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(graded O-3) differed significantly among controls, squamous cell CIS, and microinvasive carcinoma (mean 0.40, 0.83, and 1.64, respectively; P < 0.005). CONCLUSIONS: Microinvasive squamous cell carcinoma of the uterine cervix is angiogenic, but depth of invasion is not associated with increased angiogenicity. Squamous cell CIS is not angiogenic. Prophylactic granulocyte colony-stimulating factor allows escalation of chemotherapeutic dose intensity in advanced epithelial ovarian cancer Fanning J.; Hilgers R.D. us4 GYNECOL ONCOL 1996 63/3 (323-327) BACKGROUND: In an effort to discover an effective regimen for use in Phase III evaluation of the efficacy of dose intensification in advanced ovarian cancer, we performed a Phase II trial of dose intensified cisplatin, etoposide, and ifosfamide with granulocyte colony-stimulating factor (G-CSF). METHODS: Thirty patients with primary, FIG0 Stage 3 or 4, epithelial ovarian cancer underwent intensified cytoreduction followed by cisplatin 105 mg/m’, etoposide 300 mg/m’ and ifosfamide/mesna 3 g/m’, q 28 days x 6 cycles with G-CSF 5 pg/kg q day for 7 days. The dose of etoposide and ifosfamide was escalated 20% in cohorts of three patients. RESULTS: Intensified cytoreductive surgery was successful in resecting all gross tumor in 24 patients (80%). At the original dose of cisplatin, etoposide, and ifosfamide without G-CSF, 55% of cycles resulted in neutropenia and 38% in thrombocytopenia (dose intensity = 0.8). With the addition of G-CSF, neutropenia developed in 5% of cycles and thrombocytopenia in 38%. At a 20% escalation of etoposide and ifosfamide, neutropenia developed in 17% of cycles and thrombocytopenia in 50% (dose intensity = 1.2). At a 40% escalation of etoposide and ifosfamide, neutropenia developed in 33% of cycles and thrombocytopenia in 83%, which was dose limiting. The remaining 18 patients were treated at a 20% escalation and neutropenia developed in 14% of cycles and thrombocytopenia in 36%. CA125 response was 73%. At a 4.1-year median follow-up, median progression-free survival was 2.6 years and median survival was 3.0 years. CONCLUSION: In 30 women with primary advanced ovarian cancer, G-CSF allowed a 50% dose escalation of etoposide and ifosfamide from 0.8 to 1.2 dose intensity. The maximum tolerated dose of this regimen is cisplatin 105 mg/m2, etoposide 360 mg/m2, and ifosfamide 3.6 g/m2 with G-CSF. Oral contraceptives and primary liver cancer: Temporal trends in three countries Waetjen L.E.; Grimes D.A. USA OBSTET GYNECOL 1996 88/6 (945-949) OBJECTIVE: To determine if vital statistics support a temporal association between the introduction of oral contraceptives (OC) and the incidence of, and mortality from, primary liver cancer in three countries from different regions of the world. METHODS: We used Cancer Incidence in Five Continents, volumes I-VI, for incidence data on primary liver
of Gynecology
& Obstetrics
56 (1997)
301-310
cancer in the United States and Japan. The Center for Epidemiology in Stockholm provided the incidence data for Sweden. We obtained mortality data for the US from Vital Statistics of the United States, for Japan from The World Health Statistics Annual, and for Sweden from Swedish government sources. We compiled data on the prevalence of OC use in all three countries from multiple sources, including the National Survey of Family Growth, The Population Council, and original articles. RESULTS: Despite several hundred million woman-years of exposure to OCs, primary liver cancer incidence and mortality rates among women have not changed substantially in the United States. In Sweden, another country with extensive OC use, the primary liver cancer incidence trends in women paralleled those of men. The incidence of, and mortality rate from, primary liver cancer is gradually rising in Japan, where OC use has been negligible. CONCLUSION: Population-based data from three industrialized countries with very different patterns of oral contraceptive use provide no support for a measurable effect of OCs on primaly liver cancer. Although case-control studies from developed countries have suggested an increase in risk, if such an effect does exist, the public health impact appears to be negligible.
Estrogen replacement in surgical stage I and II endometrial cancer survivors Chapman J.A.; DiSaia P.J.; Osann K.; Roth P.D.; Gillotte D.L.; Berman M.L. USA AM J OBSTET GYNECOL 1996 175/5 (1195-1200) OBJECTIVE: Our purpose was to evaluate our experience with estrogen replacement in women with a history of earlystage endometrial cancer and to determine whether it increased the risk for recurrence or death. STUDY DESIGN: A retrospective review was performed of 123 women with surgical stage I and II endometrial adenocarcinoma treated between 1984 and 1994; 62 had received estrogen replacement therapy after cancer therapy. Sixty-one women received no estrogen. Variables analyzed included age, parity, surgical stage, grade, depth of myometrial invasion, presence of intercurrent illnesses, duration of follow-up, and duration of estrogen replacement, if applicable. Outcome variables assessed included recurrence rate, time to recurrence, and disease-free interval. RESULTS: The estrogen replacement therapy group had earlier stage disease (P = 0.04) and less severe depth of invasion (P = 0.003); however, the total number of deaths in each group was not significantly different. The disease-free survival in the estrogen replacement therapy group did not differ significantly compared with those not receiving estrogen replacement therapy. The data are suggestive of improved disease-free survival in the estrogen replacement therapy group, which may be related to differences in age, stage, grade, and depth of invasion. The overall recurrence rate was 6.5%, with an overall death rate of 1.6%. CONCLUSIONS: There is no evidence to suggest that estrogen decreased the disease-free interval or increased the risk for recurrence in early-stage disease.