Crossover study with cisplatin or carboplatin in advanced ovarian cancer

Crossover study with cisplatin or carboplatin in advanced ovarian cancer

Citations from Adjuvant chemotherapy cyclopbosphamide (PAC) cancer: A preliminary Stringer with cisplatin, for early-stage doxorubicin, high...

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Citations from

Adjuvant

chemotherapy

cyclopbosphamide

(PAC)

cancer: A preliminary

Stringer

with

cisplatin,

for early-stage

doxorubicin, high-risk

and

endometrial

analysis

CA; Gershenson

DM: Burke TW: Edwards

the Literature

19

quently abnormal. These data also suggest that alterations of these chromosomes may be associated with the biologically aggressive behavior of frankly invasive ovarian tumors.

CL; Gor-

don AN: Wharton JT 3320 Live Ouk. Dollu.~. TX 75204. USA GYNECOL ONCOL 1990 38/3 (305-308) Between October 1985 and January 1989.33 patients with stage I (31) or clinically occult stage II (2) endometrial cancer at a high risk for recurrence were entered in a prospective study evaluating adjuvant cisplatin, doxorubicin. and cyclophosphamide (PAC) chemotherapy. Eligibility criteria included grade 2 tumors with middle- or outer-third myometrial invasion (16). grade 3 tumors with any degree of myometrial invasion (17). presence of extrauterine disease with no gross residual (17). or a high-risk histologic subtype including papillary serous (4). adenosquamous

Crossover study with cisplatin or carboplatin in advanced ovarian cancer

Repetto L; Chiara S; Mammoliti S; Guido T; Bruzzone M; Secondo V: Donadio G; Odicino F; Ragni N; Conte PF; Rosso R Istituto Na:iunale Ricerca Cancro, Viule Benedetto XV, IO. 16132~Genoa. ITA GYNECOL ONCOL 1990 39/2 (146-149) Fifty-seven patients who had progressed during or relapsed after randomized first-line combination chemotherapy containing cisplatin or carboplatin were entered into a crossover study in which the analog not previously assigned was administered alone as salvage treatment. Carboplatin and cisplatin were ad-

(5). or clear cell (I) tumors. Patients received PAC (50/50/500 mg/m’) at 4-week intervals for six cycles. Thirty patients (90%) completed therapy. Toxicity included severe neutropenia in I4 patients. neutropenic sepsis in 2 patients, and doxorubicin-related cardiomyopathy in I patient. There were no treatment deaths. Current median follow-up is 25 months. Nine patients (27%) have developed a recurrence, 7 of whom died, after a median interval of I4 months. Eight of the 9 with recurrence initially had ex-

ministered at doses of 400 and 100 mg/m’. respectively. every 28 days. Among the 24 patients enrolled in the cisplatin arm. 6 (25%) objective responses (ORs) (3 complete, 3 partial) were observed, whereas 3 partial responses were obtained in the 33 carboplatin-treated patient (9%). Analysis of results, according to response to first-line chemotherapy, demonstrated that the patients who progressed were sensitive only to cisplatin secondline treatment (OR: 3/12). with no responders among carboplatin-

trauterine disease (P = 0.02). The resulting 2-year progression-free and overall survival rates were 79 respectively. The median progression-free interval was for patients with extrauterine disease and 45+ months

actuarial and 83%. 29 months for those

treated patients (OR: O/l I). All patients were treated on an outpatient basis and therapy-related toxic effects were mild, consisting chiefly of myelosuppression, and more frequent in the carboplatin group. In our opinion, carboplatin 400 mg/m’ per

with no extrauterine disease (P = 0.02). These results suggest that a phase 3 randomized trial comparing adjuvant PAC with radiation therapy is warranted.

cycle is scarcely effective in patients with refractory or relapsed ovarian cancer pretreated with cisplatin regimens. whereas cisplatin 100 mgIm2 per cycle appears to be an effective salvage therapy even in patients not responding to carboplatin. The dose of carboplatin should be further escalated especially in refractory patients.

Chromosome abnormalities in human epithelial ovarian malignancies

Gallion HH; Powell DE; Smith LW: Morrow JK; Martin AW; Van Nagell JR; Donaldson ES Division of Gynecologic Oncology, Depurtment of Obstetrics orid Gynecology. University of Kentucky Medicul Center, Lesington. KY 40536. USA GYNECOL ONCOL 1990 38/3 (473-477) Karyotypic analysis of tumor specimens from 29 patients with untreated epithelial ovarian carcinoma was performed at the University of Kentucky Medical Center. Twenty-three of the twenty-nine tumors had adequate cells for analysis. Seventeen of these tumors exhibited chromosome abnormalities. Chromosome alterations were complex. with an average of seven different abnormal chromosomal patterns per tumor (range 2- 14). Chromosomes I and I I were the most commonly involved. being abnormal in 89 and 83% of tumors, respectively. Chromosomes 3 and 7 were also frequently abnormal. In contrast to invasive tumors, alterations in chromosomes I and I I were not seen in the two tumors of borderline malignant potential. Evidence for DNA amplification of IGF2. Ha-ras-I. and c-ets was not observed. Amplification of the c-erbB-2 oncogene was present in two tumors. These findings indicate that multiple karyotypic abnormalities occur in untreated epithelial ovarian --alignancies. with chromosomes 1 and I I being the most fre-

Comparison of cisplatin and carboplatin

cytotoxicity

ovarian cancer cell lines using the MTT

assay

in human

Fanning J; Biddle WC; Goldrosen M; Crickard K: Crickard U; Piver MS; Foon KA Division of Clinical Immunology, Department of Gynecologic Oncology. Roswell Park Cancer Institute, Bujralo. NY 14263. USA GYNECOL ONCOL 1990 3912 (I 19-122) In this study, we compared the cytotoxicity of cisplatin and carboplatin against a panel of human ovarian cancer cell lines using the MTT assay. a rapid calorimetric test that can be used to evaluate the number of residual viable tumor cells following chemotherapy. The established human ovarian cancer cell line OVCAR-3 and the recently isolated and characterized A721. A90. A286. A I, and A I2 IA cell lines were evaluated for chemosensitivity. Each cell line was treated separately with cisplatin and carboplatin at concentrations ranging from 500 to 0. I6 &ml. Various chemotherapeutic exposure periods (I. 4. 24. and 48 h) were tested to determine maximal efl%acy. All cell lines were more susceptible to cisplatin than carboplatin at all drug concentrations and all exposure periods tested (P = 0.005). The overall median 50% inhibitory concentration (ID,,) for cisplatin was 107 &ml compared with 490 pg/ml for carboplatin (P = 0.005).

Int J Gwecol

Obster 36