Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “MITOMYCIN”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources

Mitomycin C-augmented production of I-A antigen-positive macrophages in tumor vaccine-primed mice.

Intraperitoneal inoculation of L1210 murine leukemia cell vaccine increased I-Ad antigen-positive and -negative macrophages in the peritoneal cavity of histocompatible mice. Mitomycin C, a poor producer of I-Ad antigen-positive macrophages, selectively augmented the production of I-Ad antigen-positive macrophages in L1210 vaccine-primed mice, since it did not augment the production of non-macrophage cells. Since our previous study showed that the priming of mice with L1210 vaccine and mitomycin C induced augmented antitumor response, we tested the feasibility of the association of mitomycin C-augmented I-Ad antigen-positive macrophages with the augmented antitumor response. Prostaglandin E2 suppressed the antitumor response in L1210 vaccine- and mitomycin C-primed mice and, consistent with this, it inhibited the production of I-Ad antigen-positive macrophages, although it inhibited the production of non-macrophage cells as well. This hypothesis was further tested by the use of silica. When L1210 vaccine- and mitomycin C-primed mice were further given silica on the day of and one day after live L1210 inoculation, their antitumor response was strongly suppressed, while a kinetic analysis of the cellularity of peritoneal cells showed that administration of silica resulted in a decrease of I-Ad antigen-positive macrophages, but not I-Ad antigen-negative macrophages or non-macrophage cells in these mice. These results strongly suggest, though they do not prove, the association of mitomycin C-augmented production of I-Ad antigen-positive macrophages with the antitumor response in L1210 vaccine- and mitomycin C-primed mice.

Animals↗

Mitomycin-induced chromatid breaks in HeLa cells: a consequence of incomplete DNA replication.

The formation of chromosome aberrations induced by alkylating agents such as mitomycin C has been shown to require the passage of the treated cell through S phase. However, the exact mechanisms by which mitomycin C-induced DNA lesions are translated into chromosome aberrations during S phase are not known. The purpose of these studies was to better understand the molecular basis of chromosome aberration formation after mitomycin C treatment. The morphology of metaphases of cells treated in G1 phase with mitomycin C resembled that of prematurely condensed chromosomes of S-phase cells. Consequently we postulated that chromosome aberrations resulted from cells reaching mitosis without completing DNA replication. This was tested by treating HeLa cells in G1 phase with mitomycin C and then analyzing these cells at mitosis for residual DNA damage and DNA content. Utilizing the DNA alkaline elution assay for DNA damage, we showed that HeLa cells progress through S phase into mitosis with intact DNA-DNA interstrand cross-links. These cross-links, originally induced into parental DNA, were associated equally with parental and newly replicated DNA at the time the cells reached mitosis. This suggests that recombinational events had taken place during the DNA replication process. Cells that were treated in G1 phase and allowed to proceed to mitosis in the presence of bromodeoxyuridine to density label newly replicated DNA were analyzed with cesium chloride density sedimentation. Unreplicated DNA was present in the mitotic cells of the treated populations but not in the untreated control cells. Further, flow cytometric measurements, made under hypotonic conditions in order to reduce chromatin condensation effects, demonstrated that the mitotic cells from the mitomycin C-treated populations contained 10-20% less DNA than untreated mitotic controls. These results indicate that chromosome breaks induced by mitomycin C are the result of cells reaching mitosis without having fully completed DNA replication.

Chromatids↗

New findings in the pharmacokinetic, metabolic, and drug-resistance aspects of mitomycin C.

The pharmacokinetics of mitomycin C are reviewed from reports using specific and sensitive high-performance liquid chromatography (HPLC) assays. These studies demonstrate a rapid, biphasic elimination pattern for the drug: alpha half-life of 8 minutes and beta, or terminal, half-life of 48 minutes. Urinary elimination of intact drug is minimal (8% to 10% of a dose), whereas biliary drug levels may exceed those in the plasma. There was no evidence of dose dependent pharmacokinetics over a wide range of doses and patient populations, including pediatric solid tumor patients. Metabolic studies with mitomycin C have demonstrated an absolute requirement for reductive enzymatic activation of the drug to mono- and bifunctional alkylating species. The preferred DNA target for covalent attachment by mitomycin C was found to be the N2 position of guanine. Chemical metabolites of activated mitomycin C were also demonstrated to include 2, 7 diaminomitosene and its cis- and trans-1-hydroxy or 1-phosphate analogues. Also, there was no evidence for hypoxic cell selectivity for mitomycin C in several human tumor cell lines, although some animal tumors unequivocally display this phenomenon. Finally, there are new observations of the development of the multidrug-resistance phenotype in mitomycin C-treated L-1210 cells in vitro. These cells became collaterally resistant to anthracyclines and vinca alkaloids and expressed the P-glycoprotein in cell membranes. The implications of these findings for mitomycin C use in solid tumors in humans is discussed.

Biotransformation↗

A bioassay to measure cytotoxicity of plasma from patients treated with mitomycin C.

The unpredictable clinical toxicity observed in patients treated with mitomycin C and the observation that this agent must be reduced to an active form before alkylating target molecules have led to the development of a bioassay which is capable of detecting biologically active forms of mitomycin C in the plasma of drug-treated patients. The bioassay makes use of a repair-deficient mutant of Chinese hamster ovary cells, UV-20, which is 40 to 60 times more sensitive to mitomycin C than its wild-type parent. A standard curve relating in vitro cell colony-forming ability of UV-20 versus drug concentration in the plating medium has been determined. Mitomycin C levels in patient plasma as low as 1 ng/ml can be detected, compared to the 5-ng/ml limit of detection obtained with a high-pressure liquid chromatography assay for the parent compound. This assay has been utilized to detect active drug in plasma obtained from patients with colorectal cancer treated with mitomycin C as a single agent. At the completion of drug injection, serial blood samples were collected in heparinized tubes, and aliquots of plasma were extracted and assayed for mitomycin C levels by high-pressure liquid chromatography, diluted and assayed directly for their toxicity for UV-20 cells, or frozen at -20 degrees C to be assayed at a later time. The activity detected by immediate bioassay was stable up to 2 mo in frozen samples. Plasma pharmacokinetics determined by the bioassay in seven patients were no different than those determined by high-pressure liquid chromatography. No stable, cytotoxic species other than the parent compound were detected by the bioassay in the plasma of patients treated with mitomycin C.

Animals↗

Mitomycin: its evolving role in the treatment of breast cancer.

Investigators have compiled extensive experience with mitomycin in the treatment of patients with breast cancer. Given as a single agent in intermittent schedules, mitomycin has induced responses of 26-38% in previously untreated patients and of 15-25% in those exposed to multiple prior chemotherapy regimens. Duration of response has been short. Toxicity, primarily myelosuppression, is largely dose-dependent. The dose-dependent efficacy of mitomycin has not yet been addressed. Preclinical studies suggest that optimal single-agent results are obtained when mitomycin is given in intermittent, high-dose schedules. Combination chemotherapy with mitomycin has proven more effective than single-agent therapy. Mitomycin given in combination with doxorubicin produces higher response rates than have been obtained with mitomycin alone. The 3M combination (mitomycin/mitoxantrone/methotrexate) appears effective and well tolerated at the doses described. Future research should focus on the development of polychemotherapeutic regimens that can be delivered in sequential or alternating schedules. Such regimens may yield quicker responses, and thus improve survival, in patients with breast cancer.

Antineoplastic Combined Chemotherapy Protocols↗

Effect of topical mitomycin on skin wound contraction.

OBJECTIVE: To evaluate the effect of different dosing regimens of mitomycin on skin wound contraction. METHODS: Full-thickness skin wounds were created in 5 groups of hairless mice, which represented different dosing regimens or a sterile water control: A, control; B, mitomycin (0.5 mg/mL) applied immediately after creation of the lesion (day 1); C, mitomycin (1.0 mg/mL) applied on day 1; D, mitomycin (0.5 mg/mL) applied on days 1 and 3; and E, mitomycin (1.0 mg/mL) applied on days 1 and 3. Wound surface area was measured immediately after drug application (day 1), and thereafter every 3 to 5 days until day 29 by means of computer-assisted image analysis. RESULTS: All dosing regimens of mitomycin application resulted in an initially exponential rate of wound contraction that was significantly slower than in the sterile water control group, with a significantly larger wound surface area on day 29. Wound area in the control group contracted approximately 9 times more rapidly than in the treatment groups. No difference was observed among the different dosing regimens. CONCLUSION: Application of mitomycin, at the lowest dose and frequency of application used in this study, resulted in improved outcomes with regard to contraction of full-thickness skin wounds.

Administration, Topical↗

A long-term dose-response study of mitomycin in glaucoma filtration surgery.

OBJECTIVE: To establish the long-term, dose-response relationship between the concentration of and duration of exposure to mitomycin to a decrease in intraocular pressure (IOP) and fewer complications. METHODS: We performed a prospective double-masked, placebo-controlled, 1-year study evaluating the decrease in IOP and fewer complications of fornix-based trabeculectomy surgery in 300 eyes equally divided among therapy with placebo; mitomycin, 0.2 mg/ mL, applied for 2 minutes; mitomycin, 0.4 mg/mL, applied for 4 minutes; or mitomycin, 0.4 mg/mL, applied for 2 minutes. All of the eyes had vertical and horizontal cup-disc ratios greater than 0.7. RESULTS: We observed significant treatment-related differences in IOP, with a decrease in IOP in all 3 mitomycin-treated groups for all of the times beyond 1 month. The number of eyes achieving strict IOP control and the development of cataract suggest a possible dose-response effect for concentration and time of exposure. Progressive lens opacification was the most frequent complication in 54 eyes (18.1%). The incidence of progressive lens changes markedly increased in subjects receiving 4 minutes of mitomycin therapy. Cataract formation was unrelated to IOP. Other complications were rare. Macular folds developed in 6 patients, with visual acuity returning to better than 20/40 in all but 1 patient. CONCLUSIONS: A possible dose-response relationship seemed to exist between the concentration of and duration of exposure to mitomycin. Length of exposure seems to be more important than concentration. The benefits of additional decreases in IOP must be weighed against the potential for increases in the risk of complications.

Antibiotics, Antineoplastic↗

Possible mechanism of congenital malformations induced by exposure of mouse preimplantation embryos to mitomycin C.

ICR mice were treated intraperitoneally with mitomycin C at 5 mg/kg on day 3 of gestation. On day 18 of gestation, fetuses of treated dams were inspected for external, skeletal and visceral malformations. At 6 or 12 hr after mitomycin C treatment, the blastocysts were obtained from the uteri of treated dams and the degenerated cells within inner cell mass (ICM) and trophectoderm (TE) tissues were examined microscopically. On day 5, 8, 11, or 18 of gestation, the uteri of treated dams were obtained and those including embryos/fetuses and placentae were examined histologically. Finally, on each of gestational days 5-14, the blood of the treated dams was collected and the hematological parameters determined. Pre- and postimplantation losses in the dams treated with mitomycin C were significantly increased; increased frequency of abdominal wall defects and lumbar ribs in term fetuses, decreased fetal weight, and increased placental weight were noted as well. No significant increase in visceral malformations was found in term fetuses treated with mitomycin C. Frequency of degenerated cells within ICM and TE of blastocysts from dams treated with mitomycin C was significantly increased as compared with the controls. In dams treated with mitomycin C, decidua developed insufficiently and the trophoblast giant cell layer was not separated from the uterine lumen by maternal components; hemorrhage from the denuded trophoblast giant cell layer into the uterine lumen was noted. The number of erythrocytes, as well as hemoglobin concentration, hematocrit, and the percentage of reticulocytes in blood of dams treated with mitomycin C were significantly lower from days 6-12 of gestation, as compared with controls. The results of the present study showed that an increase in number of degenerated cells within blastocysts results in preimplantation loss and both maternal and embryonic hypoxia during major organogenesis results in postimplantation loss and congenital fetal malformations.

Abnormalities, Drug-Induced↗

Influence of mitomycin C on endothelial monolayer regeneration in vitro.

This study examines the effect of Mitomycin C, a fungal toxin which inhibits DNA synthesis, on the regeneration of partially denuded large vessel endothelium in vitro. Monolayers of bovine pulmonary artery endothelial cells were treated with Mitomycin C prior to or immediately following partial denudation and were incubated in the continuing presence of Mitomycin C; the effects of this treatment on monolayer repair, cell proliferation, and other aspects of endothelial phenotype were monitored. Cell proliferation, DNA, RNA, and protein synthesis were all reduced in a dose dependent manner in treated cultures. Incubation with Mitomycin C for 48 h or longer resulted in reduced cell spreading, and rounding up and loss of cells from both intact and partially denuded cultures. Effects were less severe with lower doses and shorter incubation times. However, significant reductions in monolayer regeneration occurred within 8 h of incubation, sufficiently early to suggest that Mitomycin C may affect aspects of the regeneration process independent of cell proliferation. Polarization/spreading of cells at the denudation edge was monitored by fluorescence staining for golgi with C5-DMB-ceramide, and for centrioles with antibodies to tubulin. Centrioles and golgi rapidly reoriented to a location at the putative leading edge of control cultures. Mitomycin C treatment had no effect on centriole reorientation, but caused a significant delay in golgi localization. These results suggest that Mitomycin C inhibits endothelial monolayer regeneration by mechanisms independent of cell proliferation and DNA synthesis, perhaps by interfering with cell spreading or translocation at the wound edge.

Animals↗

DT-diaphorase in activation and detoxification of quinones. Bioreductive activation of mitomycin C.

A role of DTD in the bioreductive activation of mitomycin C was supported by indirect evidence utilizing enzyme inhibitors in cellular systems. Using a cell-free system, we have confirmed that DTD can bioactivate mitomycin C using both purified rat and human DTD. Metabolism and bioactivation of mitomycin C by DTD is pH-dependent. At pH 7.8 alkylation of DTD leading to enzyme inhibition and DTD crosslinking occurs whereas at pH values of 7.4 and below metabolite formation, preservation of catalytic activity of DTD and sequence-selective DNA crosslinking occurs. Bioactivation of mitomycin C by DTD and the cytotoxicity of this drug in DTD-rich cell lines is oxygen-independent. Mitomycin C induces greater DNA crosslinking, even after chemical reduction, at lower pH values. This suggests that if mitomycin C is used in tumors with elevated DTD activity, greater therapeutic activity may be obtained by lowering intratumoral pH. Human NSCLC has elevated DTD activity relative to SCLC and normal lung and may be a target for the development of drugs which can be efficiently bioactivated by DTD. Because of the pH-dependent inactivation of DTD by mitomycin C, however, other drugs which are efficiently metabolized and bioactivated by DTD may be better candidates for the therapy of tumors high in DTD such as NSCLC.

Animals↗

Treatment of adenocarcinoma of the liver with mitomycin, hyaluronidase, and ethanol: an experimental study in the rat.

PURPOSE: To evaluate the effect of intratumorally injected ethanol, mitomycin, mitomycin with hyaluronidase, and hyaluronidase on tumor growth in an experimental model. METHODS: A suspension of 1 x 10(6) cells of chemically induced adenocarcinoma was implanted into the liver of 52 rats. Seven days later the rats were divided into groups according to treatment and injected via a midline laparotomy with ethanol, mitomycin, mitomycin with hyaluronidase, or hyaluronidase. A control group was treated with saline. The rats were killed 7 days after treatment. The tumor growth ratio was calculated, and the results compared for the different groups. Wilcoxon's rank sum test was used for statistical evaluation. RESULTS: The tumor growth ratio was significantly reduced after injection of mitomycin (p < 0.01) but not after ethanol. Hyaluronidase alone did not reduce the tumor growth ratio and had no synergetic effect with mitomycin. CONCLUSION: In an animal model intratumoral treatment of adenocarcinoma of the liver with mitomycin was significantly more efficient than similar treatment with saline or ethanol.

Adenocarcinoma↗

Pharmacokinetic changes induced by the volume of chemotherapy solution in patients treated with hyperthermic intraperitoneal mitomycin C.

BACKGROUND: The rationale supporting the use of intraperitoneal chemotherapy in peritoneal surface malignancy relates to a large local-regional effect and low systemic toxicity. While optimizing the use of this treatment strategy, little information regarding the effect of volume of chemotherapy solution is available. OBJECTIVE: The goal of this study was to provide data regarding the effect of volume of chemotherapy solution on the pharmacokinetics of intraperitoneal chemotherapy. Data by which to optimally adjust this parameter during intraperitoneal chemotherapy treatments were sought. METHODS: Forty-eight patients with peritoneal surface malignancy were treated with hyperthermic intraperitoneal mitomycin C chemotherapy after a complete cytoreduction to remove all visible evidence of mucinous tumor. The dose of mitomycin C was always 12.5 mg/m(2) in males and 10 mg/m(2) in females. The first 12 patients were treated with 6 l of 1.5% dextrose peritoneal dialysis solution. The next 14 patients were treated with 4 l of fluid and then ten patients were treated with 2 l. In the last 12 patients the volume of fluid was 1.5 l/m(2) . Blood, peritoneal fluid, and urine samples were obtained every 15 min for 90 min; additional blood and urine samples were obtained at 120 min. Mitomycin C concentrations, urine volumes, and final intraperitoneal fluid volume were obtained. RESULTS: The intraperitoneal and the plasma concentrations were highest in the 2-l group, less in the 4-l group, and least in the 6-l group. All differences were statistically significant. Also, the percent of mitomycin C absorbed decreased significantly from 2, to 4, to 6 l of fluid. The area under the curve (AUC) ratio of intraperitoneal concentration times time to intravenous concentration times time was 27.01+/-4.92 for 2 l, 22.22+/-7.95 for 4 l, and 24.01+/-8.46 for 6 l. These differences were not statistically significant. If both the volume of chemotherapy solution and the total dose of mitomycin C were determined from the body surface area, the pharmacokinetics of intraperitoneal mitomycin C were more consistent. CONCLUSIONS: In order to prescribe a uniform treatment for patients receiving hyperthermic intraperitoneal mitomycin C, the total dose of the drug and the total volume of chemotherapy solution should be determined from the body surface area. If the volume of chemotherapy solution is not based on patient body surface area, predictions regarding toxicity are less precise.

Adenocarcinoma, Mucinous↗

Mitomycin C as an adjunct to postoperative radiation therapy in squamous cell carcinoma of the head and neck: results from two randomized clinical trials.

PURPOSE: This study was undertaken to assess the benefit of mitomycin C as an adjunct to postoperative radiation therapy in patients with operable squamous cell carcinoma of the head and neck. METHODS AND MATERIALS: Between May 1980 and May 1991, 182 patients have been enrolled in two consecutive randomized clinical trials testing mitomycin C as an adjunct to radiation therapy in squamous cell carcinoma of the head and neck. In both trials, patients were stratified by stage, disease site and intent of therapy. This subset analysis includes 113 patients entered into these two randomized trials treated with surgery and postoperative radiation therapy. In the first trial, patients were randomized to receive standard postoperative radiation therapy alone compared with postoperative radiation therapy with concomitant mitomycin C. In the second trial, patients were randomized to postoperative radiation therapy or postoperative radiation therapy with concomitant mitomycin C plus dicoumarol. RESULTS: As of November 1991, the 113 patients treated with surgery and postoperative radiation therapy in both trials had a median follow-up of 93 months. There have been a total of 12 local recurrences in the radiation therapy alone arm compared to 0 local recurrences in the radiation therapy/mitomycin C arm. There were eight regional recurrences in the radiation therapy alone arm compared with five regional recurrences in the mitomycin C arm. Patients in the mitomycin C arm experienced a superior 5-year actuarial local regional control rate (87% vs. 67%, p < .015) and a statistically significant disease-free survival benefit (67% vs. 44%, p < .03). Overall survival difference between the two arms (56% vs. 41%) has not reached statistical significance. CONCLUSIONS: We conclude from these prospectively designed randomized clinical trials that in patients with operable head and neck cancer treated with surgery and postoperative radiation therapy, concomitant administration of mitomycin C with radiation therapy will result in a statistically significant disease-free survival and local regional control benefit. We are currently investigating the value of other bioreductive alkylating agents as adjuncts to radiation therapy in patients with squamous cell carcinoma of the head and neck.

Adult↗

Effect of mitomycin C on anterior urethral stricture recurrence after internal urethrotomy.

OBJECTIVES: Urethral stricture is one of the oldest known urologic diseases and remains a common problem with high morbidity. Internal urethrotomy refers to any procedure that opens the stricture by incising or ablating it transurethrally. The most common complication of internal urethrotomy is stricture recurrence. The curative success rate of internal urethrotomy is approximately 20%. Mitomycin C has antifibroblast and anticollagen properties and in sporadic reports of animal and clinical studies it has increased the success rate of trabeculectomy and myringotomy. This study evaluated the efficacy of mitomycin C in the prevention of anterior urethral stricture recurrence after internal urethrotomy. PATIENTS AND METHODS: Forty male patients with anterior urethral strictures were randomized to undergo internal urethrotomy with or without urethral submucosal mitomycin C injection. Using general anaesthesia, the urethrotomy was performed under direct vision. Mitomycin C (0.1mg) was injected submucosally at the urethrotomy site in 20 patients. The patients were re-evaluated after 6 mo and the stricture recurrence rate was compared between the two groups (chi(2) analysis). RESULTS: Urethral stricture recurred in 2 patients (10%) in the mitomycin C-treated group and in 10 patients (50%) in the other group. This difference in stricture recurrence between the two groups was statistically significant (p=0.006). CONCLUSIONS: To our knowledge, this is the first prospective, randomized, clinical trial to evaluate the efficacy of mitomycin C application in internal urethrotomy. Submucosal injection of mitomycin C significantly reduced stricture recurrence after internal urethrotomy. Further investigations are warranted to confirm its efficacy and safety.

Adolescent↗

In vitro effect of cyclosporin A, mitomycin C and prednisolone on cell kinetics in cultured human umbilical vein endothelial cells.

INTRODUCTION: Vascular endothelial cell damage plays an important role in microvascular thrombogenesis. In vivo administration of cyclosporin A or mitomycin C sometimes results in thrombotic microangiopathy in patients. MATERIALS AND METHODS: The effects of cyclosporin A, mitomycin C and/or prednisolone on the cell cycle in cultured human umbilical vein endothelial cells were investigated to evaluate drug-induced endothelial cell damage and the protective effect of prednisolone on endothelial cells against the damage by cyclosporin A or mitomycin C in vitro. RESULTS: The addition of cyclosporin A to cultures caused proliferation arrest in the G1-phase in a dose-dependent manner, while mitomycin C inhibited DNA synthesis, which resulted in cell cycle arrest and inhibition of BrdUrd incorporation in the S-phase. The administration of prednisolone also caused cell cycle arrest in the G1 by itself, and protected the cells from the damage caused by mitomycin C. The inhibitory effects of cyclosporin A and prednisolone on the cell cycle were reversible, while mitomycin C was not. The highly phosphorylated retinoblastoma protein expressed in human umbilical vein endothelial cells decreased in the presence of mitomycin C. Soluble thrombomodulin levels in the culture supernatant were elevated by the addition of cyclosporin A. CONCLUSION: These effects of the drugs may cause the cell cycle arrest and the prolonged repair of damaged endothelial cells in patients.

Blotting, Western↗

Trabeculectomy with intraoperative 5-fluorouracil vs mitomycin C.

PURPOSE: To compare the effectiveness of intraoperative 5-fluorouracil (5-FU) and mitomycin C used adjunctively with trabeculectomy in a black West African population. METHODS: Eighty-five consecutive eyes of 85 black patients undergoing primary trabeculectomy for open-angle glaucoma were prospectively randomly assigned to receive either 5-FU (50 mg/ml for 5 minutes) or mitomycin C (0.5 mg/ml for 3 1/2 minutes) intraoperatively by soaked sponge. RESULTS: Of the 81 eyes with at least a 3-month postoperative follow-up, 41 of 44 (93.2%) in the mitomycin C group and 27 of 37 (73.0%) in the 5-FU group had a final intraocular pressure of less than 21 mm Hg (P = .01). Twenty-eight of 44 eyes (63.6%) in the mitomycin C group and 18 of 37 (51.4%) in the 5-FU group had a final intraocular pressure of less than 15 mm Hg (P = .26). Mean postoperative intraocular pressure was 13.7 mm Hg in the mitomycin C group and 16.3 mm Hg in the 5-FU group (P = .05). There were no differences between the two groups in mean age, preoperative intraocular pressure, postoperative visual acuity, and complications. Mean follow-up was 10.0 +/- 4.41 months (range, 4 to 19 months). CONCLUSIONS: The adjunctive use of mitomycin C with trabeculectomy is equally safe and more efficacious compared to 5-FU in this West African population. Use of mitomycin C in this study was not associated with a statistically significantly greater proportion of patients achieving low intraocular pressure (less than 15 mm Hg) compared to 5-FU.

Antimetabolites↗

Primary glaucoma triple procedure in patients with primary open-angle glaucoma: the effect of mitomycin C in patients with and without prognostic factors for filtration failure.

PURPOSE: To investigate the effect of adjunctive mitomycin C on primary glaucoma triple procedure in patients with primary open-angle glaucoma with and without one or more of the prognostic factors for filtration failure of primary glaucoma triple procedure. Those factors include being of African-American race, having a preoperative intraocular pressure of 20 mm Hg or more on maximum tolerated medications, and being on two or more medications preoperatively. METHODS: Study patients consisted of 197 consecutive patients with primary open-angle glaucoma who were randomly assigned to receive either no adjunctive mitomycin C (101 eyes of 101 patients) or to receive adjunctive subconjunctival mitomycin C (96 eyes of 96 patients) during the primary glaucoma triple procedure. Kaplan-Meier survival analysis comparisons were made between respective subgroups with and without prognostic indicators for filtration failures using a relatively stringent set of criteria for filtration success of primary glaucoma triple procedure. RESULTS: There was no statistically significant (P = .117) difference in filtration success of primary glaucoma triple procedure between the control and mitomycin C groups. Adjunctive mitomycin C significantly (P < .05) improved the filtration outcome of the primary glaucoma triple procedure in the subgroups with each of the three prognostic factors for filtration failure of primary glaucoma triple procedure. On the other hand, in the subgroups without the prognostic factors, adjunctive mitomycin C did not significantly (P > .05) change the filtration outcome of the primary glaucoma triple procedure. CONCLUSION: These findings establish the basis for selective use of mitomycin C in patients with primary open-angle glaucoma undergoing primary glaucoma triple procedure.

Aged↗

Effect of topical mitomycin C on glaucoma filtration surgery in monkeys.

In this study, an experimental model of glaucoma filtration surgery was used to evaluate the clinical and histologic effects of a single intraoperative topical application of mitomycin C. Argon laser treatment to the trabecular meshwork produced sustained elevation of intraocular pressure in monkeys. Eight eyes of four animals were randomly assigned to receive topical mitomycin C or balanced salt solution at the time of full-thickness sclerostomy. Surgical success was substantially increased in four of five eyes that received mitomycin C when compared with three eyes that received topical balanced salt solution. Mitomycin C was also effective in prolonging surgical success in two eyes that had previously undergone surgery and failed. No significant ocular toxicity was observed in eyes treated with mitomycin C. Histologic examination of mitomycin C-treated eyes showed patent sclerostomies and hypocellular, well-formed bleb cavities. A single intraoperative application of mitomycin C has a marked effect on postoperative wound healing after filtration surgery in monkeys.

Administration, Topical↗