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PubMed1991

A randomized trial with mitomycin-C/ifosfamide versus mitomycin-C/vindesine versus cisplatin/etoposide in advanced non-small-cell lung cancer.

192 evaluable patients with advanced inoperable non-small-cell lung cancer were treated with either mitomycin-C/ifosfamide (A), mitomycin-C/vindesine (B), or cisplatin/etoposide (C) in a prospective randomized trial. The response rates for each treatment arm were 30.0% (A), 22.7% (B), and 25% (C), respectively. There was no statistically significant difference (p = 0.4) between treatment arms. The median survival time was 27 weeks (A), 23 weeks (B), and 25 weeks (C), respectively. With regard to toxicity the combination mitomycin-C/vindesine was superior to treatment arms A and C. Nausea and vomiting (WHO 3 + 4) occurred only in 6.1% of the patients versus 43.3% of those treated with mitomycin-C/ifosfamide and 36.7% of those treated with cisplatin/etoposide. This difference is statistically highly significant (p = 0.0001). Because of its very low toxicity, especially for gastrointestinal symptoms, the combination mitomycin-C/vindesine was judged superior to the other combinations. None of these regimens, however, had a major impact on survival in advanced non-small-cell lung cancer.

Adult↗
PubMed1989

Randomized controlled study of mitomycin C/carboquone/5-fluorouracil/OK-432 (MQ-F-OK) therapy and mitomycin C/5-fluorouracil/doxorubicin (FAM) therapy against advanced liver cancer.

We have previously reported that the combination of mitomycin C, carboquone, 5-fluorouracil and OK-432, including the intra-arterial administration of mitomycin C and carboquone (MQ-F-OK therapy), was effective in the treatment of advanced liver cancer. The Cooperative Study Group conducted a controlled study on MQ-F-OK therapy and the combination of mitomycin C, 5-fluorouracil and doxorubicin, including the intra-arterial administration of mitomycin C and doxorubicin (FAM therapy), against advanced liver cancer. Forty patients with advanced primary or secondary liver cancer were enrolled in this study and randomized into the MQ-F-OK group and the FAM group. Seventeen of the 21 cases in the MQ-F-OK group and 16 of the 19 cases in the FAM group were eligible for response evaluation in accordance with the criteria of the Japan Society for Cancer Therapy. There was no significant difference in the patient characteristics between the two groups. Three cases in the MQ-F-OK group and two in the FAM group showed partial response. There was, however, no significant difference in the response rates and the prolongation of life between the two groups. As for the side-effects, only anemia was observed more frequently in the FAM group than in the MQ-F-OK group. In conclusion, we could not preferentially recommend either MQ-F-OK therapy or FAM therapy for advanced liver cancer. The performance status of the patient was one of the most important factors in the treatment of advanced liver cancer because patients with poor performance status showed poorer results.

Adult↗
PubMed1991

Reductive alkylation of DNA by mitomycin A, a mitomycin with high redox potential.

The mitomycins are a group of antitumor antibiotics that covalently bind to DNA upon reductive activation. Mitomycin A (1b; MA) is more toxic than its clinically useful mitomycin C (1a; MC). The greater toxicity of mitomycin A has been previously attributed to its higher reduction potential. In this report, the DNA alkylation products of reductively activated MA were isolated and characterized by conversion to the known 7-amino mitosene-deoxyguanosine adducts. The three major adducts formed were identified as a monoadduct, N2-(2"beta-amino-7"-methoxymitosen-1"alpha-yl)- 2'-deoxyguanosine (5), a decarbamoyl monoadduct, N2-(2"beta-amino-10"-decarbamoyl-7"-methoxymitosen-1"alpha-y l)-2'- deoxyguanosine (6), and a bisadduct, N2-(2"beta-amino-10"-deoxyguanosin-N2-yl-7-methoxymitosen-1" alpha- yl)-2'-deoxyguanosine (7). Under all reductive activation conditions employed, MA selectively alkylated the 2-amino group of guanine in DNA, like MC. In addition, both MA and MC alkylated DNA and cross-linked oligonucleotides to a similar extent. However, variations in the reductive activation conditions (H2/PtO2, Na2S2O4, or enzymatic) affected the distribution of the three major MA adducts in a different manner than the distribution of MC adducts was affected. A mechanism is proposed wherein the 7-methoxy substituent of MA allows initial indiscriminate activation of either of the drugs' two electrophilic sites. While oxygen inhibited cross-linking by MC, similar aerobic conditions exhibited little influence on the cross-linking ability of MA. Hence, the greater toxicity of MA may be influenced by increased and nonselective activation and cross-link formation in both aerobic and anaerobic cells. This effect is a direct consequence of the higher redox potential of MA as compared to MC.

Alkylation↗
PubMed1986

Conformations of complexes between mitomycin and decanucleotides. 2. Application of the model to mitomycin C derivatives. Extension to covalent binding with adenine.

Molecular mechanics simulation of the interactions of important mitomycin C analogues monocovalently bound to DNA models are presented. These analogues included substituents such as p-hydroxyphenyl, 2-mercaptoethyl, and dimethylamidinium on N7 of mitomycin C and the DNA models consisted of d(GCGCGCGCGC)2 and d(GCGCATGCGC)2. The excellent fits and strong binding affinities of these highly potent analogues support the usefulness of the model. The binding of a mitomycin-related N-phenylpyrrole with a carbamoyloxy substituent to 06 of guanine was studied. Finally, a reactive mitomycin intermediate proposed by Moore was shown to interact with DNA in a way consistent with the formation of a covalent adduct.

Base Sequence↗
PubMed1976

Effect of sodium arsenite on the biosynthesis of mitomycins by Streptomyces caespitosus and mode of action of mitomycin C on Bacillus subtilis NRRL B-543.

Addition of different concentrations of sodium arsenite to the fermentation medium used for the production of mitomycin antibiotics by Streptomyces caespitosus hindered the biosynthesis of mitomycins and led to the accumulation of 2-oxoglutarate, pyruvate and acetone. Mitomycin C isolated and purified using thin-layer chromatography in low concentration of about 0.1 mug/ml did not affect the RNA, DNA and protein biosynthesis of the growing Bacillus subtilis, while at 10 mug/ml mitomycin C markedly affected RNA, DNA and protein biosynthesis.

Acetone↗
PubMed1991

Determination of the new anticancer agent KW 2149, 7-N-[2-[2-(gamma-L-glutamylamino)ethyl)dithio)ethyl]mitomycin C, an analogue of mitomycin C.

The new mitomycin 7-N-[2-[2-(gamma-L-glutamylamino)ethyl)dithio)ethyl] mitomycin C (KW 2149) (I) proved to be active against a wide variety of experimental tumours. In order to perform pharmacokinetic studies with the new drug in Phase I sessions, a fast and reliable method has been developed based on the data of previous assays for mitomycin C. XAD-2 was preferred for isolation of I from blood plasma. The recovery of I was 50% whereas that of mitomycin C was 85%. Optimal separation was obtained on octadecyl silica columns with methanol-water (45:55, v/v) as mobile phase, while ultraviolet absorbance detection was performed at 375 nm. The assay enabled determination of I in a plasma concentration range of 20-1000 ng/ml using porfiromycin as internal standard.

Antineoplastic Agents↗
PubMed1975

Structure and stereochemistry of some 1,2-disubstituted mitosenes from solvolysis of mitomycin C and mitomycin A.

Starting with mitomycin C (1), a number of solvolytic reactions were investigated and were found to result in opening of the aziridine ring with loss or migration of the 9a-methoxy group. A careful examination of the resulting 1,2-disubstituted 7-aminomitosenes indicated that there was a strong tendency for the azridine ring on opening to furnish mainly one stereoisomer, always with the oxygen stom at C-1 and the nitrogen atom at C-2. Thus the hydrolysis of 1withdition to small amounts of the trans-aminohydrin (10). Mitomycin A (2) BEHAVED ANALOGOUSLY. Both 1 and 2 generated a cis-1-acetoxy-2-acetamide when they were allowed to react with acetic anhydride. Acetolysis of mitomycin C was found to give the cis-1-hydroxy-2-acetamide (5), the trans-1-acetoxy-2-amine (14), and a cis-trans mixture of 1-acetoxy-2-acetamides (4 and 11, respectively). Routes to cis-1-methoxy-2-acetamide (9) were possible through the methanolysis of 1 or through the methylation of 5. For comparison, the trans-1-methoxy-2-acetamide (16) was obtained through a dnown resin-catalyzed methoxy migration from C-9A TO C-1 IN MITOMYCIN C. The use of 1-H nmr spectroscopy to asign configurations to 1,2-disubstituted mitosenes is discussed.

Hydrolysis↗
PubMed2002

Randomized phase II study of irinotecan plus mitomycin C vs. oxaliplatin plus mitomycin C in patients with advanced fluoropyrimidine/leucovorin-pretreated colorectal cancer.

INTRODUCTION: Irinotecan and oxaliplatin are two new agents with promising activity in advanced colorectal cancer. Based on preclinical and clinical evidence that both drugs might act synergistically with mitomycin C, a randomized study using a 'pick the winner' design was undertaken to determine the effectiveness and tolerance of these two combination schedules in patients with fluoropyrimidine/leucovorin-pretreated advanced colorectal cancer. PATIENTS AND METHODS: Sixty-four patients with metastatic colorectal cancer, who progressed while receiving or within 6 months after discontinuing palliative chemotherapy with fluoropyrimidines/leucovorin were enrolled onto this study. They were randomly assigned to treatment with irinotecan 120 mg/m2 on days 1 + 15 plus mitomycin C 8 mg/m2 on day 1 (arm A) or oxaliplatin 85 mg/M2 on days 1 + 15 plus mitomycin C 8 mg/m2 on day 1 (arm B). In both treatment arms, courses were repeated every 4 weeks. RESULTS: The objective response rate in arm A is 7/33 (21.2%; 95% confidence interval, 9.0-38.9%) as compared to 5/31 in arm B (16.1%; 95% CI, 5.5-34.7%). Stable disease was noted in 48.5 vs. 45.2%, whereas the tumor progressed in 30.3 vs. 38.7%, respectively. Similar to the recorded response activities, the difference of the two combination regimens in terms of median time to progression (7.0 vs. 5.2 months) and overall survival (12.0 vs. 11.2 months) was only minor and clincally insignificant. The tolerance of treatment was acceptable in both arms, though severe adverse reactions requiring dose reductions (30 vs. 16%) and treatment delays (22 vs. 13% of courses) were more commonly noted with irinotecan/mitomycin C. The most common toxicities in arm A were neutropenia (85%; WHO grade 3/4 in 33%), thrombocytopenia (52%), diarrhea (45%), emesis (52%) and alopecia (92%). In arm B, common toxicities included neutropenia (68%; grade 3/4 in 13%), thrombocytopenia (81%), emesis (52%), and peripheral neutropathy (48%). CONCLUSIONS: Both mitomycin C combination regimens seem to provide an acceptable therapeutic index in patients with fluoropyrimidine/leucovorin-pretreated metastatic colorectal cancer. In view of the increasing need for a broader chemotherapeutic armentarium for second-line therapy of this common malignant disease, both regimens may be worthwhile to undergo further clinical investigation.

Adenocarcinoma↗
PubMed1996

Mitomycin C plus vindesine plus etoposide (MEV) versus mitomycin C plus vindesine plus cisplatin (MVP) in stage IV non-small-cell lung cancer: A phase III multicentre randomised trial. The "Gruppo Oncologico Centro-Sud-Isole' (G.O.C.S.I.).

PURPOSE: To compare mitomycin C plus vindesine plus etoposide (MEV) vs. mitomycin C plus vindesine plus cisplatin (MVP) in the treatment of stage IV non-small-cell lung cancer. PATIENTS AND METHODS: 204 patients were entered in a phase III multicentre randomised trial from June 1990 to December 1994 and stratified according to the ECOG performance status (0-1 vs. 2). MVP was given in the following dosages: mitomycin C 8 mg/m2+vindesine 3 mg/m2+cisplatin 100 mg/m2 i.v. day 1 and vindesine 3 mg/m2 i.v. day 8 with cycles repeated every 4 weeks. MEV was given in the following dosages: mitomycin C 8 mg/m2+vindesine 3 mg/ m2 i.v. day 1 and etoposide 100 mg/m2 i.v. days 1 to 3 with cycles repeated every 3 weeks. For both treatments a maximum of 6 cycles was planned. Response and toxicity were evaluated according to WHO. Subjective responses were assessed by numerical scales. Analyses were made on the basis of intent to treat. RESULTS: The objective response rate was 21.4% (1 CR + 21 PR among 103 patients) in the MEV and 28.7% (1 CR + 28 PR among 101 patients) in the MVP arm (P = 0.48). Symptoms were similar in the two arms. 196 patients progressed and 182 died. The median times to progression were 10 weeks (95% CI 9-12) and 12 weeks (95% CI 10-15) and median survivals were 29 weeks (95% CI 25-36) and 28 weeks (95% CI 25-35) in the MEV and MVP arms, respectively. The relative risks of progressing and of dying were 0.89 (95% CL 0.66-1.20) and 0.96 (95% CL 0.71-1.30), respectively, for patients receiving MVP as compared with those receiving MEV at multivariate analysis adjusted by sex, age, histologic type, number of metastatic sites, performance status at entry, and centre. CONCLUSIONS: In the present study, no significant differences were observed in response rate, survival or palliation of symptoms between the MEV and MVP regimens, while toxicity was significantly more frequent and severe with MVP. Thus, MEV should be considered a reasonable alternative to the MVP regimen in the treatment of stage IV NSCLC.

Adult↗
PubMed1997

KW-2149 (7-N-[2-[gamma-L-glutamylamino]ethyldithioethyl]mitomycin C). A new mitomycin C analogue activated by serum.

KW-2149 (7-N-[2-[gamma-L-glutamylamino]ethyldithioethyl]mitomycin C) is a new mitomycin-C analogue in clinical trial. This study demonstrates that KW-2149, unlike mitomycin C, is activated to a cytotoxic species by extracellular metabolism in serum. The metabolising activity differs between batches of serum and species of origin. Human serum had high activity (which resulted in a 150-fold enhancement of cytotoxicity), whereas mouse serum had low activity. In the presence of serum, the rate of uptake of 3H-KW-2149 into cells increased by 8-fold and drug binding to DNA by 32-fold. The metabolising activity of serum can partially be replaced by glutathione. No anticancer drug has previously been described whose toxicity is mediated by metabolism in serum.

Animals↗
PubMed1988

Conformations of complexes between mitomycins and decanucleotides. 3. Sequence specificity, binding at C-10, and mitomycin analogues.

Molecular mechanics simulation of the interactions of mitomycin C and certain analogues with DNA models are presented. The sequence specificity of mitomycin C binding was investigated by using a d(GCGCGCGCGC)2 decanucleotide duplex, abbreviated herein as GC10, in which the base pair was varied on either side of the covalent binding site. A CGT fragment was favored, although its correlation with the diverse findings in the literature is questionable. A model was derived for the monocovalent binding at C10 of 2,7-diaminomitosene with GC10 and for the noncovalently bound hydroquinone intermediate. Revised models were established for three highly active mitomycin C analogues: M-83, BMY-25282, and RR-150. They involved covalent binding at the 2-amino group of a guanine residue, and they accounted for enhanced noncovalent binding afforded by specific interactions of the C7 substituents with residues in GC10.

Animals↗
PubMed2002

Relative toxicities of DNA cross-links and monoadducts: new insights from studies of decarbamoyl mitomycin C and mitomycin C.

Mitomycin C (MC), a cytotoxic anticancer drug and bifunctional DNA DNA alkylating agent, induces cross-linking of the complementary strands of DNA. The DNA interstrand cross-links (ICLs) are thought to be the critical cytotoxic lesions produced by MC. Decarbamoyl mitomycin C (DMC) has been regarded as a monofunctional mitomycin, incapable of causing ICLs. Paradoxically, DMC is slightly more toxic than MC to hypoxic EMT6 mouse mammary tumor cells as well as to CHO cells. To resolve this paradox, EMT6 cells were treated with MC or DMC under hypoxia at equimolar concentrations and the resulting DNA adducts were analyzed using HPLC and UV detection. MC treatment generated both intrastrand and interstrand cross-link adducts and four monoadducts, as shown previously. DMC generated two stereoisomeric monoadducts and two stereoisomeric ICL adducts, all of which were structurally characterized; one was identical with that formed with MC, the other was new and unique to DMC. Overall, adduct frequencies were strikingly higher (20-30-fold) with DMC than with MC. Although DMC monoadducts greatly exceeded DMC cross-link adducts ( approximately 10:1 ratio), the latter were equal or higher in number than the cross-link adducts from MC. DMC displayed a much higher monoadduct:cross-link ratio than MC. The similar cytotoxicities of the two drug show a correlation with their similar DNA cross-link adduct frequencies, but not with their total adduct or monoadduct frequencies. This provides specific experimental evidence that the ICLs rather than the monoadducts are critical factors in the cell death induced by MC. In vitro, overall alkylation of calf thymus DNA by DMC was much less efficient than by MC. Nevertheless, ICLs formed with DMC were clearly detectable. The chemical pathway of the cross-linking was shown to be analogous to that occurring with MC. These results also suggest that the differential sensitivity of Fanconi's Anemia cells to MC and DMC is related to factors other than a selective defect in cross-link repair.

Alkylation↗
PubMed1986

Phase II studies of drug combinations in advanced pancreatic carcinoma: fluorouracil plus doxorubicin plus mitomycin C and two regimens of streptozotocin plus mitomycin C plus fluorouracil. The Gastrointestinal Tumor Study Group.

One hundred thirty-three patients with advanced pancreatic adenocarcinoma and measurable disease were treated with 5-fluorouracil (5-FU) plus doxorubicin plus mitomycin C (FAM), streptozotocin plus mitomycin C plus 5-FU (SMF) in the regimen originally reported, and streptozotocin plus mitomycin C plus 5-FU with 5-FU and streptozotocin administered in five-day courses. Respective response rates for all patients were 13%, 15%, and 14%, and for previously untreated patients, 14%, 14%, and 15%. Median survivals for all previously untreated patients range from 3 months (FAM) to 4 1/2 months (original SMF). Predominant toxic reactions were vomiting, leukopenia, and thrombocytopenia. Without evidence of greater therapeutic benefit, none of these regimens should be used in the routine treatment of advanced pancreatic carcinoma.

Adenocarcinoma↗
PubMed1985

[A clinical trial of a new mitomycin C derivative, KW-2083 (7-N-(p-hydroxyphenyl)-mitomycin C)].

KW-2083 [7-n-(p-hydroxyphenyl)-mitomycin C] is a new mitomycin C (MMC) derivative. Its myelotoxicity was compared with that of MMC by using colony-forming unit-spleen (CFU-S) from the femurs of C57BL/6 mice. As a result, it was estimated that the intensity of myelotoxicity of MMC was four times greater than that of KW-2083. Based on this data, a clinical trial of KW-2083 was conducted in 24 cases with various types of advanced solid tumors. KW-2083 was administered by i.v. injection at a dose of 40 mg/body every week. Out of 15 evaluable cases, a case of ovarian cancer showed a partial response. One case of each of ovarian cancer and gastric cancer showed minor response. However, as with mitomycin C, the dose-limiting toxicity of KW-2083 was leukopenia and thrombocytopenia. Other toxicities encountered were nausea, vomiting, anorexia, phlebitis and hepatic dysfunction. There were no cases with renal toxicity. Plasma concentration of KW-2083 was bioassayed in 3 cases who received 40 mg/body as an i.v. bolus injection. Plasma concentration-time curves fitted to a one-compartment model and half-life values averaged 27.6 min. The effective and low toxic dose schedules of KW-2083 should be investigated further.

Adult↗
PubMed2003

[Oral tegafur plus mitomycin versus intravesical mitomycin alone in the prevention of recurrence in stage Ta bladder tumors].

OBJECTIVE: The aim of this study is to know if the use of oral Tegafur associated to intravesical mitomycin is effective in the prevention of the relapses of Ta bladder tumors. METHOD: This is a prospective study in which we compare the recurrence rate and the disease-free interval of 2 groups of 40 patients each one, the first of them treated after the TUR with oral Tegafur and intravesical mitomycin, and the second with intravesical mitomycin alone. Tolerance of Tegafur was also studied. RESULTS: The group of the Tegafur presented a descent of the relapse rate and a continuation of the time free of illness; but it was not statistically significant. The tolerance to the drug was good, without important adverse effects. CONCLUSIONS: Tegafur seems an useful drug in the prevention of the recurrence of superficial bladder tumors, although it will be necessary bigger studies to reach statistically valid conclusions.

Administration, Intravesical↗
PubMed1991

A randomized trial in inoperable non-small-cell lung cancer: vindesine and cisplatin versus mitomycin, vindesine, and cisplatin versus etoposide and cisplatin alternating with vindesine and mitomycin.

Patients with inoperable non-small-cell lung cancer (NSCLC) were randomly assigned to receive one of three dosage regimens: (1) vindesine and cisplatin (VP); (2) mitomycin, vindesine, and cisplatin (MVP); or (3) etoposide and cisplatin alternating with vindesine and mitomycin (EP/VM). In 199 assessable patients, the response rates were VP, 33%; MVP, 43%; and EP/VM, 19%. The addition of mitomycin to the VP regimen did not significantly improve the response rate. The response rate was significantly lower with the EP/VM regimen than with the MVP regimen (P less than .01). The median survival times were VP, 50 weeks; MVP, 42 weeks; and EP/VM, 40 weeks. These differences were not significant. Grade III or IV thrombocytopenia was significantly greater (P less than .01) in MVP patients (22%) than in the VP (5%). Other toxicities were similar in the three groups. Analyses of prognostic factors showed that treatment with MVP, sex, and histologic classification (squamous cell carcinoma) were predictive of improved response. Important factors for improved survival, according to the Cox regression analysis, were the stage of disease, performance status, sex, weight loss before diagnosis, and hemoglobin concentration.

Adult↗
PubMed1989

Synthesis and antitumor activity of a novel water soluble mitomycin analog; 7-N-[2-[[2-(gamma-L-glutamylamino)ethyl]dithio]ethyl]mitomycin C.

Introducing the mercaptoethyl group at the 7-N position of mitomycin C 1 has led to the isolation of 7-N,7'-N'-dithiodiethylenedimitomycin C 2. The compound 2 showed excellent antitumor activity against sarcoma 180 (sc-ip) and leukemia P388 (ip-ip) in mice. As an extension of this study, we synthesized mitomycin dimers with symmetrical disulfide and mitomycin derivatives with unsymmetrical disulfide at the 7-N side chain. Among these compounds, the water soluble conjugate 3 with ethyl gamma-L-glutamyl-L-cysteinylglycinate was far more effective against sarcoma 180 and leukemia P388 than 1. During the subsequent stage of inquiry for the potent congeners of 3, the compound 4 (water solubility: greater than 500 mg/ml), designated as KW2149, with the gamma-L-glutamylcystamino group at the 7th position was finally selected for further evaluation.

Animals↗
PubMed2003

Comparison of single-drop mitomycin C regime with other mitomycin C regimes in pterygium surgery.

PURPOSE: To evaluate the safety and efficacy of single-drop instillation of mitomycin C (MMC) in pterygium surgery and to compare the results with both postoperative and intraoperative application of MMC. METHODS: Eighty eyes of 72 patients with pterygium were randomised into 4 equal groups: group 1--control--bare scleral excision (BSE); group 2--BSE with single-drop instillation of mitomycin C (MMC) 0.02% at the end of the surgery; group 3--BSE with postoperative MMC 0.02% drops twice a day for 5 days; and group 4--BSE with intraoperative MMC 0.02%. RESULTS: The recurrence of pterygium was observed in 14 (70%), 4 (20%), 4 (20%) and 3 (15%) eyes of group 1, 2, 3, and 4 respectively. The recurrence rate after BSE with single drop MMC regime (group 2) was significantly lower than group 1 recurrence (P=0.001) and was statistically comparable to that of group 3 and 4. Scleral defects in the bare area occurred in 4 (20%), 16 (80%) and 16 (80%) eyes of group 2, 3, and 4 respectively. The incidence of scleral defects was significantly lower in group 2 compared to group 3 (P=0.0001) and group 4 (P=0.0001). Compared to group 1 and 2, a significant delay in wound epithelialisation occurred in group 3 (P=0.003) and 4 (P=0.004). An ischaemic area in the bare sclera developed in 8 (40%) and 6 (30%) eyes of group 3 and 4 respectively, while ischaemic area did not develop in group 1 and 2. CONCLUSION: Single-drop instillation of 0.02% mitomycin C following pterygium excision appears both safe and efficacious.

Adolescent↗