. Cardiological toxicity was observed in one patient only. She developed congestive cardiac failure after an acute myocardial infarction. This regimen is active in advanced ovarian cancer that has not responded to prior treatment and warrants further study combination with other active drugs as a first-line regimen for ovarian cancer.

Adult↗
PubMed1990

Mitomycin C induces genomic rearrangements involving transposable elements in Drosophila melanogaster.

Mitomycin C was injected into the abdomen of male flies of the y2 sc1 waG strain of Drosophila melanogaster. They were mated with females bearing attached-X chromosomes, and the male offspring (F1) were analysed for the appearance of mutations in the X chromosome. We observed y+ and sc+ reversions induced either by excision of mdg4 (gypsy) with retention of one long terminal repeat (LTR) or by insertion of a foreign sequence into mdg4, partial reversion of the waG mutation, waG----waGd, and unstable f mutations. The overall mutation frequency was considerably higher than in control flies of the y2 sc1 waG strain. Possible mechanisms of genomic rearrangements induced by Mitomycin C, in particular the role of homologous recombination, are discussed.

Animals↗
PubMed1989

Expression of the dnaN and dnaQ genes of Escherichia coli is inducible by mitomycin C.

The dnaN and dnaQ genes encode the beta subunit and the epsilon subunit of the DNA polymerase III holoenzyme. Using translational fusions to lacZ we found that DNA damage caused by mitomycin C induces expression of the dnaA and dnaQ genes. This induction was not observed in lexA and recA mutants which block the induction of the SOS response, suggesting a relationship between the mechanism(s) of genetic control of DNA polymerase III holoenzyme and the SOS regulatory network. Nevertheless, there is evidence that the mitomycin C induction of dnaN and dnaQ is not a simple lexA-regulated process, because nalidixic acid (an excellent SOS inducer) does not increase dnaN and dnaQ gene expression, and the time course of induction is abnormally slow.

DNA Damage↗
PubMed1985

Mitomycin-C induced improvement in superficial bladder tumors: a morphologic and immunohistochemical evaluation.

Twenty bladder biopsies from ten patients with superficial transitional cell carcinoma were obtained prior to and following therapy with intravesical mitomycin-C. Each biopsy was evaluated histologically and immunohistochemically for A, B, H blood group antigen (BGA) expression. A, B and H blood group antigens were identified using monoclonal anti-A, B and H antibody and were localized with the avidin-biotin-peroxidase complex (ABC) technique. Particular attention was directed toward flat urothelial lesions and the urothelium adjacent to papillary tumors. Routine histologic evaluation showed improvement in post-therapy biopsies compared to corresponding pre-therapy biopsies in 7/10 cases but was equivocal in 3/10 cases. Immunohistochemical evaluation, however, showed improvement in all 10 cases, as judged by increased urothelial BGA expression. This increase in urothelial BGA expression after intravesical mitomycin-C therapy suggests a therapy induced improvement in dysplastic urothelium which was not uniformly evident on routine histologic examination.

Biopsy↗
PubMed1986

Adriamycin, vinblastine and mitomycin C as second-line chemotherapy in advanced breast cancer.

Thirty-six evaluable patients with metastatic measurable breast carcinoma previously treated with CMF or CMFVP were given second-line chemotherapy with Adriamycin, vinblastine, and mitomycin C (AVM), as follows: Adriamycin 20 mg/m2 and vinblastine 6 mg/m2 by i. v. push on days 1, 8, and 15, and mitomycin C 10 mg/m2 i. v. on day 1, every 6 weeks. Ten patients (28%) achieved partial remission (PR) lasting a median of 10 months, and eight patients (22%) experienced improvement of a lesser level than PR. An additional nine patients (25%) had disease stabilization; in the remaining nine patients (25%), persistent disease progression was observed. The median survival from the onset of AVM was 7 months for all patients; patients with PR survived a median of 13 months. Myelotoxicity was substantial and frequently interfered with the optimal administration of AVM, especially in patients with skeletal metastases; four patients were hospitalized with leukopenia and fever; all recovered promptly; one death was probably related to thrombocytopenia and CNS bleeding. Our results with AVM are similar to the average response rate published in the literature with the use of Adriamycin as a single agent in previously treated patients with advanced breast cancer.

Adult↗
PubMed1987

Prophylaxis of superficial bladder cancer with instillation of adriamycin or mitomycin C.

A multicenter trial for postoperative prophylaxis of superficial Ta-T1, G1-G2 bladder cancer was performed. Intravesical instillation using either 20-30 mg adriamycin or 20 mg mitomycin C per dose was carried out for 4 weeks or 2 years. Patients without instillation served as controls. A total of 259 patients was considered eligible for the evaluation. The instillation group showed a better disease free survival rate than the control group. Better prophylactic effects of instillation therapy were observed when one of following factors was present: multiple tumors, large tumors, T1 and G2 bladder cancer. The total dose of drug instilled seemed to correlate with the effects, but there were no differences between adriamycin and mitomycin C. The side effects were minimal and temporary.

Administration, Intravesical↗
PubMed1985

Mitomycin C-induced mosaicism in C-band regions of human chromosomes 1, 9, 16, and Y.

In order to test the hypothesis that somatic mosaicism involving C-band polymorphism of human chromosomes 1, 9, 16 may arise from mitotic crossing over, peripheral blood lymphocytes from normal males were treated with mitomycin C, which is known to induce somatic crossing over in lower eukaryotes. Evidence is presented which shows that mitomycin C is able to alter the heterochromatic pattern in human lymphocytes.

Cells, Cultured↗
PubMed1989

Mitomycin C treatment of advanced, hormone-resistant prostatic carcinoma: a phase II study.

From February 1984 to February 1987, 29 patients with advanced, hormone-resistant prostatic carcinoma were treated with mitomycin-C at a dose of 20 mg/m2 every 6 weeks (15 mg/m2 in patients greater than 75 years old and in those who had undergone previous radiotherapy). In the 27 evaluable patients, there were no complete remissions (CR), 2 partial remissions (PR), 14 stabilizations (STAB), and 11 cases of progressive disease (PRO). Ten stabilized patients showed significant pain reduction. Toxicity was minimal. The actuarial median survival was 10.8 months. In this study, mitomycin C was not active in terms of CR + PR; however, a beneficial symptomatic effect was frequently observed.

Aged↗
PubMed1995

Effects and systemic uptake of the new mitomycin C analogue KW-2149 in beagle dogs after intravesical administration.

The present study was designed to evaluate the local effects of the new mitomycin C analogue KW-2149 after intravesical instillation, together with its penetration into the systemic circulation in healthy beagle dogs. Two reference dogs were treated with two instillations of mitomycin C (30 mg in 30 ml phosphate buffer). Four dogs were given two, three, four and six instillations, respectively, of KW-2149 (60 mg in 30 ml phosphate buffer). KW-2149 concentrations measured in the systemic circulation were very low and were frequently found to be below the limit of determination. The number of instillations had no influence on the KW-2149 concentrations measured in the systemic circulation. Blood analysis showed no systemic toxicity. The histopathological findings in the bladder were comparable in both groups. The number of instillations had no influence on the severity of the lesions found in the bladder wall. On the basis of its in vitro activity KW-2149 can be regarded as a promising agent for intravesical treatment of superficial bladder cancer.

Administration, Intravesical↗
PubMed1984

Mitomycin C, melphalan and methotrexate combination chemotherapy for palliation of disseminated breast cancer.

Fifty-seven patients with metastatic breast carcinoma have been treated with mitomycin C (10 mg/m2 IV 6-weekly), melphalan (6 mg/m2 PO X 3 days, 3-weekly), and methotrexate (35 mg/m2 IV 3-weekly) to assess the efficacy and toxicity of this regimen. Of 48 evaluable patients 19 (40%) responded for a median period of 5 months and 12 (25%) had stabilisation of disease. Of the 12 patients previously treated with adriamycin only one responded, whereas 18 of the 36 patients without previous chemotherapy responded. Although healing of bone metastases was infrequent control of hypercalcaemia was commonly seen. Generally the treatment was well tolerated and treatment was stopped in only five patients because of toxicity. Cumulative marrow toxicity was observed but was not a significant problem in the first 6 months of treatment. Mitomycin C, melphalan, and methotrexate (MMM) appears to provide an effective, well tolerated chemotherapy combination for metastatic breast carcinoma.

Adult↗
PubMed1990

Mitomycin, ifosfamide and cisplatin in non-small-cell lung cancer.

Chemotherapy with mitomycin C, ifosfamide and cisplatin (MIC) is reported to produce responses of 56% and 69% in inoperable non-small-cell lung cancer (NSCLC). We evaluated the regimen in 45 similar patients who received up to six courses of 6 mg/m2 mitomycin C, 3 g/m2 ifosfamide, and 50 mg/m2 cisplatin every 3 weeks. In all, 18 patients had limited disease (LD) and 27 had extensive disease (ED). A total of 18 patients responded (40%), 9/18 with LD and 9/27 with ED; there were 4 complete responders. The median duration of response was 25 weeks, and median survival was 32 weeks (range, 2-96 weeks). Toxicity was moderate. Nausea and vomiting were controlled with i.v. dexamethasone and high-dose metoclopramide. Other toxicities included myelosuppression and alopecia. This study confirms that MIC is one of the most active regimens for treatment of NSCLC, with acceptable toxicity.

Adult↗
PubMed1996

Modulation of sensitivity to mitomycin C and a dithiol analogue by tempol in non-small-cell lung cancer cell lines under hypoxia.

We examined the mechanisms involved in the bioactivation of mitomycin C (MMC) and a newly developed MMC analogue: 7-N-(2-([2-(gamma-L-glutamylamino)ethyl]dithio)ethyl)mitomycin C, KW-2149, in non-small-cell lung cancer (NSCLC) cell lines under aerobic and hypoxic conditions. To investigate these mechanisms, we used MMC-resistant non-small-cell lung cancer cell lines (PC-9/MC4) that had been established in our laboratory from the parent PC-9 cell line by continuous exposure to MMC. We previously reported that the MMC-resistant cell line (PC-9/MC4) was poor in NAD(P)H dehydrogenase (quinone) activity and approximately 6-fold more resistant than the parent cells (PC-9) to MMC on 2-h exposure under aerobic conditions. In this study, the subline PC-9/MC4 was 6.7-fold more resistant to MMC than PC-9, the parent cell line, under aerobic conditions, and 5.2-fold more resistant under hypoxic conditions after 2-h exposure to MMC. However, on co-incubation with tempol, an inhibitor of the one-electron reduction pathway, the sensitivity of PC-9/MC4 to MMC was impaired under hypoxic conditions, but the impairment was not evident under aerobic conditions. KW-2149, the newly developed MMC analogue, was cytotoxic for both PC-9/MC4 and PC-9 cells, and the sensitivity of both cell lines to KW-2149 was not changed by exposure to hypoxic conditions or by coincubation with tempol. There were no significant differences in the intracellular uptake of MMC and the activities of cytosolic detoxification enzymes between the PC-9 and PC-9/MC4 cell lines. These results support the hypothesis that the one-electron reduction pathway plays a partial role in the bioactivation of MMC, but not of KW-2149, and that KW-2149 is excellent at circumventing resistance to MMC in NSCLC.

Antineoplastic Agents↗
PubMed1987

Potent effects of the monoclonal antibody-mitomycin C conjugate on human colon cancers.

The effects of the monoclonal antibody-mitomycin C conjugate against human colon cancers were studied, in vitro and in vivo. Mitomycin C (MMC) was conjugated with the human colon cancer-specific monoclonal antibody, using a cyanogen bromide method. The effect of the conjugate and free MMC, in vitro, was measured by incubation with human colon cancer SW1116 cells. The MMC concentration of the conjugate and of free MMC needed for 50 per cent killing of target cells was 0.11 microgram/ml and 7.00 micrograms/ml, respectively. The effect of the conjugate and of free MMC, in vivo, was assayed by the growth inhibition of human colon cancer xenografted in nude mice, after intraperitoneal injections of 30 micrograms MMC/kg. Antitumor effects of the conjugate against the cancer in nude mice were significantly more potent than that of free MMC.

Animals↗
PubMed1985

Possible enhancement of the cardiotoxicity of doxorubicin when combined with mitomycin C.

Forty-six patients with recurrent metastatic breast cancer were treated with a combination chemotherapy including doxorubicin and mitomycin C. Myocardial contractility was monitored by means of echocardiography. During therapy there was a progressive deterioration of myocardial function, and this phenomenon was found to be linearly correlated to the cumulative dose of doxorubicin. Six patients (13.8%) developed congestive heart failure during therapy; it occurred after the median cumulative dose of 322 mg/m2 (range 135-472). Possible risk factors of cardiomyopathy could be identified in only two patients. These results suggest that mitomycin C could enhance the cardiotoxicity of doxorubicin.

Adult↗
PubMed1983

Nucleotide sequence cleavage of guanine-modified DNA with aflatoxin B1, dimethyl sulfate, and mitomycin C by bleomycin and deoxyribonuclease I.

In guanine-modified DNA with aflatoxin B1, dimethyl sulfate, and mitomycin C, the nucleotide sequence cleavage of bleomycin or DNase I has been investigated using 32P-labeled DNA fragments. In contrast with cis-dichlorodiammine platinum (II) which induces intrastrand crosslinking of guanine N7 atoms, these mono-covalent modifiers did not give remarkable alteration of the DNA nucleotide cleavage mode by bleomycin and DNase I. From the viewpoint of combination drug, it is of interest that mitomycin C promoted the DNA cleavage activity of bleomycin.

Aflatoxin B1↗